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Do we know how animals refer to us, humans?
In human languages, we have "sounds" (or words) to refer to animals. For example, in English, we denominate a dog using the vocal sound dɒɡ. So, from the perspective of dogs, if they knew that the sound dɒɡ refers to them, then they "could deduce" that a human emitting the following collection of sounds is referring to them:

lʊk, ðæt ɪz ə kjuːt dɒg. aɪ ˈwʌndə ˈwɛðər ɪt ɪz lɒst?

Now, what about the reverse? Do scientists know of a particular sound (or maybe a sign, a movement, or related form of communication) used by any animal which signifies "human"? In case the current answer is no, is this ever possible to know? Maybe for animals where studies are more advances, like primates?

Downvoter(s), please comment.

The question assumes that animals (as a weirdly inclusive group) have a "word" to refer to humans. The vast majority of animals species do not use any specific signal to refer to humans. Very few species has the social intelligence needed to communicate about the the presence of individuals of a difference species and among them few have important enough direct relationship with humans to have do so. Some species make sound to indicate the presence of a flying vs terrestrial predators. If a human shows up, then the sound should be the one associated to terrestrial predator but ...

... that would not qualify as a sound to refer to humans. Outside of eventually, a very small zoo population of some vertebrate species, I doubt there is any species that would have a term for "human". If you have any reason to think the opposite, can you please try to focus on this specific species for which you think individuals might vocalize (or signal in any way) to convey the concept of "human" to its congeners. Likely the only species that has a "word" for "humans" are humans!

The only other species that actually has what we would consider words are velvet monkeys who do not have much contact with humans. Some birds appear to have a  nascent language, with something similar to words and sentences , the japanese great tit for instance but I have not seen a list of known words. https://www.nature.com/articles/ncomms10986

@Remi.b "In case the current answer is no, is this ever possible to know?" Maybe you missed that bit. Why not translate your comment as an answer?

@luchonacho Comments made into an answer as you asked! Cheers

The question seem to assume that animals (as a weirdly inclusive group) have a "word" to refer to humans. The vast majority of animals species do not use any specific signal to refer to humans. Very few species has the social intelligence needed to communicate about the the presence of individuals of a difference species and among them few have important enough direct relationship with humans to have do so.
Consider vervet monkeys as an example. Vervet monkeys make sounds to indicate the presence of a flying vs terrestrial predators. If a human shows up, then the sound should be the one associated to terrestrial predator but that would not qualify as a sound to refer to humans. See Seyfarth, R.M.; D.L Cheney; Peter Marler (1980). "Vervet Monkey Alarm Calls: Semantic communication in a Free-Ranging Primate". Animal Behaviour. 28 (4): 1070–1094. doi:10.1016/S0003-3472(80)80097-2
Outside of a very small zoo population of some vertebrate species, I doubt (but might be proven wrong, who knows?!) there is any species that would have a term for "human". If you have any reason to think the opposite, can you please try to focus on this specific species for which you think individuals might vocalize (or signal in any way) to convey the concept of "human" to its congeners. Likely the only species that has a "word" for "humans" are humans!

Do scientists know of a particular sound (or maybe a sign, a movement, or related form of communication) used by any animal which signifies "human"?

It is not a matter of knowing what sound they use. Excluding humans, animals likely don't use any sound to refer to the concept of "human".

In case the current answer is no, is this ever possible to know?

The answer is not "no, we don't know" but rather "there is nothing to be known here as animals just don't do that."

based on the work on japanese great tits some song birds use something similar to words, with combinations of sounds in specific orders, with different sequences having different meaning but we are pretty far form having a tit dictionary.

If we look at how human infants develop language skills (this is anecdotal evidence, N = 3), the first “words” spoken are nouns. For example (in English), sounds that represent mama, cookie, or ball. Verbs seem to appear later on; in the beginning we want to describe the world around us.
For me, the idea of a non-human language, does not have a clear sense.  In other words, we have no definitive evidence that any other species attempts to somehow “describe” the world they inhabit.  That is not to say that other animal species are unable to communicate among themselves with scents, pheromones, sounds, calls, vocalizations, or tail slaps (I was thinking of the North American Beaver for that last reference), just that we currently have no way of telling, or determining, if they have nouns (in the human language linguistic sense of nouns).
Consider the North American Prairie Dog communities on the Great Plains, where one, or more, individuals appear to be posted as lookouts, ever vigilant, and whom send out an alarm call when a perceived danger approaches.  It probably doesn’t really matter if the predator is a hawk, a fox, a wolf, a snake, or a human with a gun; the alert means something like “Run and hide unless you want to die, and bye-bye, it’s been nice knowing you, because I am drawing them away by making this sound.”


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How are fragments isolated during shotgun Sanger sequencing?
For a large genome (say millions of base pairs) -- we split the genome into fragments < 1000bp that are sequenced and can then be put back together computationally.
My understanding is you use some sort of shearing technique to get the DNA into fragments as in: https://en.wikipedia.org/wiki/DNA_fragmentation
Now you have a vat full of random fragments -- how do you sanger sequence these?
From what I can tell if you took the solution with the sheared DNA and ran sanger sequencing you'd get a bunch mixed of fragments mixed together resulting in a lot of noise ... you'd basically get all the runs averaged together. Don't you need to isolate each fragment before running Sanger sequencing?
How is this done?

In the original method, one would clone all of the resulting fragments into a suitable vector, and transform the collection into a bacterial host, to create a so-called library.  By plating the library clones under appropriate conditions you would have a collection of so-called clones, and each clone would be randomly selected and sequenced using the Sanger technique.

So if I understand correctly: Step 1: inject the fragmented plasmids into vectors. Step 2: Pick out an individual vector (e.g a single e-coli) and put it on a petri dish (this represents a single fragment) Step 3: Allow the individual vector to replicate (and thus replicate your fragment) Step 4: Take the culture of vectors, lyse the cells and extract the DNA. Step 5: Run Sanger sequencing

Step 0: Prepare double-stranded DNA cloning vector (usually a circular DNA Plasmid) by digesting, or cutting, it with a site-specific type II restriction enzyme, or endonuclease, and then possibly purify this uniform DNA fragment. Step 0.5: Mix the purified, linearized, cloning vector fragment with the suitably prepared sheared DNA fragments (that you want to sequence), and add ATP, buffer, and an enzyme named DNA ligase.  Specifically, DNA ligase encoded by the genome of bacteriophage T4. Step 0.9: Treat log phase E. coli cells with divalent cations, on ice (making them competent).

Step 1: Mix a small amount of the ligated DNA with the competent cells, give them a heat pulse, add some broth and grow them at 37 briefly, and plate aliquots on LB Plates containing a drug that will select for the rare bacterial cells that have taken up one of the foreign recombinant plasmids (from the DNA ligase reaction). 99.99 % of the bacterial cells will be killed by the drug in the plates, but cells that have taken up a viable copy of the cloning vector will express its selectable marker (a drug resistance gene) and be able to grow, yielding a bacterial colony on the plate).

Step 2: Pick individual colonies, grow them in broth.  Now continue with your Step 3 and Step 4

source: Stack Exchange

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

sort: votes


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Introgression vs admixture
What is the difference between genetic introgression and genetic admixture ?
Are these terms interchangeable ?
Do they apply to different population scopes or something ?
The usage seems kind of vague to me.
Looking for some clarification.

The difference is referring to the directionality of gene flow.
We talk about genetic introgression when there is some gene flow from one population (say, population A) to the other (say, population B). We would say that population A introgresses into population B. If gene flow goes both ways, then the two populations A and B are admixing.
From Wikipedia > introgression

Introgression, also known as introgressive hybridization, in genetics is the movement of a gene (gene flow) from one species into the gene pool of another by the repeated backcrossing of an interspecific hybrid with one of its parent species.

From Wikipedia > Admixture

Genetic admixture occurs when two or more previously isolated and genetically differentiated populations begin interbreeding.

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


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Its there a gene or genes for intelligence?
I don't know almost nothing of genetics but I felt a little interested in the subject of genetics and its role in intelligence and i found to reports that talk about certain genes that contribute to intelligence
https://www.nature.com/news/smart-genes-prove-elusive-1.15858 https://www.newsweek.com/how-be-smart-intelligence-linked-500-genes-large-new-study-842454
What I don't understand is if only some people have this 500 genes or all human population has this genes?

Is IQ heritable?

Let me start by saying that there is no commonly agreed upon method to measure IQ (thank you @mdperry). Keeping this in mind...
Yes, studies have shown that IQ is heritable. Or rather, IQ has a heritability that differs from both 0 and 1, meaning that both environment variation and genetic variation plays a role in determining an individual's IQ. Studies show IQ heritability varying between 0.5 (ref) and 0.8 (ref). For more information, please have a look at this post.
To understand the concept of heritability, please have a look at Why is a heritability coefficient not an index of how “genetic” something is?.

What are the genes that contribute to it?

IQ is a polygenic trait, meaning that many loci (locus = position in the genome) are affecting the variation in IQ. For more information about those loci, please have a look at this post.

What I don't understand is if only some people have this 500 genes or all human population has this genes?

Your misunderstanding comes from a misunderstanding about the concepts of gene and allele. You should start by having a look at the definition of the three following terms

gene
allele
locus

Below, I will not comment about the 500 genes claimed in this popular article and will just consider them as valid without considering the complication behind the methodology used for such estimation and about what original articles this popular article is citing.
With the exception of eventual copy number variation, the entire human population share these 500 genes but not everyone has the same allele at these 500 loci.

You say that IQ is polygenic and many genes affect IQ, but theres evidence of certain genes that certain population has but other population dont have? im not talking about alleles

I don't understand your comment. Are you making a claim or asking a question (there is a ? but the sentence is not phrased like a question)? Are you talking about CNV? Are you now talking about among population variance (which was not the subject of your question)?

Oh nevermind im just very bad at formulating scientific questions hahaha, anyway thanks for the initial response and for clarify my doubts.

@Roby If you consider that the answer has answered your question, then you can click the checkmark next to the answer so as to mark the post as answered.

I would be remiss if I did not mention that there is no accepted method to determine the IQ of an individual.


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Why are there sporadic lightly pigmented hairs in facial hair?
My body and scalp hair are entirely black. Until recently, I thought this was the case with my facial hair also, until I noticed a small handful of hairs that were anywhere from light brown to copper-orange to burgundy-red. There are hairs that are entirely pigmented like this and there are mixed along their length between different pigmentation colors (for example there are copper hairs that have black tips).
Can anyone explain why this is?
My own thoughts are that it is caused by some variation between individual hair follicles (different type/number of receptors on the melanocytes that color hair that cause them to respond differently to various amounts of hormones? But then what is causing the hormone shift in the first place? I am pretty sure that until recently all the hairs were black and only recently have these lightly pigmented hairs sprouted)

nascent gray hairs? this may be batter suited to the health and medical stack.


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Fst genetic distance: Autosomal vs. mtDNA
As far as I'm aware, mtDNA is only inherited from the mother. Hence, if I compute Fst from autosomal SNPs, then I'll get the actual genetic distance between two human populations.
If I compute the genetic distance Fst between two human populations based on mtDNA sequences, then it alone can't be used to draw conclusions on their genetic distance.
For example, an admixed population will score relatively low Fst value with its maternal ancestral population (assuming the admixture was caused by unisex migration) when computing based on mtDNA sequences. However, the Fst distance based on autosomal SNPs will be relatively higher (depending on proportion of admixture).
Is this correct?

Yes, you are correct.
$F_{ST}$ can vary among specific genetic regions considered. If for example there is a strong influx of females from population A to population B, then the mtDNA and the X chromosome (excluding the pseudo-autosomal region) would show much smaller $F_{ST}$ between the two populations than the Y-chromosome would.
Many other non-demographic processes can affect $F_{ST}$. Background selection (Charlesworth et al., 1993; Matthey-Doret and Whitlock, BioRKiv, 2018), selective sweep (e.g. Chen et al., 2010), heterozygote disadvantage (Ingvarsson and Whitlock, 2000), negative epistasis and other processes can affect $F_{ST}$ as well and cause $F_{ST}$ to differ among genetic regions. Even mutation rate variation (Whitlock and McCauley, 2001) can affect $F_{ST}$ (if the mutation rate for the loci considered is not ridiculously small compared to the migration rate).
For an introduction into the common misunderstandings of how $F_{ST}$ works, Whitlock and McCauley (2001) is a must read!

Just to complete this answer, would Fst computed from autosomal SNPs be fully representative of the genetic distance between two populations? Say for the influx of females from A to B, will the autosomal Fst correctly show that the admixed population is between A and B (depends on mixture proportion)?

The difficulty here is in the phrasings fully representative of the genetic distance and correctly show. There is no correct (true) genetic distance among populations, there is only the statistics of genetic distance that one wants to define and those statistics are affected by various processes.
Would an influx of female among populations affect $F_{ST}$ at autosomal loci? Yes. Would this effect be the same than at mtDNA? Not exactly, no. Is the entire parsing of genetic variation among population represented by $F_{ST}$? No, $F_{ST}$ is just a summary statistic (just like a mean or a variance is).
If there is a specific statistic (such as the effective migration rate, the effective population size or the location of loci involved in local adaptation for examples) that you are trying to infer from these $F_{ST}$ calculations, then maybe you should ask whether computing $F_{ST}$ by a specific method would allow you to make good inference of a specific statistic of interest.

Just to complete this answer, would Fst computed from autosomal SNPs be fully representative of the genetic distance between two populations? Say for the influx of females from A to B, will the autosomal Fst correctly show that the admixed population is between A and B (depends on mixture proportion)?

@RudyWinono See edit in my answer to address your comment.


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Measuring genetic distance: $F_{ST}$ vs. Nei's distance
As far as I'm aware, Nei's genetic distance is quite old compared to $F_{ST}$. However, I have recently read more papers that utilized Nei's genetic distance alongside with $F_{ST}$. As I'm not very familiar with Nei, what are some advantages it has over $F_{ST}$?
Does Nei's genetic distance suffer from ascertainment bias?

What do you call Nei's genetic distance? Do you refer to $D_{XY}$ or maybe to $G_{ST}$ or something else?

A note about formating: $F_{ST}$ gives $F_{ST}$.  $D_{XY}$ gives $D_{XY}$.

Nei was born about the same time as $F_{ST}$ was first defined by Wright. So, Nei's genetic distance (whatever this is referring to) cannot be older than $F_{ST}$.

Apologies, but Nei's genetic distance in this case refers to $D_{XY}$. Thanks. Nei's $D_{XY}$ might be newer than $F_{ST}$, however there have been more extensive uses and research on $F_{ST}$ to address its shortcoming. To this date, I'm wondering how Nei's $D_{XY}$ compare to the current $F_{ST}$.

The question's interesting but it will be very hard to offer a general answer. They are two different measures of genetic distance. $F_{ST}$ is better known, more studied and is more closely related with the population genetic theory than $D_{XY}$. Depending on the question of interest you might want to use one or the other. Many authors now recommend computing both to get a better picture of the genetic distances. Note that there are many other related statistics such as $\pi_S$, $\pi_B$, $G_{ST}$, $G_{ST}'$, $G_{ST}''$, $\theta$ (I mean Weir and Cockerham estimator of $F_{ST}$) and $Jost'D$.


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Time taken for species to become endemic
Is it known how long species take to become endemic? I know from examples such as Canada which have no endemics following the end of glaciation that the process must take at least 10 thousand years, but this merely demonstrates endemism must take a longer time. Has any technique been developed that provides some measure of the time needed for species to become endemic?
I am especially interested in the rate of endemism on a small and extremely isolated island such as St Helena.

From wikipedia: Endemism is the ecological state of a species being unique to a defined geographic location, such as an island, nation, country or other defined zone, or habitat type There is no time component to it. If a species is found only in Canada, then it is endemic to Canada. If it is found only in your garden, then it is endemic to your garden.

@Remi.b That can probably be an answer and is the best OP is likely to get.

From wiki: "There are two subcategories of endemism: paleoendemism and neoendemism. Paleoendemism refers to species that were formerly widespread but are now restricted to a smaller area. Neoendemism refers to species that have recently arisen, such as through divergence and reproductive isolation or through hybridization and polyploidy in plants." So the time of the former is the one of the extinction of all populations of a species but one, while for the latter is the speciation time. Which one are you referring to?

From wikipedia > endemism:

Endemism is the ecological state of a species being unique to a defined geographic location, such as an island, nation, country or other defined zone, or habitat type.

There is therefore no time component to it. If a species is found only in Canada, then it is endemic to Canada. If it is found only in your garden, then it is endemic to your garden. No matter the duration in which the species has been found in this specific location.
That being said, in conservation biology, it is common to oppose endemic species with invasive species. An invasive species
Wikipedia > invasive species

An invasive species is a species that is not native to a specific location (an introduced species), and that has a tendency to spread to a degree believed to cause damage to the environment, human economy or human health

As the linked wikipedia page explains the concept of invasive species (or if you prefer the concept of non-endemism) is open to a lot of critics and is in no way well defined. There is no time limit under which we would stop considering an invasive species as invasive. It is rather the ecological impact of this species that will people to call it invasive or endemic based on purely subjective notions.

Endemism is dependant on time and location. A long time period is required and this is what my question addresses. The role of location in endemism is self-evident.

You seem to disagree with the Wikipedia definition, then. Can you please give a trusted source that would back up your claim?

Are you sure you are not confounding the concept of endemism with another one such as the concept of being indigenous for example?

The Wikipedia statement that "endism is the ecological state of a species being unique to a defined geographic location, such as an island, nation, country or other defined zone, or habitat type" is a wordier version of my statement, which I believe to be self-evident, that Endemism is dependant on location. I also said it is dependant on time - this does not happen overnight. The question I am asking, which is not addressed by Wikipedia, is whether it is known how long a time endemism takes? I hope that makes my question easier to understand.

@user8654 I don't understand your comments but anyway. You might want to have a look at the edit in my answer. Your stance on the importance of time might come from invasive vs endemic discussions.

Could you add some non-wikipedia sources? I know this is your field, so I'm sure you have them. Wikipedia isn't reliable by it's own standards. We have access to an expert (you). I'd love to see references that represent where you learned these things. For a really basic concept, that might be an authoritative textbook.

@DeNovo Is it my field though? :) I'm a population geneticists / computational geneticist but am not an ecologist and definitely not a conservation biologist. To be fair, I have published a paper on the evolution of invasiveness in domesticated sunflowers but I have not be brought to consider the semantic difficulties behind the concept of invasive vs native species. I don't know of a reference that talk about this semantic difficlties, sorry.


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Alpine flower identification — Italy/France
I have been using the internet to try to identify alpine flowers photographed in July 2007 on a shortish walk above Chianale (1800 m), in the Italian Valle Varaita (bordering the French maritime alps).
I have managed all except the blue/lilac one shown below. It looks a bit like a scabious or perhaps a knapweed, but neither seem to correspond properly. Anyone know?

Group of flowers

Close-up with triply split petals indicated by red arrows

Just added a close-up. Thought I had done so before, but there must have been a computer glitch somewhere as there is no edit record for deletion. Anyway, this shows why I am accepting the suggestion of Phyteuma orbiculare (for what my opinion is worth).

This is not Jasione montana, but Phyteuma orbiculare, another member of the family Campanulaceae. Except for the different flowers,
Jasione has no leaves on the upper part of the stem. This plant has. And these leaves are toothed and have a heart-shaped base, unlike Jasione.
And finally: Phyteuma is resticted to calcarious soils, whereas Jasione prefers non-calcarious soils.

https://en.m.wikipedia.org/wiki/Phyteuma_orbiculare

Thanks. Looks more like it in one particular respect. That is the tips of the petals. In all the pics of Jasione I have found they seem lighter coloured and hardly split, whereas in my photo (you can see this if you zoom in) and this pic of Phyteuma (and others on-line) they are clearly split into three and curled back. I'll go back to my higher-res original and add to my question with a close-up later. This site has it in the appropriate Italian province of Cuneo (CN) at 1800 and 2500 m. Again, I'll wait before accepting.

Want to know a bit more about anatomy/morphology. What are the peripheral tri-furcate things? Are they anthers? And what is the central stalk like thing? is it the gynoecium? Btw I am not familiar with campanulaceae

@Always Confused Eh, no. Every purple stalk is a seperate flower and the tri-furcate things are the gynoecia. I don't know what this central thing is, it doesn't appear to be there in every flower. BTW: isn't this a new question?! :-)

I think the correct answer is @RHA's answer. I will leave my answer just for future reference and discussion.

Could it be Jasione montana?

Sheep's bit scabious, Jasione montana, is a low-growing plant in the Campanulaceae family found in rocky places and upland regions of Europe and western Asia. Other common names include blue bonnets, blue buttons, blue daisy, iron flower, sheep's scabious and sheep's bit.

Your flower's petals look a bit more "spiky" the Jasione montana though. As a kid (I grew up in Switzerland), I remember seeing bumblebees flying around these flowers. Have you seen any?

Thanks. Despite the difference in spikiness, it looks as if it could indeed be Jasione montane. Pity I didn't take a sharp close up, but it's my wife that's really interested in what species flowers are. I usually leave them out of photo-records, but even I find the profusion of flowers in alpine meadows stunning. I'll wait a couple of days before accepting to allow for other responses.

I think this is not Jasione, but Phyteuma, see my answer below. And about those bumblebees: could this have been a much larger blue plant: succisa pratensis? That plant I had in my garden and attracted loads of bumblebees.

I think you are correct. I will leave my post just for future reference but upvoted yours to bring it to the light.

I never answered about the bumblebees. Don't remember any. All I remember is the millions of insects that bit me, but that always happens when I'm walking as something in my sweat seems to attract them. (Same recently in California and Texas. Not a problem in Glasgow.)


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Why doesn't my rtPCR reaction work?
I am doing a rtPCR to detect the watermelon mosaic virus (WMV). My set of primers are:

WMV primer forward: 5'-TNGARAATTTGGATGYAGG-3'
WMV primer reverse: 5'-CTGCGGTGGACCCATACC -3'

both of which at the concentration of 10 microMolar.
The first step of my rtPCR reaction was looking for a positive control.
I did the rtPCR against to a field sample (In the NGS results showed a positive against to WMV) and two greenhouse samples (the first one of my greenhouse samples was inoculated with WMV and the second one it was not).
These samples were extracted with good concentrations and integrity.
After that, I did the rtPCR with rt enzyme (from Affinity company).
Following the next steps:

I added 2000 ng of my RNA samples (in different tubes; one of them to one greenhouse sample, another tube for the remaining green house sample and the latest tube with the field sample) with Reverse primer (2 ul) and H2O (until get 12.5 ul).

1.2. I incubated them 65ºC 5' and 25ºc 10'.
2.1.  I added the next volumens for 1 sample: 2ul of my buffer, 2ul of my DTT, 2ul of my DnTps, 0.5 ul RNAsa block and 1 ul of Rt enzyme.
2.2. I vortex them and I incubated them 1 hour 50ºC and 10' 70ºC.
3.1. The PCR reaction was performed with the takara polymerase enzyme.
I added the next volumen per one tube: 2.5 ul of takara buffer, 0.5 ul forward primer, 0.5 ul and primer reverse, 0.5 ul DNTPS, 0.25 ul of taq polymerase and 15.75 ul of watter. All these volume 20 ul I added 5 microlites of my rt samples (2.2 point). I did this process with my remaining two samples.
3.2. Finally I incubated them 98ºC 5', then 35 cicles of 98ºC 30'', 56ºC 30'' and 72ºC 1'. out of the 35 cicles the temperature goes to 72ºC 10'.
I run the gel and I got primer dimmer. What I am doing wrong? All help will be very useful.

Note: These protocol was following by a labmate who got good results with the same field sample. Now I am following the protocol that was written in his notebook.

RT-PCR predates the widespread availability of the World Wide Web; which means bench scientists have been troubleshooting failed RT-PCR reactions for a very long time.  I suggest you find somebody local with such troubleshooting expertise, and learn everything that they are willing to share with you.  I predict this will be both speedier and also time well-spent for your own scientific training.

@mdperry thanks for your advice, but I am looking for someone who can tell me my fault; a short time in one step or whatever

doing more assays I found what was the trouble. I used an oligodT for the rtPCR and then I amplified with my polymerase. Probably my RNA sample had not a linear conformation in the region that my reverse primer must join. The oligo dt bint to the polyA region, typical of this type of potyviruses.

Good!  I am glad that you were able to quickly identify the problem.  I suspect that it would’ve been relatively challenging for remote individuals to figure that out so rapidly.


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What flower is this? (Dolomites, Italy)
I took this picture a few days ago in Val Rendena, in the dolomitic Brenta group (2000 m). The whole plant was 15 cm tall at most, and it had a single leaf on the stem. What flower is it?

How was the leaf ? (Shape, texture...)

I had a look at white-flowered plants flowering in July in a site about the flora of the French Alps, and the best I could find was Parnassia palustris:
http://www.florealpes.com/fiche_parnassie.php

At this developmental stage, it looks quite similar to your photo, with the same kind of structures at the base of the petals.
The site says that there are heart-shaped leaves at the base, plus one on the stem. This last leaf matches your description. The site says it can grow up to 2500m.
The Italian Wikipedia says:

In Italia è presente solo nelle regioni settentrionali e centrali, nonché in Campania.[2] In montagna si spinge fino a circa 2000 m, ma sulle Alpi è stata segnalata anche a quote superiori (3000 m sul versante svizzero del Monte Rosa).

This means that it can be found in the Italian Alps too, including at 2000m.


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What moth is this and how do we get rid of them?

This bugs are everywhere in my house and we've tried so many home remedies, but they won't leave. Can anyone help us!?

Welcome to Biology.SE! I suggest you to take the tour to learn about the site and earn your first badge. Also, it is useful to include your geographical location when looking for a species identification.

Also check any cat or dog dry food if you have any.

That is an Indian meal moth Plodia interpunctella. Family Pyralidae. They are very common household pests. https://www.doyourownpestcontrol.com/indian_meal_moth.htm
They breed in grains or cereals. You need to look through your pantry, and find out what they have been breeding in. Seal up your grains and cereals in plastic, or put them all in the fridge.

They are also known in some areas as pantry moths, due to their association with that location, i.e. infestation. Note that plastic bags will not keep them out as both the adult moths and the grubs can chew though thin plastic. Infested plastic bags will have a multitude of silk threads, small uneaten food particles, and grub cases in it. The plastic containers need to have thick solid walls with an airtight lid.

Yes, you need to go through the items in your pantry, probably you will find some infested bags/boxes. Discarding them will help in getting rid of them.

This is probably a common flour moth or a similar pyralid species. It has probably laid eggs in some cereal-derived products (pasta, cous cous, but also rice, oatmeal and the like) of your kitchen. First of all, check carefully your pantry for infested food and throw it away. Then (from the above Wikipedia link):

None of the stages of the organism (eggs, larvae, adults) are very temperature tolerant and all can be killed by a week of freezing or by brief heating in a microwave or conventional oven when such treatment is practical. Scrubbing infested areas with a mixture of soap and water or vinegar is also effective. [...] Nontoxic traps are also available to monitor outbreaks. One type of trap is a triangular box with a pheromone lure and sticky walls inside. These traps are generally known as pheromone traps. In this case, male moths are attracted inside by the female pheromone (the lure) and then get stuck against the sticky walls inside the box.

From personal experience, it can be sufficient to check the pantry and seal all the cereal-derived food into plastic bags.

It's possible you had a different species to the one I encountered. Mine were capable of chewing through plastic bags and infesting them. See my comment on Karl Kjer's answer.

I know this question is old but for the possible sake of later readers, with respect to mentioning plastic bags - at least some, if not all of the moth species commonly known to infest households do have a reputation for being able to bite through thin plastic bags, both the larvae and the adult moths.
Where that's the case, or can be suspected anyway, recommendations I have found are to use hard plastic containers with a tightly (and forcefully) closing lid for endangered food etc.
Quick sourcing (I did have sufficient original reputable sources when I wrote this answer passing by, the memory of them just eluded me):
This internet article states, though rather informally,

the larvae ... can bite through plastic and cardboard, [or] work their way through a screw lid jar if it’s not tightly closed.

This official page of this U.S. National Pest Information center* states explicitly (first paragraph there as of time viewed)

Larvae can chew through plastic bags and thin cardboard, so even unopened packages may become infested.

NPIC is, from the page footer here and on other pages, a cooperative agreement between Oregon State University and the U.S. Environmental Protection Agency.
NOTE: Sourcing to continue as required...

Sources for this are pretty common across the web so no special citations here in this case (unless it gets requested and I find the time)

Please always provide citations when posting answers on this site. Otherwise, your post is likely to be downvoted or removed. Thanks!

oops - got called out within 2 minutes for not adding explicit sources and citations. Received a downvote along with a message with that. Well, received. But please, @theforestecologist and everybody, just give me some time for that, will you?

BTW, for the hygiene of the knowledgebase - which I accept - I might temporarily retract my answer but I'm uncertain about whether that would remove it irrecoverably. Would that be a way to go, @theforestecologist? Thanks again for the heads-up. - Background information: I am really right now doing my due prior research for another question that I believe is not in the system at all but exactly to make sure it really is distinct I am reading all the QAs that the system thinks they might be. That's how I came across this question in the first place.

This post was written with no other intention than to be helpful. Please.

As for the "screw lid" part, I haven't consciously read that anywhere else but here the critical factor seems to be "if it's not tightly closed". Big deal.

@theforestecologist does this qualify for this answer to be reset to +- 0 votes?

Welcome to Biology.SE! Thank you for taking the [tour], but please also consult the help pages for additional advice on [Answer] effectively on this site. Unfortunately, I think you've answered a question different from that originally posed. I would vote this up if the question was something like "Can pantry moths really chew through plastic bags?". As it stands you've made a detailed comment on a side issue rather than an answer to the OPs question. Since you've put in so much work maybe you can find a question that this does answer? Thanks!

thanks @tyersome, will try. As stated in my other comments, I was just dropping by doing adjacent research and thought I'd add a missing bit to be helpful to any latecoming readers because of other comments and I could not do that simply in a comment bc rep, however much I would have loved to. I very much appreciate your analysis and suggestion (and your not adding another downvote :-)), just if I could be allowed a little time for that?

On moving this answer: Have now checked using the site search for "Can pantry moths really chew through plastic bags?", some variations of that, and "moth chew plastic" (all yield zero), then "moth eat plastic" yielded exactly this. Now I guess this would really be an edge case as the accepted and high-rep only answer does briefly mention the essence of this answer, giving the same reputable source and link on the point. Now to look what part of the help pages would cover what to do here?

To me that question still doesn't really fit your answer. I think you might want to post a question about how to use your answer on [meta] — the moderators will often answer questions there. One possibility is for you to post a question and then answer it yourself, but I'm not completely sure how well that would be received ... ———— As for downvotes, to the extent possible it is best not to take them personally. Some users downvote ⋯ enthusiastically ⋯ without giving useful feedback, but many new users ignore feedback or respond angrily to comments. Stick around and you'll also see upvotes!

Thanks again tylersome (can't 'at' two users) - I'll take your advice to ask about that on Biology Meta, even more so as the intersecting answer I mentioned was @theforestecologist's and they are a mod. I might first complete my research on the other question I'm preparing though as it might help with explaining what I was doing in the first place (was doing my due prior research on that question by which I came across this question and noticed that it might help late readers if I added a missing bit, which could have been a comment if ...)

Thanks again @tylersome - I'll take your advice and ask on Biology Meta. Please note another comment I just added above this one (to ping theforestecologist for the reason given there, system is telling me I can't 'at' two users in one comment)

@somebody_other thanks for updating with some citations and support. I've removed the post notice. We get many unsupported posts here, so quickly responding with post notices is paramount for trying to get users to take that aspect of our site's expectations seriously. (see our help page and take our [tour]). This is an especially big problem with a topic like species ID, which is typically rampant with inaccuracies across the internet. Nothing personal. Just nipping the problem in the bud to cut down dealing with it later. Thanks Shahin for the update

Regarding rep limitations: these are in place partially to force you to get involved in our site so that you learn the ins and outs. You can only earn rep through asking, answering, or editing. Each of these are "graded" by the community here through voting. In other words, you only earn rep if the community approves. You earn more priveleges the more rep ("trust") you earn. Just a few upvotes or a handful of edits enables you to comment. So please stick around, get to know how things work a bit more, edit some posts, answer more questions, and you'll be on your way in no time!

@tyersome, apologies for consistently mistyping your username unawares so I guess you didnt get my ping. In case you're interested, see above. Thanks a lot for your helpful comments.

@theforestecologist might I get your opinion as a mod and the author of this: I 'd un-offtopic my answer as tyersome suggested by making it a separate question (that I could link to, too). I worry whether the second-last line of your above answer would make a "sort of" duplicate of it, though. AFAIS there's no "real" duplicate yet. tyersome suggested I should ask about this on Biology Meta (a bit high?) - now as it concerns your answer and you are a mod yourself, what do you say I should do? And thanks a lot for the explaining & encouraging!


text:
How to find the amino acid in the DNA protein
    3' A T A G T A C C G C A T G T A C G G G C G A G A C A T T C G A G C A T T C A T 5'

This a Template DNA.
How to find the number of amino acids amino acids in the protein encoded by the above gene?
The answer is $7$.
My Try:
First I converted the above DNA to RNA and got
   5' U A U C A U G G C G U A C A U G C C C G C U C U G U A A G C U C G U A A G U A 3'

Then I found the start codon which is A U G
5' U A U C |A U G| G C G U A C A U G C C C G C U C U G U A A G C U C G U A A G U A 3'

From here I am not understanding how to proceed.
Can anyone please explain how to solve this?

Short question: How does RNA translate into protein?

Then you just have to read the codon until you reach a stop codon. There are three stop codon UAA, UGA and UAG. So, in your example..
             Start                                                   Stop
5' U A U C | A U G | G C G | U A C | A U G | C C C | G C U | C U G | U A A | G C U C G U A A G U A 3'

Your protein is therefore 7 amino acids long (incuding the starting methionine). The genetic code is

Therefore the 7 amino acids are
Met Ala Tyr Met Pro Ala Leu

In case you are confused about having an AUG codon in the middle of an open reading frame, then you should have a look at the post Effect of a doubling of the start codon in a gene.
Of course, I assumed that the region is indeed transcribed and that the first AUG is indeed the start codon and not just a methionine in the middle of an open reading frame.

Good answer, though perhaps you should include the first methionine as the N-terminus since it is not always cleaved and the answer given in the OP is 7.

@canadianer Thank you! Edited. I did not know the methionine of the start codon was sometimes (often, usually?!) kept.

Each protein-coding gene consists of coding and non-coding regions. Coding region, a.k.a CDS (see: Coding region and Open Reading Frame), is spanned between translation initiation site (TIS), and one of stop codons. Non-coding regions include introns and non translated regions (5'UTR or 3'UTR) in the exons.
You need to know first, if (and where) your DNA template contains the information about amino acids sequence. Does your DNA template is the protein-coding region only or do you have some non-coding parts (eg. introns).
(Short remark: Methionine can be also found within the amino acids chain, not only at TIS = not every methionine is a TIS)


text:
Can a brain dead person recover?
Many times I have heard someone having to pull the plug because the patient was declared brain dead before the body healed fully? Why do they pull the plug without first waiting till the body/brain has a full recovery? What situations if not recoverable would they allow the body to fully heal before pulling the plug?

Hmm... your edit is a different question and kinda breaks the answer. The new answer is "None". Also, "shortly after trauma" is relative. What do you consider "shortly"?

@anongoodnurse revised

No.
Brain death is permanent damage to the brain. Depending on the specific definition, it may refer to either cerebral death or to failure of the brainstem to maintain functions like respiration.
It could be possible for mistakes to be made and for brain death to be declared in a patient who has not actually experienced brain death. However, this is incredibly incredibly rare: zero cases have been reported when appropriate guidelines are followed (Wijdicks et al. 2010). If someone is diagnosed as brain dead after a trauma, the medical staff involved in making that decision are stating that there is effectively no chance for recovery. Brain death is not diagnosed lightly.

Wijdicks, E. F., Varelas, P. N., Gronseth, G. S., & Greer, D. M. (2010). Evidence-based guideline update: determining brain death in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 74(23), 1911-1918.

+1. One question, though... I don't know how you can definitively say zero when there aren't detailed studies on serial examinations. I don't disagree with you, I'm just saying that patients aren't kept alive simply to answer the question; that would be prohibitive, and possibly even inhumane.

@anongoodnurse Yeah, I was really just relying on the claim made in the paper I linked. I agree that saying actually zero is probably a bit extreme. There are certainly some cases where patients are kept on life support past brain death (family wishes/disagreements, organ donation, etc), but I agree it would be inhumane to keep folk in that state for a bit just to see if a couple of them recover.

@Bryan Krause answered your question prior to the edit. Your new question is relatively easy to answer.

Why do they pull the plug without first waiting till the body/brain has a full recovery?

Some organs have a high regenerative capacity (you can donate part of your liver and it will mostly grow back), some have a high compensatory ability (you could live with one lung), etc. However, the brain isn't one of those organs.
Until relatively recently, it was thought that the brain had no regenerative ability at all. We now know that to be untrue. Still, compared with most other organs, the brain doesn't "heal" well.
It's one thing to keep a comatose patient alive (e.g. after a bad stroke) to see if time will help. Neurons do form new synapses that allow for a degree of recovery. But most times with a stroke, only part of the brain is involved, and the brain does have compensatory abilities (new synapse formation.)
But brain death is much more than a coma.
When there is so much damage that a patient can be declared to have undergone brain death, people don't recover from that. There isn't any reason to let someone heal all their other organs - or the brain - fully when the one organ that makes us who we are is dead and the only way to stay 'alive' is by artificial means (ventilators, total parenteral nutrition or a g-tube, etc.)

What situations if not recoverable would they allow the body to fully heal before pulling the plug?

Family inability to allow a hospital to "pull the plug" leads to prolonged life support and recovery time for such patients. This is not necessarily good, however. Some patients who were declared brain dead (less rigorous criteria) survived post life support, but none has gone on to become functional (and usually stay in a vegetative - or minimally conscious - state at best.)
Regeneration of Hippocampal Pyramidal Neurons after Ischemic Brain Injury by Recruitment of Endogenous Neural Progenitors

your answer had more info


text:
Looking to identify this species
I found a rather strange invertebrate...something... outside my home this evening, and I have no idea what it might be. It looks kind of like a small brown lobster, without the claws. I think it has 8 legs, making it an arthropod(?), but if I've misidentified that, please correct the tags. It's 4 or 5 inches long, head to tail. It was found in south-eastern Massachusetts. Potential nearby habitats are open grassy fields, a forest, and a cranberry bog, if that helps.

The picture is kinda fuzzy, I think the video is better.
Any ideas?

Don't know for sure, but crayfish seems plausible to me.

Welcome to Biology.SE! I suggest you to take the tour to learn more about this site and earn yourself your first badge. Have a nice stay!

@mgkrebbs crayfish is what other people elsewhere are suggesting as well. It was pretty cool, I'd never seen one before.

Yep, it's a crayfish ... given the locality and assuming it's native to the area, we're looking at a member of the family Cambaridae, which has dozens of genera and hundreds of species north of Mexico (and requires that you have a "first-form male" for genus level identification: see How to Know the Freshwater Crustaceans, if you can find a copy).


text:
How would a medication cause a one to maintain a different weight?
This isn’t really a medical question, I’m just really curious about this.
I was maintaining weight A and then started taking a medication that brought me to weight B. While on the medication, I maintain weight B. When I stop taking it, my weight goes down presumably to weight A.
The increase or decrease of weight in changing medications doesn’t puzzle me. It’s the maintaining of the weight.
Would the medication be affecting metabolism or what?

Based on my reading, weight gain, as in resetting your maintenance set-point, which is what it sounds like you are describing, is a very well-known side-effect of the serotonin selective reuptake inhibitors (SSRI).  In some cases, patients may even discontinue the medication.  As far as I know, the underlying physiology behind this specific example is not well-understood.
In recent years, the use of next-generation sequencing (NGS) of DNA has been used to characterize the so-called microbiome in the gut of individual humans (sequencing faeces).  Some studies have reported that thin, or skinny people have somewhat different microbiomes than fat, or obese people, leading to the hypothesis that some overweight people might have bacteria that are more efficient at breaking down their food such that more of the calories are available for absorption.  Some evidence supporting this interpretation comes from experiments with fecal transplants.
If a medication also affects a patient’s microbiome (in addition to the drug’s intended therapeutic effects) then that could be another, less obvious(?) mechanism for weight changes.


text:
is there an easy way to remember taxonomy?
So I have trouble remembering the order of taxonomy for classification.
i.e domain>kingdom>phylum>class>order>family>genus>species
I can never remember it, is there an good mnemonic to remember them? How do you guys remember it?

Of course, Randall Munroe has a solution to your problem: https://xkcd.com/992/

I'm voting to close this question as off-topic because it is not about biology as such.

Have a look at Wikipedia > List of mnemonics#Biology.

Dear King Philip Came Over For Good Soup
Do Kings Play Chess On Fine Green Silk?
Dumb Kids Prefer Cheese Over Fried Green Spinach
Do Kindly Place Cover On Fresh Green Spring Vegetables
Donald Kills People Cause Other Friends Get Sad

Given the current political situation I would go with the last one but it is up to your personal preferences. You can as well make up your own. Mnemonics are like soups; it is always better when homemade. For example, extending upon the last and inspired by @John's comment, here is a homemade mnemonic

Donald Kidnaps People's Children Causing Outlaw Foreigners Great Suffering

Enjoy the game!

do kill purple clowns or face great suffering.


text:
Can anyone identify this bird - small flock in ireland?
I saw small birds in a flock of about 6 or 8.
Here are details that can be seen on my best photo - The beak looks pointed and also the legs are quite long and the eye has a bar across it.

I have a recording - how do I share it??

The body shape and colour reminds me of a greenfinch (Chloris chloris). They also form flocks. However, the beak on your pictures doesn't look very 'finch-like'. Can you tell us anything about the beak shape, or do you have a picture, where it's better visible?

the beak seems to be pointed - the birds were far away - i will try for a closer shot if they return -

the beak looks pointed and also the legs are quite long and the eye has a bar across it-

Maybe edit your question add these additional information there. Not everyone reads all the comments :)

@Marzipanherz You can probably make an answer from your comment.

I also first thought of green finches, but they have a much stronger beak.

@Remi.b Richard's comment about the pointed beak made me doubt. I'm still searching for a better fit.

They're definitely not greenfinch. The horizontal bar across the eye rules that out. I think yellow-crowned wagtail (Motacilla flava ssp. flavissima) is a better fit. See https://commons.wikimedia.org/wiki/File:Motacilla_flava_flavissima,_Kingsbury,_Warwickshire_1.jpg.

@bshane I think Motacilla would have more visible stripes on the wings.

@bli: not always. Worn plumage loses a lot of the distinct scalloping. e.g., https://www.google.com/imgres?imgurl=http%3A%2F%2Fwww.hlasek.com%2Ffoto%2Fmotacilla_flava_da5089.jpg&imgrefurl=http%3A%2F%2Fwww.hlasek.com%2Fmotacilla_flava.html&docid=uMycFdL-fJqLvM&tbnid=7l0k0nvS20RrGM%3A&vet=10ahUKEwjmspmyktzcAhVSQd4KHSL5C3cQMwiHAShEMEQ..i&w=626&h=500&client=ubuntu&bih=1079&biw=1920&q=motacilla%20flava&ved=0ahUKEwjmspmyktzcAhVSQd4KHSL5C3cQMwiHAShEMEQ&iact=mrc&uact=8

Thanks Chris - If they return I will try for a recording - however the Chiffchaff, Willow Warbler and Wood Warbler are described as having black beaks - these have distinct light coloured beaks - perhaps juveniles / male-female differences??

@user45303 - You can make edits to your post using your original account (Richard). You do not need to create another account. Well, if you have forgotten your password then see here what to do. For now, Iam rejecting your edit.

With the new image it is still hard, but I think I identified the bird. I think this is a Willow warbler (Phylloscopus trochilus) which is pretty common in Europe.
The drawing from the Royal Bird Protection Society (source here) is pretty similar.

Unfortunately, there are two pretty similar birds living in Ireland which can be confused with the Willow warbler. These are the Chiffchaff and the Wood warbler. Differences are small, the Chiffchaff has dark legs and a smaller eye stripe (both of which the bird in your image has not), while the wood warbler lives in woods and has a more yellow breast (and is also much more rare). The links provide audio files with the songs of each bird, this should help you making a final decision, as they are pretty distinct.

In the US warblers typical travel in small loose flocks.


text:
Correlation between menstrual period and lunar revolution
Is it just a coincidence that the the length of the entire menstrual cycle from one flow to the other lasts almost exactly as one lunar month?

Do you mean if there is any correlation between day and night (specifically light as a zeitgeber) on menstrual cycle? Yes. There is.


text:
What is this insect found in a shower?
I hope the picture is clear enough, I've found a worm like insect like the one below a little while ago in my shower, and today I found another one. I've never seen something like this. I would say it is slightly bigger than a centimeter.
Location: Netherlands

Why do they come in my shower ?

It is a species of silverfish such as Ctenolepisma longicaudata or Lepisma saccharina for examples (thanks @RHA for correction in comments).
Silvefish are well known very resistant pest typically found in washrooms and sometimes in kitchens. They are not directly dangerous but can cause property damage. Here is a webpage giving advice on how to get rid of them

It might be a silverfish or a paperfish. And getting rid of them is, at least in the Dutch climate, virtually impossible. I speak from expierence here. Unless maybe, if you convince all your neighbours to do the same...

What is a paperfish? I could not find a wikipedia entry for paperfish except for a fish species. Yes, silverfish are really resistant and it can be really hard to get rid of them esp. in apartment building.

Sorry. It is Ctenolepisma longicaudata, called gray silverfish in English. Paperfish is my bad translation of the Dutch 'papiervisje'. It eats books...


text:
Europeans succumbing to diseases they introduced to native Americans
I am reading a non-fiction account of Spanish first contact with native Americans. The Spaniards were shipwrecked, undernourished, malnourished, and dehydrated upon their arrival. Over 75% of them died within a few months. The author writes that after their numbers were thusly reduced, the natives who they were staying with then began to die of "a sickness of the stomach." The natives blamed the Spaniards for killing them.
I am assuming that the illness the natives contracted was introduced by the Spaniards, and that it was one of the ones for which the Europeans had developed a certain level of immunity, meaning that in effect, the natives were correct that the Spaniards were killing them.
The author does not ever specifically say whether any of the Spaniards contracted this fatal stomach illness, so it is possible that all of the Spaniards who died, did so from other causes, such as malnutrition. I am basically trying to find out how likely that is.
My questions are, would the Spaniards' immunity from whatever disease this was help them in the presence of an epidemic such as this, or did their immunity only keep them from contracting it when it was in its latent form? Did their weakened and malnourished state make them more susceptible to a contracting a disease they were carrying, yet were previously immune to?
To put it another way, I'm trying to find out whether it is possible for there to have been a "feedback loop" of some sort when it came to European-introduced diseases.


text:
Reason behind using DNA primer in PCR techcnique while RNA primer use in replication in vivo?
I have went through Lehinger ( biochemistry book) and cooper ( cell Biology) but i didn't find my answer.
plese help me

Your question isn't very clear; could you please elaborate?

The (very) basic answer to your question about in-vitro vs. in-vivo primer usage is:

In-vivo - Although either (DNA or RNA primers) can be used for in-vivo primer extension biochemistry, DNA primers are not available (not made) in living cells. Therefore all natural in-vivo primer chemistries utilize RNA primers.
In-vitro - DNA primers are easily synthesized, inexpensive, functional, and substantially more stable (less likely to be degraded). DNA primers are therefore primarily used for most in-vitro purposes (i.e. PCR and other in-vitro primer extension applications).

Beyond that, all other reasons (complex evolutionary reasons vs. human choices in-vitro); involving subtle differences between RNA and DNA chemistry, structure, and function, similarly can play a role. The links below may be helpful to address some of these differences.
https://en.wikibooks.org/wiki/Structural_Biochemistry/Nucleic_Acid/Difference_between_DNA_and_RNA
https://en.wikipedia.org/wiki/Primer_(molecular_biology)

Generally speaking, initiation of DNA replication in vivo at a defined origin of replication, requires an enzyme with DNA primase activity.  DNA primase is a DNA-dependent RNA polymerase that generates short RNA primers that are used to prime DNA synthesis by the DNA polymerase holoenzyme at a so-called replication fork.
The classical polymerase chain reaction (PCR), on the other hand, is a way for humans to use an in vitro method to amplify relatively large amounts of double-stranded DNA from a specific fragment, using a DNA template target and two artificial, single-stranded DNA oligonucleotide primers (along with dNTP substrates, buffer, Mg++, a thermostable DNA polymerase, and a programmable thermocycler).
So the goals, or outcomes, of the two processes that you are trying to compare seem vastly different to me.  Replicating a chromosome is presumably to keep an organism alive, and reproducing, and dividing, to produce progeny.  Amplifying a desired DNA fragment is a tool to allow some subsequent process or assay to occur.
Your question does not have a clear sense (to me).  There is no stated requirement for biochemical reactions created by human scientists to in any way be limited, or constrained by reactions that occur inside a living cell.


text:
Can the central dogma work in reverse?
Theoretically, is it possible to obtain the original gene from the protein’s amino acid sequence as its “template”, as in, the reverse of how gene’s codons were “templates” for the amino acid sequence of the protein?
I’m curious to know if it’s possible to use enzymes such as reverse transcriptase to obtain DNA from a protein in a reversed central dogma model.

What do you mean by "theoretical"? As in could a cell do it if it wanted to, or if they are even capable of doing so? Or do you mean can we realistically envision the chemistry that would be requires for that to happen?

This can be answered in both senses, which are very interesting.

I say “theoretically” because I am not sure if it has been done before, and I am not sure if that is because of the practical impossibility of the idea. Therefore, I guess what I mean is the last phrase you proposed.

what kind of googling have you done? Have you heard of protein sequencing?

Let’s first consider what the Central Dogma[1] actually says. It is precisely summarised in the following figure[2]:

solid arrows represent transfer of information that has been observed directly; dashed arrows represent potential, not yet observed, transfer of information

In the time since the original formulation of the Central Dogma in 1958, we have been able to contribute evidence for one of the dashed lines: RNA→DNA is performed in vivo via reverse transcriptase. By contrast, note the absence of any arrows originating from “protein”. The idea of the Central Dogma was that proteins were an information transfer sink: information could only flow in, not out.
And Crick and his contemporaries had good reasons for assuming such an information sink: translation from RNA to proteins is lossy  because the genetic code is degenerate. A given amino acid can be encoded by more than one codon.
This doesn’t mean that polypeptide chains couldn’t be reverse translated into “a” RNA representation. But it wouldn’t necessarily be the original RNA. Stated like this, it’s obviously possible: we can in fact take a polypeptide chain, sequence it, and synthesise a corresponding RNA.
However, this doesn’t happen in nature — at least, it hasn’t been observed so far, and there are good reasons to assume it doesn’t happen at all. In fact, Crick’s paper[1] explains:

The transfer protein→RNA … would have required (back) translation, that is, the transfer from one alphabet to a structurally quite different one. It was realized that forward translation involved very complex machinery. Moreover, it seemed unlikely on general grounds that this machinery could easily work backwards. The only reasonable alternative was that the cell had evolved an entirely separate set of complicated machinery for back translation, and of this there was no trace, and no reason to believe that it might be needed.

The “complicated machinery” Crick mentions here consists of two distinct parts: On the one hand the ribosome, and on the other hand the aminoacyl tRNA synthetases (aaRSs, singular aaRS). The latter is essentially the physical embodiment of the genetic code in the cell. The former is the machinery necessary to decode RNAs using the codon adapters (= tRNAs) charged by the aaRSs.
Crick correctly notes that, in order to allow the transfer protein→RNA, the cell would require a system analogous to the ribosome and all the aaRSs, redundantly encoding the exact same information. And it would need to ensure that these two distinct encoding systems (translation and reverse translation) never get out of sync with each other.
It’s worth contemplating, briefly, why the cellular translation process isn’t simply reversible, given that it’s an chemical process, and thus pretty much by definition reversible in theory. The reason for this is that translation happens in two entirely distinct, and physically separate, stages: the charging of individual tRNAs with their corresponding amino acids by an aaRS, and the actual mRNA translation by the ribosome.
Simply reversing the ribosome activity would result in a polypeptide being digested from one end, yielding individual amino acids. However, the ribosome actually has no facility for capturing these amino acids, they would simply diffuse away without being attached to a tRNA, let alone the right tRNA. A successful reverse translation would have to physically couple each type of aaRS in turn to the ribosome to ensure that terminal amino acids would pair with the correct tRNA, which, in turn, would pair with a codon. There are two fundamental objections to it, which render it impossible:

Codons, which could be combined into mRNA chains, don’t swim around individually. In fact, short RNA chains are highly unstable and are quickly degraded. By contrast, individual ribonucleotides can be combined into chains — that’s what polymerases do all day, after all. But the ribosome doesn’t possess polymerase activity, and the tRNA anticodon would not provide sufficient physical support to enable a polymerase to dock to it and start synthesising a secondary strand.
Steric hindrance prevents the aaRS enzymes from interacting with the tRNAs while they are being held by the ribosome: the ribosome and the aaRSs would have to physically overlap.

It’s hard to get definitive answers in science purely from theoretical considerations, but this one’s as certain as you’re likely to get: cellular translation using the ribosome is a non-reversible process. Reverse translation, if it existed, would therefore require a separate machinery.

My answer explicitly omits the discussion of the transfer protein→protein, as this is a topic all of its own, and would increase the size of the answer unduly.

Contrary to my belief, it may be possible.
The main concern we must look at is Protein to RNA, as we know RNA to DNA can be done through reverse transcription.
Some evolutionary scientist believe that reverse translation may be a process that could have occurred naturally during the process of evolution to create the central dogma we know today. Hence, there still lies the possibility that there is a mechanism for the process that remains undiscovered. Just because we do not have proof of it does not mean it does not exist.
There is also a product under development called PeplicaTM that claims to be able to convert protein to RNA, which can then be amplified with conventional PCR. Though, I can not find much information regarding it making me a little hesitant on suggesting whether it actually works.
The following is a little bit of a review on the topic that further outlines some points I mentioned. If you are interested, do read it.
https://www.omicsonline.org/open-access/revisiting-cricks-dogma-and-the-impossibility-of-reverse-translation-jtco.1000110.php?aid=24768

+1 for finding that article, it’s certainly … interesting. And by that I may or may not actually mean that it’s absurd. At the very least it’s probably the most uncharitable treatment I’ve ever read of Crick’s work, and it provides an intellectually dishonest caricature of his arguments so that the author can dispatch them.

The key underlying concept in Francis Crick’s so-called Central Dogma of Molecular Biology is that the genetic information to create a new cell (or organism) is encoded in a cell’s DNA, and therefore it is the DNA that gets replicated when a mother cell divides to give two daughter cells, and it is the same DNA that has to be equally partitioned, or transmitted, to each of the daughter cells for life to continue.
The primary information encoded in that DNA is the sequence of all of the proteins that the daughter cells might need to make to stay alive.  And so we have:
”DNA makes RNA and RNA makes Protein”
Where the messenger RNA is a transient intermediary between where the genetic information is stored, and where the genetic information is decoded (on the ribosomes, where protein synthesis occurs).
Reversing the central dogma would be a situation where the proteins of a cell contain the genetic information that gets replicated in the mother cell and then gets partitioned, or transmitted to the two daughter cells.  If proteins could be reverse translated into a genetic mRNA (this has certainly been done in a test tube where the primary sequence of a protein has been used to create an oligonucleotide primer (admittedly made of DNA) (this required a human who could read the universal genetic code table—also assembled by humans)), then in theory that RNA could be converted into a DNA copy by RT, as you described.  But then we are left with an incomplete scenario where it is the DNA sequences which have to provide the enzymatic, structural, and regulatory roles of the resulting cells (i.e., all of the roles that proteins currently provide).
DNA does not possess any enzymatic activity (as far as we know), so at this point the model you propose does not seem viable.
You also are ignoring the fact that the genetic code is degenerate such that there are up to six different codons that can encode one of the 20 common amino acids, so any reverse-translatase would have to be imprecise.
Consider this question: where is the genetic code table stored inside a cell?

I think your answer erects a partial straw man: there’s no necessity in this model for DNA to have an active role: It could conceivably act as a passive intermediate molecule. This is in fact exactly what happens with retroviruses.

I think you make a valid point (straw man), and I like the thoroughness of your answer. I am thinking of deleting mine now.

Let's consider the following theoretical possibility of of a molecular mechanism for information transfer from protein to RNA or DNA. One can imagine having "adapters" (either protein or RNA or even DNA) that bind with high affinity to a specific protein fold. There are estimates of about 4000 possible distinct protein folds, of these ~2000 so far demonstrated) (Govindarajan et al. https://pubmed.ncbi.nlm.nih.gov/10382668/). So one could imagine ~2000 different adapters, some of which could bind simultaneously to a protein and be brought to a linear register by means of flexible linker regions of variable lengths. One then imagines that at the other ends of this flexible region is a 3-letter codon (or anticodon). Imagine then a polymerase that either polymerizes the registered array of codons (or which nucleates a growing RNA strand on the noncovalently arrayed anticodons). This fantasy is physically plausible but is rather unlikely to exist in competition with the forward transmitting of genetic information. However, in an exoplanet life could have evolved to transfer information from polymers with irregular shapes to polymers with regular features for safe storage. In other words, it is possible to imagine information transfer from complex to simple encoders, in contradistinction from the more elegant solution of transfer of earthly biological information from simple to complex encoders.

Why 2000 adapters rather than ~20 (one for each amino acid)?

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review


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What is the role of CRISPR-dCas9 in gRNA-dCas9 transcription regulator complexes?
In this paper1, I read that mutant versions of Cas proteins such as a deactivated Cas9 (dCas9) are used alongside a guide-RNA (gRNA) to form variants of CRISPR tool that can function as transcription regulators.
Since the mutant Cas9 has lost its nuclease functionality, the mutant gRNA-dCas9 complex can "block" transcription factors such as RNA polymerase from binding a certain gene, hence repressing transcription or elongation.
Another way that dCas9 can regulate transcription is by "carrying" another transcription factor - be it an activator or repressor - and this can be done by engineering a dCas9 fused to the other transcription factor of choice.
I understand how the dCas9 can block the binding of another transcription factor to repress transcription initiation or elongation, but what is the point of fusing another transcription factor with the dCas9? It seems to me that in this scenario, the dCas9 is just a passive carrier of the transcription factor that is actually doing the job, so why can't the transcription factor be fused with the gRNA instead, so that it can directly affect transcription when the gRNA forms complimentary base pairs with the target gene, instead of it being on a passive dCas9?
 1. Jusiak, B., Cleto, S., Perez-Pinera, P. and Lu, T.K., 2016. Engineering synthetic gene circuits in living cells with CRISPR technology. Trends in biotechnology, 34(7), pp.535-547.

so why can't the transcription factor be fused with the gRNA instead,
  so that it can directly affect transcription when the gRNA forms
  complimentary base pairs with the target gene, instead of it being on
  a passive dCas9?

The main reason for that is that both the gRNA and the dCas9-TF (transcription factor) combination can (each) be encoded genetically, while a combination of a gRNA with a transcription factor could only be generated chemically.
The possibility to genetically encode the dCas9-TF + gRNA unit allows one to:
a) use established methods for transferring DNA into cells,so that the cells make the Cas9 and the gRNA by themselves and
b) generate cells that will stably express the whole unit (dCas9-TF + gRNA) forever.
Neither of these options would be possible with a chemically linked gRNA-TF (which is also much harder to make for molecular biology labs that don't have the proper chemistry equipment).

Thank you. So in a more general scenario, is it more conventional to induce the synthesis of a gRNA-Cas9 complex by the cell itself, rather than deliver the already-synthesized complex into the cell?

I don't really have experience with Crispr/Cas9 myself, so I'm can't say for sure, but its is definitely easier to only transfer DNA (plasmids) in cells and let them build the proteins & RNA, since DNA transfection is one of the most common molecular biology methods. Transfection with protein &/ RNA is harder and therefore more unconventional (but still sometimes used for Cas9, especially if you DON'T want the cell to retain the Cas9 protein in any way)


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What is the adaptive significance of temperature dependent sex determination?
Why do some reptiles have TDSD ?  Is it because one of the genders is healthier than the other that only they, can survive high temperatures?

Please google search with "Temperature dependent sex determination". The search will bring up an excellent Wikipedia page on this complex topic that addresses your question. Several scientific references are also cited there as well.

To my knowledge, it is still mainly unclear what are the enviromental factors that would promote Environmental Sex Determination (ESD; incl. TSD) vs Genetic Sex Determination (GSD; incl. with and without sexual chromosomes).
Environment variability and Climate change
Generally speaking it is thought that in variable environment, GSD might be more beneficial as an ESD mechanism could lead uneven sex-ratio and hence lower fitness (Pen et al., 2010).
Climate change can be very detrimental to species that use ESD. A sudden climatic change can cause a population to have a highly biased sex-ratio to the point where persistence is not possible anymore (Boyle et al., 2014).
Differential fitness variance among sex
On the other hand, ESD can allow parents to decide the sex-ratio of their offsprings (Randy, 2005).
Consider for example a case where sexual selection lead to a much high variance in fitness among, say, males than among females. Note that parents fitness and offspring fitness is correlated (because an obvious genetic correlation but also because some environmental correlation). In such case, parents that have a low fitness would prefer to produce females (that despite being unhealthy / ugly will still manage to have a decent fitness) while parents with high fitness would prefer to produce males (because very healthy / good looking males will have a very high fitness).
Charnov and Bull model
In Charnov and Bull (1977) own words (taken from their abstract)

We propose that labile sex determination (not fixed at conception) is favoured by natural selection when an individual's fitness (as a male or female) is strongly influenced by environmental conditions and where the individual has little control over which environment it will experience. Our argument also applies to sex expression in hermaphrodites

According to wikipedia, there are a number of evidences for this model in the literature. I let you go through the cited papers for more information about what is the logic behind this hypothesis!
Evolutionary constraint
Changes in sex determination systems has not evolved that many times (in Reptilia at least; Jansen and Phillips, 2006; see this post for definition of Reptilia). It can be hypothesized that there might be a strong evolutionary constraint (see also phylogenetic signal) and hence looking for adaptive reasons for its evolution might be a moot point.


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Why should collected blood from patients be analyzed as soon as possible?
I'm looking for the possible factors influencing blood samples. What happens to the blood cells esp. WBCs/PBMCs after 8 hours of blood draw? For example, I know that granulocytes may cause oxidative stress and that may affect the viability of WBCs. What else could have an effect on blood samples that we can't store them for a long time at room temperature?  Thank you.

Biological samples, including whole blood, are not at equilibrium. Biological processes, e.g., cellular metabolism, continue. Cells interact with their environment and a tube is not the same thing as the human vascular system. For one, in humans, on average, the entire volume of blood recirculates once every minute (see Costanzo Physiology Ch 4). Recirculation, with the associated access to nutrients, waste drop off, and exposure to various different compartments doesn't happen in a specimen tube. Nutrients are consumed, waste collects, cellular stress occurs, intracellular components leak out, cellular morphology changes... You can slow this down by putting samples on ice and collecting blood in a tube with components that preserve the sample for the specific test. There's a nice discussion of this in Lange's Guide to Diagnostic Tests, Chapter 1.
Given ongoing biological process in a very different environment, you can understand how interpretation of a particular test result depends on consistent collection and storage methods. Different tests are going to be more or less sensitive to time since collection and storage methods. There's a good deal of data on this for whole blood in this review.

@biologist you're welcome. If this answered your question you should mark it the answer by clicking the gray check mark next to it and turning it green. See someone answers


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Mouse H2 allele sequences
I've been trying to find complete sequences of mouse (Mus musculus) MHC H2 locus haplotypes for quite some time now with limited success. The EBI IMGT database has a table of mouse H2 haplotypes, yet IMGT only provides haplotype sequences for human HLA genes via an FTP sever. I've found similar data for several other species at EBI's IPD-MHC, but Mus musculus is not on the list. The MGI database provides access to H2 SNPs, but I haven't found a mapping from SNP combinations to reconstruct happlotype sequences given reference genes.

Are you after amino acid or gene sequences?

@David I'm looking for nucleotide sequences: "I haven't found a mapping from SNP combinations to reconstruct happlotype sequences given reference genes". Protein sequences are readily available in the UniProt database.

I have also hit this issue. I was interested in full length amino acid sequences for the classical class I mouse MHC alleles. I was able to find a number of them on uniprot but not all. Here is my list below. Interested if anyone knows additional sequences to extend this:
H-2 D

H-2 Db
H-2 Dd
H-2 Dp
H-2 Dk
H-2 Dq

H-2 K

H-2 Kb
H-2 Kd
H-2 Kk
H-2 Kq

H-2 L

H-2 Ld
H-2 Lq

Seems a useful answer to me, but I wonder whether the poster wanted gene or protein sequences. He didn’t say.

Thank you for your effort. I've been using these UniProt protein sequences myself, but the question is about nucleotide sequences. Those are harder to find.

MGI database may give you some help about Mouse H2 complex full length sequence.
https://www.informatics.jax.org/quicksearch/summary?queryType=exactPhrase&query=H2&submit=Quick%0D%0ASearch


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How to find the amino acid that is bound to a tRNA with the anticodon?

What amino acid is bound to a tRNA with the following anticodon: $5^{\prime}$ A U G $3^{\prime}$

The answer is Histidine.

What amino acid is attached to the tRNA with the following anticodon $5^{\prime}$ A G C $3^{\prime}$

The answer is Alanine.

I also referred to this image below but unable to get the answer. Can anyone please explain how to solve this?

Each tRNA brings a single amino acid and add them to the growing peptide strand. The tRNA has an 'anticodon' which recognizes a codon on the mRNA code. How this occurs:
How to figure it out:

You have to find out the complementary bases. With DNA, A is complementary with T, and C is complementary with G. However, we are working now with RNA! It's similar with RNA, with one exception: in RNA, U (uracyl) is used instead of T, so A is complementary with U. C is still complementary with G.

Notice that the 5'-3' anticodon is antiparallel to the codon (one is 5'-3', the other is 3'-5'). This means that to find out which amino acid is being added, you have to reverse the code found on the tRNA.

Your questions, let's go step by step:

1) tRNA anticodon: AUG
tRNA complementary strand would be UAC. Reverse to get the 5'-3'
direction on the mRNA. The reverse of UAC is CAU, which is His
(histidine).

and

2) tRNA anticodon: AGC
tRNA complementary strand would be UCG. Reverse to get the 5'-3'
direction on the mRNA. The reverse of UCG is GCU, which is Ala
(alanine).

You can also reverse first and complement second. The order does not matter, provided you do both. Always visualize the process, it helps tremendously.
Let's do a final exercise to see if you understand, but in reverse and with some extra thinking. What are the tRNA sequences which bind to the mRNA strand ACUACAGUAUAC? What is the peptide sequence it will produce?
mRNA: ACU ACA GUA UAC
We can use the translation table immediately; it is used to translate mRNA into peptides directly. We find out it produces the peptide: Thr Thr Val Tyr
Reverse mRNA:  CAU AUG ACA UCA
Complement it: GUA UAC UGU AGU
(FYI: by convention, we always write mRNA in the 5'-3' direction)
The tRNA anticodons which bring (i) Thr (ii) Thr (iii) Val (iv) Tyr to build the peptide chain are (i) GUA (ii) UAC (iii) UGU and (iv) AGU.
All of these sequences are written in the 5'-3' direction, as per convention. It's easy if you are careful and clear in your working :-)


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Can supplements affect DNA? (Could 10,000% Methylcobalamin affect MTHFR genotype)
Originally titled "Could B12 supplementation affect dna test results for B12 need?" - B12 just seems like a good example question to frame the more general question of "Can supplements affect DNA?"
I recently got a DNA test done from DNAFit and found out I do not have a raised need for B12 - however - I've been supplementing with about 10,000% B12 (as methylcobalamin) for quite some time now. Been taking 10,000% every day for 5 months and like 1,000+% B12 for another 5.5 months before the increased dosage. I actually am quite dependent on my supplements, and think it's quite possible that my DNA has adapted to them, if DNA does such things. (Just looking briefly, it appears there is some disagreement as to whether DNA can change due to supplementation: google.com/search?q=CAN+SUPPLEMENTS+CHANGE+DNA )
So there's the root of the question - can supplements affect DNA - more specifically - could B12 supplementation affect the result of my MTHFR genotype (which is CC, just FTR)

What the DNAfit test does is analyse some of your genes for common variants (called SNPs - single nucleotide polymorphisms). These are hard-written in your genetic code, they won't ever change (you could in theory have mutations in some individual cells, but we can ignore that).
Taking supplements or any other environmental influences will therefore not affect these tests.
The environment can affect certain markers on the DNA, that control how active a given gene is (how strong its expressed) - this is called epigenetics. Since these markers are written on the DNA they are also potentially heritable and the two effects (the genetic code itself and the markers on it) are often thrown into one pot when some news report about 'changes to your DNA'.


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If wolves (or foxes) are fitter than rabbits, why rabbits have not become extinct?
I do not pretend to "demolish" the Darwinian theory of biological evolution and the "survival of the fittest", that's far from my intention.
I have this doubt because of the fact that humanity, as Homo sapiens sapiens, extinguished the Homo sapiens neanderthalensis because we were fitter to survive.
Please consider this question as if the humanity hadn't appeared yet (because we have domesticated rabbits).
Thanks in advance.
Edit: I have assumed that wolves and rabbits (or hares, maybe) live in the same ecosystem.

It doesn't make much sense to talk about 'the fitness of foxes' as an absolute thing, because 'fitness' is not a fixed quantity - it changes depending on environmental conditions. So the crux of the answer is 'because ecology': an environment with fewer rabbits is an environment where it is harder to make a living as a fox.

Do you agree with me in saying that no one can talk about survival without talking about a catastrophe? Like a war, or maybe an ice age.

Er. No. I talk about survival all the time, as part of day-to-day biology. Like: "the rangers have started putting out supplementary food, so the chick survival rate for [species] at [site] has increased by 15%". No catastrophe is necessary.

Neanderthals were already on the verge of extinction when they met sapiens in Europe.

Simple: wolves and foxes are not fitter than rabbits. If they were, rabbits would be extinct.
This question is like asking "If Gary Kasparov is better than Michael Jordan, why hasn't he won a chess championship against him?"
And the answers are the same:
- "what do you mean, 'better'? Better how? At what?"
- "either way, they've never played in a chess championship against each other, so..."
"Fitter" in evolutionary theory means "better at something"; in general it will be "better at surviving", but better at surviving under what circumstances? There isn't a single "fit" or "fitter". Maybe you thought that wolves are better at surviving than rabbits because wolves kill rabbits and not vice-versa, but I could as easily argue that rabbits are better at surviving than wolves because rabbits would survive fine without wolves, but wolves would go extinct without rabbits (not completely true because they have other prey, but you get the idea). The truth is, as far as we can tell wolves and rabbits are equally good at surviving because both have survived.
So you can only talk about fitness if you focus on one specific circumstance to be fit in. But then there is the other implied idea in your question, which is that fitter species drive less-fit ones to extinction. This is true only if the species are in competition. Two species (or individuals, or anything) are in competition when if one species does badly, the other will do well as a result, and vice-versa. For example, maybe they eat the same food, and there is only so much to go around, so every additional bit of food A gets is less food for B, and vice-versa. In that case it is clear that one species being better at surviving than another is bad for the other species, and can (and, according to theory, will) drive it to extinction. Like fitness however two species can be in competition in some ways but not others. For example, two species might compete for food, but have a mutually-beneficial relationship with respect  to predators, where if there is more of A the predators will go for them which is good for B, and vice-versa.
Wolves and rabbits are clearly not competitors: things that lead to more wolves will indeed lead to fewer rabbits, but things that lead to more rabbits will also lead to more wolves. As such, even if one were measurably fitter than the other by some metric, it would not necessarily lead the other to extinction. For example rabbits being better against the cold than wolves could promote the existence of wolves in cold places, because a lot of them might freeze but the abundance of food might make it worth it.
This does involve an interesting ecological paradox, which is that according to theoretical models, if you have X species in perfect competition, all but one will eventually go extinct. There is a lot of research in how and why our world's massive biodiversity exists despite this. A big factor is that as I have pointed out, perfect competition is extremely rare in nature. Most species aren't competitors at all, and those that do compete usually don't compete on everything, everywhere and at all times. But when they do or close enough, yes, one should drive the other to extinction. Whether this is why the Neanderthals went extinct is another question

It's also relevant to look at predator-prey cycles, like the Canadian lynx-rabbit cycle.  If your predator species is so "fit" that it eats all its single prey species, it starves.  So without predators, the prey species increases its numbers until it consumes all its food supply, whereupon it starves, too.  So neither species is fit in an evolutionary sense.


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What can I research for thesis on DNA data storage from math?
I'm a math researcher, I just finished a Master on Error Correcting Codes. I recently saw a presentation on DNA-based data storage that I loved.
I wish to continue my studies on (applied mathematics) in this subject.
I received a PhD offer and when I mentioned the subject, the possible director was receptive, but he is not well informed on the subject either, so he proposed that I come up with a research path ...
What do you think is an interesting research topic (and worthy of the community) about storing DNA data from the perspective of error-correcting codes?
Thanks for the help!

First, I think this question is off topic on a list about biology, as you will see if you take the tour and read the Help on questions. Any answer would be a subjective opinion of what might be interesting. You could try Stack Exchange Bioinformatics instead — you might get more informed opinions there. However I would be very wary of embarking on a PhD on the basis of opinions of unknown people on Q&A list. I can also warn you that a danger of someone in your position is doing a PhD on something that is of absolutely no interest to biologists. You need to find a live senior biologist first.

This is also duplicate of a question that you have posted on the Bioinformatics Stack Exchange website. https://bioinformatics.stackexchange.com/questions/4857/what-can-i-research-for-thesis-on-dna-data-storage-from-math

It is more based in computer science and bioinformatics as data structures and storage of information is using GATC instead of 1 and 0s. Of course, you can probably find some math application since there is math anywhere, but you need to investigate the topic throughly and find an area which could use work.... like any thesis.


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What is this bizarre looking animal we found in the forest? Bug identification
Please can someone identify this?
I can't find anything on the Internet like it. 2 cm long. North Bohemian mountains (Czech Republic).

That is the caterpillar of a lobster moth (Stauropus fagi), family Notodotidae. It is mimicking a scorpion to help protect it from predation. An amazing insect.

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


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Is it safe to autoclave seawater agar?
For an experiment I'm going to prepare an artificial seawater agar. Before use, I have to sterilize the medium of course. I imagine, that autoclaving will cause the salts in the seawater to precipitate. Can I re-suspend them afterwards, or will it irreversibly change the composition of my medium? Should I use a different sterilization method altogether, e.g. filter sterilization?

Why should they precipitate? Warm water dissolves more salts than colder.

I see no reason why it would precipitate chemically. Besides, you need to dissolve the agar via heat. Hence, auclaving is fine.
If you do not believe me these protocol allow for autoclaving of seawater agar 15min cycle 121 degrees:
1. https://www.dsmz.de/microorganisms/medium/pdf/DSMZ_Medium246.pdf
2. http://himedialabs.com/TD/M592.pdf

Hi @AdamRadekMartinez. This is a good answer. You don't need to preface your sources with "if you do not believe me", though. Just reference them. Biology.SE answers should include references, with no expectation that a poster will just be believed without them :)


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Is there any system how genes are spread across chromosomes?
Every chromosome being a wrapped DNA molecule contains thousands or more genes.
Now, is there any system why a gene A goes to a chromosome K and gene B to chromosome J?

To a first approximation, it is "not too awful" to state that genes are randomly spread. In a more detailed view, it is a little more complex.
Homochromatin vs heterochromatin
Genes are not evenly spread within chromosomes. Typically, gene density is lower at the centromeres.
Supergenes
From wikipedia > Supergenes

A supergene is a group of neighbouring genes on a chromosome which are inherited together because of close genetic linkage and are functionally related in an evolutionary sense, although they are rarely co-regulated genetically

To my understanding, such supergene may come to existence via chromosomal rearrangements or via repeated proximal gene duplication.
Supergene and synteny
From Wikipedia > synteny

In classical genetics, synteny describes the physical co-localization of genetic loci on the same chromosome within an individual or species. Today, however, biologists usually refer to synteny as the conservation of blocks of order within two sets of chromosomes that are being compared with each other. This concept can also be referred to as shared synteny.

A classical example of supergene with highly conserved synteny among vertebrates is the case of Hox Genes (Amores et al., 1998).
Sexual chromosome
A sexual chromosome is some kind of a massive supergene! Consider, for example, the mammalian case.
Consider a locus that affects sex determination (SD) such as the SRY gene (coding for TDF) in mammals for example. Any male-beneficial, female-detrimental genes would gain at becoming closely linked to this SD gene. Over time, hence genes rearrange and recombination is reduced (mainly through chromosomal inversions if I am not mistaken). As recombination is reduced, deleterious mutations can accumulate through Muller's ratchet and eventually pieces of chromosomes are being lost to get rid of these deleterious mutations. This is how a Y chromosome (to consider the mammalian case, a W chromosome in birds) evolve to become so small compared to the X chromosome (or Z chromosome in birds).
Other Y-like chromosomes
Other massive supergenes can lead to Y-like chromosomes. For example, Wang et al. (2013) report a Y-like social chromosome in fire ants.
Additional source of information on the evolution of sexual chromosome
The post Do males of all sexual species have Y chromosomes? might be of interest to you. Charlesworth (1991) and Charlesworth et al. (2005) might also be a good reads.

In prokaryotes, genes of a single pathway genes are often next to each other, and are transcribed together as a single unit.  So for those genes, their position is quite important.


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Are mosquitoes actually louder than similar flying insects, or have we evolved to hear them?
I've come across many flying insects smaller than the common housefly, but (anecdotally) the only such species that I can hear from an appreciable distance away is the mosquito, with its distinctive buzzing whine. It may just be luck that the loudest small flying insect (in my everyday experience), and therefore the easiest to detect and avoid, is also by far the most annoying. On the other hand, mosquitoes are the single deadliest animal for humans and were probably common on the African savannah in which we evolved, so maybe this apparent loudness is actually an auditory illusion, and similar-sized insects are equally loud but at frequences that we haven't evolved to hear or focus on. Are mosquitoes objectively louder than similar-sized flying insects, or might we have evolved to be particularly sensitive to their emitted frequencies?
(This question is the flip side of this one, which focuses on the mosquito's evolution rather than the human's.)