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References for historical momentum in asexual species definitions
For sexually reproducing organisms, the scope of a species is somewhat fixed by reproductive compatibility.
However, this all collapses for organisms that exclusively reproduce asexually.
Here, my impression is that historical momentum is the primary driving factor of species scopes, i.e.:
Clades continue to stay on the species level to maintain continuity, while they would be categorised with a higher or lower rank if clades had to be taxonomically ranked from scratch without respect to history.
For example, the species of Escherichia coli and Pseudomonas aeruginosa have been discovered (and thus have been made species) very early and now comprise a diversity of subspecies.
In particular, the genus of Shigella appears to considerably overlap with E. coli or is even thought to be a subspecies of it.
I am here looking for references supporting (or refuting) my impression, for example:

Has this ever been prominently noted?
Are there any instances of species being split on account of being “too large” (as opposed to other miscategorisations)?

Background: Why I care
As long as the taxonomy is phyletic, what does it matter at what level clades are ranked?
Right now, this affects me in several ways (assuming that my impression is correct):

The common way to present the composition of an ecological community is showing the abundances on a fixed taxonomic level.
For example: “Our community contained 80 % Pseudomonas, 15 % Escherichia, and 5 % Bacillus.” and analogous graphical representations.
Of course, I can deviate from this (e.g., by listing lower ranks for diverse clades), but then I have to justify it – and here the desired reference might help.

If differing subspecies of a “big” species are present in an ecological community, this may lead to a superficial underestimation of the community’s diversity.
Mind superficial:
I am aware that this does not affect any good quantification of diversity.
However, it does affect superficial diversity as estimated from representations such as that mentioned in the previous point, and the resulting discrepancies between objective and subjective diversity often demand an explanation.

Biosafety classifications are often determined on the species level, in particular, if the subspecies is unknown.
For example, even though P. aeruginosa lives on our skins, it automatically gets classified as risky on account of some black-sheep subspecies.

One issue is that I don't know what you mean by "historical momentum". Do you mean, when humans found the organisms in question?

@MaximilianPress: I mean, e.g., that E. coli continues to be a species only because of its history as opposed to what would be a more balanced taxonomy given our current knowledge.

Right- I talk about that specifically a little, below. I would then ask a different question: are species definitions themselves only still around because of historical momentum? Somewhat related: it might be helpful to read / learn more about classification, here is a video from Joe Felsenstein, old warhorse of computational phylogenetics, discussing this question (starts ~8 minutes): https://www.youtube.com/watch?v=PcD15i7yzJ8

are species definitions themselves only still around because of historical momentum? – To some extent sure, but then there is some merit to having a rough idea of how diverse a clade is by its level. Anyway, this is something I cannot change.

Our exchange has served to confuse me further regarding your question. Is your argument, basically, that E. coli is more diverse than a species first described yesterday because the type strain for E. coli was described first and it has therefore undergone more evolution since then? (That doesn't make any sense to me, but I'm having trouble understanding any other meaning.)

@MaximilianPress: E. coli is more diverse than a species first described yesterday because the type strain for E. coli was described first – Yes, though the reason is not evolution, but rather things like: 1) The definition of E. coli had to be expanded to maintain monophyly in light of new insights. 2) New insights on the properties of E. coli or strains thereof. 3) The definition of E. coli is overly broad by modern standards either due to new insights on what aspects matter for bacteria or general changes of standard as to how narrow a species should be.

I'm going to delete my answer because it doesn't seem to be helpful here. Based on our exchange, I remain puzzled about how the presentation of results at a fixed taxonomic level is methodologically enforced compared to the (to me) clearly superior phylogenetic method, there is a bunch of literature on this as we've discussed. Potentially editing the question would clarify this.

@MaximilianPress: The presentation of community composition is not methodologically enforced, because it is not about methods or quantification, but about presentation. Just to be very clear, I am talking about things like “Our community contained 80 % Pseduomonas, 15 % Escherichia, and 5 % Bacillus.” and graphical representations of similar information. I have no idea how I can make things much clearer, but am open to suggestions.

"Our community contained 80 % Pseduomonas, 15 % Escherichia, and 5 % Bacillus.” and graphical representations of similar information." I think that this is a much clearer statement of what you anticipate needing (or expect people to want from you) than I am getting from the question. I think that in your question you could take such a statement and then talk about what you think is wrong with it, and what kind of statement you would prefer to make instead. And also, to be very explicit about how it interacts with history (where I think I get confused). Also, asexuality seems irrelevant to me?

@MaximilianPress: Edited. Asexuality is relevant, because for sexual organisms species levels get readjusted based on insights on reproductive compatibility AFAIK. While this is not perfect either, it regulates the scope of species to at least some extent.

FWIW I think the question is clear, it's just hard to find the sorts of sources requested, especially reliable ones. It's more the thing that people talk about at a conference rather than writing papers on. I suspect you might find some discussion in an article arguing for a change but I've gone through several of these now and not found anything to quite back this up.

I have tried to ask a similar question from a rather different prospective: basically, whether taxonomic categories can eb defined by differentiating between quantitative and qualitative evolutionary changes.


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Has life on Earth explored the entire space of genomes?
Recently I came across a 2008 article, the authors of which argue that in fact the space of protein sequences is not as large as it might seem, and that life on Earth has most likely already explored this entire space (maybe before the appearance of eukaryotes).
Dear experts, can you explain what this means?
That life on Earth has already explored all the possible space of genomes, and all possible living organisms that are generally possible have already appeared? But after all, only the human genome consists of about 3 billion base pairs, and all possible combinations are a gigantic number, how could life explore them all, not to mention other genomes? And if life before eukaryotes tried every possible genome, then how did other life forms with a different genome come about?
I'm confused, please help.

The idea that all possible living organisms have already appeared is readily disproven, by for instance plant breeding.  Just with flowers, we see things like artificially-induced polyploidy, and interspecies hybrids that only survive because of things like embryo rescue.  WRT that 3 billion base pairs, note that in addition to the combinations, you can make it 3 billion +1 and get a new set, then repeat with 3 billion + 2 &c.

The article argues about protein space, which is orders of magnitude smaller than genomic space.  1) There are 20 AAs for 64 codon sequences. 2) Proteins average 300-600 aa depending on the organism (source); note that this is much larger than your cited article's claim of <100aa, upon which their math is dependent 3) Only a fraction of most organisms' genome codes for proteins

@Punintended How many orders of magnitude is the space of proteins less than the space of genomes?

@ArmanArmenpress To compare the two, you'd need to make approximations for both. The amount of work in that task depends on your assumptions/approximations, and would likely be a paper (or two) in its own right. A constraint like "stability" will depend heavily on your precise definition, and since proteins and DNA have different chemical properties (and therefore stability), stability constraints on one will manifest quite differently in approximations of the other. Eg, "stability = 6 months at 4dC" will give very different results for different proteins, never mind comparing it to DNA

@Punintended Thank you. That is, it is not known what proportion of all possible genomes are stable.

The answer to this question is very much no. Genomes are of arbitrary length and structural organisation (i.e. ploidy), so there isn't a fixed number of 'slots' that different base-pairs could inhabit (like e.g. rolling a dice). As a consequence (and as jamesfq mentioned in the comments), no matter what genome you have, you can always add additional levels of complexity. Take for example the human genome which is approximately 3.1bn base pairs long; you could reconfigure it by adding or removing a base-pair (also known as indels) indefinitely.
That's not even considering the total number of combinations of base pairs at each position in the human genome, which is 4^(3.2e9), which is so astronomically large that it's not even worth entertaining that all  those combinations could have occurred in nature.

There's a significant difference between "possible genomes" and "stable genomes", as the latter constrains protein sequences. As an easy example of the latter, for organisms following the central dogma of DNA -> RNA -> Protein, at minimum the genome needs to encode sequences for replication, transcription and translation

a) yes that makes it more clear, b) agreed. but the question didn't really specify (to my reading) whether or not the genomes were viable or not, but I'll edit that in to be clear.

@Punintended That is, life on Earth has explored all possible stable genomes?

@user438383 Is it known how much of the genome can be functional and stable?

@ArmanArmenpress - you mean how many combinations of nucleotides end up being stable? Not sure myself, I think that would be a hard (but interesting) question to answer.

There'll be a large difference between "chemically stable" (mostly energetic?) and "biologically stable" (proofreading, error correction, replication?).  What do you mean by "functional"?  Even with rigorous definitions, as user438383 says, it'd be hard/interesting to answer

@user438383 it seems to me that the answer to this question is generally impossible. Indeed, for genomes with different numbers of base pairs, the number of stable combinations will be different.

@Punintended: Seems like it very much depends on how you define "stable".  Logically, any functioning genome must at a minimum be stable enough for it to hang together long enough for the organism to reproduce.  OTOH, if it's not somewhat unstable, it won't mutate, and evolution becomes much more difficult.

source: Stack Exchange

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

sort: votes


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Why did ALL dinosaurs go extinct?
Why did all dinosaurs, rather than just some of them, go extinct during the K-T extinction event? Birds are an exception, but being able to fly, they are also a very special kind of creature, and specalization doesn't usually help with resilience.
My understanding is that dinosaurs filled a very broad and diverse set of ecological niches. In view of this diversity, it is counterintuitive to me that all members of such a diverse set of species would disappear, rather than just a fraction of them.
Did they have (or lack) a common set of features that distinguished them from mammals and birds and made them particularly susceptible to whatever caused the extinction? Did their niches cease to exists temporarily? (It couldn't be the case for all of their niches, could it?) Did mammals already have superior potential which could finally be realized because something upset the global ecological balance?
To sum up, my question is why a large and diverse group disappeared completely rather than partially. There must be some ecological principles that could illuminate it.
Please excuse this naive question from an ignorant but interested layman.

They didn't. Birds exist today: https://biology.stackexchange.com/questions/17546/were-there-any-flying-dinosaurs?rq=1

Most dinosaurs were bigger than most K-T survivors. A quick-and-dirty answer would be a sudden lack of sufficient foodstuffs induced by global cooling post-impact. That would off non-small herbivores, which in turn would cause most carnivores to starve

Here's a good place to start your research: https://en.wikipedia.org/wiki/Cretaceous%E2%80%93Paleogene_extinction_event  It gives a good overview with references about different species groups and the extinction event and its aftermath. Remember that although it is thought to be a single impact, the size and location of the impact led to blast effects, thermal effects, steam/cloud effects, worldwide chemical changes to oceans and land, "impact winter" temperature and sunlight decreases, etc.

@Armand Summarize and make your comment an answer.

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


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Help identify green insect with long antennae?
This was found in south Texas, USA.
It size was around 3 centimetres without considering the antennas or legs.

No, not dangerous. I think they mostly can hop and fly, so move fairly quickly if disturbed, which might startle your daughter.

Nice strategy! Good to know that google lens identified it as a Katydid (Tettigoniidae) but I think that is not exactly the Speckled bush-cricket because it body size range is 10-15 mm (wikipedia) and the one I saw was bigger.

The green, narrow body suggests this is indeed a katydid.
The red antennae, red eyes, and small, red-lined wings looks like the green form of a Paracyrtophyllus robustus (Central Texas leaf katydid) nymph.

 Credit: Mike Quinn ; Source: Bugguide.net

 Source: Austin Bug Collection


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Isolated mitochondria in glucose rich solution, what happens to ATP generation?
I'm taking intro to biology course this year, and I was thinking about this question.

Isolated mitochondria were placed in a glucose rich solution. (With ADP and Pi). How would this affect the ATP creation in the solution ?

My very simplified understanding of the process is as follows:

Glycolysis takes place in the cytosol, and converts glucose into pyruvate.
Pyruvate enters the mitochondrion and is oxidized to acetyl CoA
Acetyl CoA enters the citric acid cycle which creates NADH and FADH2
In the electron transport chain, NADH and FADH2 electrons pass through the mitochondria membrane, this flow results in active proton transport out of the matrix, creating a gradient. And the result is diffusion of protons which is coupled with synthesis of ATP.

I was unsure what would happen when isolated mitochondria and placed in a glucose rich solution.
Reasonable options are:

My book states that ATP synthesis is reversible and ATP synthase can also act as an ATPase, hydrolyzing ATP to ADP and Pi if there is too much ATP.
There is no cytosol (due to the mitochondria being isolated), There is actually no glycolysis happening, meaning no citric acid cycle, and no electron transport chain, meaning no ATP.
There is not enough ATP to start the process: break glucose into fructose and pyruvates?
Or just nothing happens and ATP is generated regularly ?

As is usual with this kind of posting, we are being asked not about a problem or principal of biology but about a contrived examination question with ambiguous wording, the expected answer to which depends on the specific level of teaching in a given syllabus. While sympathizing with the poor student, I regard this as akin to mind reading. “How would this affect ATP creation?” Creation?  Phosphorylation of ADP? biosynthesis? Abiogenesis? “Affect” it? Was it happening already? Really, if the educator wants to test whether a student knows where glycolysis occurs he should ask it straight.

While I do agree that the wording is ambiguous, I did state that my teaching level was intro to biology course. I appreciate the sympathy, and would be happy with any biological explanation that is related to my question (simplified as it might be). I think the the question indeed meant Phosphorylation of ADP.

Well for an introductory biology course (unless it's at MIT) I would imagine the answer is what you have deduced yourself in 2. As glycolysis only occurs in the cytoplasm, adding glucose to isolated mitochondria is like spitting into the wind. Phosphorylation of ADP cannot occur because there is no enzyme system in the mitochondrion that can convert glucose into a substrate that can feed into the TCA cycle.


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Blooming at moonlight
At the moment a popular question in the physics SE community is about night-blooming cereus: this flower blooms at full moon, that is it is capable of making difference between the moonlight and sunlight.
The question has attracted a lot of guesswork, with some people even claiming that the cereus doesn't know about the moon, but simply blooms at night - the blooming at full moon however seems to find experimental confirmation. It is thus more plausible that the flower distingushes between the light intensities of the moonlight and the sunlight, as suggested here.
The closest question that I found in this forum is about flowers open during the daytime and closed at night (or vice versa). I suppose one could construct a more sophisticated model based on the mechanisms described here, but I would appreciate an expert answer.
To restate the question:
How does night-blooming cereus distinguish between moonlight and sunlight?

I'd really like to get an expert answer to this interesting question. Would you consider offering a bounty?


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What is causing these lichen patterns on a tree in Scotland?
I recently saw these lichens growing on a tree in Scotland. What is causing the pattern of dark lines? Are these the boundaries between individual lichens? Or could it be something to do with the growth of the tree (which is of diameter around 15cm)?
I'm more familiar with lichens growing on rocks, where these spatial patterns can potentially be used to improve rock dating (see e.g. this article). Presumably lichens growing on tree bark are younger, but are potentially affected by other factors that don't apply on rock e.g. changes in the bark as the tree grows.


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What would an organism be like if its entire genome "worked"?
It is known that a large fraction of the genome of almost any organism "does not work", that is, it does not encode any proteins and does not participate in gene expression, in protein synthesis, and in changes in the properties of the organism during mutations (e.g., estimates of functional DNA fraction in humans).
If you imagine an organism, for example a human, whose genome consists of completely "working" parts, what will be the consequence? For example, if all 3 billion base pairs of the human genome formed fully working genes, each of which would code for some proteins or combinations of proteins.
What would a human be like if their entire genome of 3 billion sequences consisted of coding genes?

Not really since the number of genes doesn't correlated with organismal complexity. Water daphnia have ~30% more genes than humans do. Going by your last couple of posts, this article may clear up some things and be of interested to you https://metode.org/issues/monographs/the-size-of-the-genome-and-the-complexity-of-living-beings.html

@user438383 And what correlates? And yet, what would a person be like if their entire genome (all 3 billion base pairs) were working?

@user438383 That is, what would a human be like if his entire genome of 3 billion sequences consisted of coding genes?

That's impossible to answer - it's much too hypothetical, so the answer could never be known. Humans are humans because of the genes we have. It might be fun to speculate, but it' doesn't really make sense as a scientific question.

@user438383 I actually think this is quite answerable, based on the work that's been done in minimal organisms.

I think it's very important to stress that your statement It is known that most of the genome of almost any organism "does not work" is completely incorrect, as @jakebeal describes in his answer. Just because a sequence or region doesn't code for a protein gene product doesn't mean it's useless. This is a common misconception we see here, and it deserves to be vigorously refuted.

As a new contributor I would encourage you to read the guidelines on what sort of questions one should avoid asking here. If you do so I think you will realize why I think that this is one of them.

@MattDMo Your assertion is also not correct, depending on the metric. I've attempted to clean up the question without changing its sense too much.

@jakebeal in what way? I wasn't trying to say that every single base has a function, just that the notion of "majority junk DNA" is not correct.

@MattDMo The paper that I link to discusses a variety of different metrics that come up with highly divergent estimates depending on the sense in which "junk" is meant, a number of which are indeed the majority of the genome of humans and many other large eukaryotes. While the OP's phrasing was not precise, I find their question quite intelligible and reasonable.

@jakebeal ok, I'll check it out

Your question is closely related to the concept of minimal genomes, in which researchers attempt to understand the significance of genes by removing everything that isn't strictly necessary, which includes "broken" genes, redundant genes, intergenic regions, etc.
The typical result is a much more fragile and less functional organism. Much of this is due to the fact that "not strictly necessary" is not the same as "not useful."  However, there is also a lot of regulatory function outside of coding sequences, as well as implicit and unknown functionality in apparently "non-functional" DNA.
Examples of this include spacing between genes that interacts with histone positioning, decouples methylation, or other epigenetic factors, spacing that couples or decouples genes, sequences with functions that haven't been discovered yet.
So what would happen if you had a human with either all of the "excess" material removed or with the "empty" material filled in with extra genes with some intended function?  In either case, you'd probably never actually end up with a human, because the resulting organism would be so fragile and impaired by undesirable interactions due to the loss of genetic separation, that it would never even be able to make it past the embryo stage to become a fetus.

Very likely the all genes active is going to be a mass of stem cells. So more of a cancer than human.

@jakebeal Why will it be fragile? Additional genes implies coding for new forms of proteins, about which we know nothing (after all, the space of proteins is huge and grows with the number of amino acids). Maybe there will be proteins that make the body not fragile, but quite the opposite?

@RoniSaiba .
Why do you think so?

@ArmanArmenpress A genome is more than just proteins. The regulation of those proteins is critical as well, and "empty space" is part of that regulation. Break the regulation and break the organism.

@ArmanArmenpress Embryonic stem cells have the highest euchromatin to heterochromatin ratios. As cell become more specialized i.e. differentiate, they start shutting down unnecessary (for them) regions of the genome. I think Gilbert's Developmental Biology will be a book that will satisfy your curiosity.


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aneusomy vs aneuploidy
Simple question: aneusomy vs aneuploidy - what's the difference?
I tried google and PubMed, but although there are articles talking about aneusomy, I wasn't able to find a clear definition contrasting the two.
I have no formal genetics training, so sorry if this seems trivial!

Can you quote definitions for each term from the citations you've found to clarify what you don't understand about the difference between the terms?

The suffixes -somy and -ploidy mean different things. The suffix -somy translates to "body" and in genetics typically refers to an individual chromosome. Ploidy level, on the other hand, refers to the full chromosome complement.
For example, most human cells are diploid - they have two copies of every chromosome. The number of chromosomes in a diploid cell is 46. Now, if there was an extra of one of those chromosomes, we would have a trisomy of that chromosome (e.g., Trisomy 21 refers to having an extra chromosome 21, but still has only 2 of every other chromosome). If there was one extra of every chromosome, that would be called triploidy (this actually does happen in plants).
Aneuploid comes from the word euploid - which refers to the "true" amount of chromosomes that should be in a cell. If something is aneuploid (i.e., not-true), there is something wrong with the amount of chromosomes. Aneusomy would refer to the chromosomes, while aneuploidy refers to the chromosome set.
This article from NCBI gives a good overview of aneuploidy, but also monosomy, trisomy, etc.
This page from Khan Academy may be a little more non-biologist friendly.
In my experience I have encountered "aneuploidy" much more than "aneusomy" as a descriptor. It may be that in certain fields of genetics one is more relevant or common than another.


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What would cause red-haired people to become fewer?
There is this misconception that red-haired people are going to die out. This person on the Internet ("howstuffworks") also connected it to a marketing campaign of a hair dyer company. But I'm interested in a specific citation that he gives in that text, because it's cited on Wikipedia (so I want to check it):

While redheads may decline, the potential for red isn't going away. ["Red Alert." National Geographic. September 2007. Page 14.]

I don't have that National Geographic magazine, but I wonder: Why should the population of redheads decline? If it doesn't have a selection disadvantage, the frequency of the alleles causing red hair (which are recessive) should stay equal and if further assuming random mating in the human population, also the frequency of people with red hair, should stay equal, shouldn't it? So is the howstuffworks author wrong?

I don't think random mating is a realistic assumption...

The howstuffworks article notes that National Geographic did not endorse or provide any evidence for a claim that "redheads may decline". To me, that wording just means they don't know one way or another (may [or may not]).  All these sorts of silly claims may be related to the eugenics movement of a hundred years ago, which thought that "undesirable" recessive genes could be eliminated from populations by preventing homozygotes from breeding. Of course, they didn't realize that the majority of recessive alleles in a population are typically in asymptomatic heterozygotes.

Let's consider a possible scenario, with a simplified assumption that red hair is a simple Mendelian recessive trait.
Let's say we have a population that is 10% red hair. Everyone with red hair lives on one island, and they only breed among each other. They all have red hair, so we can infer they are all homozygous recessive (rr) for that trait. Everyone without red hair lives on the other island. Red hair never appears in this population, so we can infer they are all homozygous dominant for the non-red hair trait (RR).
Now, we develop inter-island transportation, and breeding becomes randomly assorted among the whole population. The allele frequencies stay the same: 10% r and 90% R. There is no selection based on the red hair trait. However, from Hardy-Weinberg we would calculate that only q^2 = 0.1^2 = 1% are homozygous recessive. 2 * p * q = 2 * 0.9 * 0.1 = 18% are heterozygous carriers for red hair, but they don't express the phenotype.
Just by changing the mating scheme, you can go from 10% with red hair to 1% without any change in allele frequencies.
It seems reasonable to infer that something like this is happening in the real world. People with red hair are much more common in certain places in the world. When people tend to mate only with people in their local communities, the likelihood of homozygous recessive individuals is higher than when people immigrate and mate with partners around the world. That doesn't mean there is any selection for the red hair allele, just a consequence of the mating scheme. That's the takeaway from the National Geographic quote you found on Wikipedia:

"while redheads may decline, the potential for red isn't going away"

In this statement, "redheads" are the homozygous recessive folks that express the red hair phenotype. "Potential for red" is a colloquial way of referring to the allele frequency, "r".
Of course you could also get actual changes in allele frequency for reasons that have nothing to do with fitness of the red hair phenotype. If you think about population growth on a regional basis, if there is more population growth in countries with lower frequency of a red hair allele, then the frequency of red hair in the human population as a whole would decrease. It seems likely this is occurring today since regions with higher frequency of red hair (northern Europe/UK/Ireland, also the US) have lower population growth than those with lower frequency (Asia, Africa, South America). There's no hint that this would result in a disappearance of the trait, though.

In the end a clear "yes/no" answer is kinda missing, I read the piece and the conclusion is not really clear to me.

@PascalVKooten I read and answered the biology question in the title and explained the National Geographic quote. If by yes/no you're meaning the question about whether the "howstuffworks author" is right or wrong, I don't really have any interest in addressing that especially because it's a long piece with a lot of different statements, most of them not about biology.

@PascalVKooten - "While redheads may decline, the potential for red isn't going away." According to this answer, that's a correct statement. And in the future there will be no redheads is almost undoubtedly false.

Thanks Bryan for this extensive answer. I will search for evidence for the changed mating patterns that you mention in the coming days and include it in this answer.


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What bird / animal has this call?
USA MA NE
I have a bird / animal coming to the trees in the backyard making this call (see link to audio file), which does not really sound like a bird - it's fairly low frequency. I have not seen it. Sometimes it sits in a young tree, where you can almost see through to the trunk. But I cannot make it out, so it's not very big (like a turkey). It comes at late afternoon and stays around until ~11PM. It switches trees fairly quickly, so I assume it can fly. The call is always the same. Sometimes another one of its kind answers.
Bird_animal_call_mp3
You don't need dropbox. Ignore "suspicious link". Close login popup. Click download arrow. Direct download.
I added a Soundcloud link:
Bird_animal_call_mp3

No idea about US bird species, but it sounds similar to a European magpie. Compare with https://www.youtube.com/watch?v=Kz4SvP0c_VE

Surely you can find a way to share an audio file that doesn't require people to ignore a "suspicious link" warning and download a file from your dropbox.

@csk, well do you have a suggestion where to upload it? You can check the url and the file on virustotal.

YouTube. iNaturalist (although that requires a login, so it's also limiting). Other options are listed and discussed here: https://www.quora.com/What-are-the-best-websites-for-audio-file-uploading-and-sharing.

I added a Soundcloud link.

Sounds a lot like a woodpecker to me. Which one, I don't know, not being familiar enough with the variety in the USA, but I think the Red-bellied might be similar.

It is a grey tree frog's mating call. See youtube link:
Grey tree frog mating call
Source for finding the answer: Audubon Society


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Unknown Issue with qPCR Standard
I am currently doing the ground work for a SELEX experiment and I am attempting to verify my standards for the starting library. I ran a reaction with samples containing 50, 5, 0.5, and 0.05ng of my starting library and the samples for the 5, 0.5, and 0.05 appear to amplify as expected, but whenever I run a sample containing 50ng of my starter library, the curves start around -2000 RFU and peak at 0 RFU. Has anyone seen this behavior before?
EDIT: Added annotated graph
Method: SYBR Green
System: Bio-rad CFX384
Software: Bro-rad CFX Manager

Can you please label your curves to make it clear which is which? Also, how are you computing RFU? Getting negative fluorescence usually indicates a process failure of some sort.

@jakebeal My apologies, I should have annotated it from the start. I've updated the post to include the annotated graph and more information. I am reading RFU with SYBR Green on a Bio-Rad CFX384. I've performed this assay several times with fresh dilutions of library DNA and the results seem to be the same each time.

I'm not too familiar with SELEX, but just looking at the curves, it seems like a baseline normalization issue. The Bio-Rad software that I use automatically normalizes amplification curves to a baseline average from the first few cycles. Since your 50ng wells were hot from the start, it looks like it took the saturated endpoint fluorescence as baseline, and normalized the rest of the curve to that. You can turn normalization off in the software, but probably still won't be able to get a good Cq value for the 50ng curves.

@MikeyC This does seem like the most likely explanation. The only thing that might make a difference in this regard is that I did run a no-template control which was stable at 0 throughout the run. It is not pictured here because it covered up a portion of the 50ng sample curve. I am new to this system so I am not totally sure how it goes about calculating a baseline. Thank you for your input.

@jakebeal The no-template control doesn't factor in. The software determines a different baseline for each well, which it subtracts from that well's fluorescence readings throughout the run so they can all lineup at 0 for the first few cycles. It's just not getting a usable baseline from those wells, so it's subtracting the saturated fluorescence instead. You can disable baseline subtraction under the Settings menu in your CFX manager software. Only problem is, you can't set a threshold for Cq determination without baseline subtraction.

@MikeyC If you're right, then yes, definitely a process failure --- and yet another example of why I never let instrument software handle calibration processes. Can you please turn your comments into an answer so that they can be voted up?


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How to convert system of equations with explicit substrate consumption into an implicit one?
I have a description of competition between two bacteria that is described by the system of equations:

S = substrate, μ = bacterial division rate, K = half saturation constant, y = yield (cells per unit of nutrient), N = concentration of bacteria.
Is it possible to convert it to a system of implicit substrate consumption such as the logistic system? For instance into this:

where μ = maximum growth rate and K = carrying capacity.
Essentially, the term Ṡ should disappear, μⱼS become μ, and Kₛ+S become K. I tried such conversion but I got the figure on the right panel instead of the original on the left:

On the left,
μ = μ₁ = 0.81
ν = μ₂ = 0.91
y₁ = 2.5*10^10
y₂ = 3.8*10^10
K₁ = 3.0*10^-6
K₂ = 3.1*10^-4
S₀ = 1*10^-4 (g/L)
N¹₀ = 1.0*10^2
N²₀ = N¹₀*200
D = 6*10^-2 (/h)
Vol = 200 mL

Obviously, the conversion I did has not included the terms y₁, y₂, K₁, and K₂. Thus, the red species never took over. How am I to bind all these variables in fewer terms into a logistic system?
Thank you

Could you explain the goal of the modification? As I see, if you model two independent logistic equation there will always look as the panel on the right. The interaction between the populations in the first set of equations is given by dS/dt which depends of both populations, while each populations only depends on S and it self.

The point is: the implicit form is present in more examples than the explicit, thus it would be the preferred way to analyze the interactions. By converting the first set into the more common way of representation, I will have a consistent data set instead of having some described in one way and other in another...

I would show an example of a numerical solution, but you don't give values for D and S0 ...

Thanks, I have updated the question to incorporate these values. The example is taken from SCIENCE 1980;207:1491 (E. coli C-8 = N₁; P. aeruginosa PA0283 = N₂).

in DOI: 10.1126/science.192.4238.463 I have found the relation μ = μmax[S/(S + K)]. This allows to convert d/dt N₁ = (μ₁SN₁)/(K₁+S) to d/dt N₁ = μN₁. Only the logistic term is missing, which I can guess estimating the carrying capacity.

There may be some way to do this, but I don't see how. My best attempt is in my answer.

By combining the parameters as shown in the science paper (actually a Monod term), I get a much larger μ for E. coli than P. aeruginosa, as expected. I estimated carrying capacity by the sum of bacteria in the original model. Yet, E. coli does not overgrow P. aeruginosa (https://u.cubeupload.com/gigux/CASE13.png).

In the previous post, I mixed up the growth rates. I actually did obtain a crossover using μ = μmax[S/(S + K)]: https://u.cubeupload.com/gigux/3cfCASE13.png

In general, no. You're trying to reduce the a three-dimensional dynamical system ({S, N1, N2}) to a two-dimensional system ({N1, N2}), which can't be done in general.
One way to approximate a two-dimensional system is to assume that the nutrient dynamics are on a fast time scale, so that for a given N1, N2 you can write down the quasi-equilibrium S*(N1,N2) and plug it back into the N1 and N2 equations.  If I've done the math right, the value of S* as a function of N1, N2, and the other model parameters is the solution to the cubic equation dS/dt = 0, or:

for S. Unfortunately, this probably means the answer (although it will have a closed-form solution) will be too complex to do anything with analytically, although you could solve it computationally.
I tried this (code below): the dynamics actually track the full system very well for a while, but then the equations seem to blow up (the lines are the full 3-d dynamics, the points are the quasi-equilibrium approximation).  It would take a lot more thought and analysis to figure out what's going on here — most likely, the equations just aren't biologically well-posed. (In the full system, S crashes down from about 1e-4 to 2e-7 very suddenly around t=12, then declines extremely slowly after that ...)
@RogerVadim suggested that one could also try the limit of slow resource dynamics, but in this case (assuming we mean dS/dt << 1) the dynamics are simple and unrealistic; slow resource dynamics means we would hold S constant at its starting value and see what happened. In this case, because the per-capita growth rates of N1 and N2 are constant at constant S, we would just get exponential growth or decay for each species (depending on whether the birth rate was greater or less than the death rate).  There are plenty of other things you could try to simplify the system - what if D=0? What if D is non-zero but << 1 ? Is there a way fix the 2-D (fast resource dynamics) system so that it works, either by changing something computational or reformulating the system? - but nothing easy is immediately obvious to me.

p0 <- c(mu1 = 0.81, mu2 = 0.91, y1 = 2.5e10,
        y2 = 3.8e10, K1 = 3.0e-6, K2 = 3.1e-4,
        S0 = 1e-4, D=6e-2)

y0 <- c(S = 1e-4, N1 = 1e2, N2 = 2e4)

library(deSolve)
g1 <- function(t,y,parms) {
  g <- with(as.list(c(y,parms)),
  {
    m1 <- mu1/y1*(S*N1)/(K1 + S)
    m2 <- mu2/y2*(S*N2)/(K2 + S)g
    c(S = (S0-S)*D-m1-m2,
      N1 = m1*y1-D*N1,
      N2 = m2*y2-D*N2)
  }
  )
  list(g)
}

Seqfun <- function(S, y, parms) {
  Seq <- with(as.list(c(y, parms)),
  (S0-S)*D - mu1/y1*N1*S/(K1+S) - mu2/y2*N2*S/(K2+S))
  return(Seq)
}

g2 <- function(t,y,parms) {
  Seq <- uniroot(Seqfun, interval = c(0, 1e3), y = y, parms = parms)$root
  cat(y[["N1"]], y[["N2"]], Seq, "\n")
  g <- with(as.list(c(y, parms)),
            c(N1 = mu1*(Seq*N1)/(K1 + Seq) - D*N1,
              N2 = mu2*(Seq*N2)/(K2 + Seq) - D*N2)
            )
  list(g, S = Seq)
}

tvec <- seq(0, 60)
r1 <- ode(y = y0, times = tvec, func = g1, parms = p0)
r2 <- ode(y = y0[-1], times = tvec, func = g2, parms = p0)

png("bact.png")
par(las=1, bty="l")
matplot(r1[,-(1:2)], type="l", log="y", lty =1, xlab="time", ylab="density")
matpoints(r2[,2:3], pch=1)
dev.off()

Probably, one could also consider the limit where the neutrient dynamics is very slow?

Thanks, I'll need some time to digest this answer...


text:
What is the term for the physical and behavioral changes that occur in an adult species due to the change in their hierarchy?
For example, when a chicken becomes a rooster its crest becomes larger and their feathers become more colorful. Dominant male lions get larger and darker manes.
Also, can these changes also occur inversely? If so, what is the term for it?


text:
Bird identification - hawk
These fledglings are learning to fly in Salt Lake City, UT. What species are they?

Welcome to Biology.SE. Please include an estimate of the size of these birds and if possible pictures of the adults that are likely to still be feeding them. To me these look like fledgling Red-tails, but the eye looks bluish rather than yellowish. However, that might be due to the lighting in your picture and this is a notoriously variable species. At any rate I think these are a buteo of some sort ...

Based on your location and the unique coloration/arrangement of the feathers near the ear area, I would say these are Northern Harrier (Circus hudsonius) chicks.


text:
The location of pulmonary valve in comparison with the aortic valve

According to most transverse diagrams of heart, the pulmonary valve, in comparison to the aortic valve, angles  towards the left side a little bit. Take, for instance, the pulmonary valve is more close to the left coronary artery than the right one. But the frontal sections, on the contrary, show that the pulmonary valve, in comparison to the aortic valve, angles toward right.
What's wrong?

They both look angled to the left to me. On the left image, left is to the left (you're looking from the top down, as if you came up behind someone and looked through their skull into the torso). On the right image, left is to the right; you're looking straight ahead at someone's chest from the front.

@BryanKrause Forget the angles, for the moment, let's talk about their location. I've edited the image.

I think you're reading too much into the picture. They're basically right on top of each other, and they are crossing along the length. In one you're emphasizing the bottom leaflets of the valves, in the other the top. I don't think there's a meaningful anatomical distinction between the two. That said, I'm a bit more familiar with porcine cardiac anatomy which is more different than these pictures. Maybe someone will have an answer I just don't see why this is important to you.

@BryanKrause One of those vague 'why' questions! I just wonder whether it is actually possible to see the aortic valve in a longitudinal section of the heart or the frontal diagrams are just trying to emphasis on showing that, on its presence.

Well it's certainly visible in some longitudinal section. The help suggests "You should only ask practical, answerable questions based on actual problems that you face." - it's hard to get good answers if you can't explain the purpose of a question.

@BryanKrause Quite agree. Though it is rather personal, let me ask, if you were to choose a frontal diagram for an atricle, what diagram would you choose, the right image, or a version in which the aortic valve is completely hidden?

The image to choose would entirely depend on the goals I had in displaying the image. I'd never put a figure in an article/paper without a purpose.

@BryanKrause It is going to be a typical illustration of the heart chambers with 15-18 year old audience


text:
How do you read the gene insert domains on a plasmid from Addgene?
This is a pretty basic question but I cannot find an answer anywhere. For plasmids on Addgene such as this one, there is supposed to be a GtCCR1 rhodopsin domain insert with a EYFP tag. However on the plasmid viewer shown below, there is only an arrow indicating the EYFP tag but not the CCR1 rhodopsin domain itself. Is the rhodopsin domain there but just doesn't show up in the image, or am I misunderstanding the nature of the plasmid? Many plasmids I have been looking at had the same issue, I am new to this so any help would be appreciated.

It should be located between the CMV promoter and the beginning of the EYFP sequence. And yes, I agree, it seems missing there.

The GtCCR rhodopsin domain is shown by the thin brown and green arrows on the right of the image that overlap with the EYFP domain and are flanked by the CMV promoter and bGH poly(A) signal. These arrows show the coding region.
The sequences for the plasmid are automatically annotated by Addgene with common features (I think they use Snapgene software for this, at least the features and way they are done are very similar). The actual insert is supplied by the depositor and is not automatically annotated, though an ORF between promoter and terminator signals can (will?) be.
If you don't have Snapgene, I recommend it for plasmids. The viewer (linked above) is free to use. It has some features that you can only use by annual subscription. I have no affiliation with this product or company.
There are a couple of ways of visualizing the sequence and features, but they all give the same result in the end. I'll take you through the most obvious:

From the front page for your plasmid of interest (POI), click on View All Sequences

A new page will load, click on the Analyze Sequence button or just click on the map of the plasmid.

This will load a new page with a number of tabs. You will be on the Map tab. In this tab you can hover over the features and get a little pop-up description and base positions. For example the gTCCR rhodopsin will pop up with ORF: 789 .. 2414 = 1626 bp as well as a protein length and mass assessment.

Now click on the Sequences tab and it will show the full sequence. You can scroll through and see all the features, base positions for each, restriction enzymes, translations etc. I've added the bit at the start of the ORF for the GtCCR and a bit of the CMV promoter.


text:
Is it even possible to cut just the phloem from the stem of a plant?
I often see questions related to this kind of diagram:

Basically, the diagram shows a that phloem is removed from the stem in the middle of the plant. Thus, the stem swells because food produced by the leaves cannot travel further. However, is it even possible to do this experiment in real life? Is it possible to cut just the phloem from the stem?

Why do you think it is not possible?

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [ask] effective questions on this site. In particular, we expect users to demonstrate that they have done the expected prior research — search for 'homework' in the help section for details. I suggest you start with this wikipedia page. After that please either delete or [edit] your question to make it on-topic for this site. Thanks.

The phloem and xylem are tissues with reinforced tubes, they are stronger than the meristematic tissue between them. This sort of splitting happens easily.


text:
What Snake is this? (Found at my door in Raebareli, North India)
Found this snake at my door in Raebareli, North India. We of course allowed it to go away peacefully.
Could someone please identify it for me?

It is the venomous Common Krait (Bungarus caeruleus), one of the Big Four Indian Snakes,  responsible for the highest number of snake bites in India.

How close was it to humans when it was noticed? Are these aggressive snakes?


text:
What do decomposers eat if they break down complex substances and make it available for producers?
I have a doubt for which I haven't found the exact answer.
Decomposers break down complex substances into simpler substances and make it available for producers. But what does decomposers get (or eat) in this process.
Answer with an example would be appreciated.
Thanks in advance!

Homework questions are off topic unless you show an attempt to answer it on your own.

There is stored energy in complex substances: that's what the decomposers use.  For instance, if you've ever made bread, you'll have seen yeast decompose sugars & starches (complex substances) into less-complex CO2 and ethanol, using the energy released to reproduce.


text:
Polymerase Cycle Assembly (PCA) is not working (Only primrs in EF Gel)
Helllo All !
I am working trying to assemble dsDNA fragments (for further golden gate domestication) via polymerase cycle assembly (PCA). After designing the required oligonucleotides with overlap regions. (Image of the design provided below).
Using
NZYProof Green mastermix x2  25 uL
Inner Oligonucleotides 2 uL of 1 uM stock
Outer Oligonucleotides 2 uL of 100 uM stock
Initial denaturation 95 ºC 2 min
Denaturation 95 ºC 30 sec
Annealing 62 ºC 30 sec
Extension 72 ºC 30 sec
Repeated by 25 cycles
Final extension 72 ºC 2 min

After performing the following protocol (based on This one) with a high fidelity polymerase mastermix, the EF gel of PCR products only shows a single "band" corresponding with the oligonucleotides introduced in the reaction.  (Ignore the blurred EF gel, it was imaged quite a long time after running the gel).

Any idea of what could actually be going wrong? Should not I observe at least some faint higher molecular weight amplicons?
Thanks in advance for your answers!
Jorge.
UPDATE: Regarding the length of overlap regions, the design considers different overlap sequences length in order to achieve roughly the same Tm for all the overlaping regions. Tm of every overlap has been calculated using the online NEB Tm Calculator tool, and all of them are in the range of 61-63 °C (Considering a Q5 mastermix, which is the closest HiFi polymerase to the one we are currently using )
UPDATE2: After trying the PCA procedure with a "touchdown" approach (reducing annealing temperature gradually after 3 succesive cycles, most of the assemblies has started to show distinctive bands of the desired lenght in the EF Gel. Annealing is a crucial parameter for PCA.

I just ran the red/right gray primer overlap sequence (gtgaggacgaaacagcctctacaaataatt) through the NEB Tm calculator at https://tmcalculator.neb.com/#!/main and got a predicted Tm of 68C.

Yes! That's actually right. The provided image is the only PCA assembly which features a weird overlap of higher Tm. However the remaining ones (the other two lanes of the EF Gel) are other sequences where all the overlaping regions are between 61 to 62 ºC of Melting temp.

I suspect mispriming due to annealing temp being too low compared to predicted melting temp of overlap regions. As the protocol in your link notes:

(3) Choose annealing temperature wisely. We recommend to use the same
as min_Tm by Primerize design, which is usually between 60-64 °C.
(4) Check PCR product on 4% agarose gel. If assembly is unsuccessful
with shorter mis-priming products, we suggest try raising the
annealing temperature to reduce mis-priming. Alternatively, splitting
the assembly into separate sub-pools (i.e. primer 1-4 and primer 5-6)
and do an additional round of full assembly (see below).

At first glance, the sample assembly in the linked protocol uses overlap regions of similar length (presumably of similar predicted melting temp as well), while your overlaps vary substantially in length (esp. red primer and bottom right gray primer).
Using the NEB Tm calculator page ( tmcalculator.neb.com/#!/main ), I got the following predicted Tms:
left gray/red primer overlap sequence (ctttccggtctgatgagt) Tm 61C
red/right gray primer overlap sequence (gtgaggacgaaacagcctctacaaataatt) Tm 68C
green/left gray primer overlap sequence (gctcgtataatgtgtggaag) Tm 60C
Based on the much higher Tm of the red/right gray overlap, I'd retry your reaction with annealing temps of 65C and 68C.

Thank you for your advise Armand, we will try to do it this way and check the resutls. However, still being strange for us not to find any other product of higher molecular weight than of the primers by themselves.

There may be a more general issue with your PCR reaction. It may be helpful to do a positive control reaction where you are doing traditional PCR, with 2 primers amplifying a segment from a template. The linked protocol also suggested breaking the reaction down into 2-primer segments, then doing a final reaction to assemble those overlapping segments. I agree that not seeing products in any of your reaction lanes suggests it's not just an issue with one sequence.

I've had experience in the past with impure primer preps that inhibited the reaction, manufacturing residue on wells that inhibited the reaction, and so forth.  Positive control reactions that let you verify the reaction components and conditions are all working can help troubleshoot more quickly.

Actually, we have already tried to perform other PCR amplifications and those reactions were succesful. Seems that it is not an issue of the PCR mix or impurities within the tubes. We have also performed a "PCA" with only 2 overlaping primers, and the results were similar to the ones posted here. I am starting to think that our HiFi Polymerase buffer leads to lower melting temperatures compared with NEB Q5 (closer to Phusion polymerases), so maybe trying with a Toucdown PCA could worh it.

Also could be that the resolution of EF gel is not enough and the "blurred spot" are multiple bands. We are going to try running the products again on a well performed 4% agarose gel and see the results. We are also planning to perform a second PCR only with outer primers using the former PCR product as template and see if some amplification occurs.  We will keep this thread updated.    Thank you for all the wise advise Armand!

It seems like you've got things covered -- good luck! I know how frustrating it can be when a supposedly simple reaction doesn't work.


text:
What book teaches you about endogenous retroviruses
I'm interest in ERVs as evidence for evolution and want to learn more about them.

The Sverdlov book is from 2005, and much work has been done in the 15 years after that. Here's a more recent review article with many useful references:
Escalera-Zamudio M, Greenwood AD. On the classification and evolution of endogenous retrovirus: humanendogenous retroviruses may not be ‘human’ after all. APMIS 2016; 124: 44–51. PMID: 26818261 DOI: 10.1111/apm.12489

can you please add appropriate links (PubMed, DOI, etc.)?

Try this one:
Retroviruses and Primate Genome Evolution - Eugene D. Sverdlov
Hope you find this answer helpful.


text:
How does auxin-inducible degron technology make it possible to observe an immediate phenotype?
I am having trouble understanding this paper, which says

Protein knockdown using the auxin-inducible degron (AID) technology is
useful to study protein function in living cells because it induces
rapid depletion, which makes it possible to observe an immediate
phenotype.

How does protein knockdown allow immediate phenotypes to be observed in general, and specifically using AID technology?

I don't think the sentence is trying to say that protein knockdown allows immediate phenotypes to be observed in general. Rather, inducible knockdown does. What is your understanding of inducible knockdown mechanics (steps taken by researcher and expected effects)?

My current understanding is that inducible knockdown (in this context) is the use of a ligand (e.g. auxin) to control the speed of proteolysis of a given protein target. I want to understand why this is used and exactly what the purpose is? I am not so much interested in that paper itself, I just want a basic understanding of how the AID2 system works

In the future you should [edit] your questions rather than reposting substantially duplicate versions of the same question.


text:
higher-order evolutionary adaptations
Most adaptations are what I'd call first-order. Cats evolve better eyesight; redwoods evolve to grow taller; male cardinals evolve attractive bright feathers. All of these changes were selected for because they directly make the organisms and their offspring more likely to reproduce. But it seems like there is a fundamentally different minority of adaptations, which I'll call second-order. Second-order adaptations do not make organisms and their offspring more fit directly, but rather they make an organisms' lineage more quickly responsive to selective pressures. Sexual reproduction is certainly the best example. The primary evolutionary benefit of sex doesn't come from increasing immediate fitness. In fact, I'd argue that many organisms' fitness is reduced by the fact that they cannot reproduce without a partner. Sex evolved not because it confers fitness to individuals, but because it confers adaptability to lineages: sexually reproducing lineages are quicker to evolve to fill new niches and avoid new threats. This is why I'd call sex a second-order adaptation, because it seems to be a rare adaptation which improves the process of evolution itself rather than the evolving organisms.
Is my understanding correct here, that sex is a fundamentally different kind of adaptation from, say, prehensile tails? If so, are there any other documented examples of second-order adaptations? Is there more accepted terminology than "first-order" vs "second-order" for this distinction?
Also, can anyone think of a third-order adaptation or pressure? Does that even make sense?
Possibly related: this post. But to be clear, I'm not asking about epigenetics.

When you say "fitness" do you mean individual or evolutionary?  Because in the context of evolution it usually means the latter, which is defined by reproductive fitness.  Evolutionarily, organismal aptitude is secondary to reproductive.  That's why there's a often a distinction, or even discrepancy, between natural selection and sexual selection

@Punintended Even "reproductive fitness" defined as something like "number of offspring" or even "copies of gene in the next generation" is an operational definition of the overall theoretical fitness concept. It works as a good estimator in many common situations, but it's perfectly reasonable to think about it on a longer time scale over multiple generations.

@BryanKrause Sure, but owls' better eyesight is an organismal fitness advantage that increases the probability / frequency with which that organism procreates.  On longer timescales it absolutely makes sense to consider organismal fitness, but I'd call reproductive fitness the end goal because of creatures like salmon, which die shortly after procreating

@Punintended I mean reproductive fitness. Changing my list of first-order adaptations to include a clear product of sexual selection.

I think that you are talking about evolvability (as I see it).
Sex is indeed a sort of a meta-adaptation, see e.g. The Evolution of Sex by John Maynard Smith. The math for this is rather well developed at this point.
In terms of higher order effects like e.g. sex, I think that you are really talking about ideas like evolvability, and questions about constraints on paths over high-dimensional fitness landscapes. Examples of this might include the evolution of genome structure, and the idea that certain genome architectures are more conducive to generating novel variation. A specific example (though one could argue about it) would be V(D)J recombination's role in the adaptive immune system.


text:
What determines the physical appearance of a tangible amount of bacteria or viruses?
As in the title, I was wondering how would feel an amount of one type of bacteria or virus, big enough to have a tangible size of the sample. What color, state (liquid, solid), textures, smell ecc. of the sample would be.
Ideally I would consider only the bacteria or virus, and none of their possible byproducts, and without any medium where they normally live in. Just the organisms in a tangible amount.
Therefore: why a set of bacteria will look like that? Why, for example, some are fluffly molds, others looks like a dough and so on. Is this representative of the physical structure of the bacteria?

Lab-grown E. coli is kind of a light-medium brown color, and smells like... E. coli. I don't know how to describe it. It's kind of squishy if you play with it, which I wouldn't recommend because you just used a lot of media to grow that much. I imagine it would get hard(er) if you dry it out, but I've never fully dried a pellet that big, just used it for protein purification.

It's going to ultimately depend on just how much you have. I'm not really seeing the practical reasoning behind this question, though. Can you explain what is directly motivating your question, and perhaps narrow it down substantially?

It has absolutely nothing practical. It is more philosophical. I've read somewhere that the total amount of covid-19 in the world is estimated to be some hundreds of grams, and I wondered how that would look like if all gathered. Question is then extended to bacteria as well. In other words, is exactly in line with the "what-if" questions.

@BryanKrause I thought you were going to refer to this xkcd, which is even more on-point.

@jakebeal Ah, had forgotten that one, nice!

@jakebeal there is always a relevant xkcd.

I was expecting a scientific answer. But I've got an equally valid xkcd link. Amazing! If that is true, if they look like that, I wonder if viruses are actually wet, or the "wettiness" is just how physically look like just the sheer amount of them. After all, water is not wet, if you take a bunch of molecule at a time. Actually, the concept of wet it would not even exist at that scale. Like a pool full of small balls: they look wet if you are big enough compared to the balls. Who knows if this applies here too. Should I move to stackexchange chemistry? :D

Is this really a question about a problem in biology at the standard of a site for professionals and serious students of biology? Or is it just idle curiosity about an unnatural situation to elicit a “fancy that!” response. Are you going to apply the information in any way? Do move the question to SE Chemistry — I imagine they will tell you what to do with it.

@David it is just idle curiosity. Moving to a place to know what to do with it, it would not help, as there is no practical reason behind. I am more active on electronics stackexchange, afaik over there humble curiosity for the sake of it is appreciated - when there is an effort shown. in this case, I did not know how to prove such effort, being illiterate in biology myself. for sure, I did not wanted to let anyone lose their time. my apologies if that was the case, although very unintended!

I am afraid that Electronics, Biology and, one would imagine, any other SE have the same statement in the Help on questions not to ask "You should only ask practical, answerable questions based on actual problems that you face. Chatty, open-ended questions diminish the usefulness of our site and push other questions off the front page." There is also the injunction "inspire answers that explain “why” and “how”" — describing the appearance and feel of something is not it. Try dried yeast in the supermarket or wet yeast in a baker's.

@David I understand now. I think the edit is more representative and more meaningful of the original question. If necessary, I will ask a new one.

There is no one answer to this question, any more than there is a single answer to the question of what color, texture, or size a mammal is.
To get a sense of some of the diversity out there, the American Society for Microbiology has a nice gallery of bacterial colony morphology, showing that in most cases, you end up with basically variously colored and shaped blobs of snot-like substance. At a larger scale, some microbial mats are formed of bacteria, and can form more fibrous mats bound together by extracellular substrate.

As mentioned in another comment, I wonder if when the sample looks "wet", is just an effect of the amount of the bacteria, or they are actually wet. Again, because the concept of wet would not exist if taking water molecules individually, maybe with bacteria is the same. I think all depends on the extracellular substrate here mentioned.

I'm not sure how meaningful it is to attempt to separate an organism from the context in which it normally lives in this manner. Consider the fate of deep sea creatures brought to the surface.

Meaningful not quite. I thought more from a physical point of view. I began to work with e-ink displays which are using very small spheres. That made me think over different type of simple particles how result at a bigger scale, just with those particles. Then the curiosity was steered toward complex, not obvious structures, like bacteria, cells or viruses. To keep the same analogy, the thought was considering just the living creature, but in neutral atmosphere - therefore is a pure hypothetical situation, where a physics can answer, but physics are unaware of living creature dynamics.

Indeed the example of the fish makes sense, it cannot be considered out of the deep sea, neither the concept of (perceived) consistency of an object might look the same in such extreme pressure. Nice catch! But I think hypothetically bacteria have a theorized "consistency" at our pressures, so I thought it would be possible to imagine it (like in the xkcd comic) - hence why I asked biologists, not chemists.


text:
Why does more melanin means harder vitamin D production if melanocytes lie deeper in the skin than keratinocytes?
From my Googling, I understand that keratinocytes are primarily responsible for generating vitamin D from UV rays, and melanocytes are for producing melanin to block UV rays. However in lots of skin diagrams I've found, such as this one, melanocytes lie deeper in the skin than keratinocytes. Wouldn't it follows that no matter how much melanin you have, it shouldn't be any more difficult for you to generate vitamin D, given that keratinocytes are more superficial than melanocytes, so vitamin-D making with keratinocytes should happen before UV blocking with melanocytes?

In your googling about melanocytes have you also read what happens to melanine after it is produced in melanocytes?

@BagiM There's this sentence, "Once synthesized, melanin is contained in special organelles called melanosomes which can be transported to nearby keratinocytes to induce pigmentation." (https://en.wikipedia.org/wiki/Melanocyte#Melanogenesis). But what does that mean? Does melanin transported to keratinocytes "cover" them up, preventing them from making vitamin D or something?

Now that you noticed term melanosomes, you can google images with "melanosomes" to see how are melanosomes distributed in skin cells. Searching for "melanosomes racial" should give you some images highliting differences in melanosomes distribution between skin types. Sadly, many general skin section diagrams show melanine distribution in caucasian skin as default, so you need to be a bit more particular/persistent in your search.


text:
Is there any reliable data about the correlation between the size of a species and number of individuals that belong to it?
I'm curious to know if such a collection of data exists, so I could visualize it with a graph, and see how humans compare to other spieces of similar size.

I don't think this question is meaningfully answerable, since the number of individuals that belongs to a species changes dramatically over time as its environment changes. Consider for example, the change in the population of the passenger pigeon during the past 200 years.

@jakebeal, I think that any graph/data is accompained by the year(s) it was collected.

I think that you are interestd in scaling laws https://physicstoday.scitation.org/doi/10.1063/1.1809090#:~:text=In%20biology%2C%20the%20observed%20scaling,the%20mass%20of%20the%20organism.

There might be something in the field of Macroecology, e.g. J. Brown's Princeton Monograph (??) on the topic ...

What exactly do you mean by the “size of a species” and how could it possibly be different from the number of individuals that belong to it?

@Wrzlprmft help me reword it. I mean the body size of the (average) individual belonging to that species.


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Gene regulation and epigenetics in specialized cells
Gene regulation is aided by epigenetics. Epigenetics determines which genes are turned off and which are switched on, and it varies throughout our lifetimes. Is it feasible that epigenetic modifications switch off the genes that determine whether a muscle cell or a neuron is a muscle cell or a neuron? I have searched this question but I could not find an explanation.

This and this may be of interest to you.

Correct me if I am wrong but it seems you are asking 'do epigenetic mechanisms influence cell fate/determination?'. If this is your question, the answer is yes. Epigenetic modifications play a key role in 'deciding' what type of cell a given stem cell will differentiate into. Here is some more information: https://www.nature.com/articles/pr2006122


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How is the possibility of beneficial mutations ensured in the genome?
To ensure natural selection and variability, the genome must have a structure in which the occurrence of beneficial mutations has a high enough probability. But how is this ensured? The space of possible genome configurations (even if we are only talking about "used" regions) is enormous. And the subspace of useful configurations is most likely negligible. That is, the likelihood of a beneficial mutation is extremely small. In this case, how does the genome provide the opportunity for beneficial mutations, which, in turn, provides for infinite evolution?
I want to add that I myself am an ardent supporter of the theory of evolution, so the question is no trick.

I think you might find this useful reading - it should answer some of your questions http://www.lifesci.susx.ac.uk/home/Adam_Eyre-Walker/Website/Publications_files/EWNRG07.pdf

OP It is not. @user438383 If you could compose an answer summarising the key points of the paper you cite, I think that would make a useful contribution to SE Biology.


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Need help identifying spider
I have been trying to identity this spider and have found nothing similar. This is the second I have found, this being the smaller at about 2cm. I want to know what kind of spider this is and if it is potentially dangerous to myself or my pets. June 2021, NW Turkey, fourth floor balcony. Thank you

A picture of the eye pattern might help with ID.

Looks to me like one of the Laceweavers: Amaurobius or something along those lines.  They rend to be fairly plain, powerful-looking ground-hunting spiders, and often have a dark reddish-brown carapace, with a dark, weakly patterned abdomen.  From what I can see of the eyes, they're consistent with that..  Unfortunately, the spider has been dead long enough to leave me uncertain, especially because my knowledge of European spiders is a bit limited.  It's definitely not a Mygalomorph tarantula, though.  No matter what, it's not one of the problem biters.

I agree with @JohnRobinson that Amauribidae is a good possibility, that it is Entelegyne (not Mygalomorph), and that its current (dried-up) state makes it hard to be sure of Family.

The spider looks very similar to Tarantulas. They are not harmful to humans but can show allergic reactions in pets when bitten by a spider.
Check out this https://en.wikipedia.org/wiki/Tarantula.

"They are not harmful to humans but can show allergic reactions in pets when bitten by a spider." Actually not only to pets and when bitten - their hairs, especially on the legs, can cause respiratory and dermatologic irritations to humans and pets..

This is not a tarantula or even in the Mygalomorph infraorder.

You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion, which is not appropriate for this site. Please consult the [help] starting with [answer] for details of what is expected.


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Why does (insulin induced) hypoglycemia stimulate ADH secretion?
Intuitively, I understand that ADH (Anti Diuretic Hormone) is responsible for maintaining osmolarity, and increased serum osmolarity is a stimulatory factor for its release-- ADH increases water reabsorbtion in the collecting ducts and DCT (Distal Convoluted tubule) of nephrons, thus decreasing the osmolarity back to normal.
But, apparently, (insulin induced) hypoglycemia also stimulates ADH secretion.
If it were hyperglycemia, it could be explained on the basis of increased osmolarity, as I have done above. I originally assumed it was a mistake in the standard book, but a quick Google search revealed several papers confirming what the book states. I still couldn't find an explanation though, most of these articles just state the observation.
Here are two of them:

https://www.jci.org/articles/view/114626#:~:text=JCI%20-%20Insulin-induced%20hypoglycemia%20stimulates,blood%20of%20conscious%2C%20unrestrained%20rams.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC296631/

Both of these also point out that Insulin Induced Hypoglycemia causes an increase in ACTH secretion. (I am not sure if that is relevant here, though.)
Also, does "insulin induced" hypoglycemia have an added significance over hypoglycemia?


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How to calculate the probability that a mutation occurred?
According to the internet, there is a 7% chance that two brown-eyed parents will have a green-eyed child. However, Dominance says that it is impossible for this to happen. Is the internet correct? If so, how is that 7% chance calculated?
source: https://www.mamanatural.com/eye-color-chart/

The "internet" is not a source. According to who on the internet?

"The internet" and "Dominance" are pretty vague sources. It'll help to specify the species and gene(s) involved.

Sadly the site you referenced is not scientific. There is no scientific basis for a claim that "there is a 7% chance that two brown-eyed parents will have a green-eyed child".  It is correct that multiple genes determine eye color, and the effects of some depend on the versions (alleles) of the other genes present, so predicting eye color is not as straightforward as it might seem.

Not to mention that it will depend on the specific family tree you are looking at and how many ancestors with different eye colors you can find in that tree. I'm sure there will  be combinations that result in a 7% chance. But there will also be various others.

https://www.mamanatural.com/eye-color-chart/ this is the source


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Is this a real "double microscope" with two stages and two sets of objectives? Is it used in biology?
In this US late night TV broadcast1 a set has been created with some "science objects" for visual impact, and right in the center is an unusual looking optical microscope.
The bottom looks like two separate microscope bodies, each with its own stage and objective turret, but on top there is a long optical block which presumably contains several mirrors or prisms and the illumination system, topped with a binocular eyepiece.
Question Is this a real "double microscope" with two stages and two sets of objectives, as opposed to something that has been created for TV visual impact alone, and is this or something similar ever used in biology?
 (cropped, zoomed and sharpened)

1Jimmy Kimmel Live, June 2, 2021

For me this doesn't make sense. Two sets of oculars is not uncommon in a teaching environment but the other way round?'

@Chris a "comparative biology microscope" perhaps?

That could work. Use two samples and then overlay images.

@Chris: But far easier to do it with two scopes with digital cameras, feeding the images into a computer.

@jamesqf four pieces of equipment (microscope, camera, computer, monitor) is not always abetter solution than one; some folks really prefer looking through a microscope directly than watching it on TV in a brightly lit room. The eyepieces may offer a 50° apparent FOV with black everywhere else, whereas staring at a monitor might offer half of that or less plus a room full of distractions. Imagine buying a nice pair of binoculars then putting a camera on them and viewing through your laptop, nobody does this because it's absolutely worse than simply looking through the binoculars.

@uhoh: I suspect the reason people don't put digital cameras on binoculars is that they don't want to carry the laptop around in the field.  As for the folks who prefer looking directly through the microscope, I would guess they don't wear contacts and/or suffer from eye floaters.  And then there's the issue of cost: unless someone else is paying for your equipment, an off-the-shelf microscope & digital camera are likely to cost a lot less than a special-purpose dual microscope - plus you can use them for other things.


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Asking for identification of biting insect

Inaturalist says it's a thrip, but my photo isn't very clear and inaturalist tries its hardest, but it can't positively identify everything, and I want to make sure it's not a flea or something else. I do know that thrips feed on the moisture of plants, and that if it is a thrip it likely mistook my bright yellow pants for a flower.
I have bites all over my legs, but mostly the left. Some bites on my midsection but surprisingly few. No bites on my arms. The bites on my legs are mostly clustered together. Anyway, when I pulled it off of my leg, it jumped out of my hand. I came back after showering to find it on the inside of my pants. At the cuffs?/bottom part of the legs of my pants, there were a lot of brown and red smears, and there weren't any bites on that part of my legs. I know that's indicative of bed bugs, so I'm worrying about that too. I need to check my mattress.
I'd argue this is still probably pretty funny.
The location is southern US. The bug is long and small. The light glints off of it. It would have been on me since this morning; I slept from probably 8 AM to 7 PM.
Mom gardens in the yard, though I haven't recently been out there. We also have a dog recovering from surgery, who went through some complications which caused her to bleed and get pus on the floor, which has only been spot cleaned, not bleached yet. She was given preventative flea meds like a month ago. I also cleaned my old beanie babies a few days ago, and while I was doing that a jumping bug landed on me, but it might have been coincidence, because I have been seeing jumping bugs on it long before that. They're dark, long, and the light glints off of them. Which means they're probably fleas, but I don't get a good look at them, so I don't know. Could still be thrips.
Thank you, in advance.
Edit:
The size is tiny. Smaller than a fingernail, but big enough to see. Mom works at an animal hospital; she said she could have definitely brought a flea home. I think it probably is fleas, but I'm still not sure. I'm used to them being smaller than this and thin. The ones I've seen are tiny and round and black

More bugs! On scenic my pants.

Fleas have a very characteristic shape, even when they are squashed they look quite round at the back end, sort of like a flat tear-drop shape. They are also quite thin  when looked at from the top, so I would guess that this is a flea. If you have one, you likely have many.

Does this answer your question? https://biology.stackexchange.com/q/56989/16866

Thrips fly; fleas jump.  The picture is certainly ambiguous, but I'd probably lean flea.


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How to identify plasma cells that only produce monoclonal antibodies?
I am studying the procedures of forming hybridoma cells for generating a large number of monoclonal antibodies.
Before the procedure of fusion (with multiple myeloma cells) happens, I would like to ask how to ensure all the plasma cells in the cell extract only contains those which produce monoclonal antibodies only but not polyclonal antibodies?
I have searched in Wiki, and it says

identifying antigen-specific plasma/plasmablast cells (ASPC) that produce antibodies specific to an antigen of interest

I would like to ask what methods are available for us to do this identification?
Thank you.

You don't do this before the fusion, you do it afterwards. First you make the hybridoma cells, which are then seeded as single cells into multiwell plates and cultivated to get enough cells for testing and further culture. This way you get only one antibody type produced per well (which is coming from a single clone, hence it is monoclonal) which then can be isolated and tested for antigen specificity.
For a schematic see the image from this publication:

Oh thanks, so using my words (to clarify my understanding), can I say: putting individual (different types of) hybridoma plasma cells into different wells, so 1 type of cell in 1 plate --> 1 specific antibody (hence prevent polyclonal Ab formed since there are no signalling of 1 cell to multiple plasma cell lines to produce them)?

And may I ask is the purpose of screening after fusion is to make all of them immortal before culturing (which takes a relatively long time)?

@Questions Your wording "...there are no signalling of 1 cell to multiple plasma cell lines to produce them)? " is confusing to me - what do you mean by "signaling"?

@Questions The purpose of screening is to identify which clonal line is making a desired antibody - remember each clonal line (each well) makes a different antibody since it is descended from a different B cell. The immortalization has already happened from the fusion with immortal myeloma cells.

@Armand Thanks for clarifying, now it is very clear to me :) and sorry that I have used the wrong phrase since I just want to confirm that in individual wells, there are no other plasma cells present to interrupt.

@Questions Sorry for the delay, I had other stuff to do. You do the screening after the generation of the immortal cells because you can expand these (theoretically at least) forever. And generation of this cells is nothing which is 100% effective. This way you screen cells which are immortal, can be used for antibody production. If you do it the other way, you cannot be sure to get immortal cells from your screened cells.


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Is this a local insect?
The monster below got into my house today (west of Paris, France). It is about 3 cm (1.2 inches) long.

I have no idea if this is a local insect that I would then let free, or some invasive species I will kill (we have from time to time alerts about invasive insect species (especially mosquitoes) that put in danger the local ones)

Incidentally it looks like it has a couple of parasitic mites on its legs

@bob1: ah, I thought that was dust (she spent sometime in the house)

I don't think those are parasitic mites - I think they are pseudoscorpions - maybe hitching a ride to new homes?

I have no expertise in (French) insects, but this looks like it might be a crane fly (family: Tipulidae) in the genus Ctenophora.  The larvae of these flies feed on decaying wood, so a lack of (partially) dead trees or other dead wood in your vicinity would suggest this is not correct.
The hunched-back with long legs are suggestive of the crane-fly family and the V-shaped groove on the back more-or-less connecting the wing-bases is (according to the wikipedia article) characteristic of this family.
In particular, this looks quite similar to many pictures online of the Cone-horn cranefly (Ctenophora pectinicornis), which is found in your area

Image by Margaret McLoughlin.
My understanding is that the simple antennae indicate that this is a female — males have feathery antennae.

Crane fly was my thought too. Looks like a case of mimicry with a wasp/bee as well.


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How can I learn botany/plant ID by myself?
I am interested in sources and methods regarding botany and plant ID, and being a self-taught person. Textbooks, sites etc.
Thank you all in advance!

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Your local public library should have books, including field guides to local plants.  For a more general view, there are lots of on-line resources, for instance a couple of OpenStax texts on biology: https://openstax.org/subjects/science

Thank you for the useful answers!

Really, start with identifying the most common plants in your area, especially weeds. try to learn family as well as genus and species - then you will see similarities within families. When I was a horticulture student I learnt ten plants each week.


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Concentration of active ingredient
For some time now, I have been wondering why, when a tablet is taken, the concentration of active ingredient undergoes an exponential decrease after the maximum concentration value in the blood is reached. For the model I refer to see.
Are there any biological reasons for this, that someone with no biological background is able to understand?

Exponential decay is a commonly observed phenomenon in nature where the rate of decay is directly proportional to the amount of stuff you start with. If you have twice as much stuff, it decays twice as fast, etc.
Another way to say it is that every molecule has an equal and independent chance of decay.
Radioactive decay is often taken as the "standard" model for exponential decay. Any unstable atom has a chance at every moment in time to decay to a more stable state. Other atoms in the universe don't influence the rate, it's just an intrinsic property of each separate atom that it has some chance to decay.
In pharmacology, the exact mechanism depends a bit on the molecule, but let's imagine a drug that's metabolized in the liver. If the drug is in a relatively low concentration (as most drugs are once they reach the bloodstream) as are it's metabolites, then the rate limiting step is the chance of an interaction between a molecule of the drug and whatever enzyme catalyzes the reaction to the metabolite. If the concentration of liver enzymes remains constant, and the low concentration of drug means there is no appreciable saturation of those enzymes, then you can think about this chance interaction as being an independent chance for each molecule of the drug. If you have twice as many molecules of the drug, you have twice as many chances for them to interact with the enzyme for a given time step.
For something filtered by the kidney, you could think exactly the same way: it's the chance of each individual molecule being filtered into the urine. Twice as many molecules means twice as many chances to end up in the urine.
Not all drugs follow this pattern. Few drugs are in high enough concentrations for the drug concentration to matter, but some are. Ethanol, for example. Other drugs have more complicated metabolic fates, induce enzyme activity that influences metabolism, or accumulate as waste products that reduce decay. There are also drugs that partition strongly into other compartments and you might need to consider different routes in which a drug might eventually leave the system.


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How are mRNA vaccines spread across the body?
Covid mRNA vaccines are injected into the deltoid. What is the process in which they spread from there to the rest of the body? Would there be a better immunization reaction if the second dose is injected elsewhere?

Why do you think the vaccine would need to spread to the rest of the body?

Mostly because of reports from Israel, US army and UK on miocardatis which may be linked to the vaccine in younger patients (although in the UK it is in low numbers compared with the others, but the age of the patients is older). If it is related, I'm trying to ascertain whether it could be from the mRNA instructions

https://meta.stackexchange.com/questions/66377/what-is-the-xy-problem

@KyuriOseetea The vaccine doesn't spread; instead, the immune system spreads its responsive elements.

https://www.docdroid.net/xq0Z8B0/pfizer-report-japanese-government-pdf#page=16
Pfizer's study for the Japanese government, cp. 2.6.5.5B. PHARMACOKINETICS: ORGAN DISTRIBUTION e.g. ovaries 23, testis 0,3 after 48 h.

The short answer to how vaccines are spread around the body is, quickly.

What is the process in which they spread from there to the rest of the body?

The reason vaccines are often delivered into muscle tissue is because muscle tissue is highly vascularized with both blood and lymphatic vessels. Immediately after a vaccine injection, the delivery vehicle (probably lipid nanoparticles or a viral vector) will quickly start diffusing into the blood, where it will be carried up to the heart, and from there begin spreading around the body (a lot of it ends up in the liver). Somewhat less quickly, in the lymph it will essentially start to generate an immune response immediately as it drains into lymph nodes and begins circulating throughout the lymphatic system (note the the desired immune response won't start until the genetic component of a vaccine has entered nucleated cells and has started being translated into the desired viral antigens).

Would there be a better immunization reaction if the second dose is injected elsewhere?

Don't know if I can definitively justify saying "no" to this question, but probably not. Muscle tissue seems to be the best injection site for vaccines. Deltoids are probably the best muscle because there's a lower chance of missing the intended injection site compared with some other muscles (e.g. glutes). And the systemic spread of vaccine components starts happening pretty fast after injection. In one animal study, researchers surgically removed a leg muscle 1 to 10 minutes after injection and still didn't prevent the related antibody response, or even really reduce it compared to animals with the muscle left intact.
Assorted References:
mRNA Vaccines: What Happens
Inadvertent subcutaneous injection of COVID-19 vaccine
The importance of injecting vaccines into muscle
Different patients need different needle sizes
Unmodified mRNA in LNPs constitutes a competitive technology for prophylactic vaccines
Differential dependence on target site tissue for gene gun and intramuscular DNA immunizations (1997)


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How long after taking a vaccine shot (Oxford–AstraZeneca) could an individual test negative for antibody (IgM)?
What I know so far about the way this vaccine works is that by encoding virus' biological signature into the vaccine and injecting it into a subject, the subject's immune system would learn to recognize the virus and develop anti-body against it. Then next time the virus wouldn't break the subject easily because the protection of anti-body.
After getting to know the theory, it looks certainly after injection, it would certainly leave some virus signature (antibody) into the body. During the early stage of virus production one would probably get IgM+ / IgG+ and after a while becomes IgM- / IgG+.
So my question is, how long does it take for an individual to get IgM-?
About IgG and IgM test (quote from here):

IgM and IgG are immunoglobulins produced by the immune system to provide protection against SARS-CoV-2. Anti-SARS-CoV-2 IgM and IgG can therefore be detected in samples from affected patients.

IgM+ / IgG+ : Recent infection with SARS-CoV-2
IgM+ / IgG- : Recent infection with SARS-CoV-2
IgM- / IgG+ : Previous infection with SARS-CoV-2
IgM- / IgG- : No infection or not enough detectable antibodies in the early infection

According to this paper, IgM antibodies can last until week 12 after infection by the SARS-CoV-2. Presumably, in case of vaccination, this time should be a lot shorter since the amounts of antigens produced are much less. It is suggested by the U.S. Centers for Disease Control and Prevention (CDC) that antibody test should be taken at least 2 weeks after each shot.
Resource

Rawat K, Kumari P, Saha L. COVID-19 vaccine: A recent update in pipeline vaccines, their design and development strategies. Eur J Pharmacol. 2021;892:173751. doi:10.1016/j.ejphar.2020.173751

https://creakyjoints.org/living-with-arthritis/coronavirus/covid-19-vaccines/antibody-testing-covid-19-vaccine-immunocompromised/


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Trying to identify a Spider found in rural Missouri, USA
I am trying to identify this spider found indoors in a rural area near Kansas City, Missouri. I cannot recall seeing one like it in my 14 years of living here but I have now found 3 inside in the past week. The one in the attached photo I found in my bed when I woke up. I would estimate that it is 2-3cm, legs included.

Sorry to be so long; I just came across this question.
There are a couple of clues as to the identity of your spider - the two-toned color pattern, with mahogany legs and cephalothorax, and grayer abdomen being the most important one.  The other is that you found it in your house.  It's been my experience that these spiders are commonly found in houses at two times of year - the adult males in the spring, and the adult females in the fall.
The most important clue is hard to see in your original photograph, but I took the step of lightening it with the Photo app, to let me see the front of its cephalothorax (see below)

What you can see is that the eyes are arranged in a fairly straight line across the fairly flat face.
The other locally common two-toned (red-and-white or red-and-grey) spider, Dysdera crocata, has a very different face.  Dysdera is a streamlined, 1950s style racing spider, with forward projecting chelicerae and a pointed-looking front end (see below)

You'll notice the pointy front end, and the way the eyes are arranged in a tighter, almost clustered, curved line.
Your spider is one of the Flat-faced Sac Spiders in the genus Trachelas.  I'd say it was probably T. tranquillis, but there are a number of western species, and I'm not sure where the ranges go to.
Here's a reference photo of a male Trachelas species to compare with yours:

Here's the Bug Guide link to Trachelas:
https://bugguide.net/node/view/26206
Note that colors and light/dark shades are not necessarily going to be the same in photographs as in real life, even above that Trachelas (like Dysdera) shows a range of color from white to grey abdomen and from red to almost brown cephalothorax and legs.

Excellent answer.

It might be this one:Dysdera crocata
(Woodlouse Hunter)
https://spiderid.com/spider/dysderidae/dysdera/crocata/
more pictures of this spider from different places in the link below.
 https://spiderid.com/spider/dysderidae/dysdera/crocata/pictures/
I know this is a bit thin as an answer but i know very little about spiders in the US,if anybody has knowledge about this spider please feel free to add the information.

I think it’s Metaltella simoni. Check it.

Image from Wikipedia

We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Answers that don't include explanations may be removed.

Hi @Mistake, I've added an image to your answer. If you can find a better image, and perhaps a reference that would be nice.


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How long will traces of mRNA vaccines stay in the cell?
Suppose a valid administration of an mRNA vaccine (e.g. Pfizer / Moderna), lipid nanoparticles with the mRNA instructions enter the cell, the lipid particles will merge with the endosome and the mRNA will release to the cytoplasm (do not enter the nucleus) before finding a ribosome.
How long will any of this stay in the cell? Is it a once off and after the production of the spike protein the mRNA evaporates from the cell? and what about the lipid nanoparticles?

Although specific time is not yet clear, the coronavirus mRNA vaccine is expected to be degraded within hours after translation, according to Rebecca Dutch, Ph.D., a virologist at the University of Kentucky.

"It’s unclear how long this degradation takes. With regular mRNA, it’s within hours. The special coating involved with mRNA coronavirus vaccines may make this take a bit longer, but how much longer is uncertain."

After entry into the cell, the LNP coated mRNA is taken to endosome, where mRNA undergoes endosomal escape and enters the cytoplasm. Eventually, LNP will be trafficked to and enzymatically degraded in lysosome, or secreted from the cell via exocytosis.
Resources

https://www.self.com/story/mrna-coronavirus-vaccine-questions

Pardi, N., Hogan, M., Porter, F. et al. mRNA vaccines — a new era in vaccinology. Nat Rev Drug Discov 17, 261–279 (2018). https://doi.org/10.1038/nrd.2017.243

Otegui, M. & Reyes, F. C. (2010) Endosomes in Plants. Nature Education 3(9):23


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What is the purpose of putting multiple blanks on a microplate reader?
I am new to biology and I saw that in the software that controls the microplate reader several targets are set, what is the purpose of this?

What do you mean by "targets"? Do you mean standards - things of known quantity used to compare your sample to? Blanks usually mean a control which has a baseline reading so that you know any value above this is "positive" for your assay (statistical significance needed!) - replicates help with this.