text:
What physiological processes give rise to a linear cell survival curve?
If we plot the number of surviving cells in a structure over time (assuming no replacement), the shape of that curve should imply something about the underlying process responsible for cell death. For example, if surrounding conditions mean that each cell has a constant probability of dying within a given interval, then an exponential decay curve should be seen. If the cell has a characteristic lifetime (with say a gaussian distribution about that mean lifetime), then (I guess) we might expect something like a logistic S-shaped curve.
In Parkinson's disease, the onset of motor symptoms is related to the number of dopaminergic neurons in the substantia nigra pars compacta, a small structure of just several hundred thousand neurons. The decline in cell numbers due to the disease process is indeed usually modelled as something like an exponential decay.
But there is also a normal age-related decline in substantia nigra neuron numbers. This decline is usually modelled as a linear decrease from birth through to old age, at something like 0.5% to 1% per year (Rudow et. al., 2008. Morphometry of the human substantia nigra in ageing and Parkinson’s disease. Acta Neuropathologica, 115(4), 461-470 http://dacemirror.sci-hub.tw/journal-article/fc4e7854ee0cef0146d60756536b2a88/rudow2008.pdf )
Note that this percentage decline per year is not a percentage of the surviving number (which would yield an exponential curve), but of the original total. In effect, it is perhaps best to think of it as a decline by a constant absolute number of neurons per year, yielding a straight line survival curve.
Exponential decline is memoryless (conditions simply conspire such that the probability of any cell's death is constant in a given interval, uninfluenced by the history of that cell or any other). The death of a cell with a characteristic lifespan, meanwhile, does have memory, as the probability of a given cell dying increases as that cell ages and deteriorates. But the death of a constant number of cells in a given interval somehow implies a sort of memory across cells, such that the number dying in a given interval is related to the initial number, and not to the current surviving population level.
My question is what general physiological processes are consistent with such a linear decline? i.e. is a linear decline a common pattern for neurons or any other sort of cell death, and in general, what sort of process governs it?

Note that linear functions are good approximations to many underlying nonlinear processes. Simply because a process is described with a linear function does not mean the process itself is linear.

Yes that’s certainly true and is perhaps what I’m getting at. i.e. could a linear model here actually be consistent with some underlying physiological process, or is it simply an approximate statistical fit to noisy data from some other more physiologically viable underlying non-linear process?

Progressive cell death along a spatial dimension would be consistent with this. For example, imagine a cylinder of tissue in which cells at one face die, inducing adjacent cells to die. This would yield linear decay in viability to 0.

Yes, a spatial process would be viable: nice approach (not for this particular situation I suspect, but it would work as a general concept).

I suspect that the comment by @BryanKrause is more likely to be correct but I've awarded the bounty to this answer, as it does provide a general and feasible physiological mechanism as requested, although it is likely not viable for the particular case I have in mind.


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What experiment for first time showed DNA is anti-parallel?
Scientists how to prove DNA is anti-parallel?

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Also, we require questions to show the previous efforts looking for an answer. What did you already do in order to find experiments for anti-parallel DNA?

@LinuxBlanket i still think thats only homowork. :)

@L.Diago I know, but let's know them the site policy :)

The definitive proof came with the crystal structure of B-DNA (see Watson & Crick, 1953). Anti-parallel strands is the configuration that best explained the diffraction data while not violating chemistry (bond lengths and angles, no steric clashes, etc.).
The relevant sentence from the article is:

the sequences of the atoms in the two chains run in opposite directions

I underlined this sentence in the following screenshot of the article:

Why are you answering homework questions that clearly do not satisfy SE Biology criteria as two comments make clear. Doing so encourages cheats and people too idle to do any research of their own.

Because I am not convinced it's a homework question. Assuming it is a homework question, it's a poorly formulated one anyway because the article containing the answer is behind a paywall, even on campus at a US university (I just checked where I work), which means no student would realistically find the answer on their own easily.

Whether or not you think the question was homework, @LinuxBLanket had explained the deficiency of the question. It is reasonable to expect the OP to respond this (and the comment about home work), and to wait until he has done so before answering. As for the unavailability of the original Watson and Crick paper, this is described in every book on biology, and is available on line in a far more comprehensible form to the student. I would wait until there is a request for access to original sources before posting, and then do so in a form that does not discriminate against the partially sighted.

You're right about accessibility: I should have retyped the sentence instead of posting a screenshot (the PDF is a scan from which I couldn't copy text, and I was lazy, hence the screenshot). Will edit the answer accordingly. Now, I disagree with the rest of your comment: answers on SE are public and therefore potentially useful to anybody (not only the OP), who would never find the information because it's behind a paywall.

Agreed about "at this point", but now their interpretation has been confirmed experimentally more than 5000 times: https://www.rcsb.org/pdb/results/results.do?tabtoshow=Current&qrid=B94C6458

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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How long could a shark breathe pepsi?
Sharks breathe seawater. Seawater isn't 100% pure water, but mostly water. Pepsi (other colas are available) isn't 100% pure water, but mostly water.
How long would a shark be able to breathe if submerged in Pepsi (other colas are available) and what, precisely, would kill them?

I don't think the dissolved $\ce{CO2}$ would do them any favours. And I doubt the chemicals from the cola would be very good for the shark (caffeine is toxic to many animals).

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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identification of differentially expressed genes in RNA-seq analysis
I am using four different packages (viz. EBSeq, DESeq2, edgeR, LPEseq) for identification of differential genes. Now I am confused whose fold change value should I take for further downstream processing.
Please give your suggestions.
Thanks in advance.

Why do you use four packages for one task?

Each package is using a different mathematic or statistical model and trying to fit that model to the data. Each model has different sensitivities and specificities, in different types of sample or experimental setup, so it can be useful to use more than one package. They are all asking a similar question in subtly different ways, so some people believe that taking a consensus can provide a more robust conclusion to the analysis.

Unless you have a good reason, stick with the ones that the community at large uses most frequently: EdgeR or DESeq2.

I would typically have an independently calculated fold-change that I use for QC and visualization.  I don't currently have a paper to reference to recommend doing some benchmarks for every project, where I would recommend testing DESeq2 / edgeR / limma-voom.  However, there are some papers that cite use of that strategy here in this acknowledgement.
In other words, one way that you could tell if a method may not be optimal for your dataset if you have a known perturbation, you can visually confirm the expected change with the directly calculated log2(FPKM + 0.1) value, but that gene isn't identified as differentially expressed with one of the methods.  It is kind of messy, but I do briefly mention this sort of troubleshooting strategy here.
In terms of comparing rlog values from DESeq2 and the direct FPKM / fold-change values, I do have this blog post: http://cdwscience.blogspot.com/2019/02/variance-stabilization-and-pseudocounts.html


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Ciliated Epithelium & Goblet Cells Lining The Trachea
My book states this - The cells produce mucus that traps particles of dirt and bacteria in the air breathed in. The cilia on these cells move this debris up the trachea and into the stomach. Isn't the stomach below the trachea? Wouldn't it move the dirt and debris up the throat so it can be removed via the mouth? My book does also state that the debris is pushed up the throat as well so does it do both?

There are two pipes from your throat, downwards. A foodpipe and a windpipe. One, called the trachea, feeds air into the lungs, i.e. connects your head with your lungs. Another pipe, called the esophagus, leads to the stomach.
Both pipes meet and share the same passageway in your throat and oral/nasal cavities. Let's call this the common pipe.
The lining of the trachea, made up of ciliated cells and mucus-producing cells, does indeed move debris UP and OUT of the trachea, away from the lungs. Once this debris is at the common pipe, it can go to the stomach or into the mouth or into your nose for clearance.

Thank you for your answer and response. I understand what you mean :)


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Where can I find datasets containing large phylogenetic networks?
There are many datasets out there for phylogenetic trees, one can example can be found here.
However, I couldn't find something for phylogenetic networks. According to Wikipedia:

A phylogenetic network or reticulation is any graph used to visualize
  evolutionary relationships (either abstractly or explicitly)2
  between nucleotide sequences, genes, chromosomes, genomes, or
  species.2 They are employed when reticulation events such as
  hybridization, horizontal gene transfer, recombination, or gene
  duplication and loss are believed to be involved.

Of course a phylogenetic tree is a phylogenetic network, but phylogenetic networks can be thought of as rooted directed acyclic graphs, meaning that more complicated evolutionary structures can be captured.

For what purpose?

I have an implementation of an algorithm that I would like to run on a phylogenetic network.

I handled your flag. This question was, however, not asked as a guest, as you have a user name and rep. So you cannot login under Jonathan?


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What on Earth is this?
Found in a field near Braga, Portugal in October 2018.

It does not look like a fungus.  It looks like an insect nest - possibly a bumble bee. Did you dig this out of the ground?

Found on the ground. May have been dug up by foraging fox?  Possibly a bee or wasp nuc. Interesting!  Thanks!

I'm voting to close this question as off-topic because without a scale bar, it's impossible to know how large the object in the photo is.

I agree that the OP should provide a scale, but I wouldn't say it's impossible to know -- look at the debris in the picture. Regardless, @Corvus, please add an approximate size of your specimen (perhaps size of each sphere) to avoid having your question closed and to aid someone in providing a good answer. Thanks.

OK, It does not look like a fungus. just going by the single close up photo - I'm pretty sure it is an abandoned bumblebee nest (or that of some similar social insect).  These bees often nest out of sight under logs or under the ground. Below is a link that may help you with a positive identification. I hope this provides at least a hint. Maybe you can fill in the blanks from your knowledge of your local fauna in Portugal.
http://www.bumblebee.org/lifeCcolDev.htm


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Small flying insects gathering around the pot flowers
Recently I spotted relatively small flying insects gathering around the pots inside my flat.
There are smaller than fruit flies, probably around 1mm - 2mm long, blackish, and fly somewhat erratically. As far as I can tell the insects are active mostly during the day.
I didn't spot any obvious damage to the plants so far, but I might have miss something.
The location is relatively warm (southern window, above heating sink), and excluding the soil in the pots, rather dry.

Geographical location: Central Europe
Time of observation: Late summer, early autumn.

I'd be grateful if someone could help me identify this species.

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Your description is rather accurate, nice first question!

Looks like some sort of fungus gnat though I won't make any attempt to ID a particular species. Note that fungus gnat describes a very wide range of species over 6 families, though yours looks most like the flies from the family Sciaridae (Wikipedia notes there are ~600 species in Europe).
Fungus gnats feed on organisms decomposing soil, which are most present when the soil is moist, especially if overwatered. The damage you will experience, if any, would be to the roots, rather than visible on the leaves, though you will see wilting if the damage becomes significant.
You say things are dry, however, the important place is the soil. You will deter, though probably not completely eliminate, the fungus gnats if you let the soil dry between waterings (in my personal experience with fungus gnats this approach was sufficient). Some specific parasitic nematodes are also used for pest control of fungus gnats, if they are available in your area.

Agreeing with @Bryan Krause even as far as family; if we're both right in that respect, species-level identification requires a compound microscope and at least some dissection (look for "Sciaridae 'sp. nov.'" in your favorite search engine; the open access results will give you some idea what specialists seek in preparing their descriptions).


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Solubility of lithium carbonate in blood
When a person with Bipolar Disorder ingests a pill of $\ce{Li_2CO_3}$ and it enters the stomach the pill cap is dissolved in the hydrochloric acid; however, when it gets absorbed in the blood how does it dissociate?  Does it dissociation is there an enzyme, is that enzyme Carbamoyl phosphate, or is it the blood that separate them. Thank you.  I have also been reading biochemistry books, and would be willing to cite the information that lead me to guess.
Reference:
Data for Biochemical Research
Third Edition
Rex M.C. Dawson, Dophne C Elliot
The book notes that the enzyme does 100 percent hydrolysis of $\ce{Li_2}$ salt in 2 min. at 100 degrees Celsius, 50 percent in 2 hours at 30 degrees Celsius.
This confused me because lithium carbonate is a salt. So I was confused.  Thanks again.

Do you have any resorses or how did you make it up?

@L.Diago Yes let me add them

Are you asking about some quote in a book? Because the uncertainty in the question about salts is a bit confusing (i.e., if you know what a salt is, and how it works in water, it's unclear what your question is). It might be better to reproduce the actual quote here.


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Light/Heavy Isotopes in Living Organisms
I was wondering, why are lighter isotopes (e.g. carbon-12 as opposed to carbon-13) preferentially used by life on Earth? Is their increased stability the only factor?
Thanks in advance!

99% of carbon is carbon-12, so it makes sense that it would incorporated by life in higher abundance. Perhaps I don't understand your question.

I appreciate your response, but I think my question is poorly phrased. I am trying to understand why a negative carbon isotopic signature is suggestive of life. For example, if the carbon isotopic ratio of the methane detected on mars was showed to be more abundant in carbon-12 than carbon-13 (negative value), why is this suggestive of life? Do living systems prefer lighter isotopes? We only have Earth as a suitable analog, but is the a biologically reason why this is (and not merely a question of abundance)? Thanks a lot :)

Hi Julian, interesting question. I look forward to reading a response.

I had never heard of this before, but after a bit of searching I think I found what you are referring to. I believe this Wikipedia article should answer your question. This is definitely out of my field, but I may try and formulate answer if someone more knowledgeable doesn’t come along. Interesting question!

Thanks for you help! I look forward to reading an answer.


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Why did scientists think humans had 100,000 genes (before the Human Genome Project)?
One of the major results of the Human Genome Project (HGP) was that humans have far fewer separate genes than previously thought. From a 2004 article about the HGP:

Francis S. Collins, director of the National Human Genome Research Institute (NHGRI), said, "Only a decade ago, most scientists thought humans had about 100,000 genes. When we analyzed the working draft of the human genome sequence three years ago, we estimated there were about 30,000 to 35,000 genes, which surprised many. This new analysis reduces that number even further [to 20,000-25,000] and provides us with the clearest picture yet of our genome."

What was the old estimate of 100,000 based on? I assume that in 1994 no one had sequenced the entire proteome...
As Remi.b points out, the 100,000 gene estimate may be based on the one gene–one enzyme hypothesis. If that's true, did people before the human genome project think that there were 100,000 distinct enzyme activities? If so, what experiments/data were used to establish that number?

Importance and amount of non-coding DNA was underestimated.

There's actually no need to speculate on the answer to this question since scientists have published their estimates and methodology, as is their way. The following paper is a good review:
Fields C, Adams MD, White O, Venter JC. 1994. How many genes in the human genome? Nature Genetics 7:345-346.
Below are some truncated excerpts from the paper but, if possible, I recommend reading the whole thing and the references therein.

In genomic sequencing pilot projects... we found... an average of about one gene in 23.4 kb... Extrapolated for the whole genome, we would predict about 129,000 genes; however, the regions that we sequenced were chosen for high-GC content and hence gene richness. At most, half of the genome, in the GC rich... bands, is likely to have high gene density; if the rest has half of the density we observed, the human genome might contain 97,000 genes. But the gene-poor fraction of the genome probably has much less than half the density of the gene-rich fraction... If we assume that the genome comprises a gene-rich half with [23.4 kb per gene] and a gene-poor half with a tenth that density, we obtain an estimate of about 71,000 genes...

Making estimations based on average gene size has been discussed in another answer. The varying estimates result from the different assumptions made: there were a lot of unknowns at this time. You can read about the correlation between GC-content and gene density in this answer.

Estimates giving much lower gene content are, however, easy to come by... Wagner and colleagues note that only about 12% of a typical mammalian genome... is transcribed. Using an average gene size of 18 kb obtained from a list of characterized genes... they estimate a total of 20,000 genes. By assuming that 2,500 housekeeping genes (from estimates of Escherichia coli) constitute 18% of the total number of genes the same authors obtained an even smaller figure of some 14,000 human genes.

I don't have access to this reference so it's hard too delve to deeply into their methodology, but the number of genes expressed really depends on the cell-type. Thymic medullary cells, for example, express 85% of the coding genome. RNAseq has also suggested that over 90% of the genome is transcribed, though this controversial. All that said, their first estimate was rather spot-on.

Measurement of RNA reassociation kinetics suggest that approximately 10,000 distinct genes are expressed in a typical mammalian cell, from which Lewin estimates a total gene number of 20,000 to 40,000.

This is C0t analysis with RNA instead of DNA (called R0t). You can read more about this here. This estimate, too, has proved reasonably accurate.

Using restriction analysis with the methylation-sensitive enzyme HpaII, Antequerra and Bird estimated that the human genome contains 45,000 CpG islands. They also report that about 56% of sequenced genes contain CpG islands, and hence estimate a total gene number of about 80,000... This number, however, may be an overestimate, as even "complete" gene sequences rarely include extensive 5' or 3' flanking sequence and hence may muss associated CpG islands.

We now know that there about 30,000 CpG islands in the genome, of which about 9,000 are intragenic and that  72% of genes have CpG islands. This would revise their estimate to 30,000 genes.

We have used a collection of 3,483 nonredundant coding sequences as an effective genome against which to compare a collection of human ESTs... If [this] set of complete cDNA... is representative of human genes in general, the fraction of known cDNAs matched by randomly-selected ESTs should equal the fraction of novel sequences matched by randomly-selected ESTs. Our human EST sequencing project has so far identified ESTs matching 1,877 of the 3,483 unique coding regions (54%). We can, therefore, estimate that the novel ESTs that we have sequenced represent about 54% of previously-unknown human genes... To estimate how many genes these novel ESTs identify, we... [clustered] the ESTs. This step reduced 65,297 ESTs to 40,077 clusters... indicating that the novel EST set was 40% redundant. We can then calculate an expected number of human genes as: 40,077 / 0.54 + 3,483 = 77,700 genes. This calculation is an over-estimate, since the clustering procedure cannot identify ESTs from the same transcript unless they overlap. If the true average redundancy is 50%, we predict about 64,000 genes; if the true average redundancy is 60%, we predict 52,000 genes.

Although they accounted for alternative splicing, assumptions were made about how representative their collection of coding sequences was. It seems that one of the problems at this time was that many of the overestimates made, using different methods, more or less agree with each other. Unfortunately, many of the assumptions did not stand up.

Human genome is 3.2Gbp (giga=billions of basepairs). If you assume there are 100k genes, this yields around 32kbp (kilo=thousands base pairs) per gene.
Before human genome project, let's say before 1990, people were isolating a lot of genes from human-derived tissues. You can use google scholar to find relevant papers. From quick search, you can see that range is pretty large:

"186,000 base-pair (bp) human factor VIII gene"
"human TF gene spans 12.4 kbp"

So you can see how one might guess "average" size of the gene to be somewhere around 30kbp, if you haven't yet found too many genes. Whereas after genome sequencing, we know that genes are 100-10000 bp long. I think the issue was that there was no enough statistics yet to judge appropriately "average gene size". And as it turns out, the distribution is very funky. You need to isolate a lot of genes to reconstruct that distribution.
By the 1990 phenomenon of the alternative splicing was already known. What perhaps wasn't quite obvious, is how many genes there are, what their real sizes, and how many genes are overlapping

I think it was rather thinking that more of DNA is coding than in reality, but that's another possibility.

From Pertea et Salzberg, Genome Biol, 2010: An estimate of 100,000 genes appeared in the 1990 joint National Institutes of Health (NIH)/Department of Energy (DOE) report on the Human Genome Project; this was apparently based on a very rough (and incorrect) calculation that typical human genes are 30,000 bases long, and that genes cover the entire 3-gigabase genome.

@tsttst thanks! i think it also interesting that today we can easily peek into the past literature (thanks google scholar :)

I don't know much about the evolution of thoughts on the subject but I would suppose that the estimate of 100,000 genes is probably caused by the one gene - one enzyme/protein ideas

The one gene–one enzyme hypothesis is the idea that genes act through the production of enzymes, with each gene responsible for producing a single enzyme that in turn affects a single step in a metabolic pathway.

The idea that genes are affecting cell functions via the protein that they code for is not so outdated. However, the idea that a gene codes for a single unique protein is a little outdated.
In reality a single gene can code for several different proteins via a mechanism called alternative splicing.

Alternative splicing, or differential splicing, is a regulated process during gene expression that results in a single gene coding for multiple proteins. In this process, particular exons of a gene may be included within or excluded from the final, processed messenger RNA (mRNA) produced from that gene. Consequently, the proteins translated from alternatively spliced mRNAs will contain differences in their amino acid sequence and, often, in their biological functions [..]. Notably, alternative splicing allows the human genome to direct the synthesis of many more proteins than would be expected from its 20,000 protein-coding genes.

The original estimate of the number of genes was hence probably alined with the observed number of proteins by assuming that there is a one-to-one function from gene to protein (as by the one gene - one protein hypothesis).

Makes sense. What I want to know though is where that particular number came from. In quantitative terms, what experiments or line of reasoning lead to 100,000? It's (basically) within an order of magnitude of the correct answer, so I'm assuming (maybe incorrectly) that the estimate was originally based on some solid numbers from somewhere. Like, was there a reason to think there were 100,000 distinct enzyme activities?

The original estimate was probably based upon the number of proteins. I'll clarify that in my answer

Thanks for the update. There's still a missing piece, though. How did they establish 100,000 as the likely count of distinct proteins? Was there an experiment that existed in the pre-omics era that was able to resolve the presence of thousands (or 10's of thousands) of proteins in a single sample? Or was it merely an informed guess based on decades of various observations?

I don't know... :D I would assume whoever found identified a protein sequence would upload it in a shared data base and comparison among protein sequences (some ancestral equivalent to BLAST) allowed one to estimate the number of proteins found in humans.


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Cichlid fish in Africa
Are the cichlid fish in Africa an example of divergent or convergent evolution? On the one hand they have evolved similar features to each other indicating convergent evolution, but on the other, they formed as a result of an adaptive radiation which indicates divergent evolution.

The level of lake malawi has dropped by 200 meters at least 20 times in the previous 1.3 million years, forcing them into small lakes, and there are lots of theories about "cichlid evolution" on google, including a 54 minute talk video. Fish have a lot of convergent evolution too, there are kinds of holotype fish forms which appear again and again in different continents and different seas, the same as an australian and european magpie. Cichlids are similar to many species like snappers, even dolphins are said to be convergent with sharks.

Writing "convergent evolution" in google images is one of the most fascinating pages out there: https://www.google.fr/search?biw=1572&bih=857&tbm=isch&sa=1&ei=-9bBW5fILoi6ac7ltrAC&q=%22convergent+evolution%22&oq=%22convergent+evolution%22&gs_l=img.3..35i39k1l2j0l8.72634.74183.0.74652.2.2.0.0.0.0.90.168.2.2.0....0...1c.1.64.img..0.2.166....0.iTe5In6n1qg#imgrc=7pBcz3R6hTpCHM: ........ and ..... https://www.google.fr/search?q=convergent+evolution+in+fishes&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwjk0OLMp4PeAhUIz4UKHXnRDOgQ_AUIDigB&biw=1572&bih=857#imgrc=u293tbb5Xe8mzM:

They have diversified to fit into many different niches.

You might want to read about adaptive radiation

Both.

Recent theoretical models, however, predict that convergence should be common within species-rich communities, such as species assemblages resulting from adaptive radiations. Here, we present the most extensive quantitative analysis to date of an adaptive radiation of cichlid fishes, discovering multiple instances of convergence in body and trophic morphology. ...

Independent adaptive radiations often produce convergent phenotypes
In Lake Tanganyika, convergent phenotypes evolved within a single adaptive radiation
These convergent morphologies are associated with adaptations to the same niche
Distantly related yet morphologically similar species coexist in the same habitat

--Convergent Evolution within an Adaptive Radiation of Cichlid Fishes


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natural characteristics of insects used as human disease model
In this paper [1], the author found that the autism-related genes are conserved between honey bee and human. Thus, this paper providing a means to further explore sociobiology theory. In my opinion, the honey bee have the potential to be developed into an model for human autism disease.
My question is: what other examples in insect like this in honey bee that the model species itself has some characteristics, which could be used as model system for some human disease studies?
Thank you!
[1] Shpigler HY, Saul MC, Corona F, Block L, Cash Ahmed A, Zhao SD, Robinson GE: Deep evolutionary conservation of autism-related genes. Proc Natl Acad Sci U S A 2017.


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Pox virus infection process
How does Pox virus duplicate it's genome? Does it bring DNA polymerase or RNA polymerase into the host cell?

Poxviruses, such as variola (the causative agent of smallpox) and vaccinia (the active constituent of the vaccine that eradicated smallpox), are very large, complex DNA viruses that replicate in the cytoplasm, rather than the nucleus. Because of this, they must carry enzymes with them to accomplish tasks that occur in the nucleus of the eukaryotic cells they infect. This includes all the proteins necessary for mRNA synthesis (e.g., a DNA dependent RNA polymerase). The enzymes for DNA replication are encoded in the poxvirus genome and are transcribed and translated as part of the "early" stage, directly after adsorption and penetration.
So, yes, poxviruses bring their own preformed RNA polymerase with them. They don't bring their own DNA polymerase with them, but they do produce it shortly after infecting a cell.
You can read more about this in Murray Medical Microbiology Chapter 54.


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Hypanthial disc
Can anyone illustrate what the hypanthial disc is?  It is descriped throughout the key to Rosa in the Flora of North America.  I think that I understand that the hypanthium is the hip which is formed from fused flower parts.  But, which part is the disc.


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Fluorescent protein tags and colocalisation
We want study if 2 proteins A and B are co-located, for that we use 2 FTP(Fluorescent tag proteins) for each protein?and after the expirement these 2 FTP are co-located. Does that mean necessarily protein A and B are co-located?

Is this a homework or test question?

It's a test question, but the correction says no, but i doesn't make sense for me!

Whel, is possible that the adittion of a FTP made them co-localize. Is that the complete question?

this question is unclear. What exactly you have problem with?

"Are protein A and B co-located?" The answer is that it depends. Since your test question included the word "necessarily", this means that the answer to the test question is no. All you have to do is think of at least one plausible counter-example.
Here's a couple:

The flourescently tagged constructs were screwed up somehow, so A, B, and each of their respective tags were actually expressed as 4 separate proteins.
(As per BPinto's comment) the tagged constructs may co-localize even if A and B would not normally do so. This can happen if, for example, the tags bind to each other, or if the tags somehow cause both constructs to get transported to a particular organelle.


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Is this long black insect with semi-long antennae and a large segmented abdomen caught in the kitchen a larva or an imago? And what is it?
This is in Northrhine Westfalia in Germany/Europe: we have those large longish and comparatively flat bugs (taking my hand below the plastic as reference, it should be about 4cm or 1 5/8in in length) or larvae in our kitchen occasionally.  For a larva, it seems to be lacking any soft parts.  It can raise its behind "threateningly" in the style of a scorpion but I doubt it's anything but mimicry.  Its large head reminds me of ant soldiers, though it is obviously out of scale.  I think it's mostly in the evening or night that we find one (and it's often because a cat stares at it in an obvious manner) and while it's usually the kitchen, that may just be because we are most frequently there.

That is an adult rove beetle (Coleptera, Staphilinidae). https://en.wikipedia.org/wiki/Rove_beetle
Rove beetles have very short elytra (forewings), so they don't look like other beetles. This one looks a lot like Ocypus olens, which is common in Europe https://en.wikipedia.org/wiki/Devil%27s_coach_horse_beetle

The Wikimedia image https://en.wikipedia.org/wiki/File:Staphylinus.olens.jpg looks so very much like my photograph (the exemplar there looks a bit less shabby) that it's almost like I copied it.  I am pretty sure that my exemplar exceeded the Wikipedia entry's given size range (up to 32mm) though.  At least the name "Devil's coach horse beetle" (though nothing in the description found there) suggests that I should have included the information that we live on riding school premises with one paddock right next to the kitchen windows.  Thanks!


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Why does this genetic pedigree show an autosomal dominant allele at one generation but not another?
Questions 186-188 of the GRE Biology Practice Test are prefaced with this genetic pedigree:

Questions 186-188 refer to the following pedigree for the inheritance of a very rare human disease over three generations.

It looks like the allele that caused the "affected" phenotype was dominant because Generation II showed a 3/4 probability of having the phenotype, and it looks like it was autosomal because it affected males and females roughly equally. This is confirmed by the answer to Question 186 ("Which of the following is the most likely mode of inheritance for the disease trait?") which is "(D) Autosomal dominant".
However, why don't the offspring 1, 2, 3, 4, and 5 in Generation III show a similar rate of expression?

Don't pay attention to probability in pedigree analysis. The number of offspring is too small. Just look for things that can't happen and use that to rule out modes of inheritance

@DeNovo I guess that makes sense, but questions 187 and 188 (see link in the question) talk about probability, so how do i go about answering them?

I don't see those questions quoted here, but that's usually a two part question. Part one may require you to determine an inheritance mode, or most likely inheritance mode from a pedigree. Part two may then require you to demonstrate some additional knowledge about that inheritance mode (e.g. what is the probability that the offspring from this individual and that individual will express some trait).

Why don't the offspring 1, 2, 3, 4, and 5 in Generation III show a similar rate of expression?

Because there are only 5 individuals in that list. The entire generation III involves 8 individuals (all the offspring of one affected and one unaffected parent). The entire pedigree involves 12 offspring of an affected and unaffected parent.
When you look at III 1-5, you see 1/5 affected (0.20).
When you look at III 1-8, you see 3/8 affected (0.375).
When you look at all offspring of an affected and unaffected parent, you see 6/12 affected (0.50).
As you increase the number of offspring you consider, the proportion affected gets closer to the expected value of 0.5. Given a very rare autosomal dominant condition (i.e., I-2 is most likely heterozygous), this is exactly what would be expected. You may have to look at fruit flies, or some other prolific organism, to see it quite so clearly. Mendel looked at tens of thousands of pea plants, if I recall.
Generally, you shouldn't use the proportion of offspring that show a trait to rule out any particular mode of inheritance, especially if you're looking at a small number of offspring. You can state the probability of a particular child expressing a mendelian trait. That doesn't mean a small sample won't deviate from that probability.
You can read more about this in chapter 7 of Thompson & Thompson Genetics in Medicine.


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White residue from ginger juice
I’ve been juicing some ginger by grating it and pressing it (by hand). A white residue collects at the bottom of the liquid. What is this?

I believe that this white residue is starch. According to Wikipedia, Ginger is 17.7% carbohydrates by weight, or 14% excluding sugar and dietary fiber.
I let the residue settle and decanted the liquid. The residue behaved remarkably similarly to wet corn starch. From this, I have concluded that it is starch of some form.

good point. You can also test it if you have an iodene antisceptic, the soy sauce colored antisceptic. if you pour it on starch it turns dark blue.


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UK insect identification
15-20mm long.
Brown legs, head, casing/wings (no flight witnessed).
Black body with protruding back part.
Long antennae.
Very fast running speed.
Seemingly keenly aware of surroundings.
Is this some sort of small cockroach?

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Have a nice stay!

The photo is not very clear, the two spikes at the back identify it as a cockroach, a "forest cockroach", probably a "german cockroach", perhaps she is pregnant? I think they prefer slightly warmer, dryer climates than the UK, whereas the UK is mostly home to slower black beetles, elsewhere in europe, you can turn a stone over and there will be 5 forest cockroaches, which are very fast, and actually quite pretty and silvery in their own way.

https://en.wikipedia.org/wiki/German_cockroach

Thank you com.prehensible. In the picture of the German Cockroach with ootheca, the ootheca looks the same shape but different colour as the one I observed. This cockroach was certainly very fast. I saw her in the kitchen in the evening so that also fits what wikipedia has to say.


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Why does the exercise level impact the nail growth rate?
I read on https://en.wikipedia.org/w/index.php?title=Nail_(anatomy)&oldid=863800434#Growth:

Actual growth rate is dependent upon age, sex, season, exercise level, diet, and hereditary factors.

Why does the exercise level impact the nail growth rate?

Had you looked up the reference that wikipedia cites?

@BPinto i tried but it's behind paywall.


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What function will survive evolution?
I wrote the following phrase in my scientific text:
X is ubiquitous in life of Y. On some occasions X might be detrimental, resulting, for example, in so so phenomena. But is it plausible that a function that takes 50% of organism resources would have only negative effects? The answer is likely "no" because such a function would have likely not survived the evolution.
But I was suggested that there a bug in my logic because if an adaptation is neutral and has no effect on reproductive fitness, it can be preserved. Would you agree with this critique? If so, how should I rephrase so that it become more correct?
Many thanks

is it plausible that a function that takes 50% of organism resources would have only negative effects? It sounds highly unlikely that an organism would invest half of its ressources into doing something that will reduce its own fitness (I should say "inclusive fitness" to be safer here). A mutation that would lead to such trait would be highly deleterious and should not raise in too high frequency in the population (unless eventually if the population size is really really small). That being said a recent and sudden environmental change could eventually lead to this type of 'maladaptation'.

On some occasions X might be detrimental, resulting, for example, in so so phenomena. Many traits can have environment dependent fitness effects and environmental heterogeneity can lead to strong variation in the trait's contribution to the individual fitness. Is this what you are referring to?

"would have only neutral and negative effects" would partly cover the critique, as it appears to me the argument hinges on the "50% of organism resources" which must have been previously firmly established.  It would be helpful to add language emphasizing that such an enormous drain on an organism cannot plausibly survive long in a species since that drain, itself, is a huge negative effect on individual fitness and hence on reproductive fitness.

Can you please let know whether my comment seem to answer your question. I am unsure I really understand your question and your feedback would help.

detrimental to what? Many adaptations are detrimental to an organisms but beneficial to their genes. Just look at social insects, or even your own somatic cells.

Detrimental for behavior. For example, sleep at night wastes our time. So, it should have some benefits.

Ia m sorry for the late reply (time zones differences). Thank you very much for the answers. So, the bottom line: do you think my phrase sounds?

@student a behavior cannot be detrimental to behavior, biologically speaking that makes no sense, it has to be detrimental to the organism, cells, or genes.


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What does the hornet do on the ivy blossoms?
We've got blooming ivy growing around a tree. Since several weeks lots of hornets have been whirring in the foliage and I wonder whether they want to feed on insects that are lured by the blossoms or whether they come for anything they get from the ivy plant.

Hornets, just like wasp in general, hunt insects to feed their larvae but feed themselves with carbohydrates like nectar (or lemonade). So it is quite probable that the hornets are feeding on the nectar of your ivy. wikipedia


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Net electrical load of a peptide
I have to determine the electrical charge of the next peptide chain:
C - E - H - P
I know that this page is not there to raise doubts about this style, but I have looked for resources on the Internet and find nothing. Please explain to me how to determine the net load according to pH and the isoelectric point, so that I can take this as an example.
My teacher told me to get the necessary data from this table:

Thank you very much for the link, it gives me the solution. But, I still don't know how to do it on my own.


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Are mutations a source of genetic variation?
Here is a question from the book SAT II Success Biology E/M (where the SAT is the exam taken by the American high school students):

Which of the following statements is true about mutations?
  (A) Rates
  tend to be very high in most populations.
  (B) generally lethal
  (C)
  irreversible
  (D) Only certain gene locations are affected.
  (E) source
  of genetic variation

In my opinion, we can definitely eliminate A, B, and D.
Then, I struggle between C and E since I think mutations are definitely a source of genetic variation but are as well generally irreversible (I've found evidence on different websites, including this http://hawaiireedlab.com/wpress/?p=154 where the author writes that only some mutations are reversible).
In the end, I think I should have probably gone with E because C can be seen as having some exceptions.
Then, here is the book explanation for this question:

The correct answer is (C). These recent conclusions about
  mutations—recall that Darwin did not know of mutations—are all the
  reverse of those listed in the choices, with the exception of choice
  (C), the correct answer. Rates, in fact, tend to be below in
  populations, mutations are generally not lethal, any gene location can
  be affected, and they are felt to be the source of genetic variation.
  Darwin felt over-production of offspring was the source of potential
  variation.

The answer is C here. However, I didn't particularly understand why E wasn't considered a correct answer.
Could you please explain why C, and not E, is correct?

The answer is clearly and unequivocally (E). Mutations introduce genetic variation. Period. As for (C), mutations are certainly reversible. If you can mutate a base to another base, you can mutate that base back to its original base. This is a simple fact of chemistry. Mutation is not an irreversible event. The answer should certainly be (E). The book is wrong!

Is the author of the book supporting so called inteligent design theory ("there is no evolution - only devolution")?

I think you need to take this book back to the bookstore and demand a refund. It's got two clear errors in it already.

@SPr They're almost irreversible in practice. It's just about the probabilities and concrete mechanisms involved. The observations we have suggest that mutations are strongly preserved throughout lineages. But that only highlights how ridiculous exams like the SAT are - you can't reduce such questions to choice answers. If you do that, the best you can do on the test is learn exactly what answers are expected on the test - not exactly something that makes you more educated :)

Going through the possible answers

(A) Rates tend to be very high in most populations.

This is a very unclear statement. What does "high" mean? In humans, the average mutation rate per reproduction per nucleotide is of the order of $10^{-8}$ (Rahbari et al., 2016) (hence of the order of 10 - 100 mutations for the whole genome). Whether someone wants to call that high or low is up to this person original intuition.

(B) generally lethal

No, that's wrong (Robert et al., 2018)

(C) irreversible

It is a little unclear. By "irreversible", do they mean that the function of the gene (or of any other functional element in the genome) cannot be restored or do they mean that a specific mutation cannot be exactly undone by a future mutation. In both cases, however, it would be wrong!
Mutations that restore the function of a gene (or any other genomic functional element) are called reverse mutations (aka. suppressor mutations; I personally don't know of any difference between the concepts of reverse mutation and suppressor mutation). Most reverse mutations are likely to act via a second mutation that restores the function of the gene rather than undoing the previous mutation. It does not mean however that it is impossible a mutation that perfectly undoes a previous mutation. Consider a substitution inverting A into T. A reverse mutation could do just the opposite.

(D) Only certain gene locations are affected.

Mutation rate varies throughout the genome but all of the genome is subject to some non-zero mutation rate.

(E) source of genetic variation

Yes, mutations are the ultimate source of genetic variation in populations, while genetic drift and directional selection removes variation.
As other users have highlighted in their answers, many mutations (incl. synonymous mutations but not only and soma mutations) do not bring up any the underlying genetic variance of phenotypic traits. These details are however mainly irrelevant; what matters is that it still remain true that (some) mutations increase genetic variance.
We could also add the complication as to wonder whether by "genetic variance", they meant "genetic variance underlying phenotypic variance" (which is its standard usage) or "genetic variance where one allele is given an arbitrary value and another (problem arising for loci with more than 2 alleles segregating). More information about the terminology and the math when it comes to quantifying genetic variance in the post Why is a heritability coefficient not an index of how “genetic” something is?
What I would have answered

The correct answer is (C). These recent conclusions about mutations—recall that Darwin did not know of mutations—are all the reverse of those listed in the choices, with the exception of choice (C), the correct answer. Rates, in fact, tend to be below in populations, mutations are generally not lethal, any gene location can be affected, and they are felt to be the source of genetic variation. Darwin felt over-production of offspring was the source of potential variation.

I disagree. To me, B and D are wrong, A is unclear, C is slightly unclear but wrong in both interpretations I can think of and E is correct. I would have answered E.
About the justification given

Rates, in fact, tend to be below in populations [..]

This piece of the sentence is not even grammatically correct. Below what? It highlights that A is unclear.

they are felt to be the source of genetic variation

The term "felt" is poorly chosen here IMO, but this piece of the sentence seems to rather give credit to answer E. I think, whoever wrote this answer mistakenly wrote C instead of E

Darwin felt over-production of offspring was the source of potential variation.

Really, who cares about Darwin thoughts on the subject here?! But in any case, this sounds like a misrepresentation of Darwin's ideas. More info can be found in Charlesworth and Charlesworth (2009) and also maybe this post

FYI, I think below is a typo for "be low". Also, I completely agree with this answer. Mutations are definitely reversible, and a source of genetic variation.

Agree about the clarity of these questions and answers, they are worded very poorly. And these are from standard US exam questions? Very concerning.

@ESR. The question is from SAT Bio exam prep book, not from exam itself.

unfortunately even the best prep books (and they do vary wildly in quality) are often written by people unfamiliar with the actual field of study, they often suffer  from being bulked out by copy pasted Q&A from other sources. Which ironically enough often suffer from distortion as they are edited over and over again.  Your prep books is just wrong.

IMO, E feels like an absolute statement, as if mutations were the only source of genetic variation.  I probably would have gone with C, arguing that E rules out homologous recombination

@Punintended The idea that recombination create genetic diversity is a common misconception (see for example this speech from Sally Otto or many of her early papers). Some people may mention migration as a source of genetic diversity but ultimately, it is still mutations who created this genetic diversity and migration just mix them up together (a bit like recombination do among different haplotypes). So, yes, it is a pretty absolute statement! Of course, by mutation, I mean any type of mutations (incl. large chromosome duplication for example).

@Remi.b That's fair.  I was also thinking about viral transposition, which results in a mutation if it chooses a site in the middle of a gene

It is true that recombination (viral transposition and some other concepts) are often causing agents of mutations.

I suspect that the question printed in the SAT Prep book contains a typo (or a deletion mutation).  If the answer to choice E. were to read “NOT a source of genetic variation” it clearly becomes the opposite of recent conclusions. Since some single nucleotide variants are clearly reversible under certain conditions (cf. Crick et al paper on the Nature of the genetic code published in the journal Nature ~ 1962) then the person who composed this question is not sufficiently familiar with the scientific literature.

Mutations are one of multiple reasons for genetic variation, hence phenotypic variation. By definition, mutations are alterations of genetic code and unpredictable changes in nucleotide sequences {in nucleic acids(level)}.
So yes, mutations are responsible for variation, but not all the time, and not all mutations actually result in variation. Silent mutations are neither harmful nor beneficial. They do not improve organisms by any means. On the other hand, nonsense mutations are readily harmful and can result in death.
Other sources of variation include:

Independent assortment of chromosomes (meiotic division), as per Mendel's first law of independent assortment.
crossing over of bivalents
environmental changes, which subsequently lead to beneficial mutations.

It depends. A mutation in somatic cells is not a source of genetic variation because they are not inherited by offspring. But mutations in the sex cells are a source of variation. Your answer key does not appear to be sure of the correct answer because it says the reverse of every answer but C is true of mutations but then agrees with answer E. Also unless part of the question is missing, what Darwin thought is not really relevant. Also, more offspring means more chances of offspring carrying a mutation.

Yes, the part about Darwin was confusing to me as well. The question or answer choices did not include any parts about his work, so I didn't particularly understand why his name appeared in the explanation...

That question was graded incorrectly.
(A) Rates tend to be very high in most populations.
That's a badly designed answer. What populations are they discussing? In lower-order life forms (viruses and bacteria for instance), mutations are the main source of genetic variation and occur often, which they thrive on (often to our detriment). Complex life forms, especially those with long life-cycles, tend to have much lower rates of mutations.
(B) generally lethal
No debate here, obviously wrong.
(C) irreversible
Wrong wrong wrong. No idea what the grader was thinking when this was picked as the "correct" answer. There's always the possibility that a base could change in a species, and later be flipped back to the wild-type in a distant descendant - by random chance alone.
(D) Only certain gene locations are affected.
No debate here, obviously wrong. Mutations can happen anywhere in the genome.
(E) source of genetic variation
This should be the correct answer. If you start with a bunch of bacteria (same species, no plasmid transfer or other shenanigans allowed), obviously they can only gain new alleles and functionality via mutations.
Now if you consider the recombination and meiosis approach: you still need mutations to produce varying alleles that can be mixed and matched. If every human had the exact same* genome (for purposes of simplicity assume there's only 1 possible X chromosome and 1 possible Y chromosome across the species, females get 2 copies of the exact same X chromosome while males get 1 each of X and Y), you can recombine all you like at each generation and everyone ends up being a genetic carbon copy of each other (all differences at adulthood would be purely chalked up to nurture as opposed to nature).


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Can I make an population genetic analysis from incomplete protein?
I have an dataset of fasta sequences. This proteins are not complete (My sequences have 700 nucleotides,while complete sequences have 1725 nucleotides)I would like to know if i can make an population genetic analysis from it(like TAJIMA-D test) and similars.

I think it is worth noting, mRNA expression does not equal protein expression.

If the sequences come from (approximately) the same part of the gene, i.e., if they can be meaningfully aligned, in order to build phylogeny.

It very much depends upon what type of analysis you want to perform. For a Tajima's D, all you would need is a single nucleotide sequences in a sample of individuals, so yes you can. Whether or not the sequence came from a gene or any other sequence is not relevant to whether you can compute Tajima's D (although the type of sequence will likely affect the resulting D).


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Will this strategy work for verifying successful cloning of a DNA fragment into a plasmid vector?
So I am in a bit of a time constraint. Essentially, I inserted a DNA fragment via molecular cloning which contains a unique RE site. I need to confirm whether my colony has or does not have the fragment.
I need to do this in one day so would this work as a confirmation strategy:

Pick colony and perform colony PCR with primers around RE site.
Cleanup the PCR product and digest using the enzyme which was inserted.
Run on a gel. If a cut is noticed, this confirms that the colony had the inserted fragment (containing the RE site).

Would this strategy work? Are there any notable issues people can for see in this strategy?

Yes, your strategy would work, with the caveats already mentioned by @Cell.
Depending on which restriction enzyme and PCR buffer you use, you might even be able to skip step 2. NEB has a good list over their restriction enzymes and their activities in some common PCR buffers. With some reasoning that information is often applicable also to restriction enzymes of other brands.
Depending on your primer availability, another quick strategy is to simply use a primer pair such that one primer binds inside your fragment, and the other binds to the backbone. This should result in a PCR product only if your cloning was successful, and also verifies correct direction (in case you used blunt-end or single-site cloning). Two possible problems with this approach is:

If you get no bands at all you may not know if what failed was your cloning or the PCR reaction. The latter can be easily controlled for with a well-thought positive PCR control.
You may detect cases in which more than one copy of your fragment have been inserted. Although such cases are rare, it sometimes happens that inverted repeats of 3, 5, 7, ... etc copies get inserted in tandem.

One issue is if your fragment amplified is too small you may not be able to see the positive result of two bands because they run off the gel. Also the RE may not cut a small fragment efficiently.
I would recommend extracting and purifying plasmid, then do a double digest using the unique fragment cutting RE and a RE that only cuts the backbone. You should either see linearized plasmid DNA or two bands that are probably both >1 kb and easily resolvable.

I would question the cutting efficiency since often PCR amplified products have restriction ends and are easily cloned into vectors.

Maybe it depends on how far away your primers are but according to this NEB article you need to some extra DNA sequences on both sides of the cut site for efficient cleavage https://www.neb.com/tools-and-resources/usage-guidelines/cleavage-close-to-the-end-of-dna-fragments Since you didn't specify I assumed the worst case where your cut site is at the very end of the amplified product.

Yes, usually its 4 to 5 bp..... my "double check" primers would amplify 500bp from each side of the RE site. It should cleave well. In addition 1,000bp vs 500bp would be very noticable


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glycogenesis, glycogenolysis and weight gain or loss
I am under the impression (from dietary websites) that when excess serum glucose is stored as glycogen, body weight is increased and the reverse: when glycogen is converted to serum glucose, body weight is reduced.
I also understand that the glycosidic bond formation in glycogenesis is a condensation reaction, releasing water, whereas the rupturing of these bonds in glycogenolysis is a hydrolysis reaction absorbing water.
Please help me here: how does the body gain weight by releasing water and lose weight by absorbing water. What am I not understanding?

shat happens to the sugar in blood stream?

Where I say ‘serum glucose’ I really mean ‘blood glucose’. Apologies.

sure, whatever. My point,  if you answer my question, you'll be able to get more intuition into your question

You ask about what happens to sugar in the bloodstream, I presume you mean glucose in the bloodstream and, if you don't know the answer to your own question, I don't think you're going to be able to help me. Sorry!

i am trying to give you a hint. If you can answer what happens to glucose in blood stream, you might be able to understand how weight loss works

Well, aaaaa, I thought I knew, but perhaps I’m missing the obvious! Please help my seventy-six year old brain, befuddled with glycolysis, Krebb’s, ketones, gluconeogenesis and heaven knows what else to get to the bottom of my question!

A point of significance - main energy storing component is fat and not glycogen. A 40 minutes - 50 minutes moderate to severe exercise is sufficient to clear up most glycogen in the body. Thus the contribution of glycogen to body weight is very insignificant if any

One face, many thanks for your comment. Many tests have shown that shortly after starting a LCHF diet there is rapid loss of up to 5 kg. For me it took about five days. The only plausible explanation is the consumption of glycogen stores, see my self-answer below. As you know, fat is hydrophobicand so no water weight is lost due to fatty-acid oxidation.

The answer to my question is that the glycogen molecule is extremely hydrophilic. For every gram of glycogen the molecule attracts 3 grams of water. When the glycogen is hydrolysed the attached water is excreted either directly in the liver or through cellular ATP processes.

you should provide links to deference where you got this information

I found this out studying the excellent biochemistry series at the Khan Academy.

I think your trouble comes from incomplete understanding of glucose life in the human body. Basically, you need to look at Citric Acid Cycle or TCA, that works with Acetyl-CoA as starting compound.
The reaction can be condensed into:

Products of the first turn of the cycle are one GTP (or ATP), three NADH, one QH2and two CO2

The weight loss that you are interested in, comes from basically releasing CO2 into the air. As far as I understand, you breath your weight away! Interestingly, trees are going to use that CO2 later to build their tissues up.
The water doesn't play central role in process of weight loss, as body tries very hard to regulate amount of water inside the cell and in the intracellular space.

I have an answer to my problem and it is thanks to Khan Academy. Of course it is SO SIMPLE!

your source is undoubtably correct regarding fat burning aaaaa, not only carbon dioxide of course but also water are the end products of cellular respiration. But that wasn’t my question which concerns the rapid weight loss experienced by folk starting a Keto Diet.


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an umbrella term for homeolog and ohnolog?
Is there a word that refer to homologous chromosomes within a polyploid species? If I have AABB species, what is A to B?
The words "homeolog" and "ohnolog" are reserved for the cases if the homologous chromosomes have diverged via speciation or whole genome duplication event. But what if we just don't know?
I hesitate to use word "homologous chromosomes" since they do not for a choromosome pair anymore, they are homologous in sense of an recent common chromosome ancestor.

I think homolog is as good a term as you'll get, though I'm certainly not an expert in this area.

In the case of (A+A'+B+B'), A and A' are homologous chromosomes. In canonically sexual species, one is inherited from each parent. "Homeology" applies to chromosomes that are related by ancestral duplication, yet segregate independently at meiosis.
https://en.wikipedia.org/wiki/Homologous_chromosome

@canadianer Hope is the last to die...
@J It's the same with ohnologs - they are also expected to segregate independently at meiosis. However "homologous chromosomes" are quite tightly linked to meiosis.

@J-- i think that this comment should be an answer. It is more appropriate IMO than Kamil S Jaron's answer.

@MaximilianPress The main problem of J's comment is that the provided reference doesn't say that homologous chromosomes are defined by shared ancestry, contrary it does say they must pair/segregate in meiosis.

@KamilSJaron I haven't looked at the paper I admit- I personally find "homologous chromosomes" to be the least confusing term (none of them are non-confusing, unfortunately), though it's possible that the rest of the world disagrees with me.

Unfortunately, there is no such term. Look at Glover et al. 2016 for a proposal how to unify the ploidy related homology terms, none of the words describes exactly what I searched for, so I at least compiled the relevant vocabulary

homoeolog/homeolog - homologous chromosomal sets in an organism diverged in isolated populations/subspecies and broght back by a hybridization event; note that the two spellings with exactly the same meaning are possible
ohnolog - homologous chromosomal sets originated from a whole-genome duplication (WGD) event; however usually this is used for ancient WGD events (like the R1 and R2 at the base of vertebrates, or the WGD at the base of bony fishes). It is not really possible to distinguish between WGD and hybridization in these ancient cases and therefome ohnologs perhaps suit "unknown" category better.
homologous chromosomes - chromosomes that pair during meiosis (does not strictly correspond to the homology in the context of molecular evolution)
homologous sequences/homologs - any sequences that have a common ancestor (as used in molecular evolution; but does not have to be on a genome-scale or within a genome; tandem duplicates or orthologs in two species are also homologous sequences)

2020 update:
I asked when I was writing this paper. I needed the term to describe the heterozygosity structure of some polyploids and I ended up calling them homolog (A <-> A' divergence) and homoeolog heterozygosity (AA' <-> BB' divergence) or composite when I was unable to set them apart (the majority of cases in fact).


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Are clones less likely to be fertile?
I know that hybrid animals like mules are infertile. What about clones? Do cloned animals show the same fertility as their original?

Do you know why hybrid animals are infertile?

@Cell Have you ever noticed that some people have a tendency to answer a question with another question?

@ImprisonedRhesus Answering questions with other questions can be a good pedagogical technique, since those questions are meant to guide your logical thinking while allowing you some creativity (i.e., without giving away the answer too directly).

Also as a curiosity - mules are typically infertile, but there are dozens of well-documented cases of mules and hinnies that have successfully reproduced, so it's not an all-or-nothing thing.

@iayork You should be more cautious before calling other people snarky and a bully. The original poster was implying that clones may be infertile for the same reasons that hybrids are otherwise why even bring it up? I know that the topics are completely unrelated hence I wanted to gauge how much the original poster knows before answering. Unlike your verbose, jargon filled, one-size-fits-all answer, I like to answer with the knowledge and expertise of the asker in mind.

@Cell and yet you clearly did annoy the original poster, so your claimed goal failed completely. Since evidence shows you don't understand how people read your comments, you should reconsider your approach. Data trumps theory every day.

Cloned animals, at least in the first generation, are often subfertile and have lower viability than their progenitors. The reasons for this are complicated but often are related to epigenetic changes that lead to altered gene regulation.
Further reading:

Although the technology of SCNT has been applied successfully by many research teams, some SCNT animals have abnormal or lethal phenotypes, including facial abnormalities, pulmonary hypertension [3], contracted tendons [9], low birth weight [10, 11], as well as distinct depigmentation of the skin and hair ... Based on previous studies, insufficient epigenetic reprogramming of somatic donor cells may result in phenotypic abnormalities in the offspring ...

--Dysregulation of genome-wide gene expression and DNA methylation in abnormal cloned piglets

The epigenetic state of the ES cell genome was found to be extremely unstable. Similarly, variation in imprinted gene expression was observed in most cloned mice, even in those derived from ES cells of the same subclone. Many of the animals survived to adulthood despite widespread gene dysregulation, indicating that mammalian development may be rather tolerant to epigenetic aberrations of the genome.

--Epigenetic instability in ES cells and cloned mice.

Because few clones survive to birth, the question remains whether survivors are normal or merely the least severely affected animals, making it to adulthood despite harboring subtle abnormalities originating from inadequate nuclear reprogramming ...  Our results suggest that many expression abnormalities are common to the NT procedure whereas some reflect the particular donor nucleus. These results further emphasize the severity of placental dysfunction and illustrate abnormalities in clones surviving to birth.

--Abnormal gene expression in cloned mice derived from embryonic stem cell and cumulus cell nuclei

Although clone D had a poorer libido and entered puberty later than those of the other cloned male cats, he produced gonadal hormones within the average range. Four of the cloned male cats had normal fertility.

--Reproductive fertility of cloned male cats derived from adult somatic cell nuclear transfer.
(Note that this paper concluded that the cloned male cats had "normal fertility", but one of four (25%) had reproductive abnormalities (reduced libido and delayed puberty); the numbers are too small for anything definite but I would say this is evidence for abnormal fertility, not the reverse)
Some early papers do claim normal fertility of cloned mice, but those are simply based on the fact that the cloned mice could have offspring (i.e. were not completely infertile) and didn't actually compare fertility of cloned vs. "normal" laboratory mice.

Wakayama, T., Perry, A.C.F., Zuccotti, M., Johnson, K.R. & Yanagimachi, R. Full-term development of mice from enucleated oocytes injected with cumulus cell nuclei. Nature 394, 369–374 (1998).
Wakayama, T. & Yanagimachi, R. Cloning of male mice from adult tail-tip cells. Nature Genet. 22, 127–128 (1999).


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Could cyanobacteria thrive with very high CO2 concentrations and almost no oxygen to start with?
Has there been research to see if cyanobacteria could live in high levels of CO2, like in the atmosphere of Venus ?
Because cyanobacteria caused the Great Oxygenation Event one might expect that they could !

Yes, there has been research. This paper asks and answers your question!
Here is the abstract of the paper. I highlighted the sentence that answers your question.

Cyanobacteria and similar organisms produced most of the oxygen found in Earth's atmosphere, which implies that early photosynthetic organisms would have lived in an atmosphere that was rich in CO2 and poor in O2. We investigated the tolerance of several cyanobacteria to very high (>20 kPa) concentrations of atmospheric CO2. Cultures of Synechococcus PCC7942, Synechocystis PCC7942, Plectonema boryanum, and Anabaena sp. were grown in liquid culture sparged with CO2-enriched air. All four strains grew when transferred from ambient CO2 to 20 kPa partial pressure of CO2 (pCO2), but none of them tolerated direct transfer to 40 kPa pCO2. Synechococcus and Anabaena survived 101 kPa (100%) pCO2 when pressure was gradually increased by 15 kPa per day, and Plectonema actively grew under these conditions. All four strains grew in an anoxic atmosphere of 5 kPa pCO2 in N2. Strains that were sensitive to high CO2 were also sensitive to low initial pH (pH 5–6). However, low pH in itself was not sufficient to prevent growth. Although mechanisms of damage and survival are still under investigation, we have shown that modern cyanobacteria can survive under Earth's primordial conditions and that cyanobacteria-like organisms could have flourished under conditions on early Mars, which probably had an atmosphere similar to early Earth's.

Thomas, D. J., Sullivan, S. L., Price, A. L., & Zimmerman, S. M. (2005). Common freshwater cyanobacteria grow in 100% CO2. Astrobiology, 5(1), 66-74.

I like this exobacteria theory question because they implement a strategy for answers that may go against or for the idea of out of space terraforming. Simply providing detail won't be enough in this case. Cyanobacteria are not very durable in Venus atmosphere. The temperature of Venus is of much higher average and they will be feeding of the atmospheric pollution as well causing an oxidative affect on the cell when too much co2 gives off oxides. But more importantly hydrogen buildup in the protein folds could cause inhibitory stress (prevents binary fission). So no I would not use Cyanobacteria as a space project. But please go against me if I'm false.

Thank you for your answer. Temperature would be no problem, at a height of 55 km, it is 27$^0$ C with a pressure of 0.5 atm. How does CO2 give of oxides ? And the hydrogen build up, is that caused by the splitting of water or the exposure to H2SO4 ? Some cyanobacteria can withstand acidity ! https://link.springer.com/article/10.1007%2Fs00442-011-2200-0

To simplify, nitromethane gives off nitrogen oxides and hydrogen carbide when in contact with nitrogen and co2. Acidity is not a problem true. But oxygen may be used up with the introduction of Cyanobacteria. Look up photosystems for more information. I am happy that I could be of help.

Thank you for the information, but there is no nitromethane in the atmosphere of Venus. And didn't you know that cyanobacteria produce  oxygen ? https://en.wikipedia.org/wiki/Cyanobacteria

Allow me to describe what I meant,

C+2H2SO4->CO+2SO2+2H2O, now add nitrogen,H2NO3+CO2->H2CNO2+O2.

I forgot to mention that iron oxide on Venus surface is harmful to Cyanobacteria.

Thank you again, but in my  original question i asked for research done


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How is the timing of gene expression controlled in developing embryo?
I understand how cell differentiation works in general (gradients of homeobox proteins etc), but how is timing controlled? Why do some genes switch on at a very specific moment of development and then switch off.
I imagine that the timing could be enabled by the same homeobox proteins (genes are switched on as soon as the proteins diffuse far enough, and switched off as soon as the homeobox is used up), but perhaps there's some special mechanism of gene expression timing?

I feel like answering this question would require more than one textbook on  developmental biology. Maybe you could narrow it down to a particular event?

It's controlled by the expression of other genes, the environment and/or maternal effect. You might be interested in this answer.

@BryanKrause, well, I am mostly interested in how it's generally possible rather than particular cases.
Say, a cluster of undifferentiated cells initiates differentiation. Half of the cells assume the fate A, and the rest assume fate B: they undergo very different steps of differentiation and transcribe entirely different proteins. And yet, in 24 hours, they all end up differentiated and forming a functional structure. How are the two completely different pathways could be synchronized so perfectly that they finish at around the same time despite having nothing in common?

@Anton Did you check out the answer that canadianer linked? I think something like that is going to be about all someone can say. I also think your conception about them "finishing at around the same time" is a bit off, there's no reason that cells have to be "done differentiating" at the same time in terms of all the maturation that goes on. Often the first steps are separating different types of stem cells which go on to differentiate in potentially multiple other separate paths, and for many tissues this never stops during the lifetime.

How can gene expression timing affect the formation of a developing embryo?
We should know that genetic imprinting is passed down. The formation of an embryo is not. Some takes on form when provoked, it is much like when oocytes are stimulated with a prod duplication
Happens automatically. The embryo is affected by the proximity of cells. Clusters, spread out, far apart. All make the cells behave automatically. But it's the first ignition of development that sets off growth. The cells have been through many phases and timing is not controlled by either proteins or genes.

Does this not answer your question?


text:
Have traditional categories such as phylum, class, genus, been dispensed with in modern taxonomy?
Looking through the one zoom and EOL projects I see no reference to such categories.

We still use these concepts because they help communication but they are mainly arbitrary. Some of the discussion in this answer might be of interest to you.

Thanks Remi, is there scope for a listing of species in terms of supersets and subsets - most likely from an evolutionary perspective.  If this has been done do you know where I could see some examples.    I don't have the required knowledge to give a detailed example but something along the lines of lion<feline<carnivore<mammal<vetebrate<chordate<etc might be one.

I am afraid any categorization of lineages of this kind will necessarily end up being somewhat arbitrary. I could picture categorizing into a <enter taxonomic level; e.g. family> everything that share a common ancestor less than  years ago. It would still lead to issues with horizontal gene transfer but that might be feasible.

But presumably some worthwhile subsets / supersets can be shown particularly from a structural point of view.   Again I lack knowledge here but I am guessing that a term like feline is arbitrary but mammal and invertebrate are demonstrable and also that all mammals are invertebrates.  Am I on solid ground with that?

Oh yes of course. What I meant is whether we choose to call mammals a class or an order is somewhat arbitrary. But we can clearly define monophyletic taxa and investigate their relationship to other monophyletic taxa. This post that offers an intro to phylogeny might be of interest to you


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How is ligand binding modeled?
I have the following exercise to solve:

To be honest, for both parts, my only idea so far would be to divide the rate expression by the sphere area and multiply by the new available areas (that of a circle for part a and that of many circles for part b). But if I do this, I will have an "a" parameter always, which makes no sense because it is representative only of the sphere.
Any ideas on how to approach this?
All help is greatly appreciated.

Consider expressing that rate in terms of surface area. For the sphere presented, adsorption rate = surface area * (DL) /a. Then extrapolate to the 2d systems.

don't use the perfect square model. You will keep getting Pi but it's not a real life formulae only used for theory. Try to use a Cartesian graph but three dimensions to take into account curve flexibility. Integral calculus is similar too or better.


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Biology and dna samples to determine parental lineage
How could you use nuclear and mitochondrial DNA samples run through electrophoresis to determine parental lineage.

Before DNA sequencing was widely available, some lineage information could be determined using restriction fragment length polymorphism, a kind of "DNA fingerprinting".
https://en.wikipedia.org/wiki/Restriction_fragment_length_polymorphism
Analyzing nuclear DNA would give information about both parents, while mitochondrial DNA would give information specifically about maternal lineage, as we inherit our mitochondrial DNA only from our mothers.


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What part of the body holds the most pain receptors?
What part of the body holds the most pain receptors or is likely to cause someone to feel the most intense pain?
I thought it was the eyes but I can't find that source anymore.

try looking at the a map of the postcentral gyrus, that will tell you which parts of the body have the most sensory neurons. I would guess the hands if I remember the homunculus right.

@John - The cornea is many times more sensitive than the fingers, with excellent reason (we use our hands to work with.) Imagine three grains of sand being rubbed between two fingers. Now imagine them getting dropped onto your cornea.

There is anecdotal evidence that the cornea is indeed the most sensitive tissue. Just think of it: our eyes well up with tears when slicing an onion. A tiny insect who flew into our eye feels enormous, and a corneal injury, say a scratch, can leave us severely compromised for a number of  days. Luckily, the cornea has rapid healing powers.
The cornea is so sensitive that part of determining the amount of brain injury one has sustained is by measuring the corneal reflex. The way this is done is to take a cotton swab and pull off some cotton fibers and twist them into a tiny tail (so to speak), and tough the cotton fibers to the cornea. If there is no reaction, that's a bad sign.
The Sensitivity of the Cornea in Normal Eyes
Evidence-based guideline update: Determining brain death in adults
Report of the Quality Standards Subcommittee of the American Academy of Neurology


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How much shorter is the short arm of a chromosome? And why?
I keep reading that the p arm is shorter than the q arm. But I cannot find an explanation of how much shorter nor an explanation for the difference.

Which chromosome in which species?

Let's say homo sapiens, any chromosomes.

@Remi.b has answered your question. The point to my comment was that "p" just means short, and "q" just means long. Just like you can't say how much shorter a short person is than a tall person, you can't say how much shorter a p arm is than a q arm. It depends on the chromosome (person).

I guess I'm looking for some data on distribution of size differences between the 2 arms. Is the average difference 1%? .00001%? et cetera.

It varies from chromosome to chromosome and from species to species. In some cases, both arms are roughly the same length. In some cases, one arm is so short that it is almost inexistant. For chromosomes with equal length arms, of course the terms p and q do not apply.

p and q are used to describe the relative size of the arms of a chromosome. According to this wikipedia article p stands for petite (french for small) and q is just the next letter in the alphabet.
So p is just defined as the smallest arm in any chromosome. How much smaller is not relevant for this definition. The names are just jargon which make it easy to refer to an arm.


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Bacteria as predators
Why do some bacteria kill each other? And how do they do that?
It's really a mind-blowing thing if you think about it. Please give me a simple answer.

Welcome. Have you done any research yourself?. I'm mod and cannot vote as such, but I would close it on the basis of underresearchedness. Adding prior research provides focus to your question. The post is too broad, which in turn attracts poor answers (and a lot of mod work :)

They do that because a bacterium contains all the molecules required for life, that is they are a source of amino acids, lipids, glucids and nucleic acids. This is the same reason why we eat in the first place: we need a source of these molecules to survive or, in other words, to allow our cells to carry out their tasks such as replicating the DNA or producing proteins.
Bacteria can kill other bacteria by a kind of infection: the predator bacterium enters a bigger prey and then start consuming the prey's molecules. By the same token, Mycobacterium tuberculosis enters the macrophages and used them for its own biochemistry, for instance.
Interestingly, this process of bacterial predation is under scrutiny for the development of a new breed of antiseptics in the age of antibiotic resistance (see https://phys.org/news/2017-03-predatory-bacteria-antibiotic.html).

Is it really always inside out? Couldn't a bigger bacteria eat and digest the smaller one?


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How many birds in this population would be expected to have either red or white feathers?
Question: The red and white feather pattern of a  bird is determined by a gene that has two alleles, band R and W,which show codominance.  Some birds have completely red feathers (RR),some parrots have completely white feathers (WW), and others have red and white feathers (RW).In a population of 630 birds that is at Hardy-Weinberg equilibrium, 202 parrots have completely red feathers. How many birds in this population would be expected to have either red or white feathers?
Is this question asking for what is the carrier proportion-2pq? The answer is supposed to be 321 but I keep getting 309. I did 202/630= p^2=0.32= 0.566. Then q=1-0.566 =0.434. Then I did 2(0.434)(0.5662)= 0.49. Then I multiplied 0.49 x 630 to get 309. If any one can point out what I did wrong I would really appreciate it!!

If this is homework, please add the homework tag.

Its nice to see someone actually do something before to post it on SE. :)

The solution
$$p^2 = 202 / 630 ≈ 0.32$$
$$p = \sqrt{202/630}$$
$$(1-p) = 1 - \sqrt{202/630}$$
$$(1-p)^2 = \left(1 - \sqrt{202/630}\right)^2 ≈ 0.188$$
There is a fraction of $202 / 630 ≈ 0.32$ of red birds. There is a fraction of $\left(1 - \sqrt{202/630}\right)^2 ≈ 0.188$ of white birds. There is therefore a fraction of $0.32 + 0.188 = 0.508$ of birds that are either all white or all red. In a population of 630 individuals, it therefore represents $630 * 0.508 ≈ 320.53$. A result that is apparently rounded up at $321$ in your answer key.
Your mistake
You computed the number of birds that have both white and red feathers (WR) while the question was asking for either red or white feathers. You calculated the expected number of heterozygotes instead of calculating the expected number of homozygotes.
Of course the number of heterozygotes and the number of homozygotes should add up to the number of individuals in the population ($321 + 309 = 630$).


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Do you have nerves on the outside of your skull?
I have a spot on my skull that feels like a nerve or blood vessel. I know that there are many to the brain, however, it is the only one I have ever felt. So do we have nerves or blood vessels on the top or outside of the skull?

Are you talking about the surface of your skull, or anything/everything "outer" to it? If there were no nerve (endings) or blood vessels outside the skull, there would be no pain or bleeding with, say, scalp lacerations or hard bumps. So wording needs to be more specific. Generally the nerves and blood vessels of the scalp aren't easily palpable. Might you be feeling a skull suture line?

A soft or hard spot (bump) on the skull part of the head can be also a skin cyst or lipoma, for example. The nerves are flat and I'm not sure if you can really feel them. From vessels you would probably more likely feel the veins than arteries.

There are a number of nuerovascular bundles that exit the skull. Three involve branches of the trigeminal nerve.


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Where does reverse transcriptase come from?
I can't figure out whether the viruses provide reverse transcriptase, or their RNA has the code for it, or the host cell normally contains it.
Multiple sources just introduce the enzyme without explaining who provides it / where it comes from. Apparently, both the host cell and viruses have processes that are dependent on reverse transcriptase, so I guess the answer is all of above / case-dependent?

Interpretation: "Where does reverse transcriptase come from" ... which is a. found in cells b. found in virus?

I was about to write an answer saying that all reverse transcriptases are viral genes/proteins, but then wikipedia reminded that the telomerase is technically also a reverse transcriptase.
To answer your (main?) question:

I can't figure out whether the viruses provide reverse transcriptase or their RNA has the code for it

Retroviruses have (almost by definition) the code for a reverse transcriptase in their genome. However, they also have the enzyme (or rather an inactive pro-enzyme) packaged into the viral capsid. The reverse transcriptase is a part of the Pol gene.
There are some other viruses that also use reverse transcription, but aren't retroviruses - in these cases I'm not sure, but I would guess that they also have an RT in their genome.
Now going back to the telomerase and retro-transposon elemnts:
These are ancient genes/elements in the eukaryotic genome, that basically do the same thing as viral reverse transcriptases: they make DNA from RNA.
Retro-transposons are generally believed to be viral additions to the genome, collected over the course of evolution. However, also the Telomerase enzyme probably has one common origin with viral reverse transcriptases (Nakamura 1998, take a loot at figure 2 at the end), (Witzany 2008). The thing about these evolutionary events is that they go way back, up the point were eukaroytes just started evolving from ... something. The sources I cited argue that many "eukaroytic" features (e.g. nucleus, RNA processing, vesicular transport) were originally taken from viruses.

As the question is not restricted to retro virus the answer might also elaborate on  any non retro virus using reverse transcriptase "being found" in cells.

It is important to note that not all viruses have a reverse transcriptase gene. These kind of genes are a defining feature of retroviruses.
Retrovirus are single stranded RNA-viruses. Once a retrovirus infects a cell it uses reverse transcriptase to convert its single stranded RNA into double stranded DNA. The genes on this DNA are then transcribed and translated into new reverse transcriptase and other protein by the host cell. When new viruses are assembled within the host cell, both RNA containing a reverse transcriptase gene and reverse transcriptase enzymes are packaged into a new virus.
So to answer your question: Host cells do not normally contain reverse transcriptase. Viruses contain both the gene and the enzyme.
Alberts

There are no double stranded retro viruses?


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Why does flatulence vary in temperature and smell?
Quite simply, why do some farts feel warmer than others?  Some feel regular, while others feel like lava.  What causes this?
If there is no real temperature difference, why do I perceive some to be warmer than others?  Does this contribute to the smell?  I've notice the hotter they feel, the worse they smell usually.

Burning sensation in the anus might also be related to decreased nerve function due to various causes including diabetes and vitamin b deficiency

a better question why would you think they would not?

Fundamentally, the smell of what comes out will depend on what goes in - primarily a function of what you ate and conditions in your gut (including the mix of bacteria).
In addition, if you ate something containing large amounts of capsaicin (the chemical that makes chili peppers spicy), it's going to "burn" on the way out. Aside from flatulence, overconsumption of capsaicin can irritate the intestines and cause diarrhea.

So you're saying the temperature fluctuates depending on the food you eat?  Does capsaicin affect temperature?

Capsaicin definitely affects the perception of temperature, but may cause localized irritation which in turn can raise actual (thermometer) temperature. Heat production is generally the product of metabolism; if something with large amounts of available energy ends up in the small intestine with sufficient bacteria to process it, expect tons of hot and obnoxious gas. If you're eating something that didn't have much of any energy in the first place, then there's nothing for the bacteria to metabolize in the first place.

I think the OP is asking about temperature in terms of the actual gas feeling warmer vs a burning sensation from capsaicin


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Are some people more 'attractive' to mosquitos? If so, is that a hereditary trait?
Mosquitos clearly love me-- but I have been told I am just more reactive to mosquito bites. Are some people more 'attractive' to mosquitos (get bit more)? Or is it just that they are more reactive? If it is an 'attractive' trait-- is this hereditary?

There is a genetic component to mosquito's attraction to humans.

Female mosquitoes display preferences for certain individuals over others, which is determined by differences in volatile chemicals produced by the human body and detected by mosquitoes. ... Overall, there was a strong narrow-sense heritability of 0.62 (SE 0.124) for relative attraction and 0.67 (0.354) for flight activity based on the average of ten measurements. The results demonstrate an underlying genetic component detectable by mosquitoes through olfaction.

--Heritability of Attractiveness to Mosquitoes

However, analysis of a comparative rating variable "compared with your twin, who is bitten by mosquitoes more often?" indicated a strong genetic influence on frequency of being bitten by mosquitoes, with no significant differences observed between males and females.

--Twin study of adolescent genetic susceptibility to mosquito bites using ordinal and comparative rating data.
There are many other influences on how attractive people are to mosquitos, including diet, alcohol consumption, and various disease conditions.

extensive anecdotal experience confirms this, for some reason, I'm always ~10x more attractive to the local mosquitos than my frequent hiking partner.

So it's a complete myth about having a higher level of blood sugar and therefore having "sweeter blood"

I would distinguish two major types of mosquito bites "risk factors": genetic predispositions and transient attractiveness.
Mosquitoes utilize different senses to localise and choose a host. Olfaction seems to be a principal stimuli (constant, gradient measure, simple sensory system). Based form experience from studying other hematophagous ("blood-eating") animals carbon dioxide (CO) is a key feature of breathing living animals. Therefore, CO is an indicator of potential host suitability. Amount of exhaled CO may increase eg. with body mass.
Preferences are made based on excretion of (S)-lactic acid and products of skin bacteria, which may vary between individuals and be attributable to genetic background (eg. the immune system that may affect the composition of skin flora) and transient factors (eg. physical activity).
Skin temperature is another possible stimuli, that mosquitoes can detect. It is correlated with individual's metabolic activity and results from increased blood flow through the skin (increasing chances for tasty meal). So all factors that affect metabolism rate may make individuals more prone for bites, eg. pregnancy, physical activity or fever. The latter is essential for malaria spreading.
Some studies suggest blood type (unlucky type 0) or even beer drinking as an important factors.
As sugar is one of the main blood nutritional resources, it is reasonable to hypothesise that the blood sugar level may correlate with the number of mosquito bites, but relevant literature supporting this is lacking.
Sources and further reading (highly recommended):
Host Preferences of Blood-Feeding Mosquitoes
Annual Review of Entomology
Vol. 58:433-453 (Volume publication date January 2013)
Landing Preference of Aedes albopictus (Diptera: Culicidae) on Human Skin Among ABO Blood Groups, Secretors or Nonsecretors, and ABH Antigens Journal of Medical Entomology 41(4):796-799. 2004
Beer Consumption Increases Human Attractiveness to Malaria Mosquitoes PLoS ONE 5(3): e9546
Limburger cheese as an attractant for the malaria mosquito Anopheles gambiae s.s. Parasitol Today. 1996 Apr;12(4):159-61.


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Two state exponential growth model
I want to write an expression to model exponential growth of a microbe that scholastically and irreversibly acquires a mutation at a fixed rate that slows growth.
I can do it iteratively, but am curious whether a simple expression can be written.
I started with:
$P_{total} = P_{wt}e^{r_{wt}t} + P_{mutant}e^{r_{mutant}t} $
How do I factor in the mutation rate that converts $P_{wt}$ to $P_{mutant}$?

Can you please explain what your variables stand for?

What is the variable you are interested in tracking? Growth rate? Population size? Do you want to model drift and selection in your model to figure out the probability of a given deleterious mutation to fix?

I want to track the number of wild-type and mutant cells over time, given the growth rate of each and the mutation rate.
P_total = total # of cells,
P_wt = # of wild-type cells,
P_mutant = # of mutant cells,
r_wt = growth rate of wild-type cells,
r_mutant = growth rate of mutant cells,  r_mutation = mutation rate
t = time,  .

$P_{total} = P_{wt}e^{(r_{wt}-r_{mutation})t} + P_{mutant}e^{(r_{mutant}+r_{mutation})t}$ ?

What do you mean by scholastically in this context?

In general
Analytic solutions only exist for special cases. Therefore a good way of approaching these problems is to first act like they don’t and be happy if you can see how to derive one. It’s also more straightforward than wild guessing.
Your problem
Notation:

$P_\text{w}$ denotes the original population and $g_\text{w}$ its growth rate.
$P_\text{m}$ denotes the mutant population and $g_\text{m}$ its growth rate.
$r$ denotes the mutation rate.

The differential equations that describe your problem are:
$$
\dot{P}_\text{w} = g_\text{w} P_\text{w} - rP_\text{w},\\
\dot{P}_\text{m} = g_\text{w} P_\text{m} + rP_\text{w}.
$$
This system of differential equations is linear as it can be written in the form $\dot{\vec{P}} = A·\vec{P}$ with $\vec{P} = (P_\text{w},P_\text{m})$ and:
$$A = \pmatrix{g_\text{w}-r & 0 \\ r & g_\text{m}}.$$
Linear systems in turn can be solved by finding the eigenvalues and eigenvectors of the matrix $A$, which are:

$\vec{v}_1 = (0,\frac{r}{g_\text{w}-g_\text{m}-r})$ for the eigenvalue $λ_1 = g_\text{m}$.
$\vec{v}_2 = \left( 1, \frac{r}{g_\text{w}-g_\text{m}-r} \right)$ for the eigenvalue $λ_2 = g_\text{w}-r$.

This means that the solution can be written as:
$$\vec{P} = c_1 e^{λ_1 t} \vec{v}_1 + c_2 e^{λ_2 t} \vec{v}_2,$$
where $c_1$ and $c_2$ are constants determined by the initial condition:
$\vec{P}(0) = c_1 \vec{v}_1 + c_2 \vec{v}_2.$
If you assume that you have no mutants at the beginning and you initial wild-type population is $1$, you have $c_1=-1$ and $c_2=1$.
With this you get:
$$
P_\text{w} = e^{ (g_\text{w}-r) t},\\
P_\text{m} = \frac{r}{g_\text{w}-g_\text{m}-r} \Big(e^{(g_\text{w}-r) t} -e^{g_\text{m} t} \Big).
$$