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Is there any evidence that humans isolated from each other genetically are less able to produce viable offspring?
I would guess that before a new species originates, members of subgroups might have difficulty in interbreeding. Is this possible?

Humans as a species are very genetically homogenous, will little genetic diversity compared to our sister species. Basically there is so little human genetic diversity this would be all but impossible to test.

@John: As a practical test, American Indians and Europeans (Africans, too) were genetically isolated for at least 10K years - probably longer considering that the Indians' ancestors came from eastern Asia - yet there are plenty of us who are descended from both groups.  I understand the same practical test has been applied in Australia, too.

@jamesqf 10K years sounds like a lot but it really isn't especially when starting with low diversity. humans lave less genetic diversity than a single subspecies of chimpanzee. which have an order of magnitude more variation. https://www.sciencedaily.com/releases/2012/03/120302101706.htm and https://en.wikipedia.org/wiki/Human_genetic_variation

@John: True, but as a practical answer to the question, we can only look at groups of humans that have been separated for various periods and see if they actually do have trouble interbreeding.  The American and Australian examples are the cases I can think of where groups of humans have been reproductively isolated for the longest periods.  Unless you include Neandertals, and I don't think there's enough data to say whether there were functional problems with interbreeding.

@jamesqf your issue will be American and Australian lines are fairly closely related. Most of human genetic diversity is in Africa. Australian and native American only diverged 70,000 years ago. If you want the longest isolation sub-Saharan African and South America would be your best bet. that will be at minimum 120,000 years of divergence, if not more. but you will run in to a big problem because human fertility rates vary drastically due to standard of living, by as much as 8 fold across all populations.

@John: But the question is not about genetic diversity, it's about reproductive isolation.  If you want to look at South American and SS-African, take the population of Brazil as your example.  I think you won't find any reproductive problems.  Fertility rates vs standard of living (however defined) is an entirely different question, one that gets into technology, culture, and individual choice, not simple biology.

@jamesqf I recognize fertility is a different question but it is a confounding to what we want to study, When you try to study cross fertilization your measurements are going to be swamped by other factors effecting fertility. Your study size would have to be absolutely massive to deal with this. this will confound reproductive isolations as well because so many places experienced colonization and establishing a lack of crossbreeding will be difficult to demonstrate for populations large enough for your needs.

@releseabe You will need to be more specific. Can you point to a specific source, or dataset, or other citation that you would like to know more about? Here is a non-technical description of reproductive isolation: https://www.sparknotes.com/biology/evolution/reproductiveisolation/section2/#:~:text=Hybrid%20Infertility,a%20horse%20with%20a%20donkey. Here is a more technical treatment: https://www.nature.com/scitable/topicpage/hybrid-incompatibility-and-speciation-820/

@MaximilianPress: i know that the Australian aborigines are a group that had been in isolation from other populations. i have never read that Europeans and this group can't have fertile offspring but i am wondering if there is any statistical effect: higher incidence of stillbirth or other issues.

@releseabe I'd suggest updating your question with that information specifically. Something like: "have human people of X group been separated from human people of Y group long enough to form reproductive incompatibilities?" I would suggest looking into this yourself also. I'm adding an answer but this may get more specific data.

@MaximilianPress: i think the question is clear and i dont want to limit it to two specific groups.

@John: Perhaps you're missing the point I have been trying to make, which is that the hypothesis of some human groups having difficulty reproducing with other groups due t genetic isolation (or indeed, anything else) has been disproven by experiment.

@jamesqf and my point is that any such experiment would likely be doomed to failure due to confounding factors. broad fertility is just too confounded by other fertility factors do do anything resembling a conclusive study. You would need hundreds of thousands of breeding pairs for just two groups to study isolated populations.

@John: But those "experiments" have been performed, naturally, when humans from long-isolated groups meet and have offspring.

@thats not the experiment the experiment is compiling that data and trying to calculate statistical significance. and if your confounding variables are powerful, you need a huge N to get useful calculation. An N that would have to be in the tens of thousands between just two isolated groups. (adding more groups would confounding and thus increase N) I don't know of any isolated groups that crossbreed in the hundreds of thousands with another group that is also considered isolated. Almost by definition if they are crossbreeding in those numbers they are not isolated.

Studies looking into this have not found any evidence of reproductive incompatibility in humans, at least not by the mechanisms other animals use.
Some studies looking at co-variation of reproductive genes find nominal positive associations between particular alleles within specific populations. This suggests (unsurprisingly) that there is functional variation of reproductive genes in humans, but again there is no evidence that it leads to the classic reproductive isolation case (e.g. here).
Some such co-occurring genetic variation of reproductive genes is also observed across populations, but again if it's across human populations it is probably not doing a great job of isolating them.
In all of these situations, the statistical evidence seems to be rather weak. If these gene-gene associations are "real", they do not seem to be very strong at all or to have much effect on fertility, echoing comments from @John.


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How do mRNAs find ribosomes?
After mRNA is released from the nucleus, the next process is its translation by ribosomes. By what physical, chemical or biochemical process does the mRNA reach the ribosome in the cytoplasm?

I didn't understand your thought experiment involving a table... Did you mean 'test tube' or 'dish' rather than 'table'?

Yes, just an assumption. It could be anything a table, a testtube or a dish. Im just trying to understand how the mRNA moves towards ribosome, how it finds the ribosome location?!?

I'm sorry, but I think the edited question is still bad. Your second paragraph is unnecessary and misleading as what you are interested in is what happens in the cell, not reconstituting the situation. Also, mRNA is a molecule — it doesn't know anything — so in science I consider it bad practice to write in a way that suggests otherwise. Finally the cell has a nucleus and a cytoplasm. The term cytosol describes an experimentally prepared cytoplasm from which organelles have been removed. I have edited your question, but the answer is basic — random collision — so I am voting to close.

Thank you @david

Consider also that (i) the nucleus has two membranes, an inner and outer one, and (ii) that the endoplasmic reticulum (ER) is continuous with the outer nucleus membrane. mRNA 'typically' leaves diffuses through pores in the outer nucleus membrane directly into the cytoplasm where free ribosomes are found, but some of it may also get into the ER. where you may also find ribosomes ('rough ER').

please have a look at this article and its images.
R. J. Jackson et al., 2010, Nature Rev. Mol. Cell Biol. 11:113.
https://www.nature.com/articles/nrm2838
In a nutshell, recognition of mRNA by ribosome occurs in multiple steps.Interaction of mRNA with (eukaryotic) initiation factors(eIF) leads to this. eIF4 complex interacts with mRNA and then an intermediate circular mRNA is formed with the aid of ATP hydrolysis.This circular mRNA attaches to the small subunit of ribosome.(the small subunit has a dozen of helper proteins attached to itself.)
After the attachment of circular mRNA to the small subunit , you can say that mRNA has "found" the ribosome as the small subunit would then form a complex with the large subunit and begin the Elongation step of Translation.

The answer to the first part of your question is: diffusion. After transcription and some processing, the eukaryotic mRNA is exported to the cytoplasm. Here it floats around until it meets a ribosome. Binding of ribosome to mRNA is facilitated by proteins called initiation factors (IFs) and the 5' cap of mRNA$^1$.
The second part of your question basically asks about cell-free protein synthesis using an RNA template. This has already been shown to work: one is reminded of the famous Nirenberg–Matthaei experiment$^2$, which ultimately led to the cracking of the genetic code. Nirenberg and Matthaei worked with bacterial cell extracts, but systems based on eukaryotic cell extracts have also been developed$^3$.

References and further reading:

Nelson DL, Cox MM. Lehninger principles of biochemistry. 7th ed (international edition). Basingstoke, England: Macmillan Higher Education; c2017. Chapter 27, Protein metabolism; p. 1077–1126.
Nirenberg MW, Matthaei JH. The dependence of cell-free protein synthesis in E. coli upon naturally occurring or synthetic polyribonucleotides. PNAS. 1961 Oct 1;47(10):1588–1602. https://doi.org/10.1073/pnas.47.10.1588
Chong S. Overview of cell‐free protein synthesis: historic landmarks, commercial systems, and expanding applications. Curr Protoc Mol Bio. 2014 Oct 1;108(1):16.30.1–11. https://doi.org/10.1002/0471142727.mb1630s108

Okay, now it makes sense! Thanks!

Ribosomes are floating around in the cytosol dissociated into subunits, they assemble around the initiation factors bound to the mRNA (and scanning for AUG), depending on the signal peptide and so on during translation they might bind to the ER membrane, after the translation they dissociate and float around again.

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Concept of mean systemic filling pressure
Mean circulatory filling pressure (MCFP) in humans was defined by Guyton as "the pressure that would be measured at all points in the entiere circulatory system if the heart were stopped suddenly and the blood were redistributed instantaneously in such a manner that all pressures were equal".
Now according to many physiologists, there must be a location in the vascular network where the pressure is completely independent of the cardiac activity, and this pressure must be equal to the MCFP. Apparently, this was already noted by Starling in 1897. The entire point is well explained in this article.
I have read this article and some others introducing the concept of MCFP to medical students; many of them report the same observations made by Guyton, Starling, etc., but a point which is never addressed is why there must be a location in the vasculature where the pressure is independent of cardiac activity.
I feel like getting a satisfactory answer to this question would greatly improve my understanding of hemodynamics, so I would be very grateful if you could explain the concept to me.

You've misread the linked article if you take this to mean there is some place that is unaffected by cardiac activity. It's just that there must be some place that is equal in pressure to the MCFP. The actual position fluctuates throughout the cardiac cycle.
The reason, though, that some place must be equal to MCFP is that pressure is continuous. Somewhere in the vasculature (i.e. proximal arteries) is definitely greater than the mean; somewhere else (i.e. proximal veins) is definitely less than the mean. Because the pressure varies continuously the function must pass through the mean at some point along the vascular path. This isn't anything special about biology, just mathematics.

Thank you very much for your answer. I am well aware that, if MCFP is comprised between mean arterial pressure and right atrial pressure, then there must be a point in the vasculature at which pressure equals MCFP. But the article I mentioned seems to say that this point does not move with cardiac activity, as illustrated with the fact that the three curves in figure 3 intersect at a unique point. This is stated even more clearly in Rothe (1993), a work cited in the article.

In Rothe (1993) the authors, citing Starling, state "Somewhere in the circulation there must be a point where the pressure is neither raised nor lowered and where, therefore, the pressure is independent of cardiact activity."

@user47679 "Rothe (1993) thought that this probably happens in small venules (less than 1mm diameter), and that it is not constant - present at different points of different organs, and changing constantly depending on prevailing conditions" - quoted from your source.

They're talking about a hypothetical location that's constantly shifting. I think you're reading too much into it or taking it too literally.

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What terrestrial Gastropod (specifically snails) has the fastest reproductive rate?
I am looking to do a series of experiments to test the adaptation of snails to different environments (Controlled environments in a lab setting. No organisms would be released into the wild under any circumstances.), and to also test the potential rates of specialization to an environment or food source, and speciation in a snail species (obviously more experiments would have to be done with many species before the results could be generalized). To do this, I need a snail species that has a very short time between the oviposition and sexual maturity of the species, and that are not extremely difficult to raise or breed in a lab. Any help or leads would be appreciated!


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Caterpillar identification - found on a coffee plant inside a house
Today, I've found a twig-like caterpillar hanging down from my homegrown coffee plant (which explained why some of the plant's leaves appear to be eaten away). What specie is this insect? It was about 2 cm long, I live in Central Europe.
Image of the caterpillar is attached below, and here is the movie of me annoying it.


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Techniques to find out which species are endangered
Most countries have a list of endangered species and international organisations too issue such lists of vulnerable and endangered species.
What mathematical or statistical models are those estimates based on?
Regardless of which techniques the lists use, what are some of the most popular mathematical models to find out whether a certain species is endangered or vulnerable given the population and/or other environmental data in the academic literature? What is the state of the art currently?
Especially, if I want to learn the models at an intermediate and then advanced level (I already have training as an Economics student on mathematical and econometric modelling), what are some books/ other sources you would recommend?

Based on the IUCN Criteria for endangered status there are two broad categories of models to help in determining endangered status. Note that no one methodology is used to determine the status of any species. Rather, a panel of experts consider all available evidence (including numerous modelling studies) and essentially make a determination based on their own judgement.

Range Estimates
Estimating the range of a species uses two primary techniques. The first is an expert range maps drawn by people very familiar with the species distribution, which involves essentially no modelling. The 2nd is ecological niche modelling, aka. species distribution modelling. See 1 and 2 for introductions on the latter. Note that the IUCN guidelines have criteria based on total range size, and well as the amount of fragmentation and patchiness of the range.

Population Size Estimates
Since it is usually impossible to count all individuals of a species, models are used to estimate total populations. These usually fall in the realm of mark-recapture models. There are numerous variations on the basic model form which account for things like an open population, varying birth and death rates, and varying capture probabilities.

1: Elith, Jane, and John R. Leathwick. "Species distribution models: ecological explanation and prediction across space and time." Annual review of ecology, evolution, and systematics 40 (2009): 677-697. https://doi.org/10.1146/annurev.ecolsys.110308.120159
2: Araújo, Miguel B., et al. "Standards for distribution models in biodiversity assessments." Science Advances 5.1 (2019): https://doi.org/10.1126/sciadv.aat4858.

Thanks a lot for your answer, it was really insightful! If it's not an inconvenience, I also wanted to know if panel data on the population estimates are or can be used to predict when would a species likely go extinct in a region. I have heard of predator-prey models in game theory, but have no idea if or how any such forecasting is done empirically. Also if any other techniques are used for forecasting

Wikipedia has an article on the IUCN Red List Categories, There are some formulae there that show how the category is determined.
For example:
https://en.m.wikipedia.org/wiki/Endangered_species_(IUCN_status)


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Is life in the open ocean homogenously spread?
Obviously around land masses or in shallow water where reefs and coral may grow, life is diverse and numerous. But how spread out is sea life in the open ocean (for example, half-way between Hawaii and California) where there is no land mass or shallow depths for hundreds or thousands of miles?
Does life exist in clusters with large swaths of oceanic desert in between or is it relatively homogenously spread?

You need to consider ocean currents. In a nutrient-rich current, density of life will be (much) higher than outside of it.

Are you purely interested in distribution across the horizontal plain? If you consider depth in your equation, around 90% of marine life is concentrated in the upper palagic zones, as sunlight can't penetrate much deeper than around 600 meters.

This is sort of a partial answer, but here is a map using chloryphyl density to map the global distribution of marine life. As you would expect, most is clustered around costal regions, but you can also see some pretty distinct zones in open ocean, with more primary production apparently in the northern and southern latitudes. Not sure how much this map projection distorts apparent distances, but it should help give you an idea.

Here's where I found this map.
And here's one of the links they references, which looks to have some more resources to explore.


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Where can I find information on the anatomy or biology of seeds?
Where can I find information on the anatomy or biology of seeds?
For example if I want to know the anatomy (some sort of drawing) of a green bean where can I go to find such information?
Searching Google does little to nothing to describe this process, let alone provide a good picture or drawing. The images of Google do return some results, but they are posts that were made by people on Twitter or Pinterest. Even Google Scholar does not have a lot of research papers on such info.
Seems like the only option is to purchase Text books which cost upwards of $200 each.
Please help....

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Well, I was able to find this on google, which seems to collect a very large amount of information on different aspects of seed biology. I don't know if it has every species/feature that you care about, but there is a lot of general information there (including images).
Note that it has an "unsafe" web address (I clicked through and my computer wasn't taken over yet).
See also this, found by google.
See also this, from a german academic source.
There are also an enormous number of technical reports like this and this from the USDA.

Hi, I guess this is my point. That there are only images but no official "safe" sites for such information.

@wwjdm If you are asking for whether there is a perfect catalog of comparative anatomy for the features that interest you in all the plants that interest you, I guess that is probably a no. However, I don't think it is too hard to look at e.g. the german source that I link to for general info, or to google scholar search "seed comparative anatomy beans" or whatever. What is an "official" site? the "unsafe" one is run by Ohio State University. The German one is also academic, the USDA is the USDA. No fancy web design in any of these places, but they are pretty official.

Thanks the USDA one you sent is good.

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Question about probability of being a heterozygous carrier
A 26-year-old woman of Norwegian descent seeks genetic counseling. Her brother died at age eight of documented cystic fibrosis. Both of their parents are deceased. The woman undergoes DNA testing for 70 CF mutations which collectively detects approximately 90% of CF carriers of northern European descent. Testing reveals that she is negative for all 70 mutations. What is the probability that she is a heterozygous carrier of CF?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. (Note that "homework" can apply to questions even if they are not assigned as homework.) Thanks!

Hi, So I have tried solving this by myself. I figured that in order for her to be heterozygous carrier, she has a 2/3 chance x by the 10% of catching a rare form of CF mutation that wasn't detected. I got a 1/15 chance, however the correct answer was 1/6, so I'm not sure what I'm missing here

Please [edit] that information into your post and include your reasoning for each step (e.g. where the 2/3 came from) — comments are ephemeral and often ignored so they can not be used to convey essential information. Please also check out the links from my first comment.

I recommend to read on Bayes theorem or maybe watch one of many videos on the subject.

I figured that in order for her to be heterozygous carrier, she has a 2/3 chance x by the 10% of catching a rare form of CF mutation that wasn't detected

Based on your comment I am guessing you have correctly identified, the correct (2/3) probability of her being a carrier prior to learning the test result. Also you have correctly identified the probability of her carrying rare CF mutation prior to learning the test result.
Now you can draw a table:
She is a carrier     She is not a carrier
c                    d                      test came out positive
e                    f                      test came out negative

In this table c, d, e and f are probabilities prior to knowing the test result. So far you have calculated the e = 2/3*10% = 1/15. I will leave to you to calculate the rest of the fields in the table.
After learning the negative test result we can cross out the fields c and d. The list of all possible options has shrunk to e and f. The new probability of her being a carrier given the test came out negative is:
probability of carrying a rare mutation / (probability of carrying a rare mutation + probability of her not being a carrier) = e / (e + f)

There are 4 possibilities:
Family has rare allele,   person is a carrier
family has rare allele,   person is not a carrier
family has common allele, person is a carrier
family has common allele, person is not a carrier
Work out all these so that they add up to 100%.  The testing allows you to eliminate one of those options, so then recalculate.


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What is the rate of bacterial cell death due to viruses on land?

"The rate of viral infection in the oceans stands at 1 × 10^23 infections per second, and these infections remove 20–40% of all bacterial cells each day." - https://www.nature.com/articles/nrmicro2644

What are the equivalent figures on land?

"On land" is pretty vague in this context. Are you just interested soil? Would you include surface waters? Wetlands? Animal-associated microbiomes? I think it's a simpler calculation for oceans, as marine biomass is largely dominated by microorganisms, whereas terrestrial biomass is dominated by plant life.

True, it is vague. I'd be interested in figures for any non-ocean ecosystems. Animal and soil microbiomes in particular.


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Hardy-Weinberg principle
The following paragraph on Wikipedia about the Hardy-Weinberg principle is bothering me.

It should be mentioned that the genotype frequencies after the first generation need not equal the genotype frequencies from the initial generation, e.g. f1(AA) ≠ f0(AA). However, the genotype frequencies for all future times will equal the Hardy–Weinberg frequencies, e.g. ft(AA) = f1(AA) for t > 1. This follows since the genotype frequencies of the next generation depend only on the allele frequencies of the current generation which, as calculated by equations (1) and (2), are preserved from the initial generation:

Why is it so that the genotype frequencies are dependant on the previous generation, but not in the case of the first as compared to the inital generation?
https://en.m.wikipedia.org/wiki/Hardy%E2%80%93Weinberg_principle#math_1

I can't think of a more succinct way to phrase it than the explanation in your post.

"...the genotype frequencies of the next generation depend only on the
allele frequencies of the current generation..."

The genotype frequencies still do depend on the initial generation, they just depend on the allele frequencies of the previous generation, not the genotype frequencies. For example, an initial generation consisting of only (XX) and (xx) genotypes will produce F1 offspring with (XX), (Xx), and (xx) genotypes through random mating. Since the (Xx) genotype frequency was 0% in the initial generation, and >0% in the subsequent generations, it can't be equal that of the initial generation. But it will still be a function of the relative frequencies of the two alleles in the population, (X) and (x).


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A mutation question from the Indian National Biology Olympiad

DNA was isolated from wild type (Gal+) and mutant (Gal-) E. coli cells and separated by density gradient centrifugation technique. DNA from Gal- strain acquired a lower position. This indicates that the mutation is caused by:
(a) deletion (b) insertion (c) mis-sense mutation (d) point mutation

Me and my friends had an extended discussion on this question and we all agreed that since the Gal- strain acquired a lower position, it was obviously more dense than Gal+ strain. Now, one of them claimed that if the volume were to remain constant, then mass is directly proportional to density hence the insertion mutation should cause increase in mass corresponding to a similar increase in density. I am not convinced by this explanation. They also said that, "Keeping the volume constant is a necessity since the experiment would lose its meaning otherwise". I am curious to know how far these assertions are correct.
After doing some research on this topic on the internet, I found a paper related to this question :
Mutations caused by the insertion of genetic material into the galactose operon of Escherichia coli
The answer given by the organizing committee of the 2nd Indian National Biology Olympiad was (b) insertion.
What could be the possible explanation for such an occurrence? Me and my friends are still unable to grasp the logic behind it even after going through different papers and books.

Volume is not kept constant as adding an insertion will definitely increase volume. In fact the volume of the object does not even matter much in density gradient centrifugation.
https://www.sigmaaldrich.com/technical-documents/articles/biofiles/centrifugation-separations.html. Look at isopycnic centrifugation in this sheet.

@RoniSaiba Yes. I get your point. It makes sense.

Would you want to win a competition run by people who are stupid enough to set this question? It’s complete and utter nonsense to imagine that the increase in mass of DNA caused by an insertion in a gene could have a significant effect on the sedimentation of bacterial DNA of 4 million base pairs, even if it is partially fragmented.

@David Sure, but the question is right:  Four gal negative mutations, which affect the expression of the gal operon severely as described in the preceding paper (Saedler et al.), are characterized as insertions of DNA by CsCl density gradient centrifugation... from https://link.springer.com/article/10.1007/BF00268890

@Bipasha — OK. But poor terminology in the question. "Density gradient centrifugation" comes in different flavours. The isopycnic flavour is something of an experimental rarity these days. There was a question on CsCl centrifugation that I intended to answer by surveying the different types of centrifugation, but I am still too busy.

@David Right, I understand, but please keep an open mind while looking at INBO questions- they are set by professors at HBCSE- the premier institution in the country for research in science. They can make mistakes, sure, but they are definitely not stupid.

Now, one of them claimed that if the volume were to remain constant,
then mass is directly proportional to density hence the insertion
mutation should cause increase in mass corresponding to a similar
increase in density.

I don't think that's quite how it works.  You don't worry about the volumes being used.  In those experiments (I don't know that anyone does them anymore)  the DNA is in a solution of really salty water.  Larger molecules get pushed more to the bottom of the tube, so the mutant DNA is larger, since it was close to the bottom.
https://embryo.asu.edu/pages/equilibrium-density-gradient-centrifugation-cesium-chloride-solutions-developed-matthew#:~:text=Density%20gradient%20centrifugation%20enables%20scientists,molecules%20based%20on%20density%20alone.

Thus, centrifugal force pushes the larger components of a mixture
farther from the rotor and closer to the bottom of the tube.

Larger DNA means an insertion.  Point mutations are not detectable with this method.


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How much ribose do we eat?
I am wondering how much ribose we ingest as food? (Deoxy)Ribose is found in the backbone of DNA and RNA. So, we eat ribose as part of the nucleic acid found in plant and animal foods. While protein, lipid, and sugar content is well analyzed for many staples we consume, I cannot find any numbers on ribose or DNA/RNA. Does anybody know of a reference to shed some light? For example, how many (milli)grams ribose is in a steak or a salad? I'm thinking about this since ribose is a more reactive sugar than glucose. It can thus cause more unhealthy additions (glycations) to other biomolecules when in circulation, so the quantity take up might matter.

PS: Maybe the lack of quantitative data leads people to the false belief that they don't eat DNA on a daily basis? ;-)

Ribose is a sugar. The "-ose" ending gives it away.

Sure, but while there's plenty of information on the weight of glucose, starch, glycogen,.. we eat, I couldn't find any on the mass of ribose consumed.

Note that DNA contains deoxyribose not ribose. I encourage you to [edit] your question to correct that and to add information about why you want to know this — i.e. why you think this is a significant question and appropriate for this site rather than one focused on nutrition. In addition, nutritional information typically describes the total carbohydrate and sugar content — neither of which is equivalent to glucose.

Who cares? Why do you want to know?  What aspect of biology will this illuminate? How would you use an answer, which is presumably related to the percent of tissues that are nucleic acids? Are you assuming the constituents of nucleic acids are absorbed as such in the gut?

Hi David, thanks for the criticism. Do you have data showing that constituents of nucleic acid are not take up and if so to which degree?


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'Big ideas' behind constrained selective breeding (optimization)
I'm looking for help in finding the 'big ideas' behind a project I'm beginning and want to make sure I'm not missing anything since I wasn't trained in Biology.
My idea is investigating constrained selective breeding, say, a farmer who wants to balance crop yield with artificially selecting a desired trait (can't select too strongly because this will reduce yield). I've found many models for selection and found Haldane's classic useful but I'm not sure how to incorporate a constraint.

I believe that you are talking about "multidimensional selection".
E.g. you are selecting on not one trait (yield) only but more than one (yield+some other trait). There's quite a bit of work done on this in crop science for example.
See e.g.

here
here
here

Figure 3 from the last talks about this in terms of evolution by reproductive isolation, which is pretty much the same thing except it's natural rather than artificial selection.

The most important thing practically is to try to measure the correlations of the traits in question. If they are positively correlated or uncorrelated, it shouldn't be too hard. If they are negatively correlated then you might have some difficulties due to constraints on the kinds of phenotypes that can exist.
For a recent technical treatment with good references, see here.


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What property of water explains how sweating helps the runner continue running?
My question I have to answer is: A runner picks up pace on a warm day and starts sweating profusely. What property of water explains how sweating helps the runner continue running?
The following are four options I have to choose from to answer this question, and below that is the uncertain answer I chose.
A. Since water molecules are polar, they adhere to the surface of the skin, which allows cooling. The skin’s outer layer of dead cells enables the adhesion.
B. At elevated body temperature, the hydrogen bonds in water break, which allows water to escape as vapor. This causes heat loss in the body, which lowers body temperature.
C. Hydrogen bonds rearrange at higher temperatures and form a lattice structure that requires energy. This energy use lowers the heat in the body.
D. Sweating is due to the high heat capacity of water. When sweating increases, heat is released and the body temperature is lowered.
I chose (B), as (A) and (C) do not make sense and that (D) I think requires too much amount of time since water has a high heat capacity. Sweating, especially during running, is more immediate than (D). Would (B) be the correct answer?

I think the answer will be B and D. B explains the process of evaporation and D explains why water is a good choice of a liquid to evaporate.

@Oosaka No, I understand the detailed explanation of how water evaporating leads to cooling. I didn't want a simple answer with no explanation, no. I suppose I was trying to ask why an answer such as A or D wouldn't work, because I feel these answers could have some merit unless I'm wrong. Finding only one correct answer choice was unclear. Do you think they have some merit, or is it definitely clear that B is correct?

@Roni Saiba: No, water is the only choice for a liquid to evaporate because there's a lot of it in humans (and other animals).  Other liquids, for instance alcohol, would actually provide better cooling since they evaporate at lower temperatures, but they don't exist in the body in significant quantities.

@jamesqf But wont same volume of water carry more heat after evaporation than alcohol because of higher heat capacity? I apologize for my shortcomings in understanding physics.

@RoniSaiba yes, water has a higher heat capacity than, say, ethanol. The point is that our bodies contain absolutely miniscule amounts of alcohols, but we are ~70% water, so the "choice" of which fluid to use for cooling is obvious.

@RoniSaiba: Also, even though water has a higher heat capacity, it cools less effectively than things like alcohol for two reasons.  First, it evaporates at a lower temperature, so it will carry away heat when water just forms beads of sweat.  Second, there's a lot of water in the environment, so in places with high humidity, it doesn't evaporate all that well.  Compare Miami to Phoenix, or a steam room to a sauna.

@Renée Thank you for clarifying. I agree with you that D sounds technically correct (as I said), and assuming the teacher sees it as incorrect for some reason, I am curious as to what that reason is. A strikes me as incorrect because the water adhering to the skin isn't useful, it is in fact its evaporation is what helps, and I don't know of dead cells helping with evaporative cooling at all. Maybe the idea is that water needs to be in contact with the skin to draw heat from the body as it evaporates, but how much does that play? IIRC skin is hydrophobic to begin with. So, seems clearly wrong.


text:
What arthropod is in the picture?
I am from Philippines and I found this in my room.
This arthropod has 6 legs and have a bit long Chelicerae like spiders that can fold to hold its food. It's about half an inch long. It also looks like a
scorpion but I could not find anything like it on the internet. Thank you!
I've also noticed that it can jump and it also produced spider silk.

It is not a pseudoscorpion as those would have 8 legs and then the two front large pincers. This is most likely a kind a jumping spider where the two large front legs count as two of the 8 legs.
Depending on your geography (not given in the question), this looks to resemble a jumping spider in the genus Chalcolecta (or some regional variant of that based on where you are). Hard to see any detail (like eyes and body segments) from your photos. But have a look at some of these and see if any of them match your specimen. Here are some pics of C.prensitans and C.simon.

This is actually the closest one. I noticed that it can jump and produces silk like a spider. However, the tip of its abdomen does bend sometimes.


text:
Plants with nutritional requirements similar to Cannabis
What are some short plants that preferably could be grown indoor which have similar nutritional requirements (in terms of N-P-K ratio, doses etc.) as Cannabis?
The purpose of this is testing a mineral fertilizer for Cannabis, without actually growing Cannabis as it is illegal in my country.
I was looking into Cannabaceae family and found out that Hops are closely related. However, due to its size/height it won't be convenient to grow it at home. Also, I'm not sure if being in the same family implies similar nutritional needs.
Plus bonus for valuable/exotic plants.

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@tyersome Although I'm not new to SE generally (been here for almost 10 years already), I've taken the tour and looked into How to Ask. I didn't find anything new or specific to this SE. There's a clear question in my post (well, I'll add a question mark). It is a general question "about biological concepts". It is not anything personal, philosophical, ethical or having many possible answers. It is well tagged. Regarding cross-posting: as I'm happy to accept both some plant names and/or directions to research myself - I'm expecting the former from Gardening.SE and the latter from here.

As for the research done - you can see I've started looking into the plant family. Of course before asking this question I've googled it only to get names of plants that have similar leaves or otherwise are visually similar. That's not what I'm looking for. With all due respect, I'm not expecting scientific papers from Gardening.SE (which I expect to get those here) and vice versa - probably there could be people with practical experience and name a plant right away which is improbable here.


text:
Difference between haemocoel and coelom
I am looking for an embryological perspective on the following question.
I know about coelom derivation, but I want to know how haemocoel is derived and how it is fundamentally different from coelom.
True coelom is formed by the cavity formed in mesoderm. It is lined by mesothelium on both sides, whereas on the other side pseudo coelom is cavity which is lined by endothelium and mesothelium. However, the formation of haemocoel is not clear to me.
I have looked for in many books, but I have not been able to find an embryological perspective and what happens to coelom in which haemocoel is present.

I was looking for the same thing and i found the answer in the anatomy of molluscs
you can clearly see that coelom is different from haemocoel and coelom is greatly reduced.
Haemocoel is a pseudocoelom it is a body cavity but not lined with mesoderm at all sides

Ca you add the source (website) of the image and add references to your answer?


text:
Which fish did modern tetrapods descend from?
Did modern tetrapods descend from Tiktaalik or Ichthyostega? While I understand that in terms of all tetrapods, the lineages of Tiktaalik and Ichthyostega both would be included, but I want to know if their lineages have continued to the modern day. Since they also have 10 million years between them, it's possible that both of their lineages have not continued to the modern day. It's also possible that neither of them have continued to the modern day and it was a later fish species altogether whose lineage has continued to this day in the form of currently living tetrapods even though Tiktaalik and Ichthyostega were the first vertebrates on land. I'm especially interested in knowing which fish species have humans descended from. I'd be grateful if anyone is able to shed any sorta light on this.

Your question cannot be answered.
One of the effects of how incomplete the fossil record is, is that it is impossible to say if a species was a member of a direct line or a side branch. we just do not have the resolution in the vast majority of the fossil record to tell. The answer could be both, neither or one or the other and we would not be able to tell. All we can say is it is likely they were closely related to or part of our ancestral line. But the working assumption is always that you have a related sister species and not the ancestor unless you can show extremely good evidence otherwise, (which is so rare you can assume it is impossible in extinct vertebrates).
Tiktaalik and Ichthyostega only give us a rough idea of what our ancestors would have been like. It is impossible to say with any certainty if either was a direct ancestor or merely a sister species to them. This is part of the reason cladograms are constructed the way they are, so that no fossil is ever put on the direct line.
Source.
Source 2
Note: Tiktaalik probably did not live on land, more likely it was a shallow water air breather.
Also whatever species was the ancestor of tetrapods, all living tetrapods would be its descendants. One aspect of population genetics is for a specific individual in an ancestral population, past a certain point in a linage  either every descendant is your descendant or you have no descendants.

You can study the reeources under "stem tetrapod tree" and tetrapod limbs. you can see the relationship in the list of the second image.
The trees suggest that tiktaalik and ichtiostega are not direct ancestors, they are close ones, so modern tetrapods descended from their common ancestors, not from their species.
vertebra:

lower jaw:

front limbs:

Technically they descended both from the tiktaalik and Ichthyostega because Ichthyostega was later, but in the same family and evolutionary line as tiktaalik.

Welcome to Biology.SE! This may be correct, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus is not considered a good answer on this site. This is a good example of how to format references. ——— Thank you for taking the [tour], but please also consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

Of all the tetrapods to have ever lived, some would be descendants of Tiktaalik and some of Ichthyostega, yes. This makes sense. However, I'm especially interested in conclusive works that posit both the lineages having continued to this day. I am not sure if there's any work of that sort, I certainly couldn't find any on my own level, hence, posted this question here. I'm also interested in knowing which of the two happen to be ancestral to human beings. I'll edit the question to reflect these.


text:
How many times did photosynthesis evolve?
Was it a 1 and done thing? Plants seem to have developed photosynthesis by the endosymbiosis of cyanobacteria. Is the latter the one time in Earth's history that the process independently came about?
Any answers would be greatly appreciated

see also some related questions: https://biology.stackexchange.com/questions/53336/evolution-of-plants-and-chloroplasts?r=SearchResults&s=3|25.0882 , https://biology.stackexchange.com/questions/36311/why-is-there-a-seeming-dichotomy-between-mobility-and-photosynthesis

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The emergence of photosynthesis has occurred rather independently in multiple organisms. One way of looking at this is to look at the taxonomic distribution of photosynthesis reaction centers, which points to 5-10 origins according to current data (mostly in bacteria). That number has some big error bars as we are talking about very deep, old branches of the tree of life.
There are other criteria that we could use- for example the evolution of carbon fixation. However, that includes also chemoautotrophy, and is thus a bit more expansive.
Note that by some definitions the acquisition of cyanobacteria in plants may not even represent an independent emergence of photosynthesis, as the cyanobacteria already did photosynthesis!
If your question is more narrowly "how many times did photosynthesis evolve in eukaryotes" (not bacteria or archaea), then you would also need to include animals that do photosynthesis in a way similar to (though I believe less efficiently than) plants. They seem to similarly use endocytosis to acquire photosynthetic machinery from photosynthetic cells that they eat.
Update
In response to comment from @shigeta, I'll add that the review that I link focuses on the reaction centers (RC) genes. They note that the RC genes probably had a single emergence, but that horizontal gene transfer is probably responsible for the current distribution of the organismal trait of photosynthesis:

Significant evidence indicates that the current distribution of photosynthesis in bacteria is the result of substantial amounts of horizontal gene transfer, which has shuffled the genetic information that codes for various parts of the photosynthetic apparatus, so that no one simple branching diagram can accurately represent the evolution of photosynthesis (Raymond et al., 2002).

Hey @maximilianPress a good citation but the conclusion at the bottom of the review is: "Current evidence suggests that the earliest photosynthetic organisms were anoxygenic, that all photosynthetic RCs have been derived from a single source, and that antenna systems and carbon fixation pathways have been invented multiple times."  you can see on their phylogenetic tree that the RC1 and RC2 appear on all these branches, which implies they came from the same ancestor, lost in time.

@shigeta a good point, which highlights the importance of whether you mean the emergence of photosynthesis (the organismal trait) or genes for the reaction centers. Indeed the RC genes are probably a single emergence, which were simply passed around by horizontal gene transfer. (Note that there is no ambiguity about eukaryotes independently evolving photosynthesis several times, through endosymbiosis!) The exact count of events comes down to a matter of how you like to parameterize your models. This exact issue is why I give a range of values. I'll edit answer.

... well in this case the structures of RC1 and RC2 and their ubiquity in photosynthesis suggest a single source, lost in time.  usually parallel evolution creates completely different protein structures for same function.  a classic example are 'crystallins' - several genes have filled in for crystallins - the protein families are quite divergent.

@shigeta the genes or proteins have a single origin. This is in the same way that e.g. Type III secretion system genes all have a single origin. However, this does not mean that Type III secretion-mediated pathogenicity has a single origin. Type III secretion systems get passed around on plasmids constantly, such that the parallel origins of this pathogenicity are certainly due to HGT. See e.g. the parallel evolution of Shigella from E. coli- Shigellas are polyphyletic in origin! Photosynthesis is like pathogenicity, only it evolves much less frequently. This is what the authors mean.

that is an excellent point @Max!  i'm going to make a supllementary answer to yours with some details.  i upvoted you tho!

Agree - you can't expect any more than this when you are looking at a ~ billion year old gene!

Im going to expand my comment into an answer because the discussion was just too interesting.
the conclusion at the bottom of the review cited is: "Current evidence suggests that the earliest photosynthetic organisms were anoxygenic, that all photosynthetic RCs have been derived from a single source, and that antenna systems and carbon fixation pathways have been invented multiple times." you can see on their phylogenetic tree that the RC1 and RC2 appear on all these branches, which implies they came from the same ancestor, lost in time.
@maximillianPress points out in his comment that lateral gene transfer is very common and this creates the exact pattern  Many gene functions can arise more than once, but when you look at the gene, if a protein is achieves a function, like RC1 and RC2 their shape and detailed sequence will not resemble each other.
A classic example is the evolution of the eye. Eyespots and photosensors with lenses have evolved many times in microbial evolution and in may have evolved separately in molluscs vs vertebrates depending on how you define it. Light detection is a microbial innovation and the opsin light sensors in animals bear a strong resemblance to those in archaebacteria.
Enzymes form a clearer example.  Studies of some of the carbohydrate metabolizing enzymes show that some specific roles are filled by multiple very divergent protein families.  The role of a protein may change over time but its very unusual for the way the protein folds to change.
An third example is the crystallins whose function is to form the lens of the eye which has to remain stable for a lifetime. In different animals these genes are radically different - distinctly different proteins can fulfill this role.  that is a gene role which may have evolved twice, but the role is fairly broad so its been filled by different proteins in different parts of the evolutionary tree more than once.
My thought is that the lateral transfer of microbial genes may confuse the evolutionary tree but the difficulty of creating a photoreaction center is much higher. There is only one bacterial reaction center protein family, so the predominance of evidence is that this phenomenon only evolved once and may have been transmitted by lateral gene transfer many times since.

I think that I agree with all this, happy that we've had a good discussion on this. With regard to the reconstruction of trees of life and the influence of HGT, a big distinction is the tree of genes vs. the tree of genomes vs. the tree of cells. Gene trees are noisy, genome trees have a central tendency but fuzzy, and the tree of cells has to exist but our only way of knowing it is the tree of genomes. For some of the (now older) work on this see https://science.sciencemag.org/content/311/5765/1283 and https://genomebiology.biomedcentral.com/articles/10.1186/gb-2006-7-10-118

i agree @MaximilianPress the good discussions are what we can all hope for in the best case!


text:
What stops myosin during muscle relaxation?
I understand that when the muscle is relaxed tropomyosin blocks myosin binding sites on actin filaments thereby preventing muscle contraction. What I am concerned with however, is whether myosin filaments - given that ATP is found in the muscle fiber- continue trying to bind to actin, and hydrolyzing ATP...
So how are mysoin filaments stopped from trying to bind to actin when the muscle is relaxed, to stop the hydrolysis of ATP?

Relaxation of vertebrate skeletal muscle is thought to occur in the absence of  ${Ca}^{2+}$ as a result of tropomyosin physically blocking the binding of myosin to actin. This steric blocking model of muscle relaxation predicts that myosin subfragment 1 (S-1) will not bind to actin under conditions where the acto-S-1 ATPase rate is inhibited.[1]
However, in a paper that questions this model, it is concluded that in the absence of ${Ca}^{2+}$, troponin-tropomyosin inhibits the ATPase activity by inhibiting a kinetic step in the cycle of ATP hydrolysis, perhaps $P_i$ release.[2]

That is the simple answer, but I think a little elaboration on the above paragraphs might help add some substance:[2]

Vertebrate skeletal muscle contraction is the result of a cyclic interaction of thick myosin filaments with the thin filaments, composed primarily of actin, troponin, and tropomyosin, causing these two sets of filaments to slide past each other. This cycling is driven by the hydrolysis of ATP by myosin in a reaction which is activated by actin.

When the sarcoplasmic reticulum lowers the free ${Ca}^{2+}$ concentration from $10^{-5}$ to $<10^{−7} m$, muscle contraction ceases and the associated actin-activated myosin ATPase activity is inhibited. The proteins troponin and tropomyosin are responsible for this effect of ${Ca}^{2+}$ on the interaction between myosin and actin.

At levels of ${Ca}^{2+}$ low enough to cause relaxation, tropomyosin is positioned away from the central groove of the F-actin filament where it appears that it might interfere with the binding of the myosin cross-bridge. This structural work formed the basis of the steric blocking hypothesis which suggests that relaxation occurs when tropomyosin, in the “relaxed” position, physically blocks the binding of the myosin cross-bridge to actin.

Three-dimensional reconstructions from electron micro-graphs have suggested that the myosin cross-bridge and the tropomyosin molecule may be in close contact with each other on the actin filament, a requirement for a steric blocking type model.

The steric blocking model predicts that in the absence of ${Ca}^{2+}$ the degree of association of S-11 should be much weaker with regulated actin than with unregulated actin. In fact, in the absence of ${Ca}^{2+}$, the binding of S-1·ADP to regulated actin is strongly inhibited in a cooperative manner.

At low levels of saturation of the actin filament with S-1·ADP, the binding of S-1·ADP to the regulated actin filament is about $10^3$ times  weaker than at high levels of saturation.

However, the fact that S-1·ADP binds weakly to regulated actin does not prove the steric blocking model since, in relaxed muscle, the cross-bridges normally exist with bound ATP (or ADP · Pi) and not bound ADP. Therefore, the steric blocking model predicts that troponin-tropomyosin should inhibit the binding of S-1·ADP·Pi as well as S-1·ADP to regulated actin in the absence of ${Ca}^{2+}$.

Using stopped flow turbidity measurements, we have previously measured the effect of ${Ca}^{2+}$ on the association of S-1 · ATP and S-1 · ADP · Pi with regulated actin. Surprisingly, in the absence of ${Ca}^{2+}$, the binding constant of S-1 · ATP or S-1 · ADP · Pi to regulated actin was only decreased to 56% of the value in the presence of ${Ca}^{2+}$ although the rate of ATP hydolysis under the same conditions was decreased to 6% of the rate with ${Ca}^{2+}$ present. These data suggest, in disagreement with the steric blocking model, that inhibition of the rate of ATP hydrolysis, in the absence of ${Ca}^{2+}$, is not the result of inhibition of the binding of S-1 to regulated actin.

1- https://pubmed.ncbi.nlm.nih.gov/27065174/
2- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1266292/#FN2


text:
The position of the macula in comparison to the blind spot
Which is located in a higher postion? Macula or blind spot?

The first image is a section of the eye. What was the plane of this section: longitudinal, transverse, or something else? Also, for the second image, what was the orientation of the camera? Are these images of the right eye or the left eye? Thinking along these lines will lead you to the answer.

@Adhish The first image is a section of the left eye and the second one is also of the left eye. Can we say that macula and blind spot are almost in the same positon or level (horizontal)


text:
Are the IRV and ERV equal in amount?
I am reading about Inspiratory Reserve Volume and Expiratory Reserve Volume in my textbook. So my general question is aren't the two terms show the same amount of air ?
I would like to tell you why I think so. Like IRV tells us about the maximum amount of air we can intake other than normal intake. So this extra amount is what going inside our lungs and I think this is the part which comes out in the form of ERV .
So shouldn't the total capacity of lungs be equal to (Tidal volume + IRV + Reserved Volume) only ? Why do we need to include the term ERV in the above equation ?

You're misunderstanding a bit. Here are some definitions from Wikipedia, where I added some bold for emphasis:

Expiratory reserve volume: the maximal volume of air that can be
exhaled from the end-expiratory position

Inspiratory reserve volume: the maximal volume that can be inhaled
from the end-inspiratory level

In plain terms, ERV is how much you can still breathe out after you've breathed out all you normally would. You can try it out yourself: when you're finished breathing out and ready to start breathing in, try to blow out a bit, you'll find there is still air there. You don't need to breathe in extra to be able to breathe out this extra.
Similarly, IRV is how much you can still breathe in after you've breathed in all you normally would.
If you were to do a "fullest possible breath" that would include inspiring as much extra as possible, plus the normal breath volume, plus exhaling the last little bit you can:
IRV + Tidal Volume + ERV
There's still a little bit of residual air left over (RV), though, so:
IRV + Tidal Volume + ERV + RV
gives you the total capacity.


text:
What does γ mean before a gene name?
I am reading the following paper and I have come across the following statement:

It has been demonstrated that the phosphorylation of histone
H2AX-Ser139 to form γH2AX.

I am not sure what the γ before the gene name H2AX means. Is γ used to indicate that H2AX is phosphorylated? Any insights are appreciated.

Yes, in this context $\gamma$ indicates phosphorylation. See e.g. "The phosphorylated form of H2AX is called $\gamma$-H2AX [18, 19]." from here, and references therein.
I am unsure of the exact basis of this, but I believe that it is because the gamma phosphate group of a nucleotide triphosphate is the one that is generally used by kinases to phosphorylate other functional groups. SEE UPDATE for derivation.
Other notations such as the $p$ prefix are more readable to me, but the usage appears to be cultural and somewhat field-specific.
Update
In response to @MattDMO comment, I read further and found that the terminology derives from this paper. They don't directly explain the terminology, but in context it's pretty clear:

At the maximum, approximately 1% of the H2AX becomes $\gamma$-phosphorylated per Gy of ionizing radiation.

In mammals, the serine in this motif is residue 139, the site of γ-phosphorylation.

When mammalian cell cultures are exposed to ionizing radiation and the acid-soluble nuclear proteins are analyzed on two-dimensional AUT-AUC gels, novel components that will be referred to as $\gamma$ (Fig. 1, A and B) are found in the H2A region of these gels.

It appears that the name probably derives from an observation that was just "whatever in this 2-D gel is $\gamma$-P32 labeled when we induce DSBs when $\gamma$-P32 ATP is present."
@MattDMO also points out that the irradiation that induces the gamma component in this context is gamma radiation. So it's all a bit of a muddle, it could also be that.

I've never heard of $\gamma$ being used to denote phosphorylation except in the case of H2AX. I suspect the nomenclature derives from its discovery, probably as multiple isoforms by some sort of chromatography or gel electrophoresis, and the phosphorylated form was the third one named ($\gamma$ is the third letter of the Greek alphabet) or the third band/signal observed. This is just a guess, but an educated one. I don't think it has anything to do with the $\gamma-PO_4$ group.

@MattDMo Turns out we're both right- it is because of the $\gamma$ phosphate, but it is also H2AX-specific, if I read the paper that first described this correctly. Editing answer.

Thanks for the link to the paper, it's been helpful. After reading parts of it, especially the 4th paragraph of the results section, I think they called the novel components $\gamma$ because they appeared after ionizing $\gamma$ irradiation, which is the primary form of radiation emitted by $^{137}Cs$, which was the rad source used in these experiments. So, $\gamma$-H2AX is a phosphorylated form of H2AX observed after exposure to $\gamma$-irradiation. Actually, it's probably both $\gamma$ irradiation and $\gamma$-ATP.

Hm. a lot of gammas here...

Which is probably what the grad student doing the experiments thought when s/he was labeling the autoradiograms of their gels.

@MattDMo tNo i was wrong! P32 is a beta emitter. sigh of relief

You're correct: the gamma denotes phosphorylation, as explained and used in this paper's abstract

H2AX is a variant of the H2A protein family, which is a component of the histone octomer in nucleosomes. It is phosphorylated by kinases such as ataxia telangiectasia mutated (ATM) and ATM-Rad3-related (ATR) in the PI3K pathway. This newly phosphorylated protein, gamma-H2AX, is the first step in recruiting and localizing DNA repair proteins.


text:
Examples of real biological applications of the Keller-Segel system
I am working on a model of aggregation behavior modeled with the Keller-Segel PDE system. I recently gave a talk on this and was asked what other examples there were of the Keller-Segel system. Since this is an obvious question, I was embarrassed to have no example other than my model and the aggregation of cellular slime molds (the application for which the Keller-Segel model was originally developed). So I did some googling and came up with bupkis. There are hundreds of papers about the system by mathematicians, but I failed to find any other biological examples.
What about it? Is the Keller-Segel model mostly just a mathematical curiosity, or is it a model with many real applications to biology?

This looks like a good starting place: Painter, K. J. “Mathematical Models for Chemotaxis and Their Applications in Self-Organisation Phenomena,” June 22, 2018. https://arxiv.org/abs/1806.08627v2 (published in Journal of Theoretical Biology, 2019). Lists examples from Dictyostelium (of course), bacterial aggregation, development, physiology and disease, ecology, social science.

In this review, I evaluate the use of PKS [Patlak-Keller-Segel] models in describing chemotaxis (and other taxes), particularly focussing on examples of pattern formation/self-organisation. I do not review the numerous excellent studies
that primarily concentrate on their mathematical analysis: a number of reviews already cover these aspects in depth [...] Next, the fundamental modelling that led to (1) is reviewed and an overview given regarding its patterning behaviour. I then proceed field-by-field, beginning with its motivations in microbiology and sweeping across areas including developmental biology, immunology, cancer, ecology and the social sciences. For each case, the historical justification for chemotaxis is described and models are discussed; a compendium
that contains many of these models is provided in the Appendix. Finally, I demonstrate how PKS models can continue to penetrate new areas, via a novel application to explain clique formation in research.

Here's a working link to the J Theoret Biol paper : https://doi.org/10.1016/j.jtbi.2018.06.019 .


text:
Is there a color changing organism that is by default translucent or otherwise "colorless"?
To illustrate a point I am trying to make in a paper I am writing it would be helpful to have an example of an organism that by default has "no color" but which can adopt the color of something in its environment (e.g., through some chameleon-like color changing ability or something like the food-derived pigments that give flamingos their pink color). I could just make up such an organism for illustrative purposes, but it would be nice if there were a non-contrived example.
By "no color"/"colorless" I'm thinking of something like translucency/transparency, but I can be flexible about the exact meaning so long as it can plausibly be construed as involving a lack of color.
Is there an animal that by default is colorless/transparent/translucent but which has the ability to take on colors present in its environment?

If you broaden the context to include all organisms then many microbes can be good candidates

@another'Homosapien' that works for me! I only specified animals because that’s what immediately sprung to mind. Any organism that doesn’t require an exhaustive description to explain its color properties semi-evocatively should work. I’ll broaden the question, thanks!

Maybe someone will have answers and I'd be curious to see examples, but I'm not sure such organisms are very realistic. Organisms typically change colors by playing on the pigments they display to the outside... But to be translucent they cannot have any pigments either outside OR inside. This organism would have to change colors based on another mechanism (like diffraction; not impossible but don't know examples), or change color by creating pigments on the fly from colorless precursors (which sounds slow), or eat colored foods (most likely mechanism to my mind but again, idk about examples).

@Oosaka when you talk about “no pigments inside” do you have in mind the way that some fish are translucent except for, e.g., certain organs? Or something a bit weirder (to me, at least) where the outside of the skin is translucent but the majority of the interior is opaque, due to something like pigmentation in an inner layer of skin or bodily fluids? I think “mostly colorless” organisms with colored organs would still work for my purposes, but an organism with, e.g., transparent skin but mostly opaque and colored interiors would not work.

@Dennis that's what I mean, to be translucent an organism has to be translucent all the way through. There is no such thing as "translucent on the outside and opaque on the inside", that's just "opaque" (I mean, if you go that way the very outer layer of our skin is translucent!). So for an organism to be translucent but change color, it needs to 1) contain pigments (because changing the pigments changes the color) and 2) not contain pigments (because pigments by definition are not translucent). If you allow isolated opaque organs that can be another workaround I guess.

Now that you say that any organism will fit just fine, there are a ton of microbes that can be good candidates. Instead of trying to list them here, I think it's better to actually have a look at some like this (instagram link; the account posts a lot of photos/videos of microbes, and the linked post shows a Rotifer with blue blobs from the algae it just ate, just mentioned that to give you some examples, not for advertisement :)


text:
When there is incomplete dominance of one allele, is one allele still considered recessive?
When you have incomplete dominance between two alleles of a gene (say, on two different tail lengths blending into an intermediate tail length or two rose colours blending together), can you still call an allele recessive or dominant? If so, how would you tell which to call "dominant" and which to call "recessive"? Do you compare protein expression or measure the difference between the phenotypes of the two homozygous variants or something?
This is purely a terminology question -- I'm aware that the distinction might be a bit meaningless in practice. The closest I could find to an answer is this question, though I'm unsure whether they're measuring tail length to determine the difference between codominance and partial dominance or what.

No - if we have a phenotype, in your case the tail, which we can measure and treat as a numeric variable, and if a heterozygote's phenotype is exactly half-way between that of the two homozygotes, the phenotype is considered not to exhibit. Dominance exists only when the heterozygote's phenotypic value lies closer to one homozygote than the other.


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Is fucus filamentous or colonial algea?
Am a bit new to biology SE. My question is wether fucus is filamentous or collonial form of algea?Does a form of algea have to be collonial or fillamentous or it can be something else?
https://en.m.wikipedia.org/wiki/Fucus_vesiculosus

I would suggest looking up some basic sources on types of algae. For example, that source that I link to says this:

Algae vary considerably in size, shape, and growth form.
They can be:

Single celled
Many celled - either colonially or as filaments of cells; or
Elaborate plant bodies with differentiated cell types

In this case, I believe that Fucus would be in the third category ("elaborate plant bodies").
But note that these are informal categories, they don't really correspond to taxonomy or evolution or anything.


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Destroying RNA of viruses using Ribonuclease
I wonder if it is possible to design some Ribonuclease to destroy only specific RNAs (like those of viruses). Then, if virus tries to infect, his RNA will be cut.
Or, instead of creating Ribonuclease, we can design suitable mRNA and let the cell do the rest.
Is this possible?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, this site is for questions and answers not discussions. We also expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). See also this sites criteria for "homework", which can apply to questions even if they are not assigned as homework. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

The human body basically does this on its own. We express various RNAses, some of which appear to have specific antiviral or bactericidal roles.
(This appears to be due to both RNAse activity and to biochemical properties of the proteins independent of RNA digestion)

How about creating some drug based on this technique? Could this help fight the infection?

@Dzery I would say rather that it does help fight infections, as part of normal human biology. And sure, you could package these RNAses up into pills or in an aerosol spray or something. I don't know of any specific examples though.

that's the point - maybe it's a way to create a new type of drug?

CRISPR/cas is used for exactly this purpose in bacteria.
The CRISPR array contains sequences from bacteriophages, which will prime various cas-nucleases to cleave either the DNA or the RNA of the virus.


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Can someone identify this worm?
The first time I saw these was in an old cooler full of water by my shed, there were 3 of them about 2 weeks ago. Now tonight I found one crawling up my door. Can anyone offer some insight? I have dogs and I'm horrified that it may be some kind of parasitic worm that they can contract.
This was observed in northwestern Pennsylvania, US. Rainy, cool fall weather currently, as it's the end of October. They're about 2 inches long. Very thin, blackish red in color and extra wiggly.

Have you never before seen an earthworm?

Yes, an earth worm has that bump thing on it. They're generally fatter.

There are several species of earthworms. For some of them the "bump" is less pronounced and some are slimmer. Everything you report (occurrence after heavy rain) fits earthworms. The picture looks like one too. But photo quality isn't sufficient to be 100 % sure.

The "bump" on an earthworm (i.e., a worm species of the order Opisthopora) is a clitellum. Clitella are only visible on earthworms when they're sexually mature [Sources: 1, 2, 3]. So the absence of a clitellum does not preclude your specimen from being a member of this order.
The species in your photo is almost undoubtedly some species of earthworm. Without clearer images or more detail, I can't imagine someone taking the time to try to ID to species.
There are many species of earthworms present in Pennsylvania (though likely none of them are native to the US: see here). Keep an eye out for a recent invader, the "Asian Jumping Worm" [read more].


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Why is a solution of cesium chloride used in Meselson & Stahl's DNA replication experiment?
Centrifugation involves separating particles of different sizes, masses, density and etc.
In the experiment, the DNA macromolecules are suspended in a solution of cesium chloride gradient and then centrifuged.
Why is cesium chloride needed? Considering the possible DNA produced in the experiment will be the same size but of different mass resulting in different density, DNA will be separated based on their density by virtue (without the need for cesium chloride) under the influence of a centrifugal force.
I noticed someone asked the same question on Khanacademy but there was no answer for it. Other websites I found doesn't seem to offer a valid answer e.g. here which says " the DNA comes to equilibrium in the gradient where its density equals the density of the surrounding CsCl" which I think doesn't really matter when considering the argument I proposed above in the third paragraph.
Here is a diagram of the experiment for reference. Thanks in advance.

In saline solution all the DNA ends up at the very bottom.
Under centrifugation, the Caesium Chloride solution forms a density gradient, each DNA rises or sinks to the equivalent density.
The same procedure is used with Sucrose solutions for other separations.

Thanks for the input. May I ask why is it that in saline solution all the DNA ends up at the very bottom? Assuming the saline premise is true, then can distilled water be used instead?

With distilled water the DNA will sink even faster.

The differences in sedimentation speed between the differently marked DNA molecules are not lare enough to allow separation in a low-density medium such as saline, or distilled water. As mentioned by @Polypipe Wrangler DNA will always completely sediment to the bottom of the tube.
To improve separation a so called isopycnic centrifugation is performed. Basically, CsCl is used to form a gradient of increasing density from top to bottom during centrifugation. The DNA molecules will float to the density zones that match their own density. This allows separating similar molecules with small differences in density.


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Reproduction in animals
Humans have acquired knowledge about their environment through many observations. Today, humans have wide variety of resources to gain knowledge about reproduction in human beings and other reproductive processes. This knowledge does not come from genes. But on the other hand the animals example pig don't have any kind of resources which teach them about reproduction, still they can perform their reproductive processes. Even an isolated mice can do so if a mate comes in his vicinity.
But the isolated mice doesn't have any knowledge about reproduction then how can they perform it?
https://animals.mom.com/how-a-pig-reproduce-2607021.html
https://oacu.oir.nih.gov/sites/default/files/uploads/training-resources/mouserepro.pdf

TL;DR: instinct. Even humans don't require any knowledge to reproduce. If you just do together what feels good, there is a good chance that it ends with sex. Behavior of most mammals is much more strongly triggered by pheromones than that of homo sapiens. You probably should start with reading about the vomeronasal organ and the response triggered in rodent brains by reception of sex pheromones.

Animals don't have any great knowledge about the processes of digestion, yet they manage to eat.  Consider that if animals (or plants, bacteria, &c) had to be taught how to reproduce, and understand all the biological details, they would never manage to reproduce at all :-)

Arguably, humans, upon learning in detail about reproductive processes and their control, seem to tend toward avoiding those processes reaching their biological ends rather than seeking them out.

Instinct
What is instinct, instinct is any behavior which did not require cognition or consciousness to perform or innate behavior that does not require learning.
BY the nature of building a brain it is possible to build in behavior by laying out neurons and connections in preset patterns. Thus some behavior can be encoded genetically.
Simple examples of Instincts include reflexes and fixed action patterns, but there is a whole spectrum of behaviors ranging from pure instinct to pure learned and everything in between.


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Water snake with a yellow criss-cross on a black background?
I saw a 60 cm long, very skinny (~15 mm diameter), black with yellow diagonal criss-cross patterned snake swimming in a pond this afternoon in northern Taiwan.
It was swimming near the top of the water and I could see it very clearly, but as soon as it noticed me it dropped most of its body to the bottom of this shallow pond and just kept part of its head above water, so the photos are not very clear.
I tried to wait for it to continue but something else disturbed it and it took off.
Is it possible to identify this snake or at least narrow down the options?
First image is cropped from the large image. I have played with contrast, color and sharpness to make the pattern and color look most like what I remember before it dropped its body lower into the murky water.

sketch of pattern as I remember it

The useful relevant facts are:
Present in freshwater
Active in daytime
Yellow patterning
(photos from wikipedia)
I used the site
www.snakesoftaiwan.com/
This gives most likely candidates of:
Rhabdophis tigrinis subspecies formosanus, the Tiger Keelback.
Grows to 0.6 to 1.0 metres long.

more photos (cannot embed due to copyright) at http://m.blog.sina.com.tw/d100vs/article.php?pbgid=30839&entryid=404413
and
Fowlea piscator  the Checkered Keelback or Asiatic Water Snake. growing 1-2 metres long.

more photos at http://m.blog.sina.com.tw/d100vs/article.php?pbgid=30839&entryid=342476

These are wonderful sites, thank you very much! Yes both of these work per the information in my question and its less-than-optimial photos, and both are compatible with what I recall. I'll have to now look for a copy of A Cobra Hijacked My Camera Bag! Snakes and Stories from Taiwan by Hans Breuer as mentioned in the site. I did surprise a 2m black Taiwan cobra myself several years ago; It was pretty close and I completely froze, never thought about reaching for my camera.


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Would there be more amino acid residues in the extracellular or intercellular space?
I am working on a bioinformatics project with HMMs and want to write some initiation probabilities for the location of amino acid residues. I know for different transmembrane proteins there will be different cases, but, in general, which regions of the protein would correspond to more AA residues: intracellular or extracellular? Or is there no general pattern?

This would probably vary a lot with cell type, is there a certain type you're interested in?

Not really, I was wondering more in general terms. It makes sense that there is a lot of variety.

Yes ,there are some patterns.
First you have to determine which group of membrane proteins you're talking about.
According to Molecular Cell Biology Lodish et al 8th ed chapter 13, there are 6 types of ER membrane proteins ( and therefore in the cell membrane)
The 6 types are type 1,type 2 ,type 3 , type 4,Tail anchored proteins ,GPI anchored proteins.
Nearly all AA residues in type 3 or  the tail-anchored type are located in the cytosolic side of the membrane ( their difference is in their N/C terminus orientation) whereas GPI anchored type has almost its entire AA residues in the exoplasmic side.
For other types there may not be a general pattern.
See E. Hartmann et al., 1989, P. Natl. Acad. Sci. USA
86:5786, and C. A. Brown and S. D. Black, 1989, J. Biol. Chem. 264:4442.
By the way , you can also think of it in another way. Antigens , Hormone Receptors , Structral proteins in exoplasmic leaflet of membrane usually have more AA in the exoplasmic side.


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What is mitochondrial run length?
I am reading the following journal paper and I have come across the following statement:

Overexpression of GSK-3β significantly increases motile mitochondria
in a Tau protein-dependent manner. However, GSK-3β does not alter
mitochondrial velocity or mitochondrial run length.

I understand what mitochondrial velocity is but I am not sure what exactly is meant by mitochondrial run length. Any insights are appreciated.

Run length means how far the mitochondria move, each time they move.
The article this references is:
"GSK3β Is Involved in the Relief of Mitochondria Pausing in a Tau-Dependent Manner".
This article has a figure showing the distances in micrometers, although I have trouble working out interpreting the error bars on the graph to see if the distances ("run length") are really different.


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Questions about Cohesin - what does the ATPase domain do, and any suggested PDBs to look at?
I've been reading about cohesin lately, and I'm confused about the head subunit interactions.  I've read a few papers, and also found this nice figure from wiki that demonstrates the crux of my question (note: SMC here corresponds to Cohesin, or am I mistaken?  I'm pretty sure this is correct, or pretty much correct):
From reading around, I'm aware generally the head subunit is an ATPase, yet from this diagram (and from the typical putative "use" of Cohesin in TAD maintenance), I'm not sure what exactly is the ATPase motif so useful for, it seems that the ATP is sort of "glueing" the the two head domains together, but that seems opposite of what ATPase would typically do, ie catalyze ATP -> ADP.  This makes me think I'm just misunderstanding something, and wondering what is the function of the Walker A/B ATPase motif.
Also, I'm wondering if there are any nice PDB files that show a cohesin loop, or elsewise are generally the most instructive about Cohesin.  I've searched through a few, but would like more informed advice about some good structures, and maybe why they are nice.

This article :
Prakash Arumugam, Stephan Gruber, Koichi Tanaka, Christian H. Haering, Karl Mechtler, Kim Nasmyth,
"ATP Hydrolysis Is Required for Cohesin's Association with Chromosomes",
Current Biology,
Volume 13, Issue 22,
2003,
at
https://www.sciencedirect.com/science/article/pii/S0960982203008042
Their conclusion is:
"Conclusions: Cohesin complexes whose heads have been connected by Scc1 must hydrolyze ATP in order to associate stably with chromosomes. If chromosomal association is mediated by the topological entrapment of DNA inside cohesin's ring, then ATP hydrolysis may be responsible for creating a gate through which DNA can enter. We suggest that ATP hydrolysis drives the temporary disconnection of Scc1 from Smc heads that are needed for DNA entrapment and that this process is promoted by Scc2/4."


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Need help interpreting Western blot data
So the paper I am reading (here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7094582/) uses densitometric units to quantify the western blots.
The authors mentioned that the unphosphorylated proteins were used as loading controls, and their quantities are represented by the densitometric graphs for each corresponding figure, but protein activity is measured by their phosphorylated counterparts which I believe is represented by the densitometric graph on the right of each corresponding figure.
Questions:

Did I interpret that correctly?
What exactly are loading controls?
I am trying to use these data for parameter estimation purposes. Is it possible to find the basal mass quantity of a particular protein?

There are several questions here, note that we usually ask for a single focused question.

Answers to each question:

Approximately, yes. In this case, phosphorylated Akt (p-Akt) is supposed to be the active form of the enzyme that goes around the cell doing its job, whereas non-phosphorylated Akt doesn't have activity that they are interested in. The authors do show that targets of Akt show characteristics of Akt activity when Akt is phosphorylated (Fig 2B, 2C).

Note that densitometry is just a way of measuring the intensity of some bands on immunoblots (westerns). In this case, it is normalized by the loading control (non-phospho Akt). So you could interpret the densitometry plots as showing the proportion of Akt that is phosphorylated. It is a little confusing because they subsequently normalize them to a specific timepoint. From the methods:

The results were quantitated by densitometric analysis (ImageQuant, Molecular Dynamics and PDSI, GE Healthcare). The ratio of phosphoprotein to its respective internal control was normalized to the control level at 0.5 h, arbitrarily set to 1.

Loading controls indicate how much protein of interest is present. For example, 1% of 100mg of protein is the same as 10% of 10mg protein (each is 1 mg). However the interpretation of 1% vs. 10% may be quite large. So if what you are interested in is a percentage or proportion, you need to have a loading control to allow unbiased comparison or normalization.

I don't really know what "basal mass quantity" means, but you could look into the molecular weight of proteins (usually measured in kilodaltons). For example the molecular weight of Akt is ~55kda. You can compute this from the protein sequence by adding up the weights of all the amino acids.


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How to estimate oxygen consumption of an average human during different activities?
I've tried to find some resource on the internet but had little luck. I'm looking to see if there's any data on average oxygen consumption of average to well trained humans during different activities.
Specifically how much more oxygen does a human consume when panicked/under pressure in comparison to other activities such as cooking, climbing etc. Even better would be if I had a formula where I could plug in weight, height, gender and receive a percentage of how much more O2 is consumed under stress/panic vs. normal functioning. Any information would be much appreciated, please include sources where possible.
NOTE: With "panicked" I mean in the state of fearing for ones safety and being in a life threatening situation with the associated hyperventilation etc.

https://i.redd.it/expf3tuhr2g01.png panicked is a vague measure, ranging from momentarily startled to buried in an avalanche.

Yeah panicked is maybe too broad, I mean like you're in a life or death situation

may be helpful. https://onlinelibrary.wiley.com/doi/abs/10.1111/1469-8986.3860961

So “average to well trained” is the average overweight shopper to the well trained sprint cyclist?


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Meaning of some unit of measurement of kinase activity
I need help knowing what $cpm \times 10^3$ means in Figure 4(C) of this paper (https://www.sciencedirect.com/science/article/pii/S0022202X15323149#f0010). It appears to be a unit of kinase activity.

It is not a specific unit of kinase activity, rather a general approach taken for following reactions where there is no change of colour. The abbreviation cpm stands for counts per minute and is a measure of radioactivity.
In this particular example a radioactive phosphate has been incorporated in the ATP of the protein kinase assay. If the protein kinase is active with the substrate, the phosphate will be transferred from the ATP to the substrate peptide/protein. If the sample mix is loaded on a SDS-PAGE gel, a scintillation counter can be used to measure the radioactivity of each band and one will be able to  show how active the protein kinase has been in phosphorylating it's substrate.

Great answer! Is there a way to approximate the mass of the active enzyme based on cpm? Thank you very much!

As a follow-up, what exactly is being counted per minute? Thanks!

Each count is one ionisation event at the detector. Assuming an excess of substrate, I guess you could use it for concentration determination of you had a standard curve to compare to.

Are these assays called "Radioligand binding assay"?

I think it would be clearer to call it a radioactive protein kinase assay, radioligand binding assay to me is more about protein-protein interactions

or "Radiobinding assay" as described here? https://en.wikipedia.org/wiki/Radiobinding_assay


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Some related questions about DNA differences in a single organism

If you took a DNA sample from someone's brain and that same persons liver at more or less the same time, would that DNA - all else being equal (e.g. no mutations from radiation) - be exactly the same?

If you took a DNA sample from an embryo, and then that embryo went on to be born, live a long life for 80 years and become an old man/woman; if you were to then take another DNA sample of this person, would that sample be exactly the same as the one which you took when he/she was in the womb? (again, all things being equal - so dismissing mutations due to radiation for example).

I don't have much of a scientific background, and am seeking your expertise so that I can consider it's relevance for both the buddhist doctrine of impermanence and christian convictions about souls, personhood, abortion etc.

What do you mean by 'exactly the same'? You should be more specific. You could be talking about the same genes, the same variants, the same heterochromatin configuration, 3-d structure, number of repeats, duplications ....

In addition to the above, what do you mean by "no mutations from radiation etc"? Do you understand that mutations accumulate due to errors in DNA replication?

No. even if you exclude the changes in DNA sequences that originate from mismatch errors in DNA replication, mutation etc.
Because
1.As a person gets old , the short repeat sequences in the telomere of a chromosome  in each cell may be lost or be reduced in amounts leading to a sequence difference.Moreover this changes in telomere sequences may cause cancer/cell apoptosis .
Telomere
2.Do not forget transposons (consisted of DNA transposons and retrotransposons). They change their position in genome and multiply their DNA over time.So they also lead to sequence differences in a person(comparing his/her younger and older DNA)
Transposons
These were the answers to question 2 .You can also think that there might be a slight difference in DNA of two different tissue of the same individual (because of the tolemere and transposons)
As a zygote starts to multiply itself ,slight changes of sequence will happen to the offspring cells .After a dozens of cell division you may encounter a little deviation compared to the original zygote sequence.

+1, but it might help to cite the mutation rate, or at the very least something else.  An overall sense of the scale of the mutation variation within an organism would improve this answer

shorter telomeres is one reason dolly died so young, she was cloned from differentiated somatic cells, so she started with shorter telomeres.


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What is the significance of running an uncut plasmid on electrophoresis gel?
What is the significance of running an uncut plasmid on electrophoresis gel?
In this case we are talking about inserting a gene into plasmid, which then goes under PCR and then electrophoresis.

So you clone you DNA, make a PCR and then run the plasmid on a gel? This doesn`t make sense, can you post your complete protocol?

It is used to determine whether the unused/excess amount of plasmid has contaminated the  final solution of the desired recombinant DNA  or not.
Electrophoresis is performed on the "Blank"(uncut) plasmid to define its bands.If the electrophoresis result contains the bands of both "blank" and recombinant DNA , it shows that your solution is not 100% pure.


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Any clue on what these tiny white bugs may be?
I would like to know what the bugs in the following pictures are, they are absolutely tiny, i would say 0.5mm at most, i can't get a really sharp picture, as they seem like to hang out in the dust on furniture (which messes with the focus) and to dislike strong lighting.
If this may help i'm located in North-Eastern Italy, i first noticed them last winter, in a home where i struggled with mold on walls, and i have moved since then (along with my furniture). During all of summer in the new home i haven't noticed them around, so i thought that they may have disliked the new "habitat", but recently when the climate started to get colder and moist i've been seeing some of them again. I see them in counts of approximately 10 - 20 on a surface, so i would assume that their total population in my room would reach the thousands.
Other than in dust on my furniture i see that they like particularly boxes aswell, my assumption would be that they're some kind of acari given their almost unnoticeable size, i've also seen someone talk about dust mites. I've also found some deposit of yellowish dust in strange formations that i would assume may be eggs or feces, i'll add the picture below.
I don't believe them to be harmfull, i'm just worried that they may be eating away at my furniture or damaging my electronics with their waste. I also believe to have seen tiny strings of material similar to spider webs around, that's why i believe them to be related to acari or some tipe of spider, rather than insects, although i couldn't actually count their appendices, they look almost "hairy" in a way. Also the smaller ones look whiteish-transparent while the biggest ones are beige as far as i can see.
EDIT: i have looked up and bought a macro lens that can be attached to the phohe's camera, here's the new pictures i got, although i'll have to wait to be able to take some pictures in natural lighting as these are overexposed