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What is the efficacy of an Ebola antibody response
There is contradictory (~?) evidence in the literature that antibody responses against Ebola are effective in clearing the virus and protecting the patient. Some time ago, I wrote a bit about the literature on this in my blog (which you can find here) that one of the primary problems faced in developing an effective antibody response against Ebola is that antibodies may actually be hijacked by the virus in order to mediate entry (Takada et al).
My question is, has this observation been supported? And, if so, how do more recent vaccines address / avoid this problem?

As far as I can see the link you reference does not support the idea that antibodies mediate Ebola entry.  There was some speculation that this might happen, but I don't think there was ever much (if any) support for it (other than analogy with viruses like Dengue).  In general, lab animal vaccine trials have shown that Ebola antibodies are pretty effective.

OK, I'm ready to be embarassed - I need to check on this and see if I may have referenced the wrong article ... or, I don't know... maybe I dreamed it. I'll look into it and repost later.

iayork - I'm sorry, I cited the wrong article. The appropriate article is Takada et al - correction made with link in text above.

Although there are a handful of papers suggesting that antibodies can enhance Ebola infection, in practice Ebola vaccines seem to be highly effective both in animal models (e.g. Aerosolized Ebola vaccine protects primates and elicits lung-resident T cell responses, VSV-EBOV rapidly protects macaques against infection with the 2014/15 Ebola virus outbreak strain, Vaccination With a Highly Attenuated Recombinant Vesicular Stomatitis Virus Vector Protects Against Challenge With a Lethal Dose of Ebola Virus) and, probably, in humans (Efficacy and effectiveness of an rVSV-vectored vaccine expressing Ebola surface glycoprotein: interim results from the Guinea ring vaccination cluster-randomised trial).
If antibodies can enhance infection, how could vaccines protect?  That's not as contradictory as it sounds.  In general, antibody-mediated enhancement of infection only works under specific conditions.  Even with Dengue, the poster child for ADE, it only occurs during a specific window of antibody titers and affinities.  Ebola is probably much less adapted to needing ADE than Dengue, so it's likely that you'd only get ADE in a very narrow range of antibody titers, affinities, and perhaps targets.  So if vaccines induce high titers, high affinities, and/or a particular set of antigenic targets, ADE may never kick in -- it may be a lab curiosity that isn't relevant in the real world.
(Alternatively, it may be an issue down the road, say if vaccine-induced immunity fades in a specific way that allows it. I don't know of any evidence suggesting this would happen, but I'm not an Ebola researcher.)

--it may be a lab curiosity that isn't relevant in the real world.                        This is exactly what I have thought as well since reading the original article that brought it up, but with all the fervor to develop new vaccines, I thought it was both something to keep in mind when fast-tracking a drug as well as a question that newly published data might answer.   Ultimately, these are the kind of data that make me pay attention because something novel might show up.


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Do bacteria develop a resistance to antimicrobial peptides at the same rate as against "regular" antibiotics?
From what I understand, antimicrobial peptides are roughly grouped into three structural sets, with large variations present between different groups as well as within the groups. Their anti-microbial properties tend to be through slightly different avenues than traditional antibiotics as well, since they can effect cell wall structure and some intracellular targets.
I have been told that antimicrobial peptides are thus able to be effective against as larger spectrum of organisms and that said organisms develop a resistance more slowly.
I do not understand why either of these cases is true, since any antibiotic sharing the same target should have the same effectiveness. Also, evolutionary pressure is what drives resistance, so why should that be reduced against antimicrobial peptides?

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Extinction of species with extant descendants
From what I've seen, species such as Homo heidelbergensis which have extant descendants are classified as extinct, which makes sense as far as it goes.
However, given that species exhibit a continuum of development throughout time, does that mean that for any given extant species and their ancestors there is an "extinction line" which moves gradually forward as small changes in the "current" gene pool render the ancestors from a given time no longer capable of producing fertile offspring with the "current" species and thus shunts them out of the current species and into the extinct species immediately proceeding it?
Additionally, does that mean that there might have existed a species (say, for argument's sake, H. heidelbergensis) with a genetic distribution such that some of them would be capable of producing fertile offspring with the "current" descendant species (in this example, H. sapiens) and some of them not, thus rendering half of the species effectively extinct and the other half not (at least, not yet)?

I don't fully understand your question. I think it is less misleading to talk about about lineage than species given that you start talking about half-species. Some lineages get extinct, others don't. The extinct lineage cannot be the direct ancestor of a extant lineage. An extinct lineage however have a common ancestor (and a Most Recent Common Ancestor MRCA) with some extant lineage.

For example, among the "big" lineage that is homo (Genera), you have several lineages (sapiens, neanderthalis, * heidelbergensis*, etc..). The lineage Homo is extant (thanks to the lineage sapiens) but all the non-sapiens lineages within the homo are extinct. I am not sure that this helped...

It is helpful, but not what I'm asking. I understand the distinction you're making, but I'm specifically interested in this particular oddity in what appears to be the common definition of "a species".

The common definition of a species (for sexual species) is based on reproductive isolation. So, if some individuals within a species die (or don't reproduce) , then only the other ones will be left. And if you consider one population (of constant size to make it easier) and look backward in time, you'll see that the number of ancestors of the currently living individuals are much less numerous that in the current time.

Maybe you are interested in coalescent theory. It is a mathematical framework that allows you (among other things) to calculate the expected to the MRCA of a sample of $n$ individuals. Here is a recent question related to this concept. Did I nail down to your interest or am I off-topic?

If any species has descendants, then it isn't extinct. Mating ceased once extinction occurred.

You are right. Consider a population at some point back in time and ask how many of the individuals left descendants that are still alive today?, the answer will be between 1 and N (inclusive), where $N$ is the population size. We call this process coalescence
A tiny introduction to coalescence
Consider a population of constant size $N$ and to the previous generation and ask the question What is the probability of two random individuals to be siblings?. This probability is $\frac{1}{2N}$ (assuming no selection and diploid population). The probability of them not being siblings is $1-\frac{1}{2N}$. We can say that, with probability $\frac{1}{2N}$, two randomly individuals coalesce in the previous generation. What is the probability that 2 random individuals coalesce $t$ generations ago? It is the probability that they don't coalesce for $t-1$ generations and then coalesce, that is $P(t) = \left(1-\frac{1}{2N}\right)^{t-1} \frac{1}{2N}$. In words, the coalescent time follows a geometric distribution with parameters $t$ and $\frac{1}{2N}$.
Because coalescent times are independent variables (and I won't prove it here), one can extend this to not only 2 individuals but $n$ individuals. There is therefore, a point in time where all individuals of the modern day population coalesce into only one individual. At this time, this one individual was not alone in the population of course.
Coalescent theory: Usages and book recommendation
The simple calculations I just made are the very basis of coalescent theory. Coalescent theory is a very powerful set of mathematical tools that one can use to make detailed predictions of the genetic patterns to expect in a population. Statistical test such as Tajima D test is based on results from coalescent theory. Coalescence theory can be extended (through approximations) to structured population (structured coalescent theory), non-neutrality (selection) and recombination.
coalescent theory: an introduction (by John Wakeley) is a good book on the subject. However, it requires from its reader some basic knowledge in mathematics and problem some knowledge in population genetics.
What is the percentage of people living in England in 1500 AD whose lineage is still alive? is a recent post on Biology.SE that is relevant to the kind of question that could be answered with coalescent theory.

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Why are carbohydrates the most common short-to-medium-term energy storage form in biology?
According to this table, gasoline has a specific energy noticeably higher than fat and more than twice that of carbohydrates; even short-chain hydrocarbons like ethanol and even methanol offer an improvement in specific energy over carbohydrates. Given this, why are carbohydrates the most common short-to-medium-term energy storage form in biology?

Two quick reasons: (1) those compounds are toxic to cells, or may give toxic metabolites when metabolized; or (2) they might actually be great energy sources, but enzymes to process them have never evolved.

I would argue that the toxicity is as much a result of the "choice" of energy storage as a cause, since toxicity is basically metabolic/physiological incompatibility; also, numerous organisms have evolved toxin immunity quite quickly where advantageous. (Also, the metabolites of hydrocarbons are simply water and carbon dioxide, the same as carbohydrates)
Secondly, my question is essentially why those enzymes haven't evolved? Complexity seems an odd reason, since straight-chain hydrocarbons are simpler than carbohydrates, so what advantage selected for the latter rather than the former?

I agree with your comment about metabolic compatibility, but toxicity is not determined simply by elemental composition. The rest sounds similar to many questions on this forum of the form "why haven't cool function X evolved". Evolution is cannot plan ahead, so it gets stuck in local optima all the time. Photosynthesis somehow (randomly?) evolved to produce sugars from CO2, and thereafter sugars became a common currency. This may well be just a coincidence. But these are so early events in evolution that we really don't have any way of knowing.

I fully understand that evolution tends to an immediate optimum rather than a long-term one, in which case the answer I am looking for would be the local optimum which made carbohydrate metabolism more (immediately) advantageous. Given that hydrocarbon-based metabolisms have evolved and currently exist, the implication is that carbohydrates offer or offered some selective advantage over hydrocarbons.


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Is a Ribonuclease Inhibitor protein the only mechanism employed by the human cell to protect cellular RNA from degradation by endoribonuclease?
Are there any other methods of protection for cellular RNA from degradation by endonuclease (specifically the Pancreatic Ribonuclease RNase II (Eosinophil-derived neurotoxin) and RNase III (Eosinophil cationic protein)) besides Ribonuclease Inhibitor Proteins? Perhaps a method that interacts with the RNA itself rather than compromising the RNase?
Would 5' end capping or 3' end polyadenylation which are normally used to protect from exoribonuclease also protect from endoribonuclease? Could a Ribonucleoprotein Particle (RNP) type strategy protect from degradation?
Thank you,
CDB

Endoribonuclease is not that high in the cytoplasm AFAIK. Yes binding with proteins does confer some protection. Secondary structures can also offer protection from certain RNAses, but not others.


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Fruit-bearing tree identification
Just moved into a new house in Puerto Rico and I found this tree in the back garden. Can anyone tell me what tree this is, and whether its fruit is edible?

Telling us where on Earth you're located would be helpful...

It is in Puerto Rico.

I think this is a Canistel (Pouteria campechiana):

The fruit are yellow when when ripe, but the form and also the leaves look very similar. The fruit are edible raw, you can find some more information here.

+1, but OP also asks if its fruit is edible?


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How are split inteins joined?
Do they form a peptide bond? Or is it just some affinity/van der Waals interaction?
Is the mechanism enzyme catalized?
Are the residues/moieties at the join site known? Could they be introduced to synthesized peptide fragments to achieve something like native chemical ligation?

Exteins are joined; Inteins are removed and van der Waals interactions are non-bonding interactions and it is definitely not the case. Can you narrow down your post to a specific issue (perhaps the last one as it seems non-trivial) but you have to add more details.

I really mean the joining of the split inteins, which in my understanding must happen before the whole intein (consisting of 2 split intein parts) can be removed. https://en.wikipedia.org/wiki/Intein#Split_inteins


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Why do cats like enclosed spaces (e.g. boxes) so much?
A recent article doesn't reach a firm conclusion, but offers two possible explanations.

Hiding is a behavioral strategy of the species to cope with
  environmental changes and stressors.

It keeps the cat at a comfortable temperature.

Can you expand on the tentative explanations (i.e. give some background), and explain what you think is lacking?

I just updated the OP. I'm looking for some more credible source to reach a firmer conclusion using better evidence.

"Cats like boxes because they are cryptic animals; they like to hide,"And a box gives them a place of safety and security."
While inside a box, cats feel that they cannot be snuck up on from behind or the side — anything that wants to approach them must come directly into their field of vision. In effect, such hiding spaces allow them to watch the world around them without being seen.
And if something interesting passes in front of the cat — be it prey or a toy — it can dash out to get the object, and then quickly return to its safety spot.
Boxes also provide cats with a cozy, safe place to sleep, which is very important given that the felines sleep for up to 20 hours a day.

authors: user1205901 - Слава Україні


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How many copies of a gene?
I am studying mathematical models of transcription and translation and I am wondering:
In a particular genome, how many copies of a gene coding for one particular protein should one expect? Are they all transcribed at the same rate?
I know humans have two copies of each chromosome, so the answer would be at least 2 in humans. But I wonder if one particular gene coding for a protein we need in abundance might be present in many copies in the genome to increase expression.

Cell cycle
Talking about physical copies of gene, we would indeed have at least 1 copy during the haploid phase, 2 copies during the diploid phase and 4 copies during the mitosis (and during the first phase of the meiosis). Of course, species having mitosis during the haploid phase would have 2 copies of the gene during the mitosis. I am not talking about polyploid species and am not talking about some fungi and other things that have all kind of crazy reproductions system. I am not talking about mtDNA either. Finally, I am not addressing the case of specialized cells that lose part of their genome or the case of tissues that are basically cells who merged together, so that the concept of cell does not even hold any more such as the Syncytiotrophoblast (in the placenta) (see also cell fusion and syncytium).
In short, the variation in the number of copies during the life-cycle is very dependent on the species of interest, the sequence of interest and may also fall under some semantic issue about what is a cell. Note another potential semantic issue result from the question "how similar two genes have to be to still be called copies?".
Mutations and polymorphism
Now, some genes can be found in several copies. When, in a given population the number of copies of a given gene varies from one individual to another, we talk about Copy-Number Variation (CNV). The increase in the number of copies is called gene duplication (or gene amplification or chromosomal duplication when a very big chunk of DNA gets duplicated). The decrease in the number of copies is called gene deletion. There are a diversity of processes that can cause deletions and duplications such as homologous recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage.
Evolution of CNV
What mutation is likely to occur first
Gene duplication does not necessarily yield to an increase in the protein concentration (but it can as it is the case for the Pelizaeus–Merzbacher disease for example). If higher expression is selected for, it "feels more likely to me" that the first mutation(s) allowing for this increased expression will affect the regulatory sequences and will not increase the number of gene copies.
Consequences of gene duplications
Gene duplication (if not loss) can yield to subfunctionalization or neofunctionalization. From wikipedia:

Subfunctionalization [is a process] in which pairs of genes that originate from duplication, or paralogs, take on separate functions

...In others words, copies are free to accumulate mutations as long as the other copy is still doing its job

Neofunctionalization, one of the possible outcomes of functional divergence, occurs when one gene copy, or paralog, takes on a totally new function after a gene duplication event

...Basically, one copy gets a totally new function... that can yield to very interesting innovations such as anti-freeze proteins (ref) or snake venom (ref).

Remi.b talked at great length in his answer about copy-number variation and the generation of new genes. However, I don't think he quite answered what I think is a pretty basic question:

How many copies of any particular gene are there in (a human) genome?

The answer to that question is also simple: two - one on the chromosome from the mother, and one from the father. The exception is genes on the X and Y chromosomes, but that's complicated so I'll ignore it :)
Now, that's not to say that there might be several versions of any particular gene, having arisen through such mutational events as Remi.b explained. So, in antiquity, gene ABC123 might have been duplicated, leading to today's genes ABC123a and ABC123b, which may or may not have different functions. But, for ABC123a, there are only two copies per (normal) cell, and the same is true for ABC123b and all the rest.

Are they all transcribed at the same rate?
But I wonder if one particular gene coding for a protein we need in abundance might be present in many copies in the genome to increase expression.

The regulation of gene expression is quite complex. However, the cell (I'm referring to eukaryotes here, I don't know how different prokaryotes and Archaea are) has mechanisms to ensure that the products of so-called housekeeping genes, which are needed in great abundance, are available to the cell. One method is to attract and keep the RNA polymerases (which transcribe the gene into messenger RNA (mRNA), which is the template for translation into a protein - the actual gene product) bound to the gene sequence through a variety of DNA "promoter" and "enhancer" sequences, which other proteins called transcription factors bind to and recruit the polymerase to the gene. These polymerases are kept active for as long as the cell needs the gene's protein product, churning out copy after copy of mRNA. There are many other mechanisms as well, ranging from how the core histone proteins that give chromosomes their shape bind near the gene, to the manner in which the translation machinery (ribosomes) bind to the mRNA and produce multiple protein molecules per mRNA copy. So, even though we may only have two copies of a particularly vital gene, the cell has evolved ways of meeting demand for its product.

Are they all transcribed at the same rate?

No, they are not. This all depends on the number, kind, and placement of transcription factor binding sequences in the DNA surrounding and within a gene, as well as the exact identity of the transcription factor(s) recruited. Some keep the polymerase machinery very tightly bound, ensuring quick and accurate transcription, while others don't bind tightly at all, allowing the polymerase to "fall off" the DNA and/or work more slowly. Each gene is uniquely and exquisitely regulated to be transcribed where, when, and in the quantity needed.


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How do catenanes form when DNA replicates?
So I am taking a course in DNA replication and repair. And we are talking about catenanes forming when DNA replicates (two circles of dsDNA interlinked) How is this possible?

The first DNA circle is double-stranded. If you could melt the double-helix completely you would not be able to pull the two stands apart without breaking the sugar-phosphate backbone of at least one of the two strands. This is a topological problem, the two strands are linked to each other.
Now consider DNA replication. In the simplest example there is a single origin of replication and there will be two replication forks proceeding around the circular genome in opposite directions. This is exactly what happens during DNA replication in the bacterium E. coli.  The DNA double helix of the parental molecule "melts", the RNA primers are synthesized by primase, and the DNA polymerase complexes initiate synthesis. Behind each replication fork there are now two hybrid DNA strands, each with a parental strand, and a new daughter strand.
Thus far no sugar-phosphate bonds have been cleaved. When replication is done each daughter ds DNA helix will have a single-stranded nick at the origin, and another one at the site where replication terminated, but those will be quickly repaired by DNA polymerase I and DNA ligase. Even if those two repair enzymes were inhibited, and you could somehow melt the DNA strands of both the daughter chromosomes, you would only be able to pull out the new DNA molecules (with the nicks), the two original parental strands are still topologically linked.
To resolve two concatenated DNA circles you need to make a double-stranded break in at least one of the ds circles. This  enzymatic activity is provided by a class of enzymes named Type II DNA topoisomerases.

Thanks for clearing that up for me, any good videos that show this in action?

When replication is done each daughter ds DNA helix will have a single-stranded nick at the origin-can you substantiate your claim with reference?

Do you have access to a recent biochemistry or molecular biology textbook? DNA replication requires a newly synthesized RNA primer, and that primer has a 5'-triphosphate.  When DNA polymerase completes the synthesis of the new daughter DNA strand, then DNA polymerase I uses its 5'-3' exonuclease activity to degrade the RNA primer (also called nick-translation).  When that is finished the daughter strand is not a covalently closed circle.  The enzyme DNA ligase (plus ATP or NAD) is required to 'heal' that nick and repair the sugar-phosphate backbone.


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Identification of a small mammal
Could someone help with identification of this small mammal? Is it a possum? A dormouse?
It was photographed in Sukhumi botanical garden, in Abkhazia (west of Georgia, on the shores of the black sea).

This is not a marsupial such as an opossum, since no marsupials are native to the region. It looks to be a rodent of some kind, probably a species in the Muridae family.
Which species is it is exactly is hard to tell, since there are many species in Muridae which look quite similar, but my best guess is that this is a Tamarisk jird. It could also conceivably be an escaped domestic gerbil or some type of mouse. The one that you found has more pronounced light areas on its coat than the photographs I found, but is within reasonable limits of what variation can be expected.
Here are some of the few pictures I was able to find that I could verify were of this species.

Klaus Rudloff (source)

Klaus Rudloff (source)


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Coalescence time: Is it different for haploids and diploids in population genetics?
I'm trying to model Cyanobacteria cells divergence in 2 populations with mutation rate $-\mu$ and I need to verify my model with a valid theory. I don't have much biology background and all the theories I can find are either valid for haploid population or mating populations. All I need to know is a theory for coalescence time/divergence for a haploid population without mating. So far I have this:
$$T = 2\times N \times d\\
D = 2 \times \mu \times T$$
in which N is the number of diploid individuals, d is the number of subpopulations (in this case 2), T is the coalescence time and D is divergence. Can I apply this to my case even though it's defined for diploid population?
Thanks

Welcome to Biology.SE. The question is a little unclear to me for the moment. $D$ is divergence. Can you tell us more about what you call divergence? You write $T=2 \cdot Ku \cdot T$, therefore, $\frac{1}{2}=Ku$. This is probably not what you wanted to write. $T$ the coalescent time is in unit of generations I suppose. You might want to let us know where this equation comes from. It is always good to follow conventions; the mutation rate is usually $\mu$, not Ku.

You should write your equations in MathJax (LaTex). Here is a quick tutorial. You might want to have a deeper look at coalescent theory. There is a wikipedia entry. Coalescent Theory: an introduction is a very good book on the subject.

Out of curiosity, what is your background (or what are you studying) if not biology?

Can you provide a background for the assumed model (the equation) and the details of the model that you want to build? Details would include assumptions, parameters to be considered etc, phenomena to be accounted for etc. If you do not include these details then your question would be too broad. There can be several ways to model a system.

Need background for those equations and need a definition for "divergence".

Coalescence time: Is it different for haploids and diploids in population genetics?

Short answer
The coalescent time is twice as high in a diploid population than in a haploid population
Long answer
Imagine you sample at random one chromosome. Then, you sample a second one and you ask the question, what is the probability that they coalesce in the previous generation. This probability is $\frac{1}{PN}$, where $N$ is the population size and $P$ is the ploidy number (1 for haploids, 2 for diploids). The probability that they do not coalesce is therefore $1-\frac{1}{PN}$. The probability that the two chromosomes coalesce $t$ generations ago is the probability that they don't coalesce for $t-1$ generations and then coalesce. That is the probability that the two chromosomes coalesce $t$ generations ago is
$$P(t) = \left(1-\frac{1}{PN}\right)^{t-1}\frac{1}{PN}$$
You might recognize here a geometric distribution, where the probability of success is $\frac{1}{PN}$. In order to simplify the math, let's assume that the population size is very large. In such case the above formulation is well approximated by
$$P(t) = \frac{1}{PN} e^{-t\frac{1}{PN}} $$
You might now recognize the exponential distribution with rate $\frac{1}{PN}$. We can now compare the mean expected time to coalescent of a diploid population and a haploid population.
The mean of the above exponential distribution is simply $PN$. Therefore, the expected time to coalescent is $2N$ in diploids and only $N$ in haploids.
Details of your post
In your post you talk about structured populations. The calculations are a little more complicated in structured populations and I don't remember on the top of my head how they work.
You talk about divergence $D$. I don't know what you mean by divergence. From coalescent results you can compute the expected heterozygosity, the number of pairwise differences, and even the whole site frequency spectrum. You can as well make those calculations for the structured coalescent model.

Yes you can, as the model speaks of allele coalescence as states the wiki article on that.

It comprises a probabilistic assessment of variation in time to common ancestry of alleles in a relatively small sample of individuals, from a much larger population.

What you are trying to check is how many generations have passed since any number of alleles were a common ancestral copy.
For that we have:
$t=\frac{4N}{n·(n-1)}$
This was developed by JFC Kingman (based on the Wright-Fisher previous model) for a constat population size of $N$ where $t$ is the coalescence time of $n$ alleles. In this equation the numerator is $4N$ because $2N$ is the total allele population size. You have to multiply it again by $2$ because the total time two alleles have been differing is twice the time it has been separating from the most common recent ancestor. Therefore for haploid populations you should use $2N$ in the numerator.
There are versions of this model that include mutation rate and non-constant $N$, but maybe it would be easier to simply look a good model to find your $N_e$ (effective size of a population, or the N that in a constant size population has the same genetic drift as your actual population) as it can be used in this formula when $N$ is not constant.

Can you please provide some equations to show how it is affected by the "only difference" you cite? You might want to add a reference for your claim as well especially if you don't provide a complete explanation. Given that $N$ is the number of individuals, I would expect the coalescence time to be $T = Nd$ for haploids (assuming $T=2Nd$ is correct for diploids).

It's T=2Nd because there are two paths by which the alleles have been changing, not because there are two copies im each genome. Anyway, let me rewrite it propperly.


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Is sequencing error a function of the nucleotide being read?
Checking out on Google Scholar, I can see that for Illumina (just to consider one example) the sequencing error rate is of the order of 0.001-0.01 per nucleotide.
Talking about sequencing error, let's consider mismatches (substitution of one nucleotide by another) only. Knowing the "true" nucleotide at a given position, is it as likely to be read as any other specific nucleotide during a mismatch or are there bias? For example, if the true nucleotide is A, is it more likely to be found being as a G (as they both are purines) than a T or a C? Are some nucleotides more likely to be misread than others?
I am hoping the answer won't depend too much on the sequencing techniques.

Actually sailorgyaru's answer is very close. The base-calling in Illumina as is different from that of Sanger sequencing. In the latter a noisy position can be assigned to different nucleotides with different probabilities. In Illumina the bad quality can be because of multiple reasons- improper washing , bad signal capture etc. Poor washing may cause overall bad quality everywhere. Perhaps you may look at the mismatch frequencies of nucleotides in reads with overall good quality (mean phred >20). I suspect the mismatch is likely to be random.

Unfortunately, it does depend on sequencing techniques.
For example, in Illumina sequencing, each sequence fragment is amplified (in order to get a stronger signal) and forms a cluster on the microarray. Each cluster is sequenced by cycles of:

Adding fluorescent terminator nucleotides. These nucleotides are modified to contain an inhibiting/terminating group and prevents more nucleotides from being added. Theoretically, only one nucleotide is incorporated into every DNA fragment in this step.
Washing off excess nucleotides.
Capturing the incorporated nucleotide using imaging techniques and determining which base was incorporated (based on the colour of fluorescence).
Cleaving the terminator from the added nucleotides, so that the reaction can continue.

Image from Metzker, 2010.
This way, each fragment is synthesized, one nucleotide at a time, and each nucleotide that is incorporated gets detected. However, the first step is not flawless: sometimes more than one nucleotide gets incorporated into a certain DNA fragment, or no nucleotides get incorporated. Eventually, the DNA fragments in a cluster (all containing the same sequence) will fall out of sync ("phasing") and the fluorescent signal will become less clear, with a mixture of different colours. This is the main cause of sequencing error for Illumina machines, and also the reason why Illumina reads are relatively short (~300bp).
So to answer your question, in this example, nucleotides may be erroneously read as nearby nucleotides in that sequence. Errors will vary using other sequencing methods and how those methods work.
The article I linked earlier explains various sequencing methods in more detail. (Unfortunately, it's behind a paywall so some may not be able to view it.)

Welcome to Biology.SE and thank you for your answer. So just to make sure, you that indeed the probability for a A to be read as a given nucleotide is dependent of the nucleotide and dependent on the technic used? You're not only saying that the error rate is dependent on the technic, right?

I can't say for sure but I don't think it's dependent on the nucleotide (at least not the chemical properties of the nucleotide). Most sequencing methods use different coloured fluorescent markers to detect which nucleotide is incorporated, and which base is called depends on the intensity of the colour signal. Perhaps certain bases are more likely to be erroneously incorporated into DNA in general, but I've never seen that mentioned as a significant factor.

In the future, we recommend linking to cited works via PubMed or DOI. Publisher's websites can (and do) change. Additionally, please double-check your links before posting. The link to the Metzker paper was broken.

@MattDMo Sorry about that; thanks for fixing it!


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Simple protein graphics software for stick models
Anybody know of a good free molecular graphics system that allows PDB file input? I prefer that it does not use Java. I also prefer that it is online, although I would consider recommended software with a simple download process.
I am looking into trying to display a stick version of one of the chains of a protein, and want a program that can help me easily do this.
I have tried using FirstGlance and Protein Workshop, but FirstGlance is difficult to navigate through and the Protein Workshop doesn’t do stick models.

Have a look at Pymol and Chimera...

There are inofficial Windows builds of Pymol, those are free. Compiling Pymol yourself on Windows is very difficult, it's pretty doable on Linux.

There's also UnityMol, reads PDBs,  Cytoscape networks, OpenDX potential maps, and Wavefront OBJ.

VMD is very powerful.

which capabilities do you expect to have?

Comments are not for extended discussion; this conversation has been moved to chat.

This is an answer simply because I can't fit it all in a comment, or several...
To install and run PyMOL, you'll need a few extras. They are all free and open-source:

Python 2.7.10: Make sure you choose to install pip during the setup process, and also choose to add Python to your PATH, if that option is given. Also, note whether you installed the 32-bit version (x86 MSI installer) or the 64-bit one (x86_64). Which you choose depends on your operating system - if you have a 32-bit OS, you only have one choice. If you have 64-bit Windows, you can do either one - there's no real difference to the casual user. I like 64-bit, but I'm a nerd :)
The numpy+mkl package: I'd get version 1.9.2, as 1.10.0b1 is a beta version. Make sure it's not one of the "unoptimized" builds! You want the cp27 (stands for CPython 2.7) package, either 32- or 64-bit, matching your choice above.
From the same page, the PMW package (choose the py2 version).
Finally, PyMOL itself (both pymol and pymol_launcher packages for cp27).

Once you have everything downloaded and Python installed, open the command prompt by hitting WinR, typing cmd into the box, and hitting Enter. Use the cd command to change to the directory where you downloaded the .whl files (paths with spaces in them should be completely enclosed in double quotes: cd "C:\Users\John Smith\Downloads"). Next, type pip -V to ensure pip works. If it doesn't, just use the whole path: C:\Python27\Scripts\pip -V. Once you get the version statement, you're good to go. For each filename, type pip install really_long_filename.whl to install it. Remember that you can start typing a long name, then hit Tab to complete it. Do this for all four wheels - numpy+mkl, pmw, pymol, and pymol_launcher - in that order.
Once you do that, you should be all set. I'm not on Windows at the moment, so I can't tell you whether you'll get an icon or not, but if you don't, then open Windows Explorer and browse to the C:\Python27\Scripts directory - there may be a PyMOL script there you can run.
If you have any questions, please ask on Stack Overflow, tagging the question with [python] and [pymol]. People are generally very quick with comments and/or answers, so please stick around on the question's page for 5 or 10 minutes to assist those who would help you.
Good luck!

Is the MKL part important? I have numy but not MKL..

I'd recommend it, as the MKL can offer quite significant improvement in some numerical calculations over standard math libraries, and since PyMOL is completely based on very computationally-intensive work (displaying molecules and proteins in 3D), I'd strongly suggest getting it. To install over your current version of numpy, just run pip install -U numpy-1.9.2+mkl-blah-blah-blah.whl. The -U flag means "upgrade".

Another good alternative is Swiss-PDB viewer. It is free, small, easy to install/use and is available for different OS (I had used it in Windows XP with 256MB RAM! Some features don't work well with low RAM but nonetheless it is not very resource hungry). It is good for the kind of tasks you are interested in. But it is not online (Actually I fail to understand why you need an "online" viewer).

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


text:
Bright green caterpillar with long white stripes, few hairs, no extensions, possibly Noctuidae
Our herbs had strange holes, and we found eight of these caterpillars to be the reason. They were mainly underneath the leafs and measured about 5 cm in length.
We collected them from the herbs, put them in boxes and also fed them (slightly rusty) crisphead lettuce, which they seemed to like just as well.
We tried to identify them, and our best guess was some sort of Noctuidae, possibly Ctenoplusia limbirena. We're located in central Germany.
When disturbed, they froze for several seconds, then slowly began to move (and eat) again. When picked up, they sometimes spit a few drops of green fluid at their attacker.

They ate "a lot" for a few days - and pooped just as much. I cleaned their box twice a day, but as you can see, they were quick to fill it up again. (I hope you don't mind the picture - at least it did not smell at all.)
Now, their behavior changed, and they folded leaves, attaching it with strings to stay in place, and hide in there - I suppose they're about to become pupas.
I would be interested in what species they are, and if they are dangerous to humans. We've always washed hands after contact and avoided touching their poo, though they most viciously attacked my girlfriend's finger with green spit (she survived without any damage).
Further, how can we help them advance to become winged? Is it sufficient to just leave them alone, or should we add more leafs or sticks to their box?
Finally, I was told they would practice cannibalism if food supply were too low - is this true? I would have thought their stomachs are specialized to leaves exclusively.
Edit: Not even a week later, they hatched, and I took some photos before setting them free:

Eisbergsalat = Crisphead lettuce

This could be one possibility, two others would be:
Scoliopteryx libatrix (The Herald (moth)), see this image (from here, contains additional information in german):

Orthosia cerasi (Common Quaker) would also fit, see here (from here, contains additional information in german):

Thank you! Is the "leg" count an indicator of species? Mine have 2x3 legs at either end, while the Common Quaker in your picture has 2x5 at the rear.


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Any examples of animal behavior in response to meteor showers?
I just spent two nights observing the Perseids and was wondering whether any animals have been recorded to exhibit unusual behaviour in response to meteor showers.
It is known that some animals change their behavior at night in response to moonlight and artificial illumination (e.g. eagle owls call more frequently at full moon), but I am not aware of any materials indicating behavioral changes in response to short-term lights like those produced by meteor showers or far away lightnings.
Any pointers would be appreciated.

There are a significant number of major meteor showers in the earth's orbit, especially in the Northern Hemisphere. Nocturnal animals have good night vision (obviously) and their acclimation to the dark plus time spent awake at night (if they look up at all) means they see many, many more meteors on average than humans do.
The year's parade starts with the Quadrantid shower.

January overall has good meteor rates restricted to the last third of the night. Rates to 20/hour can be obtained.

Meteor "showers" (if they can be called that) continue until mid-march, when they drop off to a "very poor" rate of 10/hour or less, continuing this pattern into early June, except for the Lyrids (max: April 22/23) and the Eta Aquariids (max: May 7/8).

February, March, and April evenings have another notable feature. An unusual number of sporadic fireballs come in this interval, possibly one every few nights.

In the last half of July, we get the Delta Aquariids (July 29/30) and Alpha Capricornids (July 27-28).  Then the Perseids (maximum: August 12/13), rich to our eyes at about 100/hr at their peak, moon and weather permitting.
From September to the first half of December is pretty rich.

Mid-October to mid-December is a nearly continuous period of heavy meteor activity. The Orionids (max: October 21/22) during the second half of October have a prolonged, plateau maximum for several nights, usually rich. The Taurids (max: October 11 for S. Taurids, November 13/14 for N. Taurids), active for two months, are most numerous in November’s first half, and can be rather variable in strength. This period is the best for a couple of Taurid fireballs each night, if the shower is not too weak. The Leonids of mid-November (max: November 17-19) are quite unpredictable, with rich displays occuring roughly every 33 years.

Finally there's the Geminids of mid-December (max: December 13/14) with "the strongest dependable and observable display" (usually passing 60-70/hour at maximum.)

Finally, the oft-overlooked Ursids complete the year’s activity, reaching maximum on December 22/23. Nearly half the year’s visual meteor activity is crammed into the two-month interval just described.

What does all this have to do with biology and your question? I'm guessing here that the Perseids, though rich for humans, are probably nothing exciting for animals. The diurnals and crepusculars don't see them at all (they're soundless and certainly not bright enough to wake anyone up). The nocturnals see the (or not, depending on where they're looking) all the time. So a study wouldn't likely detect much, would be challenging to design well, would cost some big bucks, and wouldn't really help humans like studying animal behavior before earthquakes and such.
As a child, I once saw some very funny chicken behavior on my grandmother's farm during a total eclipse of the sun. It was so funny that I remembered it all the years since.
I searched, as I'm sure you did, and the first hit on regular Google was this question. A scholar search brought up possible animal behavioral changes before fireballs.
Major Meteor Showers

The entire middle part of this answer seems to be an almanac and has nothing to do whatsoever with the question.

@MarchHo - How to say "Nah, it happens all the time" without proof? That's not like me.


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What are blood group determinants?
I am trying to understand if they are the same as the blood antigens. The books I have tried to read say something about them being the antigens on the surface of the red blood cell.

Blood group A expresses A antigens and anti-B antibodies etc etc, see the next figure:

Taken from the wikipedia entry on blood groups.

In immunology, determinant is another name for epitope (the portion of an antigen recognized by a BCR/Ab or TCR).


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Can stress-induced cortisol reduce diabetes type I?
Let us consider a patient with type 1 diabetes.
I think it would be safe to say that diabetes is an autoimmune disease. Now let us suppose this patient comes under stress. As far as I know, cortisol is a stress hormone and is released when a human is under stress. Now cortisol, as far as I know, increases the amount of blood sugar and at the same time is an immunosuppressant.
I would like to know whether this stress-induced cortisol can suppress the immune system, which has gone haywire, and help against diabetes - thereby rendering a suitable amount of stress useful.

Short answer
Stress is not a good candidate to treat autoimmune disease like diabetes type I.
Background
Stress indeed weakens the immune system, and diabetes type I is indeed caused by an auto-immune response against the insulin-producing beta cells in the islets of Langerhans. However, autoimmune diseases like diabetes type I need chronic treatment (i.e., insulin treatment and dietary changes).
Even if stress would help reduce diabetes type I (admittedly, theoretically it could), chronic stress would also reduce the immune response against viral and bacterial infections, it would reduce wound healing and perhaps even increase the risk of contracting cancer (Glaser & Kiecolt-Glaser (2005), as well as increase the risk of depression and cardiovascular disease (Cohen et al., 2007).
Hence, it is safe to say that deploying chronic stress as a treatment against auto-immune disease effectively means substituting one life-threatening condition with another.
References
- Cohen et al., JAMA (2007); 298(14): 1685-7
- Glaser & Kiecolt-Glaser, Nature Rev Immunol (2005); 5: 243-51

What about deliberately going through a little amount of stress everyday in a manner which is controlled enough to even reach up to the periphery of being chronic.

It is an idea, but I doubt anyone has tested it. Which patient would prefer to be stressed as opposed to regular treatment with insulin? Would you? Further, how to stress someone daily for years in a controlled way? I doubt anyone has tested it for these reasons.


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L-tryptophan in mammalian cell culture
Why must the concentration of L-tryptophan be kept to a relatively low level when culturing mammalian cells?
It's an essential amino acid, so I cannot fathom why low concentrations as opposed to higher ones are best. Does it have to do with carcinogenesis or some other dangerous side effect I wonder?

It is essential but it is also not required in huge amounts. I am not sure if it has toxic effects.

I just assumed it was due to feedback regulation that would affect other amino acids' production, but I really don't know. It's a good question.


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Use of Gene Guns
Gene guns (biolistic particle delivery systems) use gold or tungsten atoms coated with plasmid DNA and bombard it on cells. Their use, as far as I understand, is mostly limited to plant cells. From what I found out, this seems to be due to the difficulty of passing vectors through the rigid cell wall that a plant cell has. Is this really the sole reason why gene guns are mostly used for plant hosts? Fungi also possess a chitin cell wall - is the gene gun used for fungi hosts as well?

C elegans respond well. I posted a ? On here few days ago regarding the use of gene guns:  http://biology.stackexchange.com/q/36738/6061 no one cared :-( lol

I think one of the orginal reasons for using biolistic on plant cells was that it seemed to be the only method which proved to be effective.
This is due to some reasons:

A wide range of highly successful methodes for prokaryotic cells (calcium chlorid method, electroporation)
The plant cell has in comparison to animal cells a additional layer (= cell wall) that consists mainly of cellulose chains, which are stabilized by interchain hydrogen bonds to form a crystalline lattice structure (= microfibril), and thus offering the cell high mechanical defense. (book: "Plant Biochemistry", P. 4) This layer mostly needs to be removed before using other methodes than the gene gun, because it can hardly be penetrated. (chemgapedia.de on "Mikroinjektion")
The high inner cell pressure (~3 MPa) of the plant cell, which makes microinjection hard to accomplish: When the cell wall is perforated with a cannula the pressure within the cell drops dramatically resulting in cell death (chemgapedia.de on "Mikroinjektion"). I am not quite sure why the same thing isnt happening when its pierced by the gene "bullet", but I think its because of higher speed and a smaller penetration radius.
Plant cells are big (up to 0,1 mm) and packed up closly and thus an easy target (sparknotes.com on "cell differences")

When it comes to fungi cells, I don't see a reason why they shouldn't be using biolistic on them as well (besides for yeast cells, they might be to small).
The gene gun is the only way to inject even cell organelles, like mitochondria and chloroplasts, into cells. So its already huge area of application will definitly grow in the future. (wikipedia.org on "transfection")

Welcome to Bio and thanks for your answer. If you can include some supporting references I'm happy to upvote.

Can you elaborate a bit on your second point, please? Thank you.


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How to synthesize and isolate single stranded cDNA from an RNA template?
I would like to have pure single stranded cDNA of my choice. I am thinking of reverse transcription from RNA (obtained by in vitro transcription), degrading RNA from RNA-DNA hybrid with RNase-H, heating to 65C to remove any oligoribonucleotides still bound to DNA and pass the solution through G50 sephadex column buffered with elution buffer. This is what I have in mind but are there any efficient ways that are tried before? Or do you have any suggestions over this protocol?

You need a DNA template to do in vitro transcription, so I'm not really understanding what you want to do here? How long is your sequence?

You need to use reverse transcriptase and a thermal cycler. Not much more to it, follow manufacturers suggestions. Life tech makes good RT

@MadScientist I think he's talking about rna->cDNA here not invitro Txn.

Sure that will work, or gel purify the ss cDNA, or treat the rxn with alkali to degrade RNA.  The real questions in my mind are:

What will you use as a primer for the RT?
What are you going to do with this pure ss cDNA?

If you already have the target cloned (how else would you transcribe it in vitro?), then why not just do a linear PCR where you cut the plasmid to linearize it at the site of your choosing, and then throw it in a PCR machine with just one primer?
Why bother going through the T7 RNA pol and RT steps (if you don't need to)?


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What is the C765-Gal4 driver?
What is a gene driver and what does C765 stand for? Is Gal4 a transcription factor?
Source: "Dynamics of Dpp Signaling and Proliferation Control"

C765 is a transgenic Drosophila strain that has a specific Gal4 expression pattern ("embryonic salivary glands and larval wing and leg discs").
Gal4 is a transcription factor from yeast which binds an upstream activating sequence (UAS) and also happens to function in other species (like flies). In the Gal4/UAS system, a strain expressing Gal4, under the control of a tissue specific promoter or a minimal promoter in an enhancer trap, is crossed with a strain expressing a gene of interest flanked at the 5' end by the UAS. The F1 generation will thus express the gene of interest tissue specifically (ie only in the tissue(s) expressing Gal4).

[source]

Further reading:
Phelps CB, Brand, AH. 1998. Ectopic Gene Expression in Drosophila Using Gal4 System. Methods 14(4):367-379.


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Do "virgin" ant queens ever shed their wings?
In species that reproduce sexually, if an ant queen goes on a nuptial flight and does not successfully mate, will she still shed her wings and try to found a colony (although she probably won't succeed because unfertilized eggs will result in drones only)?

Good question. I tried to find a few articles to validate my answer, but it would appear that very few professional studies have been done on the matter. One of my hobbies a few years back was ant keeping and I have had several colonies started from queens over the years, so I can share some of my personal experiences.
Anyway, back to your question. For the most part, no. An infertile queen will keep her wings and either find a safe place to lay eggs like a fertile queen or just walk aimlessly until she dies/is eaten. However, there are some rare instances where an infertile queen will shed her wings after the nuptial flight and find a safe place to nest and even in some occasions will lay eggs that are, of course, unfertilized and will therefore die or become male drones.
On the subject, the same is true vice versa. In rare instances, a fertile queen will NOT shed her wings, find a nesting place and even raise a colony all with wings on. Most of the time, however, her first workers to emerge promptly remove them.
I hope this answers your question.
CDB

Actually, the thought just occurred to me that, just because a species can reproduce sexually, it doesn't mean it must reproduce sexually: what if in some species, the virgin queen can still lay eggs that are just clones of herself? She would still get her army or workers. I think I have read about one species in Japan where there is no queen and all workers just lay their own eggs that are clones of themselves. So it doesn't seem like a total impossibility for queens in other species to do the same. In fact, are we even sure that queens always have enough sperm reserve for her lifetime?

The queenless species in question seems to be Pristomyrmex punctatus (a.k.a. Pristomyrmex pungens):
http://www.researchgate.net/publication/247154220_Japanese_Queenless_Ants_Pristomyrmex_punctatus_Prefer_the_Traces_of_Both_Nestmates_and_Strangers_in_Nest_Selection
http://ant.edb.miyakyo-u.ac.jp/BE/Kingdom/2425/2425e.html


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How do plants benefit from their seeds being buried?
Common planting advice, when starting many plants from seed, is to bury the seed some small distance under the soil.  It seems like most plants (at least members of class Dicotyledonae) will grow a root, lift the seed casing out above the surface, then the cotyledons push off the seed coat.
My question then is: why is it recommended to put the seeds below ground at all?  It would seem that dirt only serves to interfere with the first stages of growth.
I can guess at a few reasons:

To keep moisture around the seed
To make sure the root hits dirt no matter which way the seed is oriented
To prevent predators from eating the seed
To keep the seed in place

Absent these reasons, is there any reason to have soil sitting on top of a seed?

Excellent question!
The main reason why us humans bury seeds seems to be to keep seed-eaters from finding them, though any historical evidence that could conclusively prove why we started doing that is probably lost to time, since we discovered agriculture before we began writing things down. Beyond that, you've rightly identified a number of advantages to burying seeds.
First, it may be helpful to note that no physical substrate is even necessary for plant nutrition. We can actually grow plants in mid-air, but for the fact that we would still need something to keep them still. Seeds will germinate if you simply spray nutrients at them - see aeroponics. This is because plants take in what would be soil nutrients via cation exchange and diffusion, as opposed to more a more active process like phagocytosis. By surrounding the seed with nutrient rich substrate, we inadvertently improved germination by exposing more of their surface area to nutrients.
As far as soil seeking behavior goes, Thomas Knight demonstrated that plants can actually find the ground by following gravity. He did this by sticking seeds onto a rotating disc to simulate gravity in another direction and germinating them there. The seeds responded by growing roots away from the center and sprouting stalk towards the center.
Of course, burying seeds too deep means that they may run out of energy before they can break the surface. However, it seems that many varieties of seed have a better chance of germinating in darkness.
Resources

On the Direction of the Radicle and Germen during the Vegetation of Seeds
A Reversible Photoreaction Controlling Seed Germination

Ahhh I hadn't thought about light coming into play


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Cause of hexadactylisim in Amish people
Is it caused by inbreeding of many generations within an isolated population?

Short answer
Yes, you pretty much nailed it. Inbreeding of (and from) an isolated population.
Long answer
According to wikipedia > polydactyly, there are 39 known polmorphic sites underlying variance in polydactyly. It is therefore not a trait with a simple mode of inheritance.
There are two important (somehow related) concepts to understand to explain the relatively high frequency of polydactyly (and other genetic disease such as maple syrup urine disease) in Amish.

High inbreeding
Important population bottleneck

If you have no absolutely no background in biology, the following might be a little bit complicated. You might want to make sure you know some concepts (such as deleterious, recessive, dominant, homozygous, Hardy-Weinberg equilibrium, locus, allele and of course inbreeding and population bottleneck) by googling them.
Inbreeding
I will, here talk only about one mechanism by which inbreeding causes those diseases.
There is a positive correlation between how deleterious is a mutation and how recessive it is (the more deleterious, the less dominant, the more recessive). The post "Evolution of dominance of alleles" will probably help you to understand why this is true.
Inbreeding increases the frequency of homozygote loci and therefore, increase the probability of a locus which polymorphism explain variance for the disease to be homozygote deleterious. Using Hardy-Weinberg formula with Sewall Wright work, if at a given locus the allele A is deleterious and is present at frequency $p$, then the frequency of the homozygotes AA is $p^2$ without inbreeding (under Hardy-Weinberg assumptions). Taking inbreeding into account, this frequency becomes $p^2 + Fp(1-p)$ (where $F$ is the coefficient of inbreeding). In words, the higher is the inbreeding coefficient, the higher is the frequency of homozygotes (including homozygotes for the deleterious alleles).
In short, inbreeding matters because of dominance. There are other reasons why inbreeding matters though but that would be the subject of another post.
Bottleneck
In population biology, a bottleneck is is a sharp reduction in the size of a population. Imagine you have a population of size $N$ and you selection a fraction $\frac{N}{1000}$ of this population, you are going to lose a lot of alleles due to random sampling. Most of the times you are going to lose deleterious alleles (as they were already present at low frequency in the original population) but sometimes you are going to pick up a deleterious allele. The frequency of this deleterious allele was maybe 0.00001 in the original population and then suddenly its frequency jumps to 0.1. This is a big deal.
The Amish went though an important bottleneck, there was a time when the descendent of the modern-day Amish reproduced with everybody and at some point, they stopped doing so as they decided to create the amish community (I actually know little about the Amish history but I assume something similar happened). This community was formed by about 200 families only (according to this not-necessarily-trustable source, so very little genetic variance) in 1693 in Switzerland (according to wiki). They probably "won" by not having the alleles coding for clubfoot, sickle-cell and cystic fibrosis alleles (just to cite a few example) but they "lost" by drastically increasing the frequency of alleles coding for polydactyly (and some other diseases).

Great answer. +1. One question: I thought that genetic drift was a slow random process http://www.nature.com/scitable/definition/random-genetic-drift-genetic-drift-201 and that it has not a diect link to a sudden reduction in #individuals in a populaton?

From wiki: Genetic drift (or allelic drift) is the change in the frequency of a gene variant (allele) in a population due to random sampling of organisms. A bottleneck is a sampling process where the number of individuals sampled is much lower than the number of individuals in the previous generation. I felt like it would lead to confusions though. I might as well just take my parenthesis away. Thnks

Short answer
Yes, the high frequency of polydactyly in the Amish is caused by inbreeding.
Background
The polydactyly in the Amish is just one of the symptoms of Ellis-van Creveld (EvC) syndrome. EvC syndrome is an autosomal recessive disorder, involving polydactyly of the hands (see figure), short stature with shortening especially of the forearms and lower legs and, in at least half of all cases, congenital heart malformation. In the Amish of Lancaster County (Pennsylvania), EvC syndrome occurs at high frequency and is caused by mutations in the EVC gene.

Source:  McKusick (2000).
The Amish have two characteristics that resulted in the high occurrence of EvC syndrome. First, they are descended from a limited number of founders who immigrated during the eighteenth century to the United States from Switserland,  via Germany in the 1690s. Second, the Amish are endogamous, i.e., they marry only within their community. Hence, gene flow is exclusively centrifugal, i.e., members may leave the community but ‘outsiders’ do not join it and thereby introduce exogenous genes.
All EvC cases in the community are traceable to a single couple, Samuel King and his wife, who immigrated to Eastern Pennsylvania in 1744, thus demonstrating
founder effect and a recessive pattern of inheritance.
Reference
- McKusick, Nature genetics (2000); 24: 203-4

Good answer, simple and without explanations of why inbreeding and founder effect can cause higher prevalence of a disease (but making a complete explanation would ask for writing a book). +1. Your first sentence says Yes, the mutation [..] is caused by inbreeding which is of course wrong.

@Remi.b - Thanks for the appreciation! And also thanks for pointing out that mistake :) I fixed it!


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Drinking soda triggers tingling on a tiny spot on my upper back... but how?
The title pretty much says it all.  Yes, I know it doesn't make sense. That's why I'm baffled.
For the past week or two, I've noticed that drinking soda seems to cause a tingling/stinging sensation on a very tiny spot on the skin of my upper-left back. It happens within a second or two after I swallow. This has been happening pretty consistently since I first noticed it. (I've noticed it at least a dozen times; I'm pretty sure I'm not hallucinating...) I think it also happened once or twice when I was drinking plain water, but not enough for me to be sure whether or not I actually felt it or if I was just imagining things...
I've been otherwise healthy and there's nothing particularly special about that spot on my back, so I'm pretty baffled at the moment. How/why could this possibly be happening?

The skin is a very richly innervated organ, and minor strange sensory phenomena are not exceedingly uncommon.
The thing about sensory nerves is that they can misfire and you seem to feel something when there's nothing there. This actually happens all over our bodies all the time (mostly our brain blocks them out, like it blocks out background noises after a while): an itch for no reason whatsoever (no bug, no bite, no reason) is the most common manifestation of this phenomenon.
Sensory nerves start their journey out of the central nervous system as relatively large bundles coming off the spinal cord, and keep on branching becoming finer and finer as they reach the periphery.

since there's a lot of muscle under the skin, most of these sensory nerves have to come up through muscle.

Sometimes an inflamed bundle of muscle fibers (aka a "knot") will entrap a small branch of a sensory nerve, and the pressure on the nerve will cause it to "misfire", causing a sensory illusion, if you will. If this is the case (if it's in the exact same spot every time) and a slender nerve branch is being squeezed by a muscle knot in your back, you can do a little test on yourself: have someone run a fine sharp object (say the end of a toothpick) softly over an area starting away from the spot going through it. If the sensation changes right on that spot - going from sharp to dull, for example - and does so consistently, that's what's going on. If you have the person map the change of sensation with a pen, the spot will be about the size of a quarter or smaller.
If, however, the sensation is only associated with swallowing, and there's no change to light touch, I have no idea what's going on.
Anyone reading this should know, though, that strange neurological symptoms can be an early sign of MS.

+1 thanks for the answer. I suspect it's just associated with swallowing, but I'll try to have someone do what you wrote just to see what happens. I'll have to wait until I get more soda though, so I can figure out the exact spot again first...


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What is possibly wrong with my gel electrophoresis when i don't see bands of DNA ladder?
![enter image description here][1]
What was possibly wrong in my gel electrophoresis when I didn't see bands of DNA ladder?
I'm running a 2% electrophoresis gel (65v for 2h) to confirm the presence of qPCR amplification products, I can see the gDNA bands, is only the ladder that don't appear.

Try a new batch of ladder, rerun the gel. Without more info this question cannot be answered.

Can you add a pic?

Already added, the ladder should appear in the first lane.

did you try rerunning with new ladder?

no, this was the last ladder available in the lab with the base pairs i needed.

As one attempts their daily Sisyphean challenge of uncovering a new fact there is one truism, or platitude, that informs all of our efforts at troubleshooting an unanticipated experimental outcome.  This can be paraphrased as:
The number one cause is pilot error.
Accumulated experience of bench scientists everywhere shows that their own human errors are the simplest explanation whenever they try to deduce what could have gone wrong.  In the real world this translates into an operating axiom:
Don't waste time and energy coming up with new physical laws, or multi-step explanations that require you to remake and test all of your reagents, just repeat the experiment and see if this phenomenon is reproducible.
With that new information, that it is, or is not reproducible, you can decide if there is any hypothesis to test. But please, don't just take my word for it. Survey experimentalists, and the more experience they have the better.


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How long do human egg cell grow up?
I read article about alcohol harm where written that child may bear with birth defect cause mother used to drink alcohol 10 years ago so egg cell stay damages that long.
I don't believe that human egg cell wait for such long time until activated.
How long human egg cell grow up until sperm fuse it?

https://en.wikipedia.org/wiki/Ovarian_follicle Eggs are paused in their development until released during the menstrual cycle.

Thanks for suggestion! It is unclear from wikipedia article (I am not biologist) but as I understand reading that number of Ovarian follicle from beginning of puberty is limited (near 300'000 - 400'000) and decreased. So I may say that human egg cell live as long as human age except childhood development time.

@gavenkoa any article that make "scientific" claims that you read that is not peer-reviewed or does not accurately reference peer-reviewed findings is at best suspect... Even articles in a source as respected as The New York Times can and do often write their articles base solely on the abstract. The problem is that abstracts to journal articles don't always tell the complete picture of the study which can lead to false assumptions that end up as articles in popular publications.

Fetal Alcohol Syndrome tends to affect the developmental process of the fetus and is not associated with actual genetic change. Ethanol is not a known mutagen, so it is not likely that it has an effect on oocytes. Oocytes are also mitotically inactive, so short of ionizing radiation, it isn't likely that any change will be made to the chromosomes of the oocytes. It is very possible that toxins such as chemotherapeutic and possibly ethanol (though unlikely) could damage or destroy oocytes, but this would likely only affect the woman's fertility and not the outcome of a pregnancy.

How long human egg cell grow up until sperm fuse it?

Ovules are made while the female is still in the uterus of her mother. The ovules (in the form of ovarian follicles) are kept in the ovaries for a long time, and just a month before leaving the ovary (ovulation), the ovarian follicle (and the future ovule) gain in size. In other words, the ovules are slightly older than the age (counting from birth/labour) than the person carrying them. You'll find more information on wikipedia > ovule > ovule Development, oogenesis, and ovarian follicle.
Does it address your interest about alcohol consumption?
Now, I don't think this question/answer address your interest about alcohol consumption. Whether or not the ovule is create by a division that happen just a day before ovulation  or many years earlier doesn't change anything to the fact that this ovule has experienced alcohol consumption (either directly or in the lineage) before.
Where to ask the question that I suspect interest you the most
If you want to question the article you read about alcohol consumption, the best you could do is to go on Skeptics.SE, link the article, quote something from the article and ask "is it true?"

Please consider editing your answer. It is incomplete from the perspective of human developmental biology. Also, I would personally question the use of "belly" over uterus on a forum on biology.

@AMR I changed "belly" into "uterus" (don't think it is quite a big deal but I guess it indeed look better this way). I realize the answer is a bit weak but it boils down to 1) the fact that the question implicitly assume a moment when an ovule is "born" which is quite an unclear concept and 2) wiki says it all. Would you think it is worth making a full description of oogenesis on this post?

No, but then don't go into partial details. Say, unlike males who do not produce sperm until puberty, and then produce them constantly for the rest of their lives, human females are born with their full complement of sex cells, which are, for the most part dormant until ovulation. You could also explain that a toxin that does not cause mutagenesis would at worst kill the cell before it could be fertilized, so it is unlikely that alcohol use outside of pregnancy would pose a risk to fetal development. It is possible that there could be diminished fertility, but that would require citation.

I wouldn't say that I am very proud of the formulation of my answer (and globally, I realize that I am not a great writer and english is not my mother tongue which probably doesn't quite help). If you don't have anything to say about the content but only about the right choice of details (and about the formulation), maybe the best is just to make your own answer, with your own formulation. Thanks for the suggestions though.

I am suggesting that an answer has a higher standard than a comment on SE sites. I gave the response I wanted to give in the comments as I did not want to get into the detail or citation necessary to answer properly. While you may not respect the OPs question or its validity for the forum, you need to remember that SE Q&A on topics rank highly on Google search, so others with the same question will be directed here. Give an answer that is representative of your training as a scientist, or leave a comment to point OP to further research. The answer represents you as much as the OPs question.


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If nerve consists of many axons, where are then their soma located?
This question has haunted me for two years.
Wikipedia mentions :

A nerve is an enclosed, cable-like bundle of axons (the long, slender projections of neurons) in the peripheral nervous system. A nerve provides a common pathway for the electrochemical nerve impulses that are transmitted along each of the axons to peripheral organs.

Okay, my book also defines like that. But if the nerve runs only with bundles of axons, where then are their soma located?
They say nerves are formed of many axons bundled together. Now, if there are axons, there must be soma, but they do not form nerve & hence are not present in nerve. So, where are they? Are they present at the beginning of the nerve?
Also, nerves communicate with each other. Books picture this as two neurons one above other; the above one sends impulse through its terminals to the dendrites of the neuron below it. So, how do these two neurons constitute a nerve?? After all, they now contain the cyton?? So, how do neurons one above other form nerve as they now contain the soma??
PLz explain.

Neurons or nerve cells typically have a dendritic region, an axon and a cell body. The axon is also referred to as a nerve fiber. The axon is typically the longest structure, while the dendrites are mostly situated close to the cell body. See the following figure 1:

Schematic of a nerve cell. Source: Prof. Brown.
Axons often bundle into nerves. For example, the peripheral nervous system contains many nerves. The cell bodies of the neurons that feed their axons into a nerve are organized into ganglions outside the nerve (Fig. 2).

The peripheral nervous system and the location of the ganglia. Source: Miami College.

Really sorry , sir. I mistook in writing nerve-fiber in place of nerve. Can you check it now??

@user36790 - how about now?

Thanks, sir, for posting the pic. So, does that mean all the cell-bodies lie in ganglions?? I urge you earnestly to please at least mark a single nerve in the pic, please. Thanks in advance:)

@user36790 : All the connecting lines are nerves in Fig.2.

Above diagram has the arrow from otic ganglion going to the VII CN ganglion. Should be ganglion just below

@user57399 - keenly spotted. The figure is a schematic only and you are right.


text:
If Tumors have lots of mutations in them how is it the immune system can't detect them?
If a cancerous tumor has a lot of mutations in them why can't the immune system detect them? If a person has cancer could this somehow alter the person's immune system so it doesn't function effectively to detect greatly mutated cells? Does the fact that a tumor is 'made' of 'mutated' non-foreign human cells help it to be undetectable?

"Does the fact that a tumor is 'made' of 'mutated' non-foreign human cells help it to be undetectable?" This is pretty much it. The more mutations a cancer has, the more likely your immune system will respond. I saw a talk by Steven Rosenburg about cancer immunotherapy, might be interesting for you.

This is a good question and I have upvoted already, but you could consider adding some more information from your own background research (e.g. on minimum and typical numbers of mutations occurring in cancers) to make it more helpful to future readers.

Have you done any research at all into how the immune system works?

This is a good question and it gets to the most basic foundations of immunology. Your immune system is made to be flexible - able to adapt to almost any challenge. However, with so much flexibility comes the potential to generate immune cells that react against the 'self'. So, at the other extreme, the immune system needs to be limited.
In order to meet these two (potentially conflicting) goals, immune (at least lymphocytes) cells have a two-step development pathway. In the first step, the body randomizes its immune receptor specificity. In the second step, it ensures that these receptors are not auto-reactive.
Doing so means that immune cells are aware of their environment at the time that they are 'born.' Take a look at this review from the Fuentes-Panana lab to read about how tumors actively cultivate the immune system of their host in order to maintain a more favorable environment.

Great question and in part, you are correct. However, you must also remember that this greatly depends on what genes have undergone mutation.
In the case of cancer, it's usually either a gene that regulates cell proliferation rates, induces programmed cell death or helps to repair damaged DNA. When one (or all) of these genes is mutated, the cell constantly proliferates and/or does not die when it is "programmed" to do so or cannot repair mutations to it's DNA, thus creating a cancerous tumor.
Now, on to the immune system. The reason a persons immune system does not target and kill it's own cells is because of a certain set of genes that is specific to each and every person called Major Histocompatibility Complex (MHC). These genes encode specific cell surface molecules that the immune system cannot produce antibodies to bind to because they are "locked", if you will (see, the immune has a sort of built-in list of genes that code for antibodies that bind to different sequences of molecules (that's how you develop immunity and fight pathogens), the genes that code for the specific molecules that your cells have on their surface are just not on that list.) In order for a person's immune system to recognize cancerous cells as a pathogen and destroy them, the cancer cell's MHC genes would also need to be mutated drastically.
For instance, breast cancer is usually caused by a mutation in the BRCA1 or BRCA2 genes. These genes assist in DNA repair. Even if this mutation happens, these cells still have the same MHC as the rest of the cells in your body because BRCA1 and BRCA2 don't really have much to do with MHC. Because of this, the immune system does not recognize the cancerous cells as a threat and is unable to destroy or even detect them.
I hope this answers your question.
CDB

This is very wrong. T-cells recognize MHC + peptide combinations. Immunogenic mutations in non-MHC genes can drive an anti-tumor response.

Did I fail to convey this? Perhaps my wording was confusing. I meant that most main CANCER causing genes do not cause a major change in the surface molecules of the cell. However you are correct, some genes that are not considered MHC linked genes can affect this, but most are not cancer causing.

It reads as if you completely misunderstand how the MHC-T-cell interaction works. MHC class I molecules on the cell-surface are loaded with the peptide fragments from intracellular proteins degraded by the proteasome. In infection, this can be proteins from viruses or microbes that are recognized as foreign. In cancer, this can be mutations that generate a peptide with novel structure. Many mutations, especially deletions, but also many oncogenic point mutations do not necessarily generate novel immunogenic peptides.

I apologize for not explaining this concept very well. It would seem, if you were that confused, I have failed completely at explaining it. I have done my best to explain and it is understandable to me, so I do not know how to clarify. Please, if you can explain more efficiently, feel free to edit my answer.

If a cell's apoptosis mechanism is not functioning would this disrupt or cause to malfunction the MHC in the cell?

Yes, quite a bit actually. Since this is a comment and I have limited characters, I would point you to this link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3489746/                             From the first paragraph after the abstract; "Moreover, many tumors downregulate the expression of MHC molecules..." read on. I would also suggest the paragraph labeled " Why Does Antitumor T-cell Responses Often Prove Defective?" located further into the article. Basically, it's a more complex version of my answer above.

A 'regular' human cell has a lot of inherent 'strategies' for 'avoiding' immune system 'attacks' unless of course there is an auto-immune disease 'situation' involved.  So if such a 'regular cell' becomes cancerous with a lot of mutations , does it  and it's daughter cells retain all the immune avoidance abilities it had before it became cancerous? Do the 'acquired mutations it has in fact  not interfere with the immune avoidance 'abilities' it has?

Do 'regular' non-cancerous cells have many traits or strategies within their genes or epigenetics or whatever ,that allows them to be unharmed by the immune system? ( assuming no auto-immune problems. )

Since a malignant tumour cell used to be 'normal' or still functioning with its mutations ; as a 'former' normal cell it would have a lot of 'in-built' strategies to avoid attack from the immune system . Then when it changes into malignancy it would still have these immune avoidance strategies to use to be 'hard to detect'. If some of these natural immune avoidance abilities that must be in all normal cells were targeted or 'temporarily shut off' by a designer virus or some special chemicals then the tumour might be made apparent and attacked by the immune system.

Answering your two questions together, all cells enjoy many mechanisms that try to prevent the mutated ones from surviving. During the cell cycle of somatic and germinative cells, for example, there are three moments of verification in which the cell will undergo a kind of internal "check up". During the interphase, this process takes place between phases G1 and S and also at the end of phase G2. In the division, as soon as the interphase ends, there is also one more verification. If during one of these three steps any mutation is recognized, the cell will undergo apoptosis (regardless of whether the identified mutation(s) were in fact to induce a neoplasm in the tissue or not.
Now, if even with these three checks any or some mutations go unnoticed, the cell in question will go through cell division and the mutation(s) will be inherited by the new lineage that will follow; but this does not indicate that the cell will be cancerous, because for a cancer to develop it is necessary for specific mutations to occur in specific genes.
This was just some information I wanted to give you, now answering your question more directly: cancers as a whole enjoy very cunning mechanisms that aim both to make tumor cells indistinguishable from normal cells for the immune system as well as they try to make it very difficult for the many proteins of the Complementary System, which is a vital part of the recognition of abnormalities of the Immune System, to get closer. There are many mechanisms that tumor cells enjoy, but one that stands out is what is called the Malburg Effect. This effect, described by the German physician Otto Walburg, in the 20th century, in a simplified way, consists in the fact that cancer cells consume a much higher amount of glucose than healthy cells and still convert a good portion of this glucose into lactose. This considerable production of lactose makes the environment around the tumor or neoplastic tissue more acidic than usual, acidic enough to compromise the activity of the many proteins that play a role in recognizing abnormalities in the immune system. This is one of the many mechanisms that many cancers use, which, directly or indirectly, makes it difficult for the immune system to recognize it.
The Warburg Effect: How Does it Benefit Cancer Cells?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783224
Another interesting point is that of the five existing therapies to treat cancers currently (chemotherapy, immunotherapy, target therapy, hormone therapy and surgery), immunotherapy consists precisely in "training" the immune system to know how to differentiate a cancer cell from a healthy cell . In a very simplified way, what they do is surgically remove a slide of your tumor or neoplastic tissue, identify the proteins present in the cell membranes of the cells that make up the collected material (among other molecules) and differentiate what is there only in the tumor. From the moment the tumor's own molecules are identified, a kind of vaccine is made, in order to introduce a cocktail with these tumor-specific molecules into the patient's body so that the immune system can then chase the tumor cells, knowing how to differentiate of healthy cells.
Cancer Treatment Vaccines - Immunotherapy - National Cancer Institute
https://www.cancer.gov/about-cancer/treatment/types/immunotherapy/cancer-treatment-vaccines
There is also an explanatory video, if I'm not mistaken from Nature, very good to introduce the idea in a very general way of how immunotherapy and cancer vaccines work: https://youtu.be/jDdL2bMQXfE

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


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Madrid, Noise by the river: Bird or cricket?
I currently live in Madrid, Spain. In July there was a loud animal near the river, in an out of town area surrounded by grassland, with trees along the river.
It's continued into August, though it has reduced.
It sounds like a cricket in general tone and rhythm, but it is always high in the trees, and sounds too deep to be an insect. It's in the frequency range of a squawking bird, so if it's a cricket it must be huge.
On the other hand, if it was a bird, I should have been able to spot one.
Does anyone have any idea what it is?
The sound is rhythmic, rasping note, with two beats of equal duration but slighly different tone, repeated over and over again without any pause.  The animal that makes it calls continuously for long periods.
EDIT: thanks to AliceD for the comment, I didn't realise we had cicadas in Europe. It could be a cicada, but it's deeper and more consistent / regular in its song than this one:
https://www.youtube.com/watch?v=DSdxm52VwOg

Sounds like a cicada to me https://en.wikipedia.org/wiki/Cicada. Btwo: with frequency range I presume you mean "loudness"? They are two very different things.

@AliceD Thanks, it could be a cicada, though of a different species than the ones in the wikipedia article and the one in the video I've added to the question. This thing is loud, but what most impresses me is how deep it is, definitely deeper than recordings in the above mentioned media. In July there were loads of them and I assumed they were birds. Now that there's less of them and I can differentiate individuals, I'm impressed by how monotonous and consistent they are - bird song is  normally more sophisticated. Also they like water, I only ever hear these things by one stretch of river.

Have you heard of the proposed Bioacoustics Stack Exchange? It seems like you might be a valuable member of that community. Please consider committing to the page so we can get closer to making it to the Beta stage. Cheers!
https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

In this case i am going to agree with AliceD, because I live in Greece and here we hear cicadas everywhere. But in Madrid, there is a other kind of cicada that its "song" is more noisy and more deep.In this video you can hear how your cicada sings.https://youtu.be/mah26og11ms

Thanks, but that is not my cicada, the rhythm of the song is different. The closest I have found is the one in the video in the question. Also the people talking on your video have an American accent, but I wouldnt discount the possibility that we have American cicadas in Madrid. It is a very cosmopolitan city with many connections to Latin America, so cicadas could be introduced. You can hear some Greek cicadas in one of the audio tracks in the Wikipedia article that AliceD linked. They are indeed much more high pitched.

That said, I was just in the park and heard a noise very much like your linked video. So I guess we have at least 2 species of cicada where I live.

Just to be clear – the cicada in the video linked just above (https://youtu.be/mah26og11ms) is Neotibicen tibicen, a genus found only in eastern North America.  See here at Wikipedia.  Sound recording on this page.

As suggested by AliceD, it does indeed appear to be some kind of cicada. I went down the river and heard one calling, unusually far from the river (30m) where there are lower, newly planted trees. I was able to approach it and take this photo which unfortunately isn't very good.
It's possible that it's even the same species as the video I added to the question. It may be that the cicada in the video did not sing with a regular pattern because it was disturbed by the observers. My cicada refused to sing at all while I was watching him, preferring not to draw attention to himself. I took 3 photos before he began to walk up the tree. On my fourth photo he became startled, flew off, and immediately resumed singing elsewhere.
The cicada in the video sounds more tinny than the ones by my river. That may be an audio effect.

The originally posted song and video suggest a cicada in the genus Cicada (the type genus of the family Cicadidae, which is known from southern Europe, eastern Asia, and north Africa); some identified recordings of this genus can be found at this page on European cicadas.  So far I can only find references to C. orni and C. barbara in Spain, but the recordings of those species given on the European cicadas site don't exactly match, although the physical appearance does suggest C. orni (keeping in mind that the white waxiness often gets rubbed off adult cicadas over time).  Since the orni recording on the website is from Slovenia, it may just be that the cadence of the song in that location differs from that of Spain (or in different temperatures, or in different courtship contexts). There are a few other Youtube videos described as orni from Spain with similar sounds (e.g., https://www.youtube.com/watch?v=3Z4STY71C-8). I don't know if there are other candidates besides orni and barbara in Spain.


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Is the swimming pool water harmful to frogs who jump in? If so, how?
Here is an odd question:
Frogs have permeable skin. Indeed, via capillary action, frogs absorb water through their skin.
Chlorine is in principle a harmful substance. I am sure what percentage of chlorine is in swimming pools usually, but the pH level is kept to around 7.4. This is the desired pH level, as a pH of 7.4 is the pH-level in human eyes and mucous membranes.
One of the "common wisdoms" I had growing up was that if a leopard frog (i.e. The Northern Leopard Frog, rana pipiens) jumps into a swimming pool, it must die soon, because the chlorine would kill it. However, I now doubt this is true.
So, do frogs die from swimming pool water? If so, why? What exactly is killing them? Chlorine poisoning?
PS: I am having difficulty finding the correct tags for this question. Any help is appreciated.

Have you considered why they add chlorine to swimming pools? If it inhibits the growth of a broad spectrum of microorganisms perhaps it also has detrimental effects on metazoans, including amphibians? If you had some water from a swimming pool and some frogs then you could test this directly. Barring that situation you could try searching for relevant studies in PubMed.

@mdperry That would be cruel, and not really answer my question. I would need a statistically very large sample of frogs, roughly the same age.

The chlorine concentration in pools is +- 0,5 mg/L.

+

0.002 mg/L will fatally damage the sensitive skin on tadpoles, frogs, salamanders and other amphibians.

another source:

Free chlorine (Cl2) is a greenish gas that is well known for its
  highly toxic properties as can be attested to by the thousands of
  soldiers that died and were severely injured from chlorine exposure
  during World War I. In water, chlorine is the most toxic substance
  that we will discuss. Ironically for the amphibian keeper, it is this
  toxic nature of chlorine and its ability to denature proteins, which
  makes its encounter inevitable. Chlorine is generally used as an
  antibacterial agent in municipal water supplies and may be present in
  concentrations of over 9 mg/1 in some tap water (measured in Houston,
  Texas as an example, although levels were generally lower). The
  concentration of chlorine in municipal water supplies can vary greatly
  from day to day, or even hour to hour, depending on conditions at the
  water treatment facilities. Concentrations as low as 0.0034 mg/1 have
  been noted to reduce reproduction in fathead minnows with 72 hour
  LC100 (lethal concentration for 100% kill) at 0.15 mg/1 (Arthur and
  Eaton,1971). LC50 (96 hour) for the shiners (Notemigonus chrysoleucas)
  was as low as 0.19 mg/1 (Esvelt et al., 1971). The concentrations
  found in municipal water supplies are many times greater than the
  minimum lethal concentrations for many aquatic life forms.

Thus, the well being of the frog in the water of the swimming pool depends on the time the frog spends in the water. Eventually, with extended exposure the chlorine concentration will exceed the one compatible will life and the frog will die. This time is multifactorial variable, thus cannot be assessed easily - the weight and the skin surface area and skin permeability will affect the frog survival in a great degree.

So what exactly kills the frog?

@the high concentration of Chlorine is toxic and causes oxidative damage to cells.

Frogs die in minutes in our subdivision pool. Usually tree frogs . I pull out about one a week ( I go first thing in the morning). Toads survive, I pull out one of them from time to time.


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Ways to fight black mold
Is it possible to introduce a microorganism to a colony of black mold that will kill off the black mold entirely and permanently? Is there a common microorganism that likes to eat them and is harmless to us?
In other words, I ask if there's a way to get rid of the mold biologically, maybe a different mold that at least won't stink?
Alternatively, will getting a UV lamp to shine in the opening once in a while be an optimal solution?
I also read that copper sulfate is a popular fungicide with plantations, will it kill and prevent the mold from coming back? Could this ruin the AC with corrosion or be harmful to people if it will be airborne?
I ask this because I have black mold in my AC and I can't take it apart and disinfect it.
PS: it's probably Aspergillus, they're black and make these white structures like in this picture:

I assume by "AC" you mean air conditioner.  What type of unit is it (car, home...?)  Why can't you take it apart to clean it?

Yes it's an air conditioner, it's a home unit. first of all, it's has a copper pipe and power cable that's connecting to the outside unit that I don't know how to disconnect properly so I could take it down. Secondly, it's built such that the fan part is really inside so taking it out means that I'll have to take out a lot of other parts fist. I don't know how to do it and I'm too afraid of breaking it in the process. @augurar

Frankly, I would suggest spraying it with some old fashioned water and vinegar. Creating an acidic environment is a pretty good mold treatment in the home. You should be able to tell if it's working- the color will fade as the mold dies. (Just unplug it first!)

@chauxvive I'm afraid this will stink more than the mold...

Bleach, borax and vinegar are good methods for fighting black mold. Don't work with bleach in the ventilation or mix it with anything! If you go w/ vinegar, you can mix salt into your solution for added effect. Borax is toxic if swallowed, as well, so vinegar is the safest option, and the smell will dissipate.

Well won't salt make it corrosive? I can order copper sulfate instead, it's pretty cheap. @Kendall

Uhh, well you're right, if it's something like stainless steel both salt and bleach would have some corrosive properties. Just be careful with the copper sulfate, too, especially in ventilation because that stuff isn't very good to get on your or in you, either. I'm not 100% in the know about cons for copper sulfate, though!

interesting question, but yet without the expected answer. The new gene editing tools might bring some hope. But until that, the most rational and effective way seems to involve Chlorine Dioxide gas (which kills -deactivates- the spores). But it's far from easy to deal with since the gas has to be produced when needed as a high concentration of the gas makes it explosive.

I write this as an answer instead of a comment because I don't have the reputation to do otherwise (frustrating!) even to edit my answer-which-is-now-a-comment
A weak vinegar solution (maybe 1:1 ratio water and vinegar) will solve your problem and will not stink up your home. Vinegar smell evaporates very quickly and are great for areas you can't reach easily to clean by hand. I promise your AC won't smell like egg salad.
Here's the first mold-cleaning with vinegar article I could find, there are plenty more where that came from

Alright, I'll give it a try.