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Does rainwater contain many fewer micro-organisms than river water?
From watching many documentaries on micro-organisms, I can tell water typically contains quite a lot of them.
But what about rainwater? (before it hits the ground). I know nothing about any micro-organisms that live in the sky or clouds. Does rainwater contain fewer, and less dangerous, micro-organisms?

If my response answers your question, please accept it. Otherwise, please leave a comment about how I could further answer your question. Thanks.

@theforestecologist It's almost a complete answer. Your last link says 80,000 bacteria per milliliter of riverwater. But I could not find a number per mL for rainwater (rain before it hits the ground).

Found a study for you and have updated my answer. Please accept if all is ok.

Who voted to close this as "homework??" 1. This question was not easy to answer, so it is not trivial (i.e., even after an initial search, very little reputable sources can be found). 2. it's already well-received with a well-received answer. I vote to keep open.

There seems to be a basic problem with the question, which is that not all rivers are alike.  Indeed, I would think that the number of microorganisms varies greatly within a single river, e.g. the Mississippi/Missouri near its headwaters, and just downstream of New Orleans.

typically something like a million times less. only think that filters water on earth is sand percolation, and the UV status of the atmosphere makes it pretty hostile to animals. it's a big UV and mechanical filter up there.

According to a number of citations listed on Kenyon College's MicrobeWiki, rain can contain microorganisms via a process called "bioprecipitation."

Essentially, microorganisms, dust and other small particles get swept up into the atmosphere, and cold temperatures cause atmospheric water vapor to freeze around the organism/particle. Once the ice-covered particle picks up enough mass, it falls from the sky and reaches earth as precipitation (likely rain if temperature is warm enough).

Here is a schematic from Wright et al. (2104) of how an increase in relative humidity, due to a cold-frontal passage, can trigger biological ice nuclei release followed by seeding of the frontal cloud band with the lofted ice nuclei:

 So How Many (and Which) Bacteria Are in Rain?
Which Bacteria?
According to Wikipedia:

The ice-nucleating bacteria currently known are mostly plant pathogens

According to MicrobeWiki, these include:

Exserohilum turcicum, Pseudomonas viridiflava, Pseudomonas fluorescens, Pantoea agglomerans and Xanthomonas campestris.
The most well described organism that demonstrates ice nucleation is Pseudomonas syringae, which was determined to specifically supply a source of ice nucleators by Leroy Maki in the 1970’s.

According to work by Natasha DeLeon-Rodriguez, Athanasios Nenes, et al. (full paper here and NPR story here), 100s of species of bacteria exist in the clouds and it's not uncommon to find almost 20 species in any given sample (60% of which on average were still living).

Here's a graph showing the relative amounts of various taxa found in their samples:

How Many Bacteria?
DeLeon-Rodriguez et al's (2013) results revealed an average bacterial concentration of somewhere between $5.1 × 10^3 cells /  m^3$ to $1.5 × 10^5 cells /  m^3$ of cloud (depending on method of counting).

Quickly doing some math (1 m$^3$ = 1000000 mL), their results suggest that, on average across a cubic meter of cloud, there is <1 bacteria / mL of moisture.

According to research by Joly et al (2014) that specifically examined ice nuclei (or "IN"):

there were 0 to ~220 biological IN/mL of cloud water (i.e. 0-22 per m$^3$ of cloudy air based on cloud liquid water content estimates) and these represented 65% to 100% of the total IN.

Comparatively, river water (and drinking water) can contain a lot more bacteria (i.e., 80,000 bacteria / mL) and other microorganisms.
However, this disparity is not always so great, especially if we focus at comparing counts of only one or a few species (and not total bacterial counts).

Based on research of a tropical reservoir by Kaushik et al (2014):

Levels of E. coli were found to be in the range of 0 CFU/100 mL – 75 CFU/100 mL for the rainwater, and were 10–94 CFU/100 mL for the reservoir water.

Note: CFU = colony forming units. (estimation of microbial numbers by CFU will, in most cases, undercount the number of living cells. [wikipedia]).

Citations

 DeLeon-Rodriguez, N., Lathem, T. L., Rodriguez-R, L. M., Barazesh, J. M., Anderson, B. E., Beyersdorf, A. J., ... & Konstantinidis, K. T. (2013). Microbiome of the upper troposphere: species composition and prevalence, effects of tropical storms, and atmospheric implications. Proceedings of the National Academy of Sciences 110(7), 2575-2580.
 Joly, M., Amato, P., Deguillaume, L., Monier, M., Hoose, C., and Delort, A. (2014). Direct Quantification of Total and Biological Ice Nuclei in Cloud Water. Atmos. Chem. Phys. Discuss 14(3):3707–3731.
 Kaushik R, Balasubramanian R, Dunstan H (2014) Microbial Quality and Phylogenetic Diversity of Fresh Rainwater and Tropical Freshwater Reservoir. PLoS ONE 9(6): e100737. doi:10.1371/journal.pone.0100737
 Wright, T. P., Hader, J. D., McMeeking, G. R., & Petters, M. D. (2014). High relative humidity as a trigger for widespread release of ice nuclei. Aerosol Science and Technology 48(11), i-v.
For further reading, also see the associated citations from MicrobeWiki.
I think you would also benefit by perusing the works of Pierre Amato.

A fairly recent study examined this as well: Microbiome of the upper troposphere: Species composition and prevalence, effects of tropical storms, and atmospheric implications

You cite two wildly disparate figures for bacteria in river/drinking water, the latter of which seems to be relatively close to the number in rain water. Is one more trustworthy than the other?

Two things to note: 1. One source presents "bacteria / mL" while the other is CFU (colony forming units) -- estimation of microbial numbers by CFU will, in most cases, undercount the number of living cells [wikipedia]. 2. Regardless, the Kaushik study looks at ONLY E coli in a reservoir (where enterobacteria such as E coli are typically managed to stay very low). I guess I could edit the answer to better contextualize all of this...

One source is talking about only E. Coli, while another source says 80k bacteria (any bacteria). They are not really comparing apples to apples. BTW in looking at the new link, I saw this: "Both rainwater and reservoir water samples were collected from the sampling locations at regular weekly intervals and within 24 h of rainfall events." This brings up a good question, namely how far apart rainfall events should be to avoid contaminating riverwater with rainwater.

@DrZ214 I've already addressed that in the above comment and in my answer edits. Your "This brings up a good question..." statement should be asked as a new question and is not relevant here.

Ofc it's relevant here. We do not want cross-contamination of riverwater with rainwater because we do not want to add the number of MOs in rainwater to the number in riverwater. Nevertheless, this latest edit answers the OP. Looks like riverwater has over 300x more MOs than rainwater.


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Relation between bases while changing into a SNP
Is there any relation or influence among the bases (A, C, G, T) while they are converted into a snp? Such as, is A converted into T, similar to converted into C or G? Or is this all random and no way to evaluate?

Interesting question. You can start here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1790724/ and here: http://www.nature.com/nature/journal/v505/n7485/full/nature12861.html I may convert this into answer later, time allowing.

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Quantity of genetic material in humans vs nonhuman animals
I am using a simple, rigorous definition of genetic material- the total number of base pairs in all of the coding regions of a species' genome.
For example, take human genome H and snake genome S. H has some genetic sequence of 5 bp. S has an identical sequence followed by a different sequence of length 2. Thus H and S have 5 bp of genetic material shared with humans, and 2 bp of genetic material not shared with humans.
We can take the set of genetic material in all studied animal species, and count the number of unique sequences in this set. Call this variable A.
What percent of A consists of sequences shared with humans?
Certainly not all species' genomes are documented, so this number will be biased toward a high value. It would also be too much work for anyone here to compute such a value, even though the data is well cataloged. But I am interested in knowing if anyone has performed a similar calculation and what the results were.

There have been plenty of calculations of genetic similarity between all sorts of organisms. Are you unaware of those, or does your question and the description of what you want calculated specifically exclude them ?

Nevermind, I understand your question now. There is still an issue with it though: when you describe your calculations it's clearly a difference in raw base pair sequences, however you then ask "what percentage of A consists of genes"; differences in genes and in nucleotide sequences are two very different things. Did you mean that switch, and if not is it sequences or genes you're asking about ?

I've edited your question slightly to make it clearer, hopefully the meaning of your question wasn't lost.

@DapperLad Please do not spam! This comes in reaction to your, now rather obvious, recent spam where you make the question and the answer and then delete both once I highlighted the spam. Such behaviour is a bit of an insult to the user of this site and could result in your account being blocked.

OK, that's a very confusing question but I think I've figured it out (uncertainty about "genes" vs "genetic material" notwithstanding).
I am almost certain that this calculation has not been made, for these reasons: as you say we don't have nearly enough information to make the calculations, even a partial calculations would be an enormous amount of work, which raises the question of what the purpose of this work would be, and I don't really see a use biologists might have for this number.
The reason it is an enormous amount of work is that most comparative genomic studies are done between a few species; to put all that information together you'd have to trawl through all those different studies. This is more feasible now with huge genomic databases, but it leads to the big issue: you can't just add all the genes in the different organisms, because most of those genes are shared between them. The closest thing I've found to a calculation of your "A" number is this paper:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4466264/
If that were the total number of distinct genes in the biosphere then you could approximate the percentage you're looking for by dividing the total number of genes humans have by the total number of genes in the biosphere. Or you could get a better approximation by substracting from the total number of human genes the number of genes humans don't share with chimpanzees; I doubt it would change the number much though.
However that paper has an estimation of the total amount of DNA in the biosphere, a completely different issue from the number of genes, which is itself completely different from the number of distinct genes, which would itself rely on completely arbitrary distinctions because almost all genes vary between species, but if we count those small variations as "different genes" then obviously none of them are shared with humans at all, but there isn't a sharp line between "genes with different sequences that code for the same protein", "genes with different sequences that code for basically the same protein", and "genes with different sequences that code for similar but different proteins". The question is a bit easier with genetic material, but it's still clear that cross-comparing ALL genomes we have to list ALL of the distinct sequences is a computationally monumental task. And we're already using those computers for more immediately useful genomics analyses.
As for the issue of biologists having no use for the number, I simply don't see how knowing that number can increase our understanding about life, animals or humans compared to things we already know or are investigating, such as what genes humans have, what genes exist out there in the world, what relationship any specific human gene has to the genes of other relevant animals, etc.
I would like to know more about why you're interested in this number. You must certainly have a question in mind that having this number would help answer, and if we know that question it might be that there are other numbers, that have actually been calculated, that could inform it.
EDIT: Having said that it occurred to me you could still find things like the total number of distinct genes that have been identified by biologists in all living things, since that's more about counting the entries in various gene databases (this could also make a gene-based calculation actually easier than a sequence-based one). This would give at least bounds on the number you're looking for. In that spirit I found this paper about the total number of distinct genes in human gut bacteria:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0006074
Which appears to be 9,000,000, which would put an upper bound for the percentage human genes make up out of the total number of genes at 0.00025 or so. (you said nonhuman ANIMALS though, I don't know how strict you were about that factor)
REDIT - The number might be very different in animals actually, given these two papers :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3130542/
http://www.nature.com/nature/journal/v476/n7360/full/nature10249.html
Looking at the sequenced genome of a sponge and a coral respectively. The latter in particular has a convenient phylogenetic tree that illustrates how the sponge is the furthest branch away from us (i.e. our common ancestor with that sponge is pretty close to the common ancestor of all animals) and the corals branch off soon later. The former was estimated to have 30000 genes, of which 20000 were homologous to genes in other animals. The latter they found 25000 genes, of which 93% matched the genes of other metazoans. So we have something like 10000 genes that sponges don't share with us; 2000 genes that corals don't share with us; the numbers get smaller as we get groups that are closer to us, and presumably most of the genes, say, sponges have that are different from us are common between sponges, so you could get a ratio of genes in humans/genes in all animals that's as high as one half.

It would be interesting to know the distributions of differences as well. For example, how many of those nonshared genes are completely identical except for a single base pair, two base pairs, three base pairs, etc. Would further describe how similar the DNA of all animals is.

Again, I would really like to know why you think those things would be interesting, because I don't really know why you want to know those completely non-standard things as opposed to the things the field of genomics measures as a matter of course ? I feel like I would better know how to answer the question if I knew. (...)

As for "how many of those nonshared genes are completely identical except for a single base pair", the answer is none, because genes that differ only by a single base pair would be considered "the same gene", or more specifically homologues. To quote the paper on the sponge : "18,693 (63%) have identifiable homologues in other organisms in the Swiss-Prot database". Emphasis added by me: if the standard for "same gene" were "identical sequence" you wouldn't need to use the word "identifiable" which suggests a bit more effort and judgement than "checking if they're identical or not".

For more detail on how biologists identify gene homologues : https://en.wikipedia.org/wiki/Sequence_homology and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820096/. While the Wikipedia page leaves some ambiguity as to whether "similarity" usually means "identity" or not, the paper clearly gives the standard for "similarity" as being statistical significance, i.e. being more similar than you would expect from chance.

@rozzen Because they provide genetiticists have no idea

@DapperLad ????

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How is vitamin B12 stored in the body although it is water-soluble?
Vitamin B12 is stored in the liver for a long time.
How is it stored?

Compounds are not necessarily lost from the body just because they are water-soluble. Cell membranes serve to sequester water-soluble molecules in the cytosol. It more depends on whether cells have transporters or binding proteins that lets them retain a given compound.

Yeah ! I researched about that . That's why I deleted the last comment. Thanks for your answer

Vitamin B12 (cobalamin) is a cofactor required by the enzymes methionine synthase (MTR) and methylmalonyl-CoA mutase (MUT). These are the only known enzymes that use B12 in humans, and are abundant in the liver. Since it is a cofactor, B12 is not consumed by any reactions, and hence there is no need to store large amounts of B12 beyond that bound to MTR and MUT. (In contrast to major nutrients like glucose and fats, which are stored in large amounts.)
Early biochemical studies showed that B12 isolated from cells was bound to an unknown large protein complex, called the intracellular cobalamin binding protein (ICB). It was later found that ICB actually consisted two separate proteins, and that these were identical to MTR and MUT.
So B12 is "stored" by simply being attached to the enzymes that require it. But, as @jzx also pointed out, perhaps "storage" is not an accurate description --- cobalamin is an integral part of these enzymes; it is not present in excess, and not kept in some storage compartment from where it can be mobilized (like glycogen, for example).

B12 is stored as mitochondrial 5-deoxyadenosylcobalamin, primarily in the liver (2 to 5 mg) but also about another 1/3rd in muscle. It's estimated that 0.1% of reserves are turned over per day, and the reference values for serum B12 are 180 to 914 ng/L.
While the literature tends to use the term "storage," this coenzyme form of B12 would still be taking an active role in metabolism. As the liver and muscles have the most mitochondria per cell, they are apparently considered the de-facto reserves.
Note that my source (1) indicates that it wasn't fully understood how this stored AdoCbl is released.
Source:

Nutrient Metabolism: Structures, Functions, and Genes. 2015.
Mayo Clinic: Vitamin B12 Assay, Serum

A good start, but how is the vitamin stored? Is there a major binding protein, for example? Also, I think the 5-deoxyadenosyl form is a radical that occurs in some reaction mechanisms, so I doubt that is a storage form. To my knowledge, adenosylcobalamin and methylcobalamin are the two forms that are active cofactors.

It does seem like "storage" could be a misleading term. Admittedly, it might be more correct to say that it's stored in several forms if you were to take a broad view of the process.

I think that's right. I posted a second answer just to detail the binding proteins a bit more.


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Can DNA sequencing of food provide quantitatively the fraction of protein from chicken vs soy?
update: New York Times  X, 2021: The Big Tuna Sandwich Mystery:

For about $500, his lab could conduct a PCR test — which rapidly makes millions or billions of copies of a specific DNA sample — and try to tell me whether this substance included one of five different tuna species.

There is some news about a report from Canada's CBC about fast-food chicken items containing as much as 50% soy protein, based on DNA testing. I won't do the report the service of linking to it directly, but you can search for the news "What's in your chicken sandwich? DNA test shows Subway sandwiches could contain just 50% chicken."
Isn't quantifying ratios of various DNA sequences fairly difficult, requiring rigorous sample preparation? Could results vary dramatically by varying cooking times, and the independent processing of the animal protein and the vegetable protein? Is there an reason to expect isolated DNA ratios to be a good indicator of protein ratios?
I'm also curious, is there a better way to at least try to do this study - perhaps search for key sequences of amino acids within the proteins to at least try to distinguish animal from vegetable proteins quantitatively?

edit: Here is a newer, more reliable, independent news item not written by the agency who paid for the testing.
The NPR news article DNA Tests Find Subway Chicken Only 50 Percent Meat, Canadian News Program Reports says:

The tests were conducted by a DNA researcher at Trent University's Wildlife Forensic DNA Laboratory, for a CBC Marketplace episode dedicated to testing fast-food chicken dishes, and have not been independently confirmed.

Later in the same article a strong statement by one of the companies refuting the results has also been provided.

Looking at the article, which didn't provide a link to anything published, they used several control sources (McDonald's, Wendy's, etc.) so assuming their method was truely the same in each case there is reason to suspect it contains significantly less chicken. "Just 50%" might be a stretch, though. It does seem like a good place to start at least, although the lack of actual publication and the rush to the press seems pretty unethical.

@jzx the history of the food - the chicken and any soy could be very different. Quantitative DNA analysis requires very careful and controlled sample preparation. Cooking temperature and time, chemical environment, pH, all these things are totally uncontrolled. Even if they pay lip service to the word "control" the samples are totally uncontrolled in a variety of factors that could impact final DNA concentration, in a way that differs between soy and chicken, for each tested product.

Exactly @uhoh - without a paper outlining their methods and observations it's hard to say. Although I'd have to assume the chicken would be uncooked, possibly frozen.

@jzx I'd guess they are cooked and purchased over the counter, the only caveat is that no sauces were added (e.g. "hold the sauce"). If you read farther down and see the discussion, most of this stuff is "restructured product" - even if it feels like it is cooked muscle, most of this stuff was a slurry or even a liquid at some point. That's how the soy gets mixed into the "meat" - the stuff is usually mixed as a "goo" and then pressed and moulded into suggestive shapes that remind you of real meat. Go look for veins, ligaments, nerves, etc. all you'll find are air bubbles.

@jzx Here is a paper: X. D. Sun (2009) Utilization of restructuring technology in the production of
meat products: a review, CyTA - Journal of Food, 7:2, 153-162, DOI: 10.1080/19476330903010193 here is a pdf: http://www.tandfonline.com/doi/pdf/10.1080/19476330903010193 I have no idea about the level of peer review, but it helps explain what "restructured product" is like and the processes that can be used to prepare it. Not exactly what one would do for a quantitative DNA analysis in an analytical laboratory.

Mm, yes. It would be interesting, then, to repeat with uncooked product. I would hope that any reputable business would want to know if their supplier's meat doesn't match their policy, which they'd have to have agreed on previously.

I'm not saying your question is bad, in fact it's quite interesting. I also agree that methodology of any "study" should be published. But, the way you phrase the question makes it sound like you already have your mind made up on the answer before asking it. Anyways, my previous comment is not particularly relevant, so I have deleted it. Good day to you, sir.

@canadianer I've cleaned up too. For sure i believe that a method that tries  to use chicken/soy DNA ratio as an accurate proxy for chicken/soy protein ratio in restructured meat product is flawed. But instead of making my mind up, I've asked here in bio SE, where science reigns - at least most of the time :)

Importantly, if you look at the lab that did the testing, most of their work seems to involve identification, rather than quantification. Without more insight into their methods I can only say that there is a huge difference between determining whether a steak came from a moose or beef and determining that a hamburger is some % moose...

http://s3.documentcloud.org/documents/3477610/DNA-Report-Chicken.pdf

In reference to the update in the question three years later, I'll include additional quotes from the same New York Times article.

“No amplifiable tuna DNA was present in the sample and so we obtained no amplification products from the DNA,” the email read. “Therefore, we cannot identify the species.”

The spokesman from the lab offered a bit of analysis. “There’s two conclusions,” he said. “One, it’s so heavily processed that whatever we could pull out, we couldn’t make an identification. Or we got some and there’s just nothing there that’s tuna.” (Subway declined to comment on the lab results.)

With all testing, there are major caveats to consider. Once tuna has been cooked, its DNA becomes denatured — meaning that the fish’s characteristic properties have likely been destroyed, making it difficult, if not impossible, to identify.

While this question falls somewhat between biology, chemistry, and food science, the use of quantitative DNA analysis as a proxy for estimation of relative protein fractions from two different species (in this case plant vs mammal) is probably on-topic here considering it is biologists who have invented, use, and interpret results of DNA amplification and sequencing analysis, and can best speak to their correct use and potential problems when used outside their accepted protocols.
I am not a trained biologist myself, so I can not state with authority that starting with a food product whose plant and animal components may have started from different places on Earth, been processed differently, then combined and further processed involving major excursions in heat (cooking) and in pH deviate substantially from accepted protocols for DNA quantitative analysis, but I have a strong hunch that this is probably so.
As @BryanKrause has noted in a comment, the laboratory in question's primary expertise is in animal identification - does a carcass or piece of meat or fish come from the species claimed or not, and this is a laudable service. But using relative fractions of DNA within a single sample of prepared food as proxy for relative contribution of protein is far outside that kind of service, and as far as I know, is not an accepted practice anywhere.
Ars Technica is a popular technical news source that generally does a excellent job of summarizing scientific topics when they do cover them, in my opinion at least. In an update to the article Subway releases data after scientists weigh in on 50% chicken test [Updated] they summarize released information from two independent laboratories using an "ELISA methodology designed for food products to quantify soy in the chicken." ELISA is a quantitative method that can be used to measure the presence of various proteins directly, and does not use DNA as a proxy.

Update, March 6: Subway has released the lab reports from both of its independent tests. Both Maxxam Analytics in Ontario, Canada and Elisa Technologies, Inc. in Florida used enzyme-linked immunosorbent assays (ELISA) designed for food products to quantify soy in the chicken. ELISA's are a standard type of assay that generally detect and quantify substances based on binding by an antibody. In the assay, antibody binding kicks off a detectable chemical reaction, commonly resulting in a color change. In the case of Elisa Technologies, the lab used an antibody that binds to soy flour proteins and the lab used known concentrations of those soy proteins for comparison to determine the quantity of soy protein in Subway's chicken samples.
In all samples, Elisa detected 3 parts-per-million or less of soy proteins, which is well below one percent of the chicken. Maxxam detected 5.3 ppm of soy protein in the chicken, which is still well below one percent. (emphasis added)

The testing by subway only raises more questions since they, too, did not release their methodology. Also, what does ppm mean in this context?

@canadianer these are very good points, thanks! I am not sure how much has been released in toto, this is the best source I could find so far. It is possible a more complete report has been released elsewhere. I'll keep looking.

I'm going to tentatively accept my own answer in this case. Please flag me if there's a change or new information that I've missed, or just leave an improved answer!

I now read the article. They don't include/show a standard curve so take it with a grain of salt.
It's possible to do Carbon Isotope analysis to distinguish plant vs. animal carbon from an isolated protein fraction.
Besides that you could also do quantitative mass-spectrometry and look for animal vs. plant peptides.
If you want both cell number, protein abundance of known targets there's the fancy Mass Cytometry that could do this.
That being said, IMHO: DNA-sequencing is probably fine and definitely robust. If you set-up a standard curve (mix soy and chicken at known ratios and DNA sequence it) then that's probably the easiest/cheapest way to do this. Without a standard curve testing this though you can't draw a definitive conclusion.
Also from the NPR article; analysis from other fast-food sources of meat gave lower Soy DNA ratios with Subway being an outlier. That's an important distinction to make. Subway subsequently claiming that it's 100% chicken appears more misleading after previously saying there was soy as a stabilizer.

Can you provide some evidence to support the "probably fine"? The mix is processed at high temperature with several added chemicals, none of which are directly related to standard laboratory procedures for handling and preserving DNA samples for quantitative analysis. Can you also support that a DNA ratio can serve as a quantitative proxy for a protein ratio? I appreciate your answer, but right now as written, it's looks like an unsupported opinion.

Temperature and chemical treatment wouldn't matter since all the DNA is being treated the same. Maybe if it's heavily degraded the values are low you get into a non-linear problem. One way or another there isn't enough information to say what they did is correct or not, so yeah it is partly based on opinion, the methods I outline are ways to definitively test it. My opinion is also that fast-food places will serve junk if it's cheap, subway chicken in particular barely resembles a chicken breast.

That's not necessarily correct. Animal and plant DNA start out in very different types of cells, with different ratio of protein to DNA. They are processed separately for quite a while before being added together. The chicken will probably be sterilized fairly quickly (compared to soy) due to the risk of salmonella or other dangerous organisms.

Sure, if you want to find flaws in this study they are there I'm not denying it. Is that difference enough to explain the 1.5 order of magnitude discrepancy (1% vs. 50%) between what the company vs. researchers are saying? I'm skeptical.

Deviations from carefully established protocol can lead to loss of DNA. The stuff that is likely to be most carefully cooked and sterilized is the stuff who's DNA is "low". Cook it long enough and hot enough it could drop much further, and who knows what pH excursions happen during the "restructuring" process. I'm just explaining why I think your answer could use some factual support

I could also imagine different outcomes depending on the standardization procedure. For example, if the products from soy are mostly protein isolates, different procedures might leave more or less DNA intact. If Subway's process left 50x more DNA than the preparation used in the standards, that could also lead to an overestimate. I think overall it is going to be hard to interpret these results without a full publication-style report.

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Why do Great White Sharks not survive in captivity?
Keeping any large marine predator in captivity is a challenge. While it has been done with both mammals and some sharks, it has never been successful with Great White Sharks. The longest a Great White Shark has survived in captivity is something like 4 – 5 weeks, if I am not mistaken.
I have heard this can be because they are used to swimming such great distances in the wild. However, both Killer Whales and Dolphins also swim great distances per day in the wild and are known to survive (sometimes even breed) in captivity.
So why is it that Great White Sharks are so hard to keep in captivity?
I am aware that most large predators kept in captivity live less long than in the wild, with some the exceptions (crocs just chill). It just seems extreme to me that Great White Sharks die within such a short period of time.

Most of the reasons why Great Whites are hard to keep in captivity are actually quite practical in nature:

Great White Sharks are expensive to keep because they eat a lot of food; their tanks need continuous re-stocking;
They refuse to be fed by humans, leading them to die of starvation. They do not seem to accept dead small fish for food;
The correct saline balance seems very important and difficult to maintain;
Logistics are difficult; they have to be safely captured in the wild, transported to a tank and that all the while keeping them in appropriate living water;
Due to their size and aggressive nature, great whites are hard to handle;
As you said already in your post; they are open water fish and cannot be confined. Sharks can swim hundreds of kilometers within a matter of days. This exercise and freedom may be essential to their well-being. A small 4-feet 'Great' White was kept alive for 6 months in a 1-million gallon tank. And even that was hardly enough;
They seem to get depressed in captivity. Great White Sharks that are kept within tanks have been known to head butt their noses into the glass walls and lose their appetites. It has also been noted that they get increasingly aggressive in their depressed state.

Sources
- IFL Sciece
- Science Alert
- Shark Bookings


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Molecules responsible for reading amino acid language

The molecules responsible for reading the language of amino acids and nucleotides is:

RNA polymerase enzyme
mRNA
tRNA
DNA

I don't actually understand what "reading amino acid language" means!
Does saying nucleotides refer to those on the DNA molecule? If so then RNA-polymerase is then responsible for synthesizing mRNA molecules which carries the same genetic code of the amino acids; or is it something else?

Is this a homework question?  I guess that "amino acid language" refers to the genetic code,  https://en.wikipedia.org/wiki/Genetic_code

This is a homework question I assume? You should show what effort you've made so far to be well received on the site. I agree it's not very well worded, however. My interpretation is that you can think of the question as asking you: "What molecule is responsible for converting between the 'code' of DNA and the 'code' of Amino Acids"

It means which molecule participates in the process of turning a sequence of nucleotides into amino acids, i.e. "reads" the sequence of nucleotides and "knows" to which amino acids it corresponds.

It is not a homework question unless studying for un upcoming exam is considered a homework question.... sorry for any inconvenience and thank you

Do you mean which molecules turn RNA into amino acids? Because that would be those in the ribosome complex.

@KoenvdH Unfortunately, I don't fully understand the question. Also it's u multiple choices questions....

Yeah, that’s one badly worded question! I’m assuming that the required answer is one/all of: ribosome/tRNAs/aminoacyl tRNA synthetase. However, this would actually be inaccurate or even wrong: these molecules read the codon language, not the amino acid language. I’m not aware of any molecule which actually reads amino acids, except maybe immunoglobulins. However, I’ve never heard of “language” in this context. Another candidate would be post-translational modification (e.g. glycosylation). But, once again, I don’t know of anything that would qualify that as a language.

Please use commas to separate the choices or bullets, it makes your question more clear.

Clarifying the premise
As mentioned in my comment, the term “amino acid language” doesn’t really make sense as far as I’m concerned. Worse: nothing, to my knowledge, is ever reading an amino acid sequence in living systems.
Yet here we are. The term “amino acid language” itself is definitely used (though, once again, I’ve never heard of anything “reading” this language).
So, to answer the question, let’s define a meaning for the term “amino acid language”:

The amino acid language is a language written by amino acids. In other words, a set of sequences consisting of amino acids.

The candidates
Now, your question is multiple choice so it’s sufficient to go through all possible choices and see if they fit:

RNA polymerase enzyme

RNA polymerase reads either DNA (DNA-dependent RNA polymerase) or RNA (RNA-dependent RNA polymerase) and produces RNA. There are no amino acids involved. This is clearly not the right answer.

mRNA

mRNA is an information-carrying molecule. But it does not “read” anything (at least not in its canonical function). Note that other RNAs are involved in recognising/reading things, but not mRNA. So, not the answer.

tRNA

tRNAs (transfer RNAs) are RNAs that carry individual amino acids. Each individual tRNA recognises a codon on an mRNA via complementary base pairing and thus “translates” the codon into a specific amino acid by the rules of the genetic code. In the context of this question, it’s fair to say that tRNAs (in combination with other molecules) are writing the amino acid language.

DNA

DNA, like mRNA, is an information-carrying molecule that does not read anything. Moving on.
The answer
tRNAs do not read amino acids in the conventional meaning of the phrase. But it’s the closest candidate here: not only does it indeed read a language, it translates symbols into amino acids. This is therefore almost certainly the expected answer, unless an acceptable answer is “none of the above”.

Thank you for your effort..... This was really confusing as I got like 3 different answers from 3 different people and I never actually came across the word reading an amino acid language which made the question far more confusing... thanks again.

I think what the question was trying to get at, though I agree it was poorly written, is that the "codes" in DNA, RNA polymerase, and mRNA have no direct connection to the amino acids; when we say a given sequence "codes for" a particular amino acid, the only thing mediating that code, connecting it to a particular amino acid, is the tRNA (though the aminoacylation process is at least if not more important).


text:
Is palmitic acid really that dangerous?
According to Wikipedia,
"Palmitic acid is the most common saturated fatty acid found in animals, plants and microorganisms. It is also the first fatty acid produced during fatty acid synthesis and is the precursor to longer fatty acids. As a consequence, palmitic acid is a major body component of animals. In humans, one analysis found it to make up 21–30% (molar) of human depot fat, and it is a major, but highly variable, lipid component of human breast milk."
(https://en.wikipedia.org/wiki/Palmitic_acid)
Yet, specifically palmitic acid is also said to be "harmful" (that it increases LDL levels and puts people at risk for heart disease), per the World Health Organization (http://www.freezepage.com/1348239076FHWAJDADVT).
So, I am skeptical --- possibly most ubiquitous saturated fatty acid in nature and a central component of our fatty acid metabolism, is somehow "more" dangerous/unhealthy compared to other saturated (or unsaturated) fatty acids? I'd suspect the opposite should be true -- it seems to me it should be the saturated fatty acid we should be most capable of handling well!

Let's first clarify some concepts. Free fatty acids, including palmitic acid, are not present in animal tissues (or in the diet) to any large extent; they are esterified with glycerol to from triglycerides (fat), which is the storage form. This is a very important distinction, because triglycerides are chemically inert molecules that can be stored in very large amounts in cells without causing problems (adipocytes are pretty much just one big fat droplet), while free fatty acids are dangerous to organisms because they disrupt cell membranes --- fatty acids are basically soap.
When nutrition studies like the WHO report talk about dietary intake of "palmitic acid", they really mean intake of triglycerides that contain a large proportion of esterified palmitic acid as side chains. There is a large body of epidemiological studies indicating that intake of fats rich in palmitic acid correlates with cardiovascular disease and other "metabolic" disorders, although some reports show no significant effect. In clinical trials, replacing saturated with unsaturated fat seems to provide some health benefit; but there also are studies indicating that monounsaturated fat can be worse than saturated fat. So there is some evidence that too much saturated fat is problematic, although the issue is not straightforward.
The causal mechanism is to my knowledge still not clear. You are right that cells are normally perfectly capable of handling palmitic acid; it is a good substrate for beta-oxidation and a common fuel source for human cells. However, in pathological situations, free fatty acids can accumulate in cells and in the blood, probably because of excessive lipolysis. Many studies show that this can cause insulin resistance and trigger inflammatory signals, and even cell death by apoptosis. Some reports show that palmitic acid in particular causes these effects, whereas oleic acid (monounsaturated) does not, but I don't think there's any consensus on why palmitic acid is special.
My own hypothesis (if I may be so bold :) is that palmitate only appears to be special because cells have evolved to sense it as a "proxy" signal for free fatty acids in general. Since fatty acids are clearly dangerous to cells, sensing them is important, and because palmitate is the naturally most abundant fatty acid, it would be the easiest fatty acid to detect. It is known that palmitate is recognized by toll-like receptors, in particular TLR2 and TLR4, and that sensing by these receptors trigger "proinflammatory" signalling. But this alone doesn't prove my "proxy" hypothesis, of course.

Nice answer, +1! Can you add some resources which make you think "palmitate only appears to be special because cells have evolved to sense it as a "proxy" signal for free fatty acids in general"? I mean, at least a verified basis for a hypothesis is better :)

Sorry, I don't really have any reference for that last paragraph --- it's just a hypothesis, purely based on reasoning from principles. It is clear that palmitate does causes signalling responses (it's known to be sensed by TLR4), but I know of no clear rationale why palmitate would be physically more dangerous than other long chain fatty acid. This leads to my "proxy" hypothesis. As I said, it's just a hypothesis, I have no proof. (I actually hesitated to put this part in, as it is pure speculation, but I thought it could be interesting to share.)

@another'Homosapien'   Done, but that is not really the key part of the argument ...

+1. Only one thing to say - no one will disallow you to be bold; men often do that. Being too bald, however, may be arguable in science ;-)

+1 great answer indeed : ) I'm aware that fats are both generally consumed (eaten) and stored as triglycerides, not as free fatty acids (though i did not explicitly state that in my question, since i thought that was obvious/well-known). But, I was not sure why nutritional research seems to specifically single out (triglycerides with) palmitate chains with such criticism/disdain (especially for such a common and centrally important fatty acid).

@ManRow,  Yes, it is a bit strange. To some extent this could also be experimental bias: most experiments are done using palmitate only, and so any effects discovered are reported for palmitate, although they could actually be evidence of a more generalized response to fatty acids.

What is the reason for free fatty acids being detrimental? If in excess? What about the  triglyceride uptake mechanism of muscle cells/adipocytes.


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Why is the internal capsule dark in this transverse section of the brain?

Why is the internal capsule dark in this transverse/horizontal section of the brain?
If it is white matter, then why isn't it white?
P. S. : Formalin was used for fixation.
Why the same color was not for remaining white matter.

Short answer
White matter is called white matter because it is relatively white compared to gray matter. However, in fixated specimens it is not as snowy white as in textbook pictures.
Background
The internal capsule is a paired V-shaped structure that is visible in horizontal brain slices (Fig. 1). It is a subcortical structure mainly consisting of fiber tracts connecting the cortex to the brainstem.

Fig. 1. Horizontal (transverse) brain slice showing internal capsule. source: Utah University
In Fig. 1 the structure is quite white'ish, but in the following two images you can see it is not always the case.

source: The Human Brain: Chapter 5: The Cerebral Hemispheres

Fig. 3. source: Medicos Notes
As you can see, the internal capsule is not always nice and white. Fig. 2 particularly shows a reddish taint of many white matter structures.
The internal capsule is well-vascularized (Schamann, 2003) and strokes in this region are associated with muscle weakness and loss in sensory sensitivity (source: Stanford Medicine). Hence, the red coloration may well be due to red blood cells that have not been completely washed out of the brain beore it was fixated. Also, non-specific coloring may happen over time in fixated specimens and many fixation artifacts can occur that lead to alterations in gross morphology (Chatterjee, 2014).
References
- Chatterjee, J Oral Maxillofac Pathol (2014); 18(S1): S111–6
- Schamann, Stroke (2003); 34: 2264-78

That is fine and something that is obvious.  Can you please be little more specific, why is it grayish (its not reddish)?  What was effect of formalin on internal capsule and tapetum only, and not on remaining white matter?

Hard to say,  really. Was it formalin treated? How old is the prep?  How often was it used?

In aged fixed tissues, red blood cells appear much more brown than red, though I am not sure if that's a likely explanation here, I am not familiar with @AliceD's suggestion that the internal capsule is particularly vascularized. In general, the specimen pictured does not look like it is in great shape. There is very little color distinction between white and gray matter, for example. It's possible some of the change in coloration is simply because of the orientation of different fiber tracts and the resulting susceptibility to drying/aging, really more of a texture difference than color.

It was fixated in Jan 2016 using formalin.

It was used last year for one month and again this year for one month.

@AnubhavGoel I'm surprised it looks so bad after that little time, but maybe it was not as fresh when initially fixed - just in general, it does not look good. Was it stored in formalin, too, or in ethanol?

@AnubhavGoel - I'm also surprised by the bad state it is in. I think this is part of the reason the coloring may be off

@BryanKrause It was Stored in formalin

@AnubhavGoel I think it is typically thought to be better to preserve tissues long-term, especially brain, in ethanol rather than formalin (after intial fixation in formalin/paraformaldehyde). Long-term formalin storage can essentially "overfix" the tissue. I'm not certain that is what happened here, but without seeing the tissue before and around the initial fixation that's my best guess.


text:
How nasal hairs filter particles of micron size?
This book says:

The larger particles (> 10 μm diameter) are filtered by hair in the nostrils

If we see the anatomy of nasal hairs and its density in the nostrils then it seems that its impossible for such a structure to filter particles in micrometers, So how does the nasal hairs filter them?

That's not strictly true. Particulate matter of less than 10μm in diameter (expressed as PM˘10) reach lower airways, and 10μm diameter reaches the bronchial tree, Hair disturbs airflow allowing for deposition, is moist and can catch small particles; mucus on surface epithelium and hair can as well. But it's a combination of a lot of mechanisms that keep out larger particles. Shape of the particle also matters. But pollen of 20μm has been found in lung periphery.


text:
Help me identify this insect found in fishtank

This bug appeared in my fish tank,transparent 6 legged with 3 tail insect. Anyone able to identfy this, please help. Many thanks

Please add some more images, including a better close-up, some morphological details, your location, etc.

This is a Damselfly, suborder Zygoptera. Together with the Anisoptera (true dragonflies) they belong to the order Odonata, usually also named dragonflies.
Damselflies are smaller and more slender then Dragonflies, both as larva and as adult, although there are exceptions (mostly tropical species).
It can be distinguished from mayflies by it's broad head and the broad, flat lamellae; the 3 'tails' as you call them.
Some beautiful pictures can be found here


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What is the difference between the evolution of fins in whales and fish?
For a homework assignment I received the following question:
Which statement best explains the evolution of fins in whales and fish?
a. The common ancestor of whales and fish possessed genes for fins.
b. Whales and fish possess the same mutations in their genomes.
c. Fins evolved in whales and fish because they both use them to swim in water.
d. Fins evolved in whales and fish because of different mutations that occurred
in their genomes.
e. Fins evolved in whales and fish because their most recent common ancestor swam in water.
My answer is (c). Of the given options, it seems most accurate. I feel that the language is unclear as many organisms who do not have fins swim in water. That can be a logic against the option. But, the given answer is (d). That seems too bizarre as even humans and fishes have different mutations in their genomes. (c) seems more appropriate as it can exemplify convergent evolution.

FWIW, I agree that C is a better answer, because it demonstrates that you understand the concept of convergent evolution, and "different organisms have different mutations" is a pretty trivial observation.  It could be the answer to virtually any question you could ask about different organisms evolving differently.

It sounds like "d" isn't saying that having different mutations caused fins to evolve, but it's making a contrast to "b" - both whales and fish fins evolved via mutations that occurred in their genomes, but they weren't the same mutations in both lineages. Which is accurate. Is there a single answer or is this a "select all that apply" situation ?

I'm curious, have you asked your instructor about this question? Did they explain the reasoning for the correct answer and their reasoning why another answer is incorrect?

Short answer
d) is definitely correct.
Background
The crucial element is that whales returned from land to the sea and re-evolved fins.

a) is incorrect, as the common ancestor may not have had fins. In fact, it is thought it was a sea squirt, a sedentary species without fins, that was the most recent ancestor of fish.
b) is incorrect, as they may share some mutations but overall they have very different mutations and very different genomes altogether, being fish and mammals;
c) is incorrect as they have to develop fins first before they can use them;
d) is correct, as the emphasis in the answer is on

Fins evolved in whales and fish because of different mutations that
  occurred in their genomes.

Fins in whales have developed from arms and feet. Hence there are different mutations going on, as fish don't have arms and feet.

e) The common ancestor from fish and whales may have been in the water, but may not have had fins.

I disagree that "c" is incorrect. First, by the logic of "they have to develop fins before they can use them" nothing would ever evolve. Both whales and fish started out swimming with things that weren't fins (arms/legs for whales, some kind of appendage for fish), so selection pressure developed for swimming ability and those whose limbs were better for swimming did better, presumably swam more, leading eventually to the evolution of fins. "c" might be meant to be incorrect because it sounds Lamarckian as written, but the fact is, whales and fish swimming is integral to why they have fins.

Also for e): I'd say whether the common ancestor of fish and whales had fins is irrelevant - "e" is wrong because that common ancestor being in water isn't the cause of whales having fins. After all, it's our common ancestor too and we don't have fins. Whales have fins because their mammalian ancestors became aquatic, not because the first vertebrates lived in water.

actually all tetrapods have the genes for fins, limbs form as fins first then apoptosis kills the cells between the individual digits turning a flipper/fin thing into a hand or foot with individual toes. That's why thalidomide did what it did it intercepts the pathways for apoptosis.

@Rozenn Keribin: Also ichthyosaurs.  And FTM penguins started out swimming with wings.  So our original fish ancestor develops fins, which evolve into legs as Tiktaallik and friends move onto the land.  Ichthyosaurs and cetaceans go back to the sea and the legs re-evolve into flukes.  (Note intermediate cases like seals & otters.)  And penguin ancestors evolve their front legs into wings, and then into flippers...

Your answer is almost correct.. I do not like how you say "whales returned from land to the sea and re-evolved fins." Or how you said "Fins in whales have developed from arms and feet.".. These statements are basically the equivalent of saying that humans transformed from chimps. That is not how evolution works..

@Bob I'm trying to get a message across and I adapt the answer to the level of the question. Thanks for the lesson, but I'll leave at at this :-)

I agree with you that the question is ambiguous, and also that the most sensible answer would be C.  However, one could make a more or less reasonable argument in favor of several other answers, too.

a. The common ancestor of whales and fish possessed genes for fins.

Technically, this statement is true.  At least some of the fins of whales and fish are even distantly homologous, even though the lineages leading to tetrapods (including whales) and to ray-finned fishes diverged quite early in their evolutionary history.
(Specifically, the flippers of whales are modified tetrapod forelimbs, which are homologous to the pectoral fins of ray-finned fishes.  Whether one should also consider the tails fins of whales and fish to be homologous is a bit more debatable: the actual fin structures are very different, and presumably share few if any developmental pathways, but the tail and the spinal column which they attach to and are powered by is clearly a shared feature of both groups.)
However, while shared evolutionary history may explain why fish and whales have similarly placed flippers / pectoral fins, and why they both have a flexible spine that supports undulatory swimming with the help of a tail fin, it does not explain the convergent evolution of whales' forelimbs (which were formerly adapted for walking on land) into fin-like flippers.  So in that sense, while perhaps partially correct, this answer is also quite incomplete.

b. Whales and fish possess the same mutations in their genomes.

It's hard to even tell what this statement means.  Insofar as it's a restatement of the fact that whales and fish share some of their evolutionary history (up to the divergence of the bone-finned and ray-finned fishes), it's no more or less correct than statement A above.
However, I suspect that the intended meaning of this statement is that whales and (ray-finned) fish would've separately evolved the same "fin-making" mutations after their lineages diverges, which is both clearly incorrect and also, even prima facie, statistically very unlikely.  So I would rule this one out.

c. Fins evolved in whales and fish because they both use them to swim in water.

This statement is written using teleological language, which some may consider misleading, as it could be misinterpreted as implying that evolution was a directed process: it could be interpreted as saying that whales needed to be able to swim, so they chose to evolve fins (or that some guiding consciousness granted them fins).  This is, of course, incorrect — or, at least, we have no scientific evidence of there being any such conscious force guiding evolution, or of any organism (with the arguable exception of humans) being able to deliberately direct their own evolution.
However, it's quite possible to interpret this statement in a way that makes it perfectly correct: as both whales and fish move around by swimming, possessing fins (or something similar to fins) is an advantageous trait for them, and has thus been favored by natural selection.  If pressed, I would thus choose this one as the most correct answer out of the given options.
In particular, note that the argument made by AliceD that "they have to develop fins first before they can use them" is not really true: the ancestors of both whales and fish were swimming long before they evolved fins, and thus the selection pressure in favor of having fins (or fin-like structures) was already present before the fins themselves evolved.
In particular, the first aquatic ancestors of whales are believed to have swum much like modern-day otters and seals, using their flipper-like limbs as makeshift fins.  While there's no discrete transition point where one could definitely say that whale limbs turned into proper fins, it is clear that the fins, and their direct evolutionary predecessors, were being actively used for swimming, and that this fact directly drove their evolution into the actual fins that modern whales have.

d. Fins evolved in whales and fish because of different mutations that occurred in their genomes.

While technically correct, this statement is so vague that it's all but meaningless.  All evolution is driven by mutations, and those mutations, being basically random, are rarely if ever the same in any two lineages.
Certainly, it would be silly to claim that "different mutations occurring in their genomes" is an explanation of why whales and fish evolved fins: humans also constantly have different mutations occurring in our genomes, but we clearly don't seem to be evolving fins.  Neither are pigs or bumblebees or sunflowers, even though all of those species (and, of course, all others too) are also constantly experiencing different mutations in their genomes.
Really, this answer reminds me of the story about a person in a car who gets lost and stops to ask a passerby where they are; the passerby, after a moment's thought, replies "you're in your car."  While technically correct, that answer is absolutely useless — and so is this one, too.

e. Fins evolved in whales and fish because their most recent common ancestor swam in water.

Again, this answer could be interpreted as basically a restatement of answer A, and thus as being partially correct.  However, it completely ignores the convergent selection pressure described in answer C, which is responsible for the more recent evolution of whale flippers into something resembling fish fins more than, say, human hands or the feet of hippopotamuses (currently believed to be the closest living relatives of whales and other cetaceans).  Thus, I would not pick this answer, for the same reason that I wouldn't pick answer A.

Nice one +1. Great answer

While technically correct, [d] is so vague that it's all but meaningless. All evolution is driven by mutations, and those mutations, being basically random, are rarely if ever the same in any two lineages. Depending on the education level that the course was pitched at, the mere recognition that whales and fish have different lineages, and have not inherited fins (in their present form) from their common ancestor but rather evolved them separately, might actually be non-trivial hence credit-worthy. Many High School students would even go so far wrong as to think that whales are fish!

[Having said that, my first instinct on reading the question was the same as yours. The theme of the question suggested the examiner wanted to know if students understood the idea of convergent evolution, and (c) at least seemed to describe this, albeit in a verbally slightly clumsy way. I just felt that (d) is not entirely without substance, depending on the background the students are coming from!]

This was a question on the 2016 Toronto Biology Exam, precisely question 42.
Though the question was asked vaguely, d is the best answer. It's quite obvious that if animals are in water, fins will eventually evolve to improve fitness, that's pretty obvious.
However, if they are both in water, why are their fins different? This touches on the more complex concept of analogous structures; structures that perform similar functions but are anatomically different.
Well, why are they anatomically different? Different mutations in their genomes resulted in those differences.
Therefore, d is the better answer. It does ask which "best" explains.

It is far from inevitable that all aquatic animals evolve fins: marine invertebrates (jellyfish, crustaceans, octopus, starfish etc), sea otters etc (and possibly sea snakes, depending on your definition of 'fin').

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


text:
Book request: systematics and evolution of vertebrates
Would you recommend any good vertebrate systematics & evolution book?
The main goal is to teach a Master's level class - mostly focused on amphibia, reptiles and fish.

I'm tempted to recommend Alfred Romer's The Vertebrate Body , but it's quite out of date now.

If nobody is able to offer recommendation on Biology.SE, you can look at reviews on Amazon by search Vertebrates Evolution. This book has many good reviews for example

I really like Liem et al.'s Functional Anatomy of the Vertebrates: An Evolutionary Perspective.


text:
How to preprocess htseq counts for gene expression (TCGA)
I want to prepare a matrix of gene expression to analyse TCGA LAML data.
The required data is available at TCGA LAML - Gene expression quantification.
The following is an example of the kind of data retrieved from the TCGA data portal:
ENSG00000000003.13  9
ENSG00000000005.5   1
ENSG00000000419.11  661
ENSG00000000457.12  1434
ENSG00000000460.15  1211
ENSG00000000938.11  405
ENSG00000000971.14  251
ENSG00000001036.12  786
ENSG00000001084.9   4423
ENSG00000001167.13  5038
ENSG00000001460.16  246
ENSG00000001461.15  2773
ENSG00000001497.15  1932
ENSG00000001561.6   1693
ENSG00000001617.10  55
ENSG00000001626.13  8
ENSG00000001629.8   4629

Each row displays, for each gene, the quantification of read counts by the htseq tool.
My question is, how do I have to preprocess the data (e.g. regarding gene length) before using data for subsequent analysis?
In this case I will not consider normalisation (such as loess) and batch effects removal (e.g. with combat).

This entirely depends on the type of subsequent analysis so the question isn’t really answerable without more information. However, in general I recommend you familiarise yourself with a standard RNA-seq analysis workflow.


text:
Examples of creating a new animal species by humans
So recently, I was arguing with my friend who happens to be creationist. As he does not believe in the "theory of evolution" I asked him how he can explain such a big diversity in the dog Canis familiaris sppecies. (The example taken from Charles Darwin's on the Origin of Species saying that humans made to dogs what mother nature has done to every species)
My friend replied something like:

Well, having chihuahuas or huskies is one thing but, getting a tetrapod from a fish is a something which can never happen.

I realized that indeed the Darwin's example isn't perfect... Even though, due to size chihuahuas and hounds can't copulate efficiently their semens and ovaries can start a new life.
I can't give a counterexample of a species which was bred artificially by human for so long in a new direction that a new species (whose specimens by definition were not able to reproduce with the specimens of the base species) was created.
It's not that I am becoming creationist... but is there any exception from that rule for any artificially bred animal species?
[Edit]
This question has nothing to do with this
I am strictly asking about examples of an artificially bred animal species which got bred into two species.
[Edit 2]
Also to be exact, I am not interesed in specimens that can't reproduce due to various "external" circumstances like environment's temperature or size (chihuahuas&hound example). I am interested in specimens which come from the same base species and can't reproduce even with the help of in vitro fertilization (I know this is not exactly the definition of species). I just want to avoid getting answer similar to this.

Note that there are many definitions of "species", and you've chosen one that was specifically devised for evolutionary theory. In any case, rather than animals you might look into crops such as corn and its ancestor teosinte, the Brassica family, etc. It's pretty pointless, though, to try to reason someone out of a position they didn't reach by reason.

On top of the marked duplicate which seems very central to your misunderstanding, you might want to consider having a look at Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?. Of course, crops are also examples that come to mind (such as corn and teosinte for example).

@Remi.b,  I don't agree this is a duplicate of the ancestor-of-birds question that you marked up; this one asks about humans breeding organisms, not natural evolution. The drosophila question you mention in you comment does answer this question though.

That is exactly my point

@Roland. Ok, I've reopened the post. Thanks for feedback. The question might arguably be a duplicate of Have we ever observed two drosophila lineages that evolved reproductive isolation in labs? though but an answer based on some crop would probably be a better fit. Note that there is likely reproductive isolation between a chihuahua and a wolf despite taken as example of something of no interest in the question

You many want to tell your friend that saying evolution can happen but not to the point of new species is like saying you can walk around the block but its impossible to walk across the country. The mechanism is identical all that changes is how long the mechanisms runs.

This page contains a list of observed speciation events including a breakdown by mechanism and starts with a rather good introduction to the concept. http://www.talkorigins.org/faqs/faq-speciation.html

Why - and I'm not saying your question is wrong - but why does it have to be a new species? Doesn't any significant mutation (e.g. the mutation allowing lactase to be expressed into adulthood) suffice? Does not the fossil record suffice? Your friend's arguement is based on the difference between selective breeding and the cumulative effect of many mutations. I don't think you finding a new species through selective breeding proves anything. imo.

@John I’d like to give you some advice in order to be more effective when talking to creationists.  As I pointed out in this post , creationists challenge evolutionists with what they call the bait-and-switch (see their link I posted).  AGAIN, creationists fully believe in adaptation via genetic variation and NS.  To them this is NOT evolution that will turn worms into women.  Your ‘walk around the block/across the country’ falls directly into that, and is completely ineffective against a creationists.

No offense Runz but I know all this, I also know that if what the believe is wrong you do them no service by pretending it is not. The mechanisms are identical are the same thing and pretending otherwise only helps them deny reality. It plays right into their false belief in "kinds" by acting as if there is some great diffrence between a change in a population and and change in population we happen to label as speciation.

@John, No offense as well, but do understand that there IS a difference between N.S. based on variation of existing genetic variety, and the CREATION of new phenotypes via genetic material that did not exist before.  Creationists are well aware of this difference.  You need to be as well.

Yes there is a difference new genetic material and existing.  However new genetic material is NOT speciation and new genetic material  is actually quite common in the "population level" evolution they accept. furthermore new material is not necessary for speciation. Again both "types" of evolution are the same mechanism both may or may not have new genetic material but do have a selective process. They are trying to create an distinction where there is not one and using ambiguous terminology to make it seem as if they are not. If you want to continue this in discussion feel free.

There are indeed many examples of new species created by humans, and observed to arise by humans. Many via deliberate experimentation. You can find examples googling "examples of speciation", looking at the Wikipedia page for speciation or the Talk Origins one:
http://www.talkorigins.org/faqs/faq-speciation.html
http://www.talkorigins.org/faqs/speciation.html
https://en.wikipedia.org/wiki/Speciation
The issue is that there are two events of interest in "the origin of species" that are related but not the same thing: there is speciation, and then there is overall change. And as far as change itself goes you can have genetic change and phenotypic change which themselves aren't perfectly correlated.
Speciation is a very important evolutionary event, as it's the point at which genetic material is no longer exchanged between two groups and so they start evolving independently, meaning differences will accumulate over time (steadily and inevitably for genetic differences, more variably for phenotypic ones as that depends on the environment). But you can have differences accumulating without speciation (especially not with your "in vitro fertilization" criterion, which allows gene flow to be stopped for a long time without "speciation" by that definition happening), and you can have speciation happen without much genetic or phenotypic change.
And so on our human timescale we'll tend to see three categories of events:
1) large phenotypic change without speciation (especially by the in-vitro definition), because natural selection can cause large phenotypic change but random mutation cannot be rushed and that genetic drift is usually what will make groups no longer inter-fertile,
2) Speciation without large phenotypic change, again because speciation is just the beginning and all you need for "speciation" is just enough change to make interbreeding impossible or difficult, and so many examples of observed speciation involve just that, and
3) Speciation with large phenotypic change, which will usually be single-generation events with hybridization and polyploidy. Those are the most likely to fit your criteria that in-vitro fertilization shouldn't work. And they are legitimate and important evolutionary processes; polyploidy has happened many times in our lineage, it's an important source of genetic diversity, and hybridization and polyploidy are a major mechanism in the evolution of plants in particular. But they're not the major mechanism for the evolution of large vertebrates, so it's easy for Creationists to dismiss them.
Still, looking at the links I gave you I see a few examples that involve genetic change sufficient to block even in-vitro fertilization. The second Talk Origins link in particular refers to examples where speciation was determined by the offspring being sterile. There is also an article in the notes of the Wikipedia page about a recent discovery about the kind of genetic changes that can lead to speciation:
https://www.scientificamerican.com/article/wandering-fly-gene-suppor/
The general problem with giving Creationists examples though, is that the examples they want don't exist (and would usually contradict the theory of evolution anyway) and the ones that do exist they're not satisfied by (because the change involved isn't dramatic enough, or IS dramatic but as a result makes the dramatic look trivial because it happened via a small gradual underlying change - which, you know, is how evolution is thought to work).
I notice in fact that you are the one asking about the speciation with in-vitro fertilization, not your friend; your friend apparently just said that huskies and chihuahuas are not comparable to fish vs tetrapods. If this is personal curiosity from you then that's fine; if you are looking for arguments for your friend specifically then it looks like you're on the wrong track, since no amount of lack-of-interbreeding will make flies any less flies, which is usually the issue for people who focus on "fish to tetrapod" as a scale of change.
You might have better luck figuring out exactly what claims your friend makes, where they set the boundaries of what they think is possible and what they think it isn't, and then find an example that breaks that specific boundary. So they say "speciation can't happen !", you reply "speciation happened in fruit flies", and they answer "so what, fish haven't become tetrapods" - but, what is it they meant by "speciation can't happen" ? What mechanism do they think makes it impossible, what do they think this "speciation" is that's impossible, where do they set the boundary for themselves between "ordinary change that can happen" and "stuff that can't happen so evolution is false" ? They probably don't know clearly themselves, but figuring it out and addressing it is a better way of moving forward, and you both can learn things. And it makes it a bit easier for you too - you don't have to worry about finding proof that fish can become tetrapods, you can be like "OK fish can't become tetrapods whatever, but you said that new species cannot arise through genetic change, but here is a paper saying that a gene transposition makes it impossible for those two flies to interbreed, wouldn't that be an example of speciation via genetic change ? What do you think ?"


text:
Which frequency of UV light damages DNA?
I have read that UV light can damage pure DNA (DNA that has been extracted and purified). Is there a particular frequency threshold where this damage occurs or is it more of a gradient where the high frequency, the more damage. I want to understand how much damage light can do at what frequencies.

Not only pure DNA, UV radiations are one of the main causes of skin cancer because they damage cellular DNA in skin cells. Talking about frequency range, two different types of UV radiations damage DNA in two different ways:

UV-A radiation damages DNA in indirect ways. UV-A radiation easily generates free radicals, such as hydroxyl and oxygen radicals, which in trun cause the main damage1. The damage caused by such radicals is mostly single-stranded breaks in DNA. In fact, it has only recently been established that UV-A radiations do damage DNA, while these were originally considered as not (or less) harmful2. UV-A also has immunosuppressize effects on the entire body and is also mutagenic for keratinocytes in skin.
Wavelength range: 315 - 400 nm
Effect: source
UV-B radiation is in fact what causes most damages and deadliest damages to DNA. UV-B radiation directly attacks DNA, it excites atoms of adjacent thymine molecules, which in turn form covalent bonds with each other and lead to formation of thymine dimers. These dimers, because of being bonded side-by-side instead of being bonded to opposite strand base, form a bulge which interrupts structure and function of DNA. Such dimers are removed by a process known as nucleotide excision repair, which involved about 30 diffeeent proteins3, meaning UV-B is more harmful for the body than UV-A. UV-B also causes double-stranded breaks in DNA, which are a major problem for DNA replication and a threat for cell's survival.
Wavelength range: 280 - 315 nm
Effect: source
Other effects of UV radiation on the body include damage to collagen fibers and vitamin-A in the body and accelerated ageing effects 4. Apart from this, UV radiations, because of harmful effects on DNA, are used for sterilization as they destroy microbes' DNA and thus prevent them from replication.
Wavelength range: 10 - 400 nm (complete UV spectrum)

References:

Svobodová AR, Galandáková A, Sianská J, et al. (January 2012). "DNA damage after acute exposure of mice skin to physiological doses of UVB and UVA light"
Halliday GM, Byrne SN, Damian DL (December 2011). "Ultraviolet A radiation: its role in immunosuppression and carcinogenesis"
Bernstein C, Bernstein H, Payne CM, Garewal H (June 2002). "DNA repair/pro-apoptotic dual-role proteins in five major DNA repair pathways: fail-safe protection against carcinogenesis"
Torma, H; Berne, B; Vahlquist, A (1988). "UV irradiation and topical vitamin A modulate retinol esterification in hairless mouse epidermis"


text:
Probability of carrier for recessive trait given parents are carriers and sister affected
I'm trying to understand more about inheritance of an autosomal recessive trait that runs in my girlfriend's family. How could I start looking at this?
My girlfriend's sister, C, is affected with a recessive trait. Her parents, A and B, are confirmed unaffected carriers. Am I correct to assume my girlfriend, D, is a carrier with probability 50%? Or must I take into consideration that we know the state of C given she is affected.
Furthermore, if I (E) have a child with my girlfriend, what is the probability that our children are either carriers or affected? My carrier status is unknown.

Welcome to Biology SE!  Although questions on human genetics are most welcome here, please note that we do not answer personal medical questions or give health advice at this site.  For advice on genetic testing etc, you should consult your physician.

@Roland Sure thing. More interested in the probability aspect of inheritance, and how it works in general

Real life is not always as simple as the paradigms you learn in high school.
However, the high school level answer is this:  Since you know your girlfriend is not affected, there is a 67% chance she is a carrier, and a 33% chance she is not.
The state of the sister is irrelevant, if you are sure both parents are carriers.
Without knowing the prevalence of the recessive allele in your population, it is impossible to know the odds of you being a carrier.  But if you are not, then your kid has a 33% chance of being a carrier.

Assuming the trait is caused by a single gene, she would indeed have a roughly 50% chance of being a carrier. If both parents are carriers but unaffected they will both be Aa (with a being the recessive mutation). For your girlfriend to be a carrier she will have to be Aa, of the 4 possible combinations her parents could have passed on (AA,Aa,aA,aa) two lead to this outcome, thus 1/2. If you are sure that she is unaffected the aa option is eliminated and she thus has a 2/3 chance of being a carrier.
If you are not a carrier but your girlfriend is it will be impossible for your child to express the trait (but would still have a 50% chance to be a carrier!). If you are both carriers you loop back to the original situation of her parents, your child would have a 25% chance of being affected and have a 50% chance of becoming a carrier. I must emphasize that real life genetic inheritance is more complex than these textbook calculations, chromosomal crossing over and whatnot can seriously alter these percentages.
I am not a health professional, consult your physician and/or get your girlfriend tested (if possible).

That calculation is only correct if the girlfriend does not know whether or not she is affected.

@swbarnes2 Yeah I apologize I misread carrier for affected.


text:
Are there any bacterial lineages which are particularly well adapted to becoming endosymbionts?
Is there any particular bacterial lineages which contain a large number of endosymbiotic species and that inhabit a large range of eukaryotic hosts? To me, this would seem to suggest that they are particularly well adapted to becoming endosymbionts.

Can you give some more background? Which endosymbiotic bacterial linages do you know of from before, and are you interested in any specific types of endosymbiosis in particular?

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0027909

Members of the genus Xenorhabdus are entomopathogenic bacteria that associate with nematodes. The nematode-bacteria pair infects and kills insects, with both partners contributing to insect pathogenesis and the bacteria providing nutrition to the nematode from available insect-derived nutrients. The nematode provides the bacteria with protection from predators, access to nutrients, and a mechanism of dispersal. Members of the bacterial genus Photorhabdus also associate with nematodes to kill insects, and both genera of bacteria provide similar services to their different nematode hosts through unique physiological and metabolic mechanisms.

While that's definitely an interesting example of symbiosis, I think the question was more focused on whether there are bacterial lines that are more prone to forming endosymbiotic relationships with diverse species.


text:
Isn't biological immortality strictly speaking impossible?
This question relates to both immortal cells such as cancers and organisms like the Hydra genus. Isn't it technically impossible for these "immortal" biological systems to live forever, even disregarding accidents and disease?
I am aware that they are considered immortal because they do not exhibit the usual degradation of functionality as they chronologically age. In cancer's case an up regulation of telomerase prevents the usual gradual depletion of DNA at the chromosomal ends limiting a cell's lifespan. But at the same time cancer cells and immortal organisms still undergo DNA damage and thus mutation (cancer cells even mutate faster as far as I know), wouldn't the stacking of these mutations at some point kill off the cancer cell line/immortal organism as some vital part of their metabolism is inevitably damaged?
Wouldn't true biological immortality require an organism with DNA that is either impossible to damage or if it could would always be perfectly repaired? (creating an evolutionary dead-end as well)

It sounds like you're actually defining immortality as perfect self-replication. With that definition, yes, it's practically impossible, as no DNA replication machinery is perfect. Is it a rhetorical question?  :)

@Roland It wasn't intended as a rhetorical question hahah, I'm just wondering if I'm missing something obvious. I read about achieving human biological immortality by engineering up regulation of telomerase and this question popped in my head as a caveat to human immortality.

Keep in mind that all living things are the result of an unbroken chain of replications going back to the first cells. If "immortality" is defined to include "the ability of cell lines to replicate indefinitely" (and if we bring in the "immortality" of cancer cells, then it is) then all evidence points to biological immortality being possible - I mean, not really, the heat death of the Universe will get us if nothing else does, but 3-odd billion years isn't a bad run so far. This is different of course from the question of the immortality of any given multicellular organism.

I don't think you're missing something. The word "immortality" is used to describe cell lines that have bypassed the normal replication limit of normal ("mortal") cells, but you're right it's technically not true. If you culture a cancer cell line for a very long time, it will degrade in various ways and at some point it will stop growing and die.

I think part of the confusion between where your question wants to be and a purely rhetorical question is that there are two different types of immortality here: perpetual life of an organism, like a human - who contains many cells that proliferate and die all the time, and immortality when referring to lines of cultured cells: the definition of an immortal cell line is a line which will not stop replicating due to intrinsic mechanisms to limit cell division. (edit: while typing this comment @Roland commented effectively the same exact thing)

Cancer isn't 'human' but more of a 'human-derived organism'. It in essence becomes a unicellular eukaryotic organism growing in the ecosystem of an animal (or a dish). As such consider that a group of cancer cells are just related to one another in the same way a colony of bacteria are and thus are 'immortal' in the same sense that bacteria would be considered immortal. Cancer cells are constantly evolving in the same way as bacteria. Immortality is more of a philosophical concept then a biological one down at the cellular level.

Good question.
There are many organisms that are technically biologically immortal. However, I would like to point out that the definition of biological immortality is this:

...cells that are not limited by the Hayflick limit, where cells no
  longer divide because of DNA damage or shortened telomeres.

(That's from here.)
So biological immortality doesn't really cover disease or physical trauma, which would actually include damage to DNA. I know what you're thinking: But wait, doesn't biological immortality literally mean cells that don't die because of DNA damage? Nope. Close, but no. Look back up at the definition. You probably caught it this time (by the way, it's not listing two different reasons (DNA damage and shortened telomeres), just rewording the Hayflick limit (DNA damage aka. shortened telomeres)). Biological immortality does not mean that the cell will not die because of excessive mutation (which would fall under physical trauma mind you, be it from chemicals, radiation, or just plain mistakes during replication), it means that the cell will not die from excessive programmed mutations, aka. its Hayflick limit, aka. telomere degradation. A molecular biology course summary from Berkeley says:

However cells that express telomerase still undergo cellular senescence in response to DNA damage, oncogenes, etc.

Ok, sidetrack time (go ahead and skip this part if you already know what telomeres are). A telomere is a repeated DNA sequence at the end of a chromosome that protects the coding regions from deletion (the reason for these deletions is complex and off topic, but long story short, RNA primers cannot attach to the very end of a chromosome, so a little of the lagging strand is lost during every replication). So the telomere takes the hit instead of the important coding DNA further up the chromosome (see this article.) As you can imagine, there is only enough telomere to go around, so cellular aging exists unless the organism has active telomerase, which is an enzyme that adds telomeres every time they are lost (see this article).
So, short answer, biological immortality is very possible in its actual definition (see above).
Concerning your definition (immortality regarding all mutations, programmed or otherwise), an organism comes to mind: Physarum polycephalum. It is biologically immortal in the way we have just defined, but also avoids DNA mutation by sharing DNA (constantly comparing and fixing sequences) among thousands to millions of nuclei through homologous recombination, which repairs DNA mutations at a freakishly high efficiency when you include millions of strands bearing what should be the same sequence (see this article). Physarum polycephalum is a slime mold, meaning that when cells meet each other, they fuse. This particular slime mold actually prefers to be a plasmodium, which is a constantly growing mass that is technically a multinucleated single cell but can grow to be potentially infinitely large as far as we can tell. Because of its extreme ability to correct mutations, this organism has been referred to as, exactly like you said, an "evolutionary dead-end." I'm sure it still sustains some mutations over a very long period of time, but you might want to check it out nevertheless.

Nice answer, +1! I recommend that you add some more references in the answer, like about telomeres and Physarum, etc.

Thanks, I do find it a bit weird that aging in this context is solely defined as shortening telomeres instead of overall DNA damage. Also that mold seems fascinating.

@another'Homosapien' Thank you. Done. And thanks for the italics, not sure how I missed that... :)

@KoenvdH My pleasure :) Keep in mind, that's just the definition of cellular senescence (aging). While we're pretty sure it has a lot to do with the aging of the whole organism, we still don't know for sure if that's the entire story. But alas, that is a discussion for a different question. To avoid confusion, slime molds are very inaccurately named; they are actually protists. They were named when we still thought they were fungi... But yes, they are quite fascinating. :)

The whole "science" behind telomeres is rather flaky, for example:
Is Telomere Length a Biomarker of Aging? A Review

Although telomere length is implicated in cellular aging, the evidence suggesting telomere length is a biomarker of aging in humans is equivocal...
They observed that the change in telomere length at follow-up was highly variable with some participants showing an increase in telomere length.

So like most questions in biology, there's no answer.
Also P. Physarum has many strains, it is in no sense an "evolutionary dead end" simply because it can't mutate.
http://www.genetics.org/content/78/4/1051.short

"There is no answer" is not an answer. A more accurate description of your situation would be "I do not know the answer, nor do I care to seek one out." In which case, it would be better to not answer at all. Regarding your links, see my answer. I said nothing of mortality rates, like the article you cited was discussing. Rather, I was speaking purely of cellular senescence, which was the OP's question. The correlation between telomere degradation and mortality rates has so many variables (disease, trauma, lifestyle, etc.) that it is very difficult to substantiate, as we see in that article.


text:
A way to measure ripeness of a fruit
I'm doing an experiment how fast fruits ripen and decay
I'm wondering how to measure the ripeness of a fruit(banana, mango, tomato, kiwi etc.) so that I will get a quantitative results.
I have looked at using penetrometer to see how squishy it is. Is there any other ways to do it?
If not, I'm thinking of getting qualitative results. Is there any tips of making good qualitative results?
thanks

Sorry, I am not sure if this falls into Biology category

I suspect the answers will depend greatly on which fruit(s) you are considering measuring.

At what stage of development will you be observing the fruits? Are they going to be fruits from the supermarket, or do you have access to the trees?

Just a fruit from the supermarket

Asides from just eyeballing the change in color/consistency, Wikipedia suggests using iodine for a qualitative measurement (though without reference):

Iodine (I) can be used to determine whether fruit is ripening or rotting by showing whether the starch in the fruit has turned into sugar. For example, a drop of iodine on a slightly rotten part (not the skin) of an apple will stay yellow or orange, since starch is no longer present. If the iodine is applied and takes 2–3 seconds to turn dark blue or black, then the process of ripening has begun but is not yet complete. If the iodine becomes black immediately, then most of the starch is still present at high concentrations in the sample, and hence the fruit hasn't fully started to ripen.

A quantitative method applicable to many kinds of fruit is going to be tricky. If you have a spectrophotometer you could measure the changes in light absorption as the fruit ages. You will probably want to measure the absorptions of control fruits as they age and then compare them to fruits from whatever experiment you perform.
Another possibility is measuring ethylene and/or carbon dioxide production. As fruits ripen they produce more of both these gasses, but this increase does not follow a neat linear correlation with time to put it lightly. Non-climacteric fruits, if you use them, may also be problematic here as they do not show such increase in gas production.

Merzlyak, M. N., Gitelson, A. A., Chivkunova, O. B., & Rakitin, V.
Y.    (1999). Non‐destructive optical detection of pigment changes
during    leaf senescence and fruit ripening. Physiologia plantarum,
106(1),    135-141.
Burg, S. P., & Burg, E. A. (1962). Role of ethylene in fruit
ripening. Plant Physiology, 37(2), 179.


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How to derive rate of product formation for an allosterically inhibited enzyme?
I'm working through Mathematical Modelling in Systems Biology: An Introduction by Brian Ingalls, and in Chapter 3 there's an example of a simple allosterically inhibited enzyme with reaction scheme shown here:
$$\ce{S + E<=>[k_1][k_{-1}] ES->[k_2] E + P}\\[2em]
\ce{I + E<=>[k_3][k_{-3}] EI}\\[2em]
\ce{I + ES<=>[k_3][k_{-3}] ESI}\\[2em]
\ce{S + EI<=>[k_1][k_{-1}] ESI}
$$
where E is the free enzyme, I is the allosteric inhibitor, S is the substrate, P is the product, and ES, ESI, EI etc. are the various complexes between them. The book goes on to state that the rate of formation of P is
$$\frac{V_{max}}{1+I/K_I}\frac{S}{K_M +S}$$
where
$V_\text{max}$ is the maximal rate of reaction ($k_2$ * Total enzyme concentration), $K_I$ is the dissociation constant of the inhibitor $k_{-3}/k_3$ and $K_M$ is $(k_{-1}+k_2)/k_1$
No proof for this is shown, although the book says the solution is assuming a quasi-steady state of the complexes ES, EI and ESI. I've attempted to work it out, and arrived at almost, the same equation, except I have I/Ki * (k-1+k3)/k1 instead of I/Ki * KM. I have no idea how to get to the equation present by the book. Can someone explain how their equation was derived?

If you apply quasi-steady state approximation for the complexes then you will get three equations for each of the complexes. Then you have to use the conservation law for enzyme to obtain the equation with respect to just substrate and inhibitor. If you try solving these algebraic equations, it gets very complex and difficult to solve by hand. However, in this system of chemical reactions, you can notice one thing: the binding of the inhibitor is not affected by the binding of substrate. In other words, the amount of enzyme inhibited will not depend on the amount of substrate present. So, in the absence of substrate:
$$\frac{d}{dt}(EI)=k_3I.E - k_{-3}EI = 0$$
So the total uninhibited enzyme ($E_u$) would be:
$$E_u=\frac{E_0}{1+\frac{I}{K_I}}$$
When the substrate is present, the amount of total enzyme available for catalysis would be $E_u$. Now, apply the Michaelis-Menten equation for uninhibited enzyme but substitute total enzyme ($E_0$) with total available enzyme ($E_u$):
$$V=\frac{k_2S\left(\frac{E_0}{1+\frac{I}{K_I}}\right)}{K_M+S}$$
From here you can get the equation given in the book.
The above logic works only if the rate of inhibitor binding is much faster than that of substrate binding. If not, the dynamics of product formation will depend on the different reaction rates and this simplistic equation would not be valid.