text:
Would someone lose some of their traits if they stop using them for some time?
A co-worker of mine told me, that there are some mutations in the genome during the life of a human body. So, the body changes genes to fit better into the surrounding environment.
My thought is now, if it is true, every generation of human beings loses some abilities which the body has not needed till the time.
A hypothetical example: in a time where education takes even more time and importance than now, would human beings lose their mechanical skills because they do little physical work?

You seem to have several major misconceptions about evolution and mutations. I strongly suggest reading through Understanding Evolution from the University of California, Berkeley.

@MattDMo: this is ablolut true, thats why I'm asking.

This question is relatively clear and easy to answer. I disagree with the close votes and with the down votes.

It has been substantially edited since I voted to close, retracted vote now.

A co-worker of mine told me, that there are some mutations in the genome during the life of a human body. So, the body changes genes to fit better into the surrounding environment.

Yes mutations accumulate during the lifetime but they are random. They are not targeted in a way that the organism adapts to the environment. Evolution happens through multiple generations and not in a single lifetime.

... every generation of human beings loses some abilities which the body has not needed till the time.

No. That does not happen.
It was once actually hypothesized by Lamarck that an organism gains or loses traits based on the use and disuse of those traits, respectively.
We now know that it is not true. A trait is not removed from the population unless it imposes a strong survival disadvantage to the population.
For more details see Why do some bad traits evolve, and good ones don't?


text:
Poisonous plants, animals, mushrooms: is this always a kind of defense?
I wonder whether developing deadly toxins in the organism's body is always or usually a defensive strategy rather than a by-product.

I don't understand the question, spiders, snakes, etc... use it for external digestion of their prey.

@inf3rno I wouldn't say it that generally. Animal venoms tend to be a complex mixture of ingredients, with some components that paralyze a victim, while other components may cause death or digest tissues. Snakes don't use external digestion, they swallow the prey whole.

@inf3rno I do not refer to venom used as a weapon. I mean toxins in somatic tissues.

There's certainly a spectrum here, from the monarch butterfly(and others) who find their poisons in the environment and store them in their tissues, to some kinds of shark that have high urea contents as a result of their metabolism. The sharks probably retain some of the urea they would otherwise excrete for defense, but I'm not actually certain. If I understand the question correctly it's asking about poisonous organisms, not venomous ones. The difference is crucial to addressing this question.

@JeremyKemball +1 venom and poison are different terms, I forgot that too...

I think it always starts as byproduct, and after that if it is an evolutionary advantage it will help the organism to survive.

related: Why are some fungi poisonous?

Developing anything by the body takes energy so generally only useful products are conserved. If some sort of mutation caused an organism to produce some sort of by-product that also happened to be toxic to its predators, then that organism is more favored to survive. No species ever starts producing something with the intention of toxicity in a predator/consumer of said species.
These xenobiotics that the plant/animal produces then can either be selected for because they're useful in whatever pathway they are a by-product of. Or they can be conserved because then this by-product has a defense use, regardless of whether the pathway its part of is necessary. Or both could happen, it could be doubly selected for.

needs references..

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text:
Controlling for phylogenetic signal - what is statistically appropriate?
I am currently collaborating with a fellow PhD student. We are both in the same Biology department, but my collaborator is more of a natural historian, so I am handling the statistical side of things.
He has published a few papers using only Brownian models and Pagel's $\lambda$ (with a different collaborator). However there seems to be a plurality of different methods available - Grafen, Blomberg, and Martin, to name a few. OU models seem inappropriate for our data since we have relatively small phylogenies (Cooper 2016). The literature seems to indicate that Pagel's $\lambda$ is more robust than Blomberg's $\kappa$, and in general an okay method to check for phylogenetic signal. I've also found that some people throw everything and the kitchen sink at their data, and then compare log-likelihoods, AIC, BIC, with log-likelihood ratios for any nested comparisons.
My first question is then, should you have any a priori assumptions of which method will be appropriate for your data?
I am still new to PCM so I used old R scripts and an AmNat paper (from 2019) as my reference. I am also using the same phylogenies as that AmNat paper. From that paper, and from those scripts, only two models were used, a Brownian model (which is essentially $\lambda$ = 1, anyways) and an estimate of $\lambda$. They compared the two models, chose the more appropriate model by log-likelihood ratio and that was it.
My second question is, shouldn't you always compare your models to a model with fixed $\lambda$=0?
For example, I have the following output in R,
#Brownian Model

pglsModel_BM <- gls(sum_dep ~ ContGroup, correlation = corPagel(1, phy = UltTree, fixed = TRUE), data = temp, method = "ML")

#Estimated Lambda Model

pglsModel_E <- gls(sum_dep ~ ContGroup, correlation = corPagel(0.50, phy = UltTree, fixed = FALSE), data = temp, method = "ML")

###Output of comparison is...

             Model df      AIC      BIC    logLik   Test  L.Ratio p-value
pglsModel_BM     1  3 528.4584 534.5344 -261.2292
pglsModel_E      2  4 528.0454 536.1468 -260.0227 1 vs 2 2.412992  0.1203

###ANOVA output of preferred model

Denom. DF: 54
            numDF  F-value p-value
(Intercept)     1 7.039370  0.0104
ContGroup       1 6.480427  0.0138

And the Brownian model got the go ahead. It seems that Brownian is treated as a null model, but I can't wrap my head around why $\lambda =0$ isn't also a null model or the null model. Moving forward with my assumption,
###Adding in a lambda=0 model

pglsModel_0<- gls(sum_dep ~ ContGroup, correlation = corPagel(0, phy = UltTree, fixed = TRUE), data = temp, method = "ML")

###Using anova for model comparison

             Model df      AIC      BIC    logLik
pglsModel_0      1  3 524.0962 530.1723 -259.0481
pglsModel_BM     2  3 528.4584 534.5344 -261.2292

###checking out the 0 model...

Denom. DF: 54
            numDF   F-value p-value
(Intercept)     1 289.67228  <.0001
ContGroup       1   0.21234  0.6468

I realize the differences are rather small, but all methods point to $\lambda  =0$ as the 'more likely' model.
My third question is -- although, possibly answered by the second question -- do we assume that there must be some amount of phylogenetic signal due to shared history, such that it is suffiecient to only test for $\hat{\lambda}$ and compare to $\lambda = 1$?
Note: Just to be sure, I compared all Brownian models with corBrownian to their $\lambda = 1$equivalents, and got the exact same outputs.

I have a tentative answer to my question.
In the publication for the R package phylosignal (Keck, 2016), they state:

To test the presence of phylogenetic signal, the null hypothesis is that trait values are randomly distributed in the phylogeny. Another null hypothesis might be that trait values follow a Brownian motion model but it is less often used and implemented.

So it would seem there are indeed two null hypotheses, however it seems disingenuous to not test for both, especially since it is relatively simple to do. And of the two, should you for some reason be limited to one, testing for $\lambda = 0$ (or the log-likelihood of a general linear model) should be your first choice.
Another issue was with corPagel from the package ape. It requires an initial value to estimate Pagel's $\lambda$ (Unless you fix the value, of course). Convergence is not guaranteed, and sometimes requires some fine-tuning of the initial value. This set off a bit of a red-flag, so I collected the median lambda from 5000 subsets of my data (I am using a different family/phylogeny/dataset, where the $\hat{\lambda}$ model is preferred over a Brownian, but not $\lambda = 0$).

I think this is stronger argumentation for a phylogenetic signal, albeit a weak signal.
#output of comparing lambda=0, lambda=1, and median lambda

                 Model df      AIC      BIC    logLik
pglsModel_0          1  3 636.9876 643.6899 -315.4938
pglsModel_1          2  3 681.9784 688.6807 -337.9892
pglsModel_MEDIAN     3  3 636.4812 643.1836 -315.2406

#output of comparing median lambda to the estimated lambda from the full dataset

                 Model df      AIC      BIC    logLik   Test   L.Ratio p-value
pglsModel_MEDIAN     1  3 636.4812 643.1836 -315.2406
pglsModel_FULL       2  4 637.7024 646.6388 -314.8512 1 vs 2 0.7788265  0.3775

By the evidence of the distribution of lambdas, and the median model's AIC, BIC, and log-likelihood, we can argue in favor of the median model. Residuals also look normal and random. Confidence intervals should also be obtained. But, in reality, here, the difference here between a weak phylogenetic signal and none at all are vanishingly small.

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What's this parasite?
Any microbiologists or parasitologists recognize this? It's from my pet bearded dragon in the eastern US and the vet's never seen it before.

Welcome to Biology.SE! Identifications questions should include: 1) the location (e.g. country and region — the more specific the better) where you observed this organism; 2) habitat information — e.g. from what type of lizard and from where in/on the organism it was isolated; and 3) an estimate of the size of the organism. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

It could be a whipworm, a common parasite in dogs with a flagellum.
Check the image here:
Image at:
https://www.texaswestveterinarian.com/whipworms/

Thanks. Afraid it's probably not that. What my lizard has is microscopic, whipworms are 3-5 cm.

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Why does the structure of RNA change?
RNA only has one strand, but like DNA, is made up of nucleotides. RNA strands are shorter than DNA strands. RNA sometimes forms a secondary double helix structure, but only intermittently. Why does RNA change structure? We see that DNA has a well-defined structure of a double helix. Why does RNA have to change it's own?
EDIT - My main focus is on this line "RNA sometimes forms a secondary double helix structure, but only intermittently."

Please clarify. 1. Are you talking about a particular type of RNA — ribosomal RNA, mRNA, virus genomic RNA? 2. What do you mean by “change structure”? Form secondary structure, suffer mutation? Or are you asking why RNA is usually single stranded, or what advantages RNA genomes have for viruses? At the moment your question is unclear to me.

...or perhaps you are asking why different RNAs have different structures rather than a single structure like DNA, or why mRNA doesn't have a distinct structure but can adopt different structures? If you can clarify we can help you. It's what you mean by "change" that seems to be the root of the problem.

@David My main focus is on this line "RNA sometimes forms a secondary double helix structure, but only intermittently." Why does this double helix structure form intermittently?

Intermittently conveys to my the sense of change in so far as sometimes it’s one structure, sometimes another. This would be true for mRNA. For rRNA and tRNA the situation is that some parts of the RNA are double-stranded, others not. I can answer regarding either or both, as you wish.

@David it would be great if you would answer for both. Thanks!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, quotes must be referenced — this is considered good practice in scientific communication and will help other users understand the context for the quote. Thanks!

I have now provided an answer, which really is to the question "Why do different nucleic acid species have different structures". If my answer addresses your problem, I think this would be a better title for your question in which I think the word "change" is misleading, and their is an implication that all DNA is double-helical and all RNA is not, which is incorrect.

Summary
Most nucleic acid species have specific structures (or a limited number of alternative structures) which may involve a greater or lesser amount of double helix through complementary base pairing. The extent of such helical components depends primarily on the availability of sequences of complementary bases, which is obviously greatest for the two distinct strands of a double-stranded DNA or RNA genome, but also occurs in a specific manner within RNA species where base-pairing has been evolutionarily conserved in particular regions.
Two ways of interpreting “why?”
When responding to questions about biomolecular processes and structure, I think it important to differentiate between two meanings of “why”, and I shall distinguish these by appropriate numbering in my answer.
1. The mechanistic “why”
This is generally easier to answer objectively, as it is request for a physico-chemical explanation for the formation of a structure (RNA or RNA in this case) or operation of a process.
    It is worth emphasizing that just as different macromolecules of the class “protein” can adopt different particular structures — globular or fibrous with many variants on each — so can different RNA, and even DNA, species, as described below.
2. The functional “why”
By this I mean “what function(s) can a particular structure serve?”.
    This is more difficult and beset with dangers. Whereas, we can say that the structure of myoglobin allows it to bind oxygen and release it as the partial pressure in tissues falls, with some macromolecules the function of their structural features may be less clear. The dangers here are in thinking that suggestions of function are facts, and that a particular function can only be accomplished or is best accomplished by a particular structure or structural feature.
The physico-chemical principles governing structure of macromolecules
Put simply, the structure adopted by a macromolecule in a particular environment is that in which it has the lowest thermodynamic energy (Gibbs Free Energy) in that environment. This is the structure in which the sum of the individual interaction energies (generally hydrogen bonds and Van der Walls interactions) is greatest.
    Thus, a macromolecule is able to adopt alternative structures when these structures have similar energies, and the equilibrium between such structures can be changed by action of or interaction with other molecules.
Genomic DNA Structure(s)
Double-stranded DNA (dsDNA) genomes
1. Double-stranded genomic DNAs form an anti-parallel helical duplex structure (double-helix) primarily because they consist of two perfect complementary sequences that allow maximum hydrogen bonding of A–T and G–C base-pairs. The helical structure of the duplex allows the maximize the energetic π– π interactions of the stacked bases.
2. The function of genomic DNA is to maintain the genetic information of an organism and allow it to be transmitted to daughter cells. The double-stranded structure protects the bases from external modifying influences, to some extent, and allows the semi-conservative replication of the strands when a cell divides.
Single-stranded DNA (ssDNA) genomes
Some small viruses of bacteria and eukaryotes have single-stranded DNA genomes, illustrating that this particular function can be served by different structures.
1. Although the replication of ssDNA viruses involves production of a strand complementary to that of the genome, the genome is not double-helical — negating the generalization in the question. The simple reason for this is that the replication mechanism generates many more copies of the genomic DNA strand than the other: complementary nucleic acid sequences are required  to form a double-helix! One could imagine a ssDNA having local regions that could base pair to one another, but this is prevented by the compact supercoiled structure that they adopt, which is a consequence of their closed-circular nature.
2. The compact super-coiled structure of such ss genomic DNAs (e.g. φX174) is suitable for encasing in a viral capsid (although ds circular viral genomes also supercoil).
    The question of why some viruses have ssDNA genomes whereas most have ssDNA genomes is neither a mechanistic nor a functional  “why”. It may be worth discussing, but falls into the realm of hypothesis.
Genomic RNA structures
1. To a large extent, the remarks above about the structure of genomic DNA apply to the genomic RNA of viruses. Genomes of dsRNA viruses have an anti-parallel helical duplex structure because two perfect complementary sequences are available in equal proportions from replication. Genomes of ssRNA viruses do not have this structure because replication generates primarily one type of strand. The ssRNA viruses, unlike the ssDNA viruses, have linear, rather than circular genomes.
2. I have nothing to say about the relation of these structures to function. Both are packaged into viral particles. Both can be replicated.
Transfer RNA (tRNA)
1. The single-strand of tRNA has a clover-leaf stem-loop structure with three short double-helical stems formed by Watson–Crick base pairing, folded into a three-dimensional L-shape by other hydrogen bonds. The sequence of bases in tRNA determines that this self hydrogen bonding can only occur in a manner to produce the particular structure.
2. The purpose of tRNA is to bring an amino acid onto the ribosome in response to a particular mRNA codon. The non-hydrogen bonded loop at one end of the folded molecule contains the anti-codon, allowing it to interact with a complementary mRNA codon; the free 3′-end at the other extremity is covalently attached to an appropriate amino acid. The compact hydrogen-bonded ‘L’ is of a shape that can be accommodated in the A or P site of the ribosome.
Ribosomal RNA (rRNA)
1. The single strands of the two major rRNAs are folded into a complex of stem-loops formed by short stretches of internal double helices involving either Watson–Crick (A–U, G–C) or single hydrogen-bond G–U base pairs. There is conservation of base pairs in the helical regions, without necessary conservation of particular bases. This determines that a specific structure is formed.
2. The double-helical stems are thought to play a structural role in the ribosome. The unpaired regions are free to interact with the various substrates of protein synthesis on the ribosome, and the catalytic centre is constituted of such unpaired bases. In this respect the ribosome represents catalytic RNA in which double-stranded regions have a functional role but the catalytic bases need to be unpaired.
Messenger RNA (mRNA)
1. mRNA is generally thought to lack hydrogen bonded secondary structure or have a limited amount of such structure, depending on the particular mRNA. This presumably reflects a general lack of complementary stretches of nucleotides in mRNAs. In eukaryotic mRNAs there is significant secondary structure at the 5′ end in the untranslated region. Phage RNAs (and perhaps other mRNAs) do have significant double-stranded regions.
2. This can be rationalized as arising from the fact that the primary role of the bases in mRNA is to specify the sequence of a protein, and the mRNA must be capable of being translated by the ribosome. The secondary structure regions that do occur limit this, and may allow the control of translation. This latter point illustrates RNA flexibility — the potential for a switch from one structure to an alternative. This can only occur if the alternative becomes more energetically favourable, e.g. by unwinding of the helical region at the 5′ end of eukaryotic mRNAs.′


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Aquatic forest insect identification
I found it in the forest but I've never seen anything like it so I took it home to see what it is. Does anyone know?

There are few things a species identification query must fulfill; locale, dimensions of the species and clear picture(s) (ideally from as many angles possible - so that all parts of the specimen are conspicuous to the one trying to ID your specimen).

This is a caddisfly larvae (Trichoptera). They live in streams and other water that are rich in oxygen.
They protect themselves by building there own 'house', with whatever is available, e.g. plant or wood fragments, gravel or even snail shells (see picture below)

Picture from Dutch wiki
https://en.wikipedia.org/wiki/Caddisfly

Id to species level probably requires microscopic work.

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text:
What is this fruit / nut?
These were found in a park in Pittsburgh, PA. From a distance they looked almost like plums, but they're actually hollow, paper-like covers that contain a hard pea-sized seed.

Thanks for the good description of the fruit, but could you also give an approximate size? And was it a tree or a shrub that you found them on?

Thanks for your edit in astronomy but I could use all your up votes

Most likely a member of the genus Staphylea. Since you are in Pittsburgh, PA, it's most likely Staphylea trifolia L., or an introduced species.

That is it! I've never heard of (or seen) a "bladdernut" before.

By the looks Of it,it mostly is a hop hornbeam Which are indeed found in pittsburghBut i Still cant confirm it because
they are no photos of their leaves and any twigs or the whole tree, this info would be great to identify it and do you mind mentioning the name of the park you've been to
Can you confirm whether the tree looked like this

Ostrya Virginis

Nope, definetly not an Ostrya species.


text:
What is this animal?

Can someone tell me what is the name of this one? Then I can check a little more about it.

How big is it and where did you find it?

It is not a beast :P

@RHA The bug in that question looks pretty different from this one...

@Cactuswoman same family, different species.

It looks like a squash bug to me (Pyrrhocoris apterus). If not apterus, I'd say it is at least in the Pyrrhocoridae family. Note, they must not but confounded with Corizus hyoscyami. Here is a picture of Pyrrhocoris apterus:

Pyrrhocoris apterus have a very broad range covering a big part of Eurasia, from France to China. Is it where you found it?

This seems to be a species of the genus Pyrrhocoris, most probably the firebug Pyrrhocoris apterus. Its quite common in Europe, but according to the Global Biodiversity Information Facility there are also some occurrences in the US.


text:
What species of conch are these?
I found these in one of my pots in the garden (Gujarat, India) after a few days of heavy rain possibly munching on some algae grown on the side of pots.
The biggest one of them is around 1cm in size. Smallest one is about a 2mm.

Hi Nijraj Gelani. I think it will be almost impossible to answer your question. There are many species of snail, especially in warm countries such as India and they often look much alike.


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What is the name of the bird which feeds on penguin blood and meat in Tristan island?
I just watched a National Geographic documentary "Unseen Islands: Atlantic Arks" and there was some thing strange in Tristan island. Some small bird which changed its diet to feed on the blood and meat of the penguins on this island.
I want to know more about this bird - or its name so I can search it - and if there are other examples of this behavior of changing diets.

You almost certainly mean the Tristan Thrush, Turdus eremita, which is endemic to Tristan da Cunha. The species is considered to be an opportunistic omnivorous scavenger, but their diet includes the eggs and chicks of many seabird species, as well as the adults of some smaller seabird species.
The Wikipedia page for the species mentions that Tristan Thrush has been recorded drinking penguin blood, citing a BBC documentary which I don't have access to. Five species of penguin have been recorded on Tristan da Cunha, but only the Northern Rockhopper Penguin breeds there (the others are rare visitors to the island). Given the nature of penguin colonies (i.e., densely-packed, and with abundant chicks as well as occasional sick adults), there would be many opportunities for an opportunistic omnivorous scavenger to eat penguin blood, chicks, eggs, or carrion.

The BBC documentary is “Southern Ocean”, the second of three episodes in the BBC Four series Britain’s Treasure Islands. A YouTube upload is available here; the Tristan thrush is introduced at 13:22, and at 13:54 you can see one pecking at a live(!) penguin and drinking blood from the open wound.


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What is the percentage of true bugs compared to all animal species on the plant?
Also, what is the percentage of True Bugs compared to the insect population?
I’m writing a children’s book on bugs and I’m comparing the true bug to the insect. All population info seems to combine the two. Please list sources.

Wellcome to Biology SE. Please could you explain what you mean by "bug" and "true bug". I'm no entomologist so I can only go on my Chambers dictionary, which defines bug as "a name loosely applied to certain insects…and specific to one (Cimex lectularis) that infests houses and beds". Is this what you mean? But it has nothing to do with plants. Or do you mean "on the planet"? Unless you clarify your question, I'm afraid you are not going to get the answer you are after.

@David I think "True Bugs" are usually defined as Hemiptera. Also, that article lists an estimate of 50,000 - 80,000 species of hemiptera. If you find estimates for total insect species and total animal species, you could get your own estimated percentages for each.

@user137 — Many thanks for providing this information. I'm sure many others besides myself will have been enlightened.


text:
Plant species ID, Bangladesh

This plant is quite common in vegetations near swamp areas in Bangladesh. I have included multiple picture hope that compensate for the bad quality.

Any chance you could give a close-up of the flower?

Probably Salvia genus: https://en.wikipedia.org/wiki/Salvia but that's just a guess, I never learned botany.

These pictures are terrible. The best I can tell is that the plant has inconsistently perfoliate leaves. this might help with the ID


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Why does the T7 RNA Polymerase require a reducing environment ie. DTT
Every bloody protocol suggests adding in DTT when doing in vitro RNA transcription. Why? The rationale seems to be that the cytoplasm traditionally has a reducing environment but as the only protein we care about is the T7 polymerase, why is this necessary.

A quick search on T7 cysteines gave some clues:

Bacteriophage T7-induced DNA polymerase is composed of a 1: 1
  complex of phage-induced gene 5 protein  and Escherichia coli
  thioredoxin. Preparation of active  subunits in the absence of
  sulfhydryl  reagents  indicates  the reduced form of thioredoxin  is
  sufficient for formation of  the  active holoenzyme. The oxidized
  form of  thioredoxin, thioredoxin modified  at  one  active  site
  sulfhydryl by iodoacetate or methyl iodide, or thioredoxin modified
  at both  active  site  sulfhydryls  by N-ethylmaleimide,  are  all
  inactive,  being  defective  in  complex formation with  gene 5
  protein.

Adler and Modrich, J Biol Chem 258:6956 (1983)
There's a more recent paper (Aguirre et al, Inorganic Chemistry 48:4425 (2009)) that mentions the "the enzyme critical sulfhydryl cysteine groups", but unfortunately I only have access to the abstract.
Update: It seems to be an old finding, rather than a rationale concerning the cytoplasmic redox state. According to Chamberlin and Ring, JBC 248:2235 (1973),

General Requirements-The general requirements for T7 RNA
  synthesis directed by T7 DNA polymerase are shown in Table
  I. As expected for a template directed polymerase, RNA
  synthesis shows an absolute requirement for DNA, the 4
  ribonucleoside triphosphates and Mg++.

(no surprises there ;)

The activity of the
  enzyme is reduced significantly if a sulfhydryl reducing
  agent such as b-mercapto-ethanol is omitted from  the
  reaction. The addition of 10^-5 M p-hydroxymercuribenzoate to
  the assay system in the absence of b-mercaptoethanol
  abolished all activity, indicating that the enzyme contains a
  sulfhydryl group necessary for activity.

However, if you see the table I, the remaining activity after removing bme is still 74%
There seems to be 7 exposed cysteines (Mukherjee et al, Cell 110:81 (2002)), but I could not find any paper discussing their roles.

Here's a copy of the paper. Enjoy.
http://cl.ly/101U380b3r261i0w0v1d

How strange. I'm looking at the crystal structure (1QLN) and there aren't a lot of cysteines near the active site. Will have to take a look at those papers.

@jp89 Thanks for the copy of the paper. I'm not sure though if this is allowed here, since it is breaking copyrights. Anyhow, for now I believe it is still fair use. Regarding to the question, I'd follow citations 59-62 from there (last paragraph on page 2/first on page 3). Cheers.

Bacteriophage polymerase is active within the cell, which has a reducing environment.  Most protocols of intracell proteins include DTT or glutathione for this reason.   Disulfides are mostly for secreted proteins.

@Aleadam Yeah, that is the sad case. I honestly don't understand the concept of copyrighting human knowledge.

@jp89 it is slowly improving, with the PLoS effort, and NIH manuscript requirements, but there is still a long way to go

I always assumed it was because DTT is useful in inactivating ribonucleases (by reducing their disulfides) which are notoriously stable and pervasive. It would be pretty unfortunate to get your RNA synthesized only to have it immediately be destroyed by a contaminating RNase.

Welcome to Biology.SE! This may be correct, but answers are much more likely to receive a favorable response if they are based on research rather than speculation. Consequently you should include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


text:
Which cryogenic vials and caps are ideal for storing glycerol stocks?
There are internally threaded, externally threaded, natural caps. For the vials, there are skirts, star-footed, and various bottoms. Why do any of these things matter?

I routinely store my stocks in plain vanilla 1.5ml eppendorfs and see no issues with it. I would be curious also to know what/why these special vials are "special"

Hence the question. Do companies just charge us more to make us think that they are "necessary"?


text:
Is bootstrapping an acceptable way to determine standard error for binding constants?
I'm measuring binding constants my system and I appreciate the usual methods of using replicates to measure standard errors and using those errors to calculate propagation of error. I'm curious if bootstrapping is a reasonable alternative to calculate uncertainty?

This is probably more suitable for stats.stackexchange.com, or do you think biological assumptions will influence the answer (I'm not familiar with binding constants)?

I approve this move. @fileunderwater Please let me know how to make that transition. I was under the impression that this was a fairly regular question that was relevant to the biochemistry community?

I've flagged it asking for migration, but I don't know if it is possible. This is not my topic, so I cannot say anything about methods/problems in biochemistry. To me, it feels like a clearcut statistical issue though.


text:
When has an organism evolved enough to be called a new species?
Imagine that we take a population of horses, split them in half and place them in completely different environments. The two species will evolve separate from each other and because the environment is different, the outcome of evolution will be different.
But at what point can you say that these horses have evolved into two different species?
(I do know that they would probably go extinct if we conducted this exact experiment, but this experiment is just to give an example)

I think LuketheDuke's answer is an oversimplification of the biological species concept (possibly resulting from the dictionary having a poor definition). The definition he gives is one of many which are in current use, and is made redundant by many types of organism.
It is important to recognise that because reproduction is not the same process in all organisms, genetic differentiation between individuals occurs in different ways for different groups.
Let's take the definition given in LuketheDuke's answer...

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but are not able to breed with members of another species.

Under this definition, lions and tigers (see ligers and tiglons, which are sterile hybrids between the two) would be considered one species, as would donkeys and horses (see mules and hinnys, again sterile hybrids). There are hundreds of other examples of pairs of animal species which can hybridise to produce sterile offspring.
However, these animal hybrids usually only take place with human intervention, by delibrate breeding efforts. Thus we could extend the previous definition to include them...

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but do not breed freely with members of another species in the wild.

That last part takes care of the ligers and tiglons. But what if we consider plants? Under the definition I just gave, most grasses (around 11,000 species) would have to be considered as one species. In the wild, most grasses will freely pollinate related species and produce hybrid seed, which germinates. You might then think we could just modify the definition to specify that the offspring must be fertile (i.e. able to reproduce with one another)...

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but do not breed freely with members of another species in the wild to produce fertile progeny.

Unfortunately, the situation is still more complicated (we've barely started!). Often wild hybridisation events between plants lead to healthy, fertile offspring. In fact common wheat (Triticum aestivum) is a natural hybrid between three related species of grass. The offspring are able to breed freely with one another.
Perhaps we could account for this by taking into account whether the populations usually interbreed, and whether they form distinct populations...

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of populations or meta-populations of related individuals that resemble one another, are able to breed among themselves, but do tend not to breed freely with members of another species in the wild to produce fertile progeny.

This accounts for the grasses, but it still leaves a messy area when you have a hybridisation which establishes - until the hybrid population is segregated away from the parent populations it is unclear whether they still count as the same species.
We could probably live with this situation, except for the fact that bacteria refuse to conform to it at all. Bacteria of the same species, or even very different species, can freely transfer genes from one to the other in conjugation, which combined with fission can result in perfectly replicable hybrids. This is such a common occurence that it breaks even the 'tend to' part of the previous definition, and members of a population can be doing this almost constantly, which negates the segregation requirement.
Richard Dawkins had a go at defining around this, by stating that...

two organisms are conspecific if and only if they have the same number of chromosomes and, for each chromosome, both organisms have the same number of nucleotides

This partly gets around the bacterial problem and means that bacteria which result from conjugation are a new species. Unfortunately under this definition we might as well not ever bother trying to classify bacteria as billions of new species would be created every day - something which the medical profession might have something to say about. This definition would also mean that those with genetic diseases like trisomy 21 are not human. The final nail in the coffin of this attempt is that there are many species, including frogs and plants, which are very certainly considered a single species by taxonomists but which have some variety in the presence of small accessory chromosomes, which occur in different combinations between individuals.
Let's consider one last option. We now live in the era of genomics where data about genomes of thousands of organisms is accumulating rapidly. We could try to use that data to build a species definition based upon similarity at the nucleotide level. This is often used for bacteria, by considering organisms with less than 97% nucleotide similarity to be different species.
The major point I've been trying to make, though, is that species is not a natural concept. Humans need to be able to classify organisms in order to be able to structure our knowledge about them and make it accessible to people trying to link ideas together. But the natural world doesn't care about our definitions. Ultimately the species concept is different for different groups of organisms and will continue to change over time as our analytical methods and the requirements of our knowledge change. Note that I've deliberately skipped over many historical species concept ideas.
The direct answer to your horse question is "it depends how you want to define a horse".

So you're saying that it is incorrect to say that the horses are no longer the same species when they can no longer successfully breed (successfully here meaning 'producing fertile offspring'), as stated in my answer? I would say this is 'correct', even if it is a simplification. If the example had been bacteria (that do not 'breed' per se) then I would not have given this definition.

That being said, yours is a very interesting and informative answer. But it does not really answer the question. If you were to test whether the horses had sufficiently divereged to become 2 new species, would the test not be to see if they could successfully breed?

@LukeTheDuke yes I'm saying that's incorrect. Firstly because the definition you gave doesn't specify that 'successfully' means 'producing fertile offspring'. And secondly because there are many situations in which two populations of horses can't breed to produce fertile offspring, for example if they are geographically separated. Accounting for those to things, we could get a workable definition for a horse.
For horses, then, we could say they were no longer the same species if, when cohabiting, they did not breed to produce fertile offspring.

@LukeTheDuke I hope it's clear that I don't think you've done anything wrong, but that the dictionary gives an insufficient definition.

Not a problem, as you say there is no definitive way to draw the line between species, but the line is much easier to draw in animals like a horse. Yours should be the 'correct' answer for this, as the title to the question is not about horses, but species as a rule (the horses were just an example). But therein lies the problem - using one definition (the 'classical' definition?) we can distinguish between 2 closely related animals, but this same definition is not adequate for other organisms. Is it possible to clarify your answer to include separate definitions for plants/animals/bateria?

Sure thing, when I get home this evening I'll add a summary at the end of appropriate definitions for major groups.

Wow, I didn't imagine it would be this hard to draw a line between two species (should I even call them species now?).

Hence why you end up with huge discussions about whether there are human races etc. Words like species, races etc. are just words, they are mutable and it is pretty much impossible to provide a biologically funded universal definition. Hence why definitions usually say things like 'should be considered' or 'differences[...]warrant'

As another example of why the dictionary definition is not always applicable; the two breeds of dog, great dane and chihuahua are unable to breed successfully but are still considered to be the same species due to their genetic similarity.

Amongst taxonomists - who define and name species - there are 'lumpers' and 'splitters' who choose larger taxa with more diversity, and smaller with less respectively. The problem exists even for professionals where it ultimately becomes a personal preference.

I registered to the site just to say that this is a great answer.

The story of the ability to interbreed is even more complicated than the ambiguity posed by horses, donkeys, lions and tigers. In California and Mexico, there are a series of species of lizards which form a geographical 'horseshoe'. Neighboring lizards can interbreed, but species at either end of the horseshoe cannot breed. In other words, lizards at the ends of the horseshoe are clearly of different species, but any pair of geographically close groups of lizards can be argued to be the same species. There's no place to draw the line to say where one species ends, and the next begins.
I think that this lies at the heart of the question... the concept of a species is an artificial construct. By and large, there are large enough separations of space and time that the lines are easy to draw, but during the split, the lines are in no way clear.

The biological definition of a species on Dictionary.com is as follows;

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but are not able to breed with members of another species.

So what we take from this is that a species, by definition, are those individuals/organisms that can successfully breed together. It is worth pointing out that some members of closely related species can breed together (e.g. a male horse and a female donkey can produce a 'mule'), but these animals are not fertile, so this is not considered 'successful' breeding, and the two organisms (in this case the horse and the donkey) are of different (if closely related) species.
In your example, the populations of horses would be said to have sufficiently diverged from one-another when they can no longer successfully breed.


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Do humans sneeze or cough in their sleep?
As far as I know, I've never seen anyone sneeze or cough while they're sleeping. Google wasn't very helpful either; a lot of contradicting claims.
So the questions remains: do humans sneeze or cough in their sleep? (a few other things I've never seen with sleeping people are yawning and vomiting) If they don't, why?

Babies may sneeze, cough and vomit while asleep, but it is not common even when they are ill. No reference, this is just my personal experience. I would think it's a matter of control over body muscles, babies have limited control (my kids would very often burp or sneeze and pass gas at the same time), but as they grow they learn to keep certain muscles in a certain state while asleep.

I've heard people sneezing and coughing in bed a lot. I can't be certain they were really asleep that moment though. They might have been woken up for just a minute by the discomfort that then caused the cough or sneeze.

Sneezing does not occur during REM sleep, due to REM atonia.(1)
The coughing reflex is  also suppressed during sleep, but coughing may still occur occasionally during sleep. (2).


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What is the role of acetylcholine in blood pressure regulation?
What is the role of acetylcholine in the cardiac cycle and in blood pressure regulation?

I hope this answers your question:
So the heart is an electrically excitable tissue: it pumps due to action potentials that start  from specialized heart cells called nodal cells and these nodal cells spread the action potential to surrounding heart cells. These nodal cells are found throughout the heart and they make up what's called the conducting system. These nodal cells don't need neural or hormonal input for them to spread action potentials, they have this mechanism to spontaneously start action potentials on their own called a pacemaker potential, BUT they can be influenced by neural (think sympathetic and parasympathetic) or hormonal input. These external inputs change the frequency (the pace) of the heart beat by influencing the pacemaker potential of the nodal cells.
The sympathetic nerve fibers send out epinephrine which cause the pacemaker potential to occur at a faster rate, that's why during exercise (when epinephrine is released... hopefully) the heart beats faster. Parasympathetic nerve fibers send out acetylcholine which causes the pacemaker potential to occur at a slower rate, thus slowing down the heart. What does this mean in regards to the cardiac cycle? It influences how much blood (the volume) is ejected during the cycle. The volume of blood that is ejected from the ventricles, called cardiac output (CO), which is also how many liters/min, is determined by 2 other factors: stroke volume (volume of blood ejected during each ventricle during systole) and heart rate (CO = HR x SV). And therein lies a part of the answer to your question: when heart rate decreases because of parasympathetic stimulation, cardiac output should also decrease, granted stroke volume stays constant.
I unfortunately do not know how acetylcholine affects blood pressure. I've read a paper of how acetylcholine induced relaxation in hypertensive rats, but I'm not sure of the mechanism, like how it affects systolic or diastolic BP.


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Somatosensory System
I have a test in my upcoming Neuroscience class, one of the items on the study guide is:
Identify 2 means by which a maintained, constant stimulus produces only a transient excitation of the Pacinian corpuscle (phasic receptor). How does adaptation occur?

I would consider physical filtering properties of the corpuscle sheath as well as adaptation of the neuron or downstream targets.


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Measuring the density of surface antigens
I'm trying to get a sense of the variety of methods used for determining the number of cell surface antigens and receptors. This is notably different from determining the affinity of these surface markers.

Are you looking for extraction techniques, or techniques to analyze your extracted molecules?

Do you mean to count numbers of both antigens and receptors in live cell?
Possible ways:

FRET (unlikely to work)
imaging of receptors with single molecule resolution
western blot to roughly estimate amount of receptors
single cell proteomics techniques (not very suitable)

FRET could work. He'd have to tag both the antigen and antibody, though He probably would be better off with standard fluorescence spectroscopy.


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Determine secondary structure (per residue pair) from a protein contact map
Given a protein map contact map (which for this particular case is a matrix of all Ca-Ca atoms in protein 1a3a that are less than 8 Angstroms):

Question: For each contact, is there an established heuristic to determine what kind (alpha, beta, or tertiary) of contact this is?
Observations: The contacts along the diagonal +4 clearly belong to alpha-helices, but I'm struggling to find a way to identify the parallel and anti-parallel beta-sheets and to differentiate these from a long range tertiary contact.


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Visual receptive fields
What I know about centre-surround type receptive fields is that depending on whether the region is on or off, the response to being stimulated is either excitatory or inhibitory respectively. So if a light shines on the centre of an on-centre/off-surround and off-centre/on-surround fields, spikes would be detected in the first case and not the second.
To my understanding, if both centre and surround areas are simultaneously stimulated, no spikes would be detected in either of the above-given fields. However, that means that if I am staring at what is essentially a blank white wall, I shouldn't be able to see anything. But that is obviously not happening. What am I missing here?
Also, on a related note - do on-centre & surround or off-centre & surround fields exist? What function do they serve, if any? What are the other types of visual receptive fields in humans, or other animals? Is there a major difference in properties of visual fields across species?
Edit: While browsing a few resources on receptive fields, I found this very-helpful image here.

This image perfectly illustrates my question: what happens to the grey areas in the right image? How are they processed by the retinal ganglion cells?

The centre + surround do not cancel completely, as you can see from these mudpuppy recordings. [Image 1] (Werblin and Dowling, 1969, I believe)

One function of a centre-surround set-up is to highlight the contrast at borders.  Most of the useful visual information is from borders/outlines, so this is a method of ignoring redundant information.  The highlighting of contrast borders and ignoring of redundant information explains why the neural image appears different. [Image 2 - right].
Another function of centre-surround fields is to avoid saturation, but this is more complicated to explain. [Image 2 - left] (Diagrams from Cambridge MVST Part IB lecture series by Hugh Matthews)


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Which DNA sequence will have higher melting temperature: CCCCCC... or GCGCGC...?
I tried this service to calculate temperatures. The nearest neighbour method consistently gives larger results for sequences like GCGCGC over sequences like CCCCC or GGGGG, while other methods don't give a difference. Is it nearest neighbour's feature or is there indeed a difference in melting temperatures?

The dependence of melting temperature on different dinucleotide pairs was experimentally measured; the meting temperature calculator is based on those results. Based on these results, you would see that a GC dinucleotide pair would differ from GG and CC pairs. Possibly, this is because of steric effects and stacking conformations.
SantaLucia (1998; author of the nearest neighbour model) has referred to different experimental studies from which the values were obtained, in the Table-1 of the paper.

That answers my question, but I am curious whether triplets and longer sequences of nucleotides have also been tested experimentally for melting temperature?

@СашкоЛихенко I haven't checked if studies with triplets have been performed. However, I think that with longer stretches of nucleotides, there would be additional factors that would affect the binding (mostly arising from steric factors). For longer sequences (oligonucleotides) people do isothermal titration calorimetry (ITC) to calculate binding energy and other theromodynamic parameters. People also perform melting analysis by slowly increasing the temperature. This would provide the most accurate in-vitro estimate of melting temperature.


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How ants handle the huge "data" from multiple pheromone trails?
We know that every single ant produces pheromones to communicate and inform others. When there are millions of ants, how do they handle that many signals without getting confused?

Why expect every signal to be different? Many would be redundant or boosting, along a trail leading to much food or in the presence of predators, for example. Then there's likely a priority system that would let "colony in danger" signals block out everything else.


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Measuring Bioluminescent Algae Intensity
For a science project, I am required to measure the intensity of the light given off by the Algae, Pyrocystis lunula. Can a photometer with a range of 1-50000 lux be able to pick it up? If not, what are some tools to measure the intensity(without costing to much money.)?

As stated here:

The lunate cysts of Pyrocystis lunula have a bioluminescent emission spectrum with a peak intensity of 477.5 ± 1 nm.

So, almost any spectrophotometer should be able to detect it, it's just bluish visible light.

So even the cheap ones?

Even a phone camera


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Travelling with tissue samples in RNAlater
I've been in Brazil collecting some samples (ants) and need to travel back to to the UK with - I've got their brains stored in RNAlater, which have been in the freezer at -4C for a bit less than a month. On the Fisher Scientific website it says that they can be left at 37C for a day in solution before the RNA can begin to degrade. I've got a long journey home which could take up to 3 days in the heat (it's around 38C at the moment here) and involves stopping off through Morocco.
Has anyone travelled with samples in RNAlater like this before in elevated temperatures and got good results from their RNA extractions? Would you reccomend trying to source some dry ice for the journey?

Though I have not really tried it, I think that keeping the suspended tissues at 37⁰C for three days is not a good idea. You can try getting some ice from local shops and keep the samples in ice inside a thermocol box. IMO, the best option would be to courier your samples from Brazil to UK.


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How can I change my buffer system for protein purification?
I have a protein that I purified in PBS buffer, pH 7. I will do dialysis to remove salt and will then further purify the protein with ion exchange chromatography.
I will need to use another buffer (Tris-HCl) with pH 8 in the chromatography, and so my question is: Can I change the buffer system for my protein in the dialysis step? Or would you recommend me to use the Tris-HCl buffer from the very start and then just adjust the pH for the chromatography?
Thanks in advance!

There are a number of ways to address this, and the other answers are certainly correct. Another strategy, especially if you already have the sample in PBS, is just to dilute it in the low salt ion exchange buffer. This works because you don’t need to completely remove the phosphate or salt, just get it low enough so that it doesn’t interfere with binding to the column. This method also has the advantage of minimizing the exposure of your protein to low salt, which can destabilize it, and is often used for ion exchange chromatography.
As an aside, if you’ve never done IEC with this protein before, you may want to do a trial run first with a small aliquot of your sample so you can make sure the conditions you’ve decided upon are suitable.

Good point, dilution of the sample might be the easiest way forward, if feasible in regards of sample volume and flowrates.

Assuming that your protein can handle being in the new buffer, you have multiple options.
Dialysis will work although you might want to consider using a centrifuge spin filter with a suitable MW cutoff to gradually switch buffer and concentrate the sample. Be aware that some of your protein will stick to the filter, giving a loss of sample.
Alternatively you can perform size exclusion chromatography to switch into the new buffer, but you better be sure that the sample will remain stable or you may clog the column. If you can perform affinity chromatography, you can also opt to change buffer in this step.
You can of course try to start with a Tris based buffer and simply adjust pH by dialysis in a tris buffer with the desired pH. Just make sure that the dialysis volume is large enough to counteract the buffer in the sample.
Instead of using PBS you can also try with TBS (Tris-buffered saline), see wiki for details. https://en.wikipedia.org/wiki/Tris-buffered_saline

Two accepted methods of 'desalting' a protein and/or changing the buffer are dialysis and gel-filtration. Dialysis is time-consuming, and gel-filtration usually requires a concentrated sample (It is difficult to gel-filter a 250 ml sample unless a very large column is available, for example, but dialysis of such a volume is relatively easy).
You do not say whether you are using cation- or anion-exchange chromatography, but note that the charge on the buffering species is positive with Tris, but negative for phosphate, and it is usually desirable that the charge  is the same as that of the ion-exchange column, as you do not want the buffering species to be exchanging and possibly exposing your protein to 'local' extremes of pH, especially if your protein is sensitive to pH changes: use a positively charged buffer for anion-exchangers such as DEAE-cellulose, but a negatively-charged buffer for cation-exchangers such as CM-cellulose.  (This is the 'strategy' adopted in Chromatofocussing, and I'll bet that is why the protocol requires a change in buffer as well as pH).
Note also that a protein that binds to an anion-exhanger at pH 8 may not bind at pH 7: in Chromatofocussing on an anion-exchange column, for example, we lower the pH to elute the protein.
Ref: Protein Purification. Theory and Practice, R.K. Scopes

Impossible to answer this in detail without knowing why you started with PBS, but simpler is better so if you can start with a buffer that is compatible with the ion exchange step then I would try that.
Dialysis is a reasonable way of changing buffers, but do you know whether your protein is soluble in Tris at pH 8 without salt?
If you have a relatively large sample you might consider doing a test dialysis using a small fraction using something like this kit.


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How can I get the yield of my purified immunoglobulins?
In order to get the yield of IgY through a set of purification steps, what method can I use?
Thanks in advice!

Do you know the antigen of the Ig and can you make it and use it for assays?

Someone asked a similar question recently.

You can use western blotting with a anti IgY secondary antibody conjungated to  a HRP (or other reporter), this method will primarily help with troubleshooting your purification and locating IgY in the different fractions and flowthroughs.
If you want to quantify, consider using an ELISA kit. Here is one such kit (https://www.antibodies-online.com/kit/1563240/IgY+ELISA+Kit/)


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Is the salt obtained from meat (as the primary diet) nutritionally sufficient?
This post is derived from that one, where someone says

if you meant salt as a nutrient such as carbs, protein and all, there is salt in the stuff one eats already.

The background is "Naked and Afraid", a Discovery Channel survival show, where a group of people survive for 21 or 40 days without any cloth or food.
They are not next to a shore. They are in amazon jungle or Solani River Basin in Africa.
The footage shows that the candidates got food by hunting but never got additional salt.
They are hunting in Africa. Don't they need additional salt? Is the amount of salt they got from animals like impala sufficient?

Hunter-gatherers rarely if ever added salt to their foods, and studies of salt-free Yanomamo Indians have shown these indigenous people to maintain low blood pressures that do not increase with aging (Oliver et al, 1975).

--The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. European Journal of Clinical Nutrition (2002) 56, Suppl 1, S42–S52 (PDF link)
(The Yanomamo Indians were/are hunter-gatherers, but that doesn't necessarily mean their diet was mainly meat - plants and fruits are important components. However, meat is likely to be higher in salt than plants, so this just supports the general principle.)


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How many phosphates are in the 5' end of a DNA strand?
I know that the pyrophosphate of a NTP is hydrolysed so that it can create enough energy for the synthesis of DNA. But if we want to get specific we can know for sure that the 3' end of the DNA strand has got one phosphate because the phosphate is having a bond with another nucleotide. But what could be the reason for the 5' end to have only one phosphate and not 3? Could it be the energy providing or that the structure has to be consistent or something else that I can't think of?

The DNA polymerase can only extend a primer and therefore almost all lifeforms have a primase (which is a type of RNA polymerase) that synthesizes RNA primers at the replication origins that the DNA polymerase can extend.
As you guessed, the 5' end would indeed have a triphosphate.

Organism            Template Sequence        Primer Synthesized
Herpes simplex-1        3′-GPyPy                 pppPuPu
T4                      3′-TTG                   pppAC
T7                      3′-CTG                   pppAC
E. coli                 3′-GTC                   pppAG
S. aureus               3′-ATPy                  pppAPu
S. aureus               3′-ATPy                  pppAPu
A. aeolicus             3′-CCC, CCG, CGC         pppGG, pppGC, pppCG
B. stearothermophilus   3′-ATPy                  pppAPu
Human                   3′-PyNN                  pppPuNN
Calf                    3′-PyNN                  pppPuNN

Initiation sites used by primase from different sources. Pu = purine, Py = pyrimidine, N = any base ppp = the triphosphate on the 5′-end of the primer. Those bases that are required but do not code for a base in the primer (“cryptic” nucleotides) are underlined and in bold.
Kuchta and Stengel (2010)

In the final stages of replication, these RNA primers are removed by RNAseH and DNA polymerase I in bacteria and the gaps are filled by the latter (Cooper (2000) The Cell). In eukaryotes, the primer is removed by the action of Fen1 and Dna2 exonucleases and the gaps are filled by DNA polymerase δ (Burgers 2009).
In PCR, it is quite straightforward: the product will have whatever 5' modifications the primers have (usually none).


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How to estimate mRNA counts from Relative Promoter Units (RPU) or RNAP per second (PoPS) in E. coli?
I need a rough estimate on how to translate RPU or Polymerases Per Second (PoPS) to mRNA count (or even better protein count) in E. coli.
I understand that any number we come up with will be a very rough estimate of it, but for now, I need a placeholder value to do some modeling on genetic circuits in E. coli until a more verifiable number comes about.

Can please you explain (or provide a link to) what you mean by these terms as they are not very common? In general, mRNA count is easier to estimate than calculating the speed of polymerase. So you are better off counting mRNAs directly instead of extrapolating from these parameters. Protein count is even more difficult to estimate using these parameters. You can't have a good estimate of protein counts unless you know about translation initiation and elongation rates and protein degradation rates.

Yes, of course, I added the links just now. I know it would be much better to have mRNA numbers and then simply estimate protein numbers using an average ratio for E. coli. However, there is a study I am basing of my work and we only are going to have RPU or PoPS to base of, so was wondering if anyone had any references or rough estimates as to how to translate these into mRNA numbers for E. coli

I could not find any paper that discusses these issues. So this answer is just based on my guess.
From the this page:

Transcription rate is generally a parameter associated with a
  particular transcript and has units of transcripts per unit time. In
  contrast, PoPS is essentially transcription rate at a particular
  location on the DNA. The value of PoPS just downstream of a coding
  region should be equal to the coding region's transcription rate.
  However, there are certain positions at which a transcription rate
  doesn't necessarily make sense yet PoPS does. For instance, as
  biological engineers, we care about the rate at which RNA polymerase
  moves through a terminator (or the PoPS downstream of a terminator)
  but yet most people don't talk about the transcription rate of a
  terminator.

What we want is the transcription rate for every gene. You can estimate it using PoPS corresponding to that terminator.
Now, at steady state the mRNA concentration would be the rate of formation divided by the rate of degradation (removal): rf / rd.
Since the study that you are referring to, calculates PoPs, I would guess that it is based on some standard BioBricks parts. You are likely to have have mRNA degradation rates associated with these transcripts (even protein formation and degradation rates, possibly). If you don't have the mRNA degradation rate then at least for long lived mRNAs, you can assume the rate of removal to be same as the dilution rate (loge2 / doubling time). Substitute this in the equation for steady state and you should get mRNA concentration.
Steady state protein counts would be: mRNA counts × protein formation rate / protein removal rate.


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What is the genetic background for fast metabolism?
I am wondering if it is possible that people with very fast metabolism have some genetic mutation. There are people who can eat a lot while others would definitely get fat with such a diet. In other words, they seem to have very fast digestion and never feel so much full after eating but what's surprising is that they still stay very skinny?
Can it be a result of some disorder/mutation?

Are you asking about the genetic background for fast metabolism or for underlying diseases? I am asking, because a) not all genetic deviance from the 'norm' is a disease and b) not each possible underlying diseases are caused by genetics. Could you please edit your post (and/or title) to clarify this?

For medical advice, it is better to ask a physician.

The expression "fast metabolism" is very general and makes the question hard to answer. I will hence answer in the most general sense possible and then just give one example.
Yes, it is most definitely the case that there is genetic variation underlying the variation in metabolic abilities in the human population (btw, this post summarizing the partitioning of phenotypic variation might be helpful to you). For example, Greenlandic Inuits have a series of mutations that affect their ability to digest polyunsaturated fatty acids allowing them to cope with the impressive amount of animal fat that is/was found in their traditional diet (Fumagalli et al., 2015).


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Identify a spider
This spider was making a web on the back porch.
Just wondering what kind of spider it is?

Please tell us about your location and if possible, the weather conditions when the picture was taken.

Did you have a look at my answer?

Seems to be a Barn Spider (Araneus cavaticus).

(photo from here)


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Does the preservation fluid (ethanol or formaldehyde) leach heavy metals from mollusc tissue?
In a thread on researchgate, the concern was raised that long term exposure to unbuffered preservation fluids such as ethanol or formaldehyde may leach heavy metals from biological samples due to a reduction in the fluid's pH. Can anybody tell me if this also applies to mollusc samples? I would assume that carbonate shells function as a pH buffer and thus keep the fluid's pH relatively stable over a long time.
Edit: Link to the researchgate thread. No research articles were mentioned in that thread.


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Can radiation exposure cause cancer later in life even if no traces of radioactive material are present in the body anymore?
I had a long-lasting debate with a friend of mine about the Fukushima incident.
The question that we tried to solve was if radiation or toxin exposure can cause cancer later in life even if no traces of radioactive material or toxins are present in the body anymore.

Yes it can, because exposure alone can cause mutations in your genes which is usually the main cause of cancer.
For example, when we get exposed to UV light for longer periods of time, we can get skin cancer/melanoma. Here , of course no traces of these rays are present in our body, its just all due to prolonged exposure.
Now to the fact that why does it even happen , according to wikipedia is

Cancer is a stochastic effect of radiation, meaning that the probability of occurrence increases with effective radiation dose, but the severity of the cancer is independent of dose. The speed at which cancer advances, the prognosis, the degree of pain, and every other feature of the disease are not functions of the radiation dose to which the person is exposed.

So since once induced, it just keeps on increasing even though you are not exposed to that particular rays anymore, you most probably are going to have it. This is the reason why cancer is so dangerous, because once it is there you can't stop and even can't make any precise stats about it until a certain stage.
For more details , visit https://en.wikipedia.org/wiki/Radiation-induced_cancer#Mechanism
I hope this answer helps you :)


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The Hawk-Dove game: why is the average payoff half of the difference between reward and cost?
My question is about the well known Hawk-Dove model used in game theory. It concerns two strategies: the Hawk, which always fights the opponent, and the Dove, which does not fight and will either retreat or share. The payoffs for each of the possible encounters are presented in a matrix. Now, say that the reward (R) is 10 units and the cost of fighting (C) is 5 units. When a Dove meets a Hawk, it will retreat: Dove gets 0 and Hawk gets R=10. Vice versa, when a Hawk meets a Dove, Hawk gets R=10 and Dove gets 0 because it retreats. When two Doves meet, they will share the benefits; both Doves get R/2, in this case 5. These three, I have no problem understanding.
My issue is with the payoff when two Hawks meet. I understand that, under the assumptions of the model, both Hawks have a 50% probability of winning. I also understand that the winner gets R and loser pays C. But I'm completely stuck at why the average payoff is given as (R-C)/2. When you input the numbers above, it gives you a value of 2.5. How is the average payoff in an encounter between two Hawks 2.5 if one receives 10 and the other loses 5?

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

$\frac{(+10)+(-5)}{2}$, isn't that how an average is calculated?

It's about evolutionary game theory and it is considered a part of evolutionary biology. It cannot be considered off-topic.

One hawks gains 10, the other loses 5. So together, they gain only 5 (=10-5). On average, they gain 5 / 2 hawks = 2,5


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How do wild animals get rabies?
I can see the chain of spreading disease: Humans usually get rabies from domestic animals, those usually get it from wild animals, wild animals in their turn get from the other wild animals and here I'm stuck. Well, so where do wild animals get it from initially?
I know that rabies is a virus and it needs warm-blooded animals to live out. Also according to Wikipedia once an animal is effected it lasts, let's say, no longer than for 2 weeks.
In other words, does it mean that there is a constant population of rabid animals that exists in order to pass this virus from one animal to another every 2 week on the average?

Such viruses have a natural host, which might get sick, but is usually not killed by the virus. From there, the virus can get zoonotic (jump over species barriers) and infect other animals when it comes to contact. For Rabies the reservoir hosts are different, for the US these are bats, skunks and racoons. For more details, have a look on this PDF.
Another example for this is the SARS virus (a corona virus) which most likely lives in bats naturally and has jumped from there onto birds and from there infected humans.

Thank you very much for this PDF. The only section I found which explains virus origin is "Mechanisms of Attachment". Still I'm not sure I get it, could you rephrase it in layman's terms?

@dVaffection For example, ticks can carry lime disease, they're not affected by it but can still pass it on to you. Similarly mosquitoes and malaria. The latter is explained nicely in wikipedia. You can have a similar situation with viruses, that's what Chris means by "natural host".

@terdon Also "Natural hosts" are referred as reservoirs - I totally get it. But somehow those animals get this virus in the first place and this virus stems from somewhere!

@dVaffection that one is the age old question of the chicken and the egg, not really within the scope of this site :) Anyway, many viruses can survive outside a host (for a given value of "survive") so some can be airborne and picked up by the host that way.

Or host and reservoir come in contact somehow and transmit the virus. It is only present for some time in the intermediate host (and will either kill him or simply leave him) before the virus gets either transmitted to another (probably better) host or the spreading stops here.

I wonder what is the reason a virus strives to find a host? My guess so it can replicate itself. Am I right here?

@terdon As far as I understand virus of rabies if transmitted only through saliva.

@dVaffection no, you're anthropomorphising, a virus doesn't "strive" to find a host any more than an Oxygen strives to find two Hydrogens to make water. We are at the frontier between life and chemistry here.

Well, so from your words I may infer that a virus (rabies in this case) is just a poison scattered all over the earth which animals pick up on occasion. And this virus has no any intention to hit any animal but this is just a way it exists?!

A virus has a host for which it fits. If it doesn't meet this host, nothing will happen and over time it will be deactivated. It is a bit more than a poison though, since it can replicate (given the right conditions) and spread. But outside its host viruses are not alive.


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What kind bottom feeder is this?

It’s about 2 1/2 inches long and had a little tail on the end. Also has short feelers that almost look like a moles.

By the first look it seems to be a lamprey. But I would suggest to give some more context to the place you took the animal. (see the species-identification tag wiki.

It's a kind of loach. You have to include the location in your query.
i.e. a black khuli loach:

a weather loach:
http://badmanstropicalfish.com/profiles/profile103.html


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Spine found on the beach
Can someone please tell me which animal does this spine belong to? I found it today on the beach..

Where in the world is this beach located.


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Is this 12+ foot plant a sunflower or hogweed?
I'm trying to determine what this is. The plant is well over 12-feet tall, had huge leaves, and a very thick stalk. People near me say it's a giant sunflower plant, but it hasn't bloomed or shown sign of flowers. My moral ag-knowledgeable friends say it's hogweed, which is very dangerous. Thoughts?
This is the plant .
Here's another picture .

Looks exactly like a sunflower.  Though I've never seen hogweed in person (I assume you mean Giant Hogweed?), the leaves are much different, as in this picture: https://www.goodhousekeeping.com/home/gardening/a21598753/giant-hogweed/#15323659656822&%7B%22sender%22:%22offer-0-1WjsT%22,%22displayMode%22:%22modal%22,%22recipient%22:%22opener%22,%22event%22:%22resize%22,%22params%22:%7B%22width%22:800,%22height%22:792,%22iframeId%22:%22offer-0-1WjsT%22%7D%7D  Also, if it's a sunflower, it simply may not have bloomed yet.  Mine are just starting.

Never listen to those friends anymore (concerning plants that is).

The plant in your photo is a sunflower (Helianthus annuus).  The large, heart shaped leaves and stiff, hairy stem are very characteristic of the sunflower as seen in your plant. These form a single flower head on top when mature - about 90 days after planting.  They typically grow to 10 feet in height, so 12 feet would not be unusual.  The tallest recorded specimen was apparently 30 feet in height. Please see links below for more information.
https://en.wikipedia.org/wiki/Helianthus_annuus#Cultivation_and_uses
https://homeguides.sfgate.com/time-year-sunflowers-bloom-67915.html
http://www.illinoiswildflowers.info/prairie/plantx/an_sunflowerx.htm

That’s definitely a sunflower. Hogweed has very large lobed leaves and has more maple or oak look to it. Most sunflowers bloom at different times. For most sunflowers- August to early October is flowering time. Peak is usually September. Hope this helps.


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What type of moth is this?
 What type of moth is this that was on my wall in Spain

please provide the approximate size of your moth. Also, indicating a bit more info about your location (urban, suburban, rural, etc.) and time (of day; of year) can be helpful in getting an accurate ID

It looks very much like Manulea palliatella, Family Erebidae, Subfamily Arctiinae.
https://commons.wikimedia.org/wiki/Category:Eilema_palliatella
These are present in Spain.


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What species of mushroom is this?

Growing up in Oregon I don't remember ever seeing these. There are different mushrooms growing all over my backyard right now, but these look way different than all the others and there was only a small cluster of them in the corner, which caught my eye. Searching online and trying to match pictures it keeps coming back to Psilocybe Semilanceata aka Liberty Caps, which apparently are hallucinogenic.  Like I said  I've never seen these before growing up in Oregon, so I'm curious as to what they really are. I tried to upload a better picture, but it was too big of a file, so hopefully this one is good enough. Thanks in advance.

Hi and welcome to the site. Your mushroom is a bit old for identification I'm afraid. Try to take a picture when they are fresh and preferably at the place where they grow.


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What type of tree is this? (Coyote Hills)

I found this in Coyote Hills, Los Angeles, USA. Please provide the common name.

Size: You can probably tell by the fence post; the tree is probably about 3 times normal human height

I guess it is Schinus molle (Peruvian pepper)

This does not provide an answer to the question. To critique or request clarification from an author, leave a comment below their post. - From Review

the person don't search a name of this tree? in facht i don't understand why it is not a answer of the question.

We like to see sources. A random species name doesn't say much.

which source could answer this question? i see no other possible like i did. and indeed it is not much, but better than not answer the question. we can discus this answer but i don't know the reason to don't give it a try.

Add a link to wikipedia is enough?


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Why is this spider wound in such a dense web?
I saw this thing yesterday on my window curtain, and I've been wondering what this is.
It looks like a dense network of spider web, and the spider inside it is visible. I thought the spider was dead, but I saw the spider making very small movements inside it. So, that made me more curious to know what it is.

This is probably made to protect eggs and young spiders, a sort of nest.

From the look of the spider outline, it looks to have short legs and is dark. A yellow sac spider is quite light-coloured and has long legs. Yellow sacs and clubionids will sometimes make themselves a sac for resting or eating or molting or laying eggs. Yours is probably a jumping spider, and here is a youtube timelapse video of a jumping spider laying eggs while inside its own protective sac:
https://www.youtube.com/watch?v=yoqMNX0RWuc


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Veins in Plant Leaves (terminology)
Why do we call the vascular bundles in plant leaves "veins"? I think its probably because the xylem and pholem serve circulatory function analogous to the human body's circulatory system with arteries and veins. But why don't we call the vascular bundles arteries instead or veins?
In the human body, we call a blood vessel "vein" when it travels blood to the heart and an "artery" when a blood vessel travels blood away from the heart. Is there a similar reason or significance as to why we call vascular bundles "veins" instead of "arteries"?

It's just a colloquial term and not a well thought of/standardized term. So there is nothing much to reason here.

I think this is a valid question with valid historical (not simply colloquial) usage and I think that potential answers could definitely be based on more than just an opinion. I disagree with both close voters and vote to keep open.


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How do people measure how many calories or proteins/fats/сarbohydrates are in some food?
How is the composition (in fats, proteins or carbohydrates) of a certain food estimated and how is the amount of calories provided by the food calculated?

https://www.scientificamerican.com/article/how-do-food-manufacturers/

https://carolina.com/teacher-resources/Interactive/food-calorimetry+/tr23949.tr

Hi! Welcome to StackExchange. Question is nice but would be better if you add some research you've done

Messured by the amount of energy it will take to raise 1 degree celsius in 1 kg of water. You really can never go by what the packaging says either. All depending on how food is prepared, even your digestion differs the count person to person.


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Resting membrane potential in cells
My textbook says “Among K+, Na+ and Cl-, K+ contributes to the resting membrane potential the most, because it has the greatest permeability across the membrane.”
I agree with this, but I’m just curious: why is the equilibrium potential of Cl- (-75mV) closer to the resting membrane potential (-70mV) than that of K+ (-90mV)?

This is only true because the chloride concentration happens to be slightly less negative than potassium, therefore the weighted (by permeability) average of all the other ions is near the reversal potential for chloride.
Even if you assume the permeability of every ion except sodium and potassium is zero (i.e., if chloride doesn't contribute at all), you will end up with a resting potential near chloride's reversal potential.


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Wax layer destruction from seed coats
I'm working with some orchid species, and i encounter a specific issue. Some of those species deposits upon their seed coat a wax layer. This layer makes seeds behave in a very hydrophobic way. You cannot dispense them in a pour water.
That behavior has many impacts. One of the most significant is that it does not let water come in touch with the actual seed and then with embryo to make it sprout.
So i tried many ways to remove that layer but nothing actually seemed to work out.
I treated seeds with the following chemicals:
a) 1% NaOCl with some dish soap water solution for 10min. After throwing seeds into this solution you could see that they can be evenly dispensed in it and come in touch with the solution. But if you wash them up with pure water for example 3 times they are getting back their hydrophobic behavior.
b) 1% H2SO4 water solution for 10min. I thought that with this treatment waxes will be removed from the seeds but nothing like that happened. Maybe they had been better dispensed in the pure water comparing to the previous treatment but nothing significantly changed.
c) 93% ethanol solution for 1, 2, 3, ... 30min. results here were also very disappointed. While the seeds are immersed into ethanol, they were very well dispensed into the liquid without any hydrophobic behavior. After three washes with pure water, hydrophobic properties came back.
Treatment time seems not to play any significant role on the results.
My conclusion is that there is no destruction of the waxes with the above chemicals. The only thing that happened probably, is the creation of a Micelle around the seed, which make it for a while (the time that it was in the solutions with soap and ethanol) non hydrophobic.
Finally my question is, if there is any way to destruct chemically, to some grade the waxes. So even when you put the seeds in a pour water not be so much hydrophobic.
Thank you.

Using H₂SO₄ is not a nice idea for dewaxing. Try ether or chloroform. Have a look at this page.

I 'm thinking if it's possible these chemicals to harm the embryo of the seed. Maybe if they are in small concentrations to not harm them. I'll read your page suggestion and maybe there is an answer. Thank you very much.

This paper describes dewaxing of sunflower seeds using various solvents. As you have already shown for yourself, using hydrophilic substances such as bleach and acids do not work well in removing the waxes.
Waxes are highly hydrophobic substances, and must be removed with either hydrophobic solvents (much like washing away acids with water at the emergency eye-shower) or detergents and water. The hydrophobic solvent mixtures used for lipid extractions recommended in WYSIWYG's link will likely work as well.

Waxes look something like this:

ref: http://lipidlibrary.aocs.org/Primer/content.cfm?ItemNumber=39369

So you will never be able to dissolve them with a polar solvent like ethanol or water. You need a detergent or an apolar solvent.
If I were you I would try out gasoline to dissolve the wax and soap + water after that to remove the gasoline remnants from the surface of the seed. They are cheap, but they might damage the seeds. If gasoline would be too strong for the seeds, you can use plant oils, like sunflower oil as apolar solvent too, but you might need to rub the surface with that, because it is very slow otherwise.
Using hexane and ethanol like in the article March Ho linked is somewhat more sophisticated, but chemicals are harder to procure at least in some countries.

Try a nonionic detergent like NP-40, it is a very good surfactant.


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mFOLD prediction result interpretation
I am trying to predict the secondary structure of certain predicted pre-miRNAs through mFOLD which is the generally accepted technique for structure prediction in most studies. I am finding it hard to interpret the result and accept if the pre-miRNA which I have picked and the miRNA I have can be accepted and included in my result.
This is one predicted pre-miRNA structure with the predicted miRNA position shown in green.

Is this a good/bad structure and if so, can anyone give me a reason why. Thank you.
edit: I understand that energy levels are also something that is looked for in the prediction. In this particular figure, ΔG = -75.00 kcal/mol which I think is fine.
Sequence used for folding is
AAAAATAAAAAACAGAACCATGAGGCAGCGCACCAAGAGCGTCGTGAACGTCCGCGAATA CTTCCGCATGGACGGCAGTGGCGCCCCCGAGCAGGAGGACGACGATGACAACGATGACTG GATGGCCATCGCCATGCAGGGCGCACCGCGTAAGGTCAGCGTGGAAGTCGTTAAGCCTGG CAAGAAGGCACGCGCTCGTACGTCGACGTGTGACTCAC

and the highlighted match area is
ACGATGACAACGATGAC

So this structure should be fine because the sequence lies along a stem-loop structure.

I am worried about that bulge on the left top corner though. That doesn't affect the predictability of this structure does it?

As a non-specialist reader, I wonder when you say mMFOLD is a "technique" if you mean it's software?

@daniel yup software

Can I know more about the settings of this prediction? Temperature, ionic strenght, molarity etc? You could post the link to the job results on the mfold server so I can better evaluate the likelihood of this structure.

@alec_djinn I have moved past this project but I generally stick to default parameters for prediction. The paper titled "Bioinformatic discovery of microRNA precursors from human ESTs and introns" gave me a guideline for identifying a viable precursor which I follow currently. But it would of course be helpful to know how the prediction is done. I will make sure to contact you the next time I do a precursor prediction and give you a link. Thank you.

The green region will definitely not make an miRNA: It is not a part of a stem loop. See typical miRNA structures from miRbase.
EDIT
Bulges can sometimes determine which strand is chosen as mature miRNA. However, this green region is also is unlikely to form miRNA because the stem is just 15bp.

Please look at the edit of the question.

I didn't know if I should ask this as a separate question so, I am posting it as a comment. In one paper (http://bioinformatics.oxfordjournals.org/content/21/18/3610.abstract, I found that ~70 nt of the matched flanking area was taken as pre-miRNA while in this paper (http://www.hindawi.com/journals/ijg/2012/957607/) ~100 flanking nt of the match area was taken for pre-miRNA structure prediction. Any idea why so?

no idea.. it is best to take 60-70 nt from either side (because you don't yet know that your read is -3p or -5p). I suggest that you use a machine learning algorithm to predict the right miRNA structure. Co-incidentally a friend of mine was working on similar problem and was talking to me about it (for a moment I thought you and her are same people :P ). I'll let you know if we make some progress.

I'll post it as a question then to see if anybody else could get some light on the issue..


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Is there a maximum amount of antibodies your body can keep?
I am wondering if you were theoretically able to get vaccinations or antibodies for any and every diseases and/or illness, would there be a limit to how many you can get and keep in your body at one time? If so, what is the limiting factor?
What would be the possible effects of this on the body and immune system? Thanks.

Everyone has an estimated number of around 10^12 (1 trillion) different antibodies, without counting any immune reaction to vaccines or other antigens (http://www.ncbi.nlm.nih.gov/books/NBK26860/).

Textbooks tend to quote different numbers whatever you read, our recommended one (http://www.garlandscience.com/product/isbn/9780815341468) comes up to 10^16 for example. But the number itself isn't useful anyway, the point is that it's a lot.

Antibodies are simply proteins and like any other protein have a relatively short "life", so after clearing out an infection, they are not retained for long (most of them anyway). What the body keeps is memory cells which can produce a much more rapid response if they come in contact with the same pathogen again.
You could see it as a selective process: the body produces immune cells, one or more specific cells for nearly every potential antigen that might exist in the world (there are more steps involved of course but they are of little relevance here). Only those which are used at some point mature into memory cells.
Unfortunately, I just realised that I can't explain why the immune system goes through this selective process; producing cells equivalent to memory cells in the first place would make the immune response much stronger. One explanation I can think of for why the body produces naive cells first is that either a) their production or b) their maintenance is less costly.
The other explanation I could think of is that even immune cells in the periphery which have undergone the proofing mechanisms of immune cell development already, may not be perfect and target body cells every now and then - in that case it would be devastating if they would go all-out like a memory cell.
From my three explanations, only alternative b) would mean there could be a limitation to how many vaccinations our immune system can bear (if memory cells take more effort to maintain than naive cells, having too many of them may overstrain whatever systems maintain them). Otherwise I don't see any limiting factor for how many memory cells you can retain; except if their numbers become so large that your lymph nodes swell and that causes problems.
Edit note: I'm not aware of any research about that question and couldn't find anything either.

I just realised that I can't explain why the immune system goes through this selective process; producing cells equivalent to memory cells in the first place would make the immune response much stronger. It would also mean making an essentially infinite number of cells, since there are an infinite number of potential antigens in the universe. Memory cells are only produced when they see a target, thus proving that their antibody sequence has potential utility.

@iayork My thought process came more from the fact that our bodies do maintain exactly that large number of naive cells specific for potentially useless antigens, so I don't see much sense in an argument based on maintaining a lower number of cells. If that was the case, it would be even more desirable to have naive cells being fully potent already. This argument to me only makes sense if naive cells die relatively quickly.

There is an extensive literature on this subject; if you are "not aware of any research about that question and couldn't find anything either", I suggest you delete your answer since it's simply your idle speculation based on mis-informed guesswork.

I wouldn't be surprised if the literature situation has changed in 6 years. It seems at the time, idle speculation based on misinformed guesswork was the best I could offer without spending disproportionate amounts of time on literature search. Particularly if it's so extensive, I suggest you post a better answer and then we can upvote it.

so I work in a B-cell and Antibody Memory lab and the answer to your question is no. First of all, your body does make a B-cell against every possible target conceivable and if they don't bind to their target, they will die within a few weeks. If they do bind to their target however, they turn into long-lived plasma cells, which are stored in the bone marrow and constantly pump out antibodies, and memory cells which are pretty much the same as B-cells except they're way more powerful in their response and they live forever. So, yeah, don't hold back on the vaccines (but careful of any autistic side effects)

Memory does have limits; it's been shown that adding new specificities eventually does start to crowd out old specificities. The point at which this happens is unclear and probably has complex determinants, and the vaccine schedule doesn't come close to touching it. Hopefully your "autistic side effects" comment is a joke, but given that a non-scientific audience reads this I hope you'll edit it out.