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Multiple clones Sanger sequencing analysis
I am doing a 96-well arrayed cloning. I have done Gibson, transformations and minipreps in a 96-well format, then sent out the plate for sequencing. Normally, I sequence 3-4 clones and check if the sequencing looks good manually with Benchling cause it has nice visualization tool that highlights mismatches but also displays sequence quality. Now I have to check the sequences of 96 individual clones. Obviously I can write a simple script that would do alignments and report the alignment quality. However, I am guessing there should be already tools available that work with Sanger clonal sequences and provide nice visualization for many alignments at once. Any recommendations for specific tools I should use?
Thank you!

I haven't personally used it but seqtrace seems to be targeted for this purpose. It seems to be able to do alignments and facilitates multiple trace file analysis.
I worry a little bit about not visually inspecting trace files for sequencing of clones, but I may be a relative dinosaur (about sanger at least).
Here is the abstract:

Modern applications of Sanger DNA sequencing often require converting a large number of chromatogram trace files into high-quality DNA sequences for downstream analyses. Relatively few nonproprietary software tools are available to assist with this process. SeqTrace is a new, free, and open-source software application that is designed to automate the entire workflow by facilitating easy batch processing of large numbers of trace files. SeqTrace can identify, align, and compute consensus sequences from matching forward and reverse traces, filter low-quality base calls, and end-trim finished sequences. The software features a graphical interface that includes a full-featured chromatogram viewer and sequence editor. SeqTrace runs on most popular operating systems and is freely available, along with supporting documentation, at http://seqtrace. googlecode.com/.© 2012 ABRF.


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Can this toad be approx 1cm long?
Recently the toad from this video has been identified as an American Toad inside this post in Reddit. The original video mentions it was filmed in White Clay Creek State Park, Newark, Delaware, USA.

Calculating the water's wavelength based on the sound yielded a value of 0.5mm. Using the image's ratios, the toad's length can be estimated. The result was 7mm. Yes, a toad being 7mm long.
The purpose of this question is to ask both if it effectively is a species of American Toad and if it's plausible for it to be 7mm long.
Thanks

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — photos must be uploaded (not links) — e.g. post stills captured from the video; 2) habitat information. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

source: Stack Exchange

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Could a mutation on neutral part of genome become deleterious?
I know that silent mutations are neutral because they dont affect function of the protein/gene, and a missense mutation would. But lets say both occur on a neutral portion, could one or the other become deleterious? I remember my prof stating that a mutation can become deleterious if on a neutral portion. I just dont remember what would cause this.
Thanks!

several related questions: https://biology.stackexchange.com/questions/73286/neutral-genetic-mutations-in-eukaryotic-cells/73293#73293, https://biology.stackexchange.com/questions/92575/how-do-we-formulate-the-mutational-load-for-junk-dna, https://biology.stackexchange.com/questions/8809/what-is-neutral-genetic-differentiation/92960#92960

@ManonValiquette can you better define "neutral portion"?  Are the "neutral portions" of genes the bases that correspond to the wobbly positions of codons? Is noncoding DNA considered "neutral" by your definition?

Of course. There are tons of ways this could happen. A trivial example:
CTA codon encodes leucine.
CTA --> TTA mutation will still encode leucine.
CTA --> CTT mutation also still encodes leucine.
By your definition, each of these mutations is "silent" or "neutral" independently.
However, if you combine both mutations, they lead to a TTT codon, which encodes phenylalanine aka missense mutation.
The fancy name for this kind of genetic interaction is "epistasis". THere are many other ways in which this kind of theoretically neutral mutation becomes non-neutral, but this illustrates it simply.

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


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why does water go from high to low osmotic pressure to decrease the size of the nucleus?
I am reading this paper "Volume regulation and shape bifurcation in the cell nucleus" (linked below)
https://jcs.biologists.org/content/joces/128/18/3375.full.pdf
I am confused by this sentence "During cell detachment, because the cytoplasmic osmotic pressure decreases dramatically, water flows out of the nucleus and the nuclear volume shrinks."
Since water flows from low to high osmotic pressure, I would have thought that this decrease in osmotic pressure of the cytoplasm would cause water to flow into the nucleus, not out of it. Why does the opposite happen here?
The article also states that the volume of the cytoplasm will decrease. So is this something to do with the extracellular space?

After reading a snippet of the article, it seems like you just found a simple mistake that wasn't caught during review, but really shouldn't cause much confusion in the context of the paper. It's clear enough from the preceding paragraphs what they concluded is happening. Cell volume is reduced after detachment, primarily due to water efflux. Because of that change, the difference in osmotic and hydrostatic pressures between the cytoplasm and the nucleus favors water flux from the nucleus to the cytoplasm, reducing the volume of the nucleus and causing it to shrivel.


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Are the y-axis values informative when performing biolayer interferometry?
I am currently reading  an this article by Alexandra C. Walls et. al.
I would like to ask a question about a graph that is being used in the article and I wanted to know if my analysis was correct.

I was wondering if for the Binding Response versus Time graphs of SARS-CoV-2 (panel A), and SARS-CoV-1 (panel B), can we infer that SARS-CoV-2 was more adept at binding to the human ACE2 because the y-axis has larger numbers than for SARS-CoV-1? If not, why not?

@EnlightenedFunky You cannot assume that a particular user downvoted you. Votes are anonymous and there is basically no obligation for a voter to explain their vote. However, I can understand that it is can be annoying as well as discouraging but it's better to ignore it for your own happiness.

I've tried to clarify what your question is about this figure, and to use an informative question title that makes clear what type of question this is. Please feel free to edit if you think these changes did not capture what you were after.

From the linked article:

We found that hACE2 bound to SARS-CoV-2 SB and SARS-CoV SB with respective equilibrium dissociation constants of 1.2 nM (Figure 2A) and 5.0 nM (Figure 2B).

An equilibrium dissociation constant (commonly called Kd) represents the propensity of a complex to dissociate into its constituent pieces.  A smaller value represents a smaller propensity to break apart, i.e. a stronger interaction.
So, yes, considering only the data presented, domain B from the SARS-CoV-2 spike protein shows a slightly higher affinity for hACE2 than the equivalent domain from SARS-CoV.  Note, however, that the authors are careful with their wording, and state in multiple places that the relative affinities of the homologous domains are comparable.

The SARS-CoV-2 SB engages human ACE2 (hACE2) with comparable affinity to SARS-CoV SB from viral isolates associated with the 2002–2003 epidemic (i.e., binding with high affinity to hACE2).

What's more telling are the binding constants (kon and koff) given in Table 1:

$$\begin{array}{c|c|c|}
\text{} & \text{SARS-CoV-2 S}^{B} & \text{SARS-CoV S}^{B} \\ \hline
\text{K}_{D} \text{ (nM)} & 1.2 ± 0.1 & 5.0 ± 0.1 \\ \hline
\text{k}_{on} \text{ (M}^{-1} \text{s}^{-1}\text{)} & 1.4 × 10^5  (2.3 ± 1.4 × 10^5) & 1.4 × 10^5  (1.7 ± 0.7 × 10^5) \\ \hline
\text{k}_{off} \text{(s}^{-1}\text{)} & 1.6 × 10^{−4}  (1.7 ± 0.8 × 10^{−4}) & 7.1 × 10^{−4} (8.7 ± 5.1 × 10^{−4}) \\ \hline
\end{array}$$
Values reported represent the global fit to the data shown in Figures 2A and 2B and the averages obtained from five (SARS-CoV-2) or four (SARS-CoV) replicates carried out with different protein preparations are shown in parentheses.

Note that Kd is the reciprocal of the association constant, Ka, which is equal to the ratio of the binding constants.
$K_{a} = \frac{k_{on}}{k_{off}}$, $K_{d} = \frac{k_{off}}{k_{on}}$
Since the values given for kon derived from the global fit are the same for SARS-CoV-2 and SARS-CoV, the observed difference in Kd is due to the different values of koff.  So, at equilibrium, SARS-CoV-2 SB and SARS-CoV SB will associate with hACE2 at the same rate, though SARS-CoV SB dissociates faster.

Can you explain how the y-axis values relate to Kd? I'm not sure this answer is correct based on what you've written here (you've explained what is written in the text, but not the figure). I'm also not particularly familiar with this technique, but I'm assuming the Kds come from a parametric fit to some aspect of the curves displayed and would depend on the spacing at different concentrations rather than the Y-axis.

@BryanKrause I understand and agree with your concern. The problem I've encountered in trying to better understand how binding kinetics are derived from the raw Δλ is that the software associated with biolayer interferometry appears to be proprietary.  All the "guides" and literature I find give the sequence of operations in the software GUI without stating what those operations do.  I'll update my answer if and when I find better resources.


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How do *Polistes sulcifer* (cuckoo paper wasp) eggs hatch so quickly?
The Polistes sulcifer wasp is a brood parasitic species, which parasitizes colonies of the paper wasp Polistes dominulus. During an extremely brief time window in the spring, just before the P. dominulus workers have emerged, the P. sulcifer female will invade a P. dominulus nest. Once inside, it will kill or evict the host queen, ensure its cuticle hydrocarbon profile will not lead to its being attacked, and then lay its own eggs. It will rely on the host workers to tend to these.
(Note: I don't know whether it just alters its own hydrocarbon profile, or whether it also alters that of the nest. It's tangential to this question.)
The P. sulcifer wasp needs to time its attacks precisely. If it invades too late, the workers will have emerged and the colony will have a lot more wasps to defend it. If it invades too soon, there will not be enough host workers emerging to tend to its brood, especially if the host queen has not laid many eggs. P. sulcifer itself does not have a worker caste, and so is entirely reliant on host workers.
Research published in 2004 (paywalled, unfortunately) showed that the parasite wasp eggs took an average of 5 days to hatch after being laid, with the minimum observed being 3 days. This was in marked contrast to the host eggs, with average time 8.6 days in an unparasitized host colony, and 9.1 in one which was parasitized. Likewise, the parasite larval stage was much shorter, lasting an average of 9.8 days as opposed to 16.6 for host larvae in a parasitized nest (14.8 in an unparasitized colony) and the pupal stage also slightly shorter.
The parasite larvae were able to attract more attention from the workers than the host larvae - including being fed more often - which would appear to offer an explanation for the faster larval development and shorter larval/pupal stages. But this does not explain the shorter egg stage. Rapid development is clearly advantageous in terms of maximising the number of offspring produced, so a shorter egg stage is advantageous to the parasite, but the mechanisms behind this short incubation period are not known.
In the famous example of an avian brood parasite, the cuckoo, the parasite eggs also hatch more rapidly than the host eggs. This is, at least in part, because the female cuckoo holds the egg in her oviduct for an additional 24 hours prior to laying, at a higher temperature than an egg being incubated in the host nest. This gives the cuckoo egg the equivalent of a 30 hour head start on the host eggs.
In the aforementioned 2004 research paper, it was speculated that the wasp might use a similar mechanism, but this was not known, and no research into this had been carried out. A later 2006 paper also stated that no information was known about this, and I have been unable to find any further research on the topic.
Has there been any subsequent research into how P. sulcifer has been able to ensure its eggs hatch abnormally soon after being laid?
Sources - paywalled:
Cervo, R., Macinai, V., Dechigi, F., & Turillazzi, S. (2004). Fast growth of immature brood in a social parasite wasp: a convergent evolution between avian and insect cuckoos. The American Naturalist, 164(6), 814-820.
Ortolani, I., Turillazzi, S., & Cervo, R. (2008). Spring usurpation restlessness: a wasp social parasite adapts its seasonal activity to the host cycle. Ethology, 114(8), 782-788.
Sources - non-paywalled:
Cervo, R. (2006, January). Polistes wasps and their social parasites: an overview. In Annales Zoologici Fennici (pp. 531-549). Finnish Zoological and Botanical Publishing Board.
Cervo, R., Dani, F. R., Cotoneschi, C., Scala, C., Lotti, I., Strassmann, J. E., ... & Turillazzi, S. (2008). Why are larvae of the social parasite wasp Polistes sulcifer not removed from the host nest?. Behavioral Ecology and Sociobiology, 62(8), 1319-1331.
Other sources:
Davies, Nick B. (2015). Cuckoo: Cheating by Nature. Bloomsbury. ISBN 978-1-4088-5658-1.


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What is the current state of research on the relationship between sponges, ctenophores, and other animals?
I've been reading about the basal taxonomy of animals recently, and it seems as though there is some controversy surrounding the classification of sponges, ctenophores (comb jellies), and all other animals. One proposal has it that sponges form a monophyletic group, sister to all other animals. Another proposal is that sponges are polyphyletic, with the rest of the animals descended from some group of sponges or another. A third proposal is that in fact ctenophores are the sister group to the rest of the animals.
What does the current state of research on this topic look like? What are the arguments for and against each view? Is there a general consensus?


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Which ant/wasp species is that?
Anybody knows which species (or genus, family...) of ant/wasp is that?

It's from Brazilian Amazon (Upper Negro River, Amazonas state). About 2-3 cm long (about one inch), maybe. It was walking on the sandy road around noon. Don't know the month of the year.

I think this is a Cryptus wasp, and from the googling I've done it looks very like Cryptus leechi, but I don't know which parts of the world that's found in.

It looks even more like Cryptus rufovinctus. OP, take a look at the Cryptus species on this webpage: https://v3.boldsystems.org/index.php/Taxbrowser_Taxonpage?taxid=213691 and see what you think.

@Astrid_Redfern I'm not sure, but the waist on mine has two segments, and the abdomen seems more like an Aculeata.

@Astrid_Redfern The wing venation is different too.

What do you think of this Cryptus albitarsis : http://www.knowyourinsects.org/Ich1_Sarah.jpg The legs are the wrong colour, but I can't tell whether one part of the image I'm seeing has the extra waist segment.

@Astrid_Redfern No. The waist, the tip of the abdomen and the wing venation are all different.

Great photo! I see 12 or 13 segments total on the antennae, so not Ichneumonidae (includes cryptus) which have 16 or so.

@PolypipeWrangler Thank you! Does this also exclude the remaining Ichneumonoidea? I'm not sure, but to me its abdomen looks like Aculeata.

Given the presence of a petiole and postpetiole, this is most likely a winged ant (drone or queen), such as this similar one here:
https://bugguide.net/node/view/57281

Indeed it looks like an Attini ant, though the antenna does not seem to be geniculate, and the first flagellomere seems to be the same size as the others. But that's probably just an impression, because the photo is not so clear.

For this to be an ant, the antennae MUST be geniculate ("elbowed"), with the first segment the longest (see here for some identification tips); this is not true of the OP photo.

I wondered about this too, and if this insects antennae had a very short elbow.  I couldn't quite decide from the image

@ArthurJFrost, this is what I was thinking regarding the scape:
https://cdn.britannica.com/s:700x500/21/188721-050-3D55AD79/leafcutter-ant-species-fungus-substrate-Atta-cephalotes.jpg
Rodrigo I do agree regarding the flagellomere.  What an intriguing insect you've happened upon!

Regarding the very short elbow - take a look at the very short "elbow" on the antennae of the male Monomorium minimum in this picture: https://www.antwiki.org/wiki/File:Monomorium_minimum_queen,_male,_Austin_Texas,Alex_Wild(1).jpg . Then look closely at the antennae on OP's mystery specimen - the antenna that's further away does appear to have a noticeable joint of some sort near the head. Perhaps the angle of the shot obscures such a joint on the closer antenna too. Anyway, I think these could be ant antennae, though not that species.

There's a similar short "elbow" and eleven-segment-thereafter antenna on this Dacatria templaris winged male: https://www.antwiki.org/wiki/File:Dacatria_templaris_male,_South_Korea,_Minsoo_Dong.jpg . Though otherwise that's even less like OP's photo.

Could be some other winged male ant of the Monomorium genus?

The "elbows" on male Crematogaster ants are even shorter - see http://cle.fourmis.free.fr/male-crematogaster-2.html and https://bugguide.net/node/view/1327317/bgimage

The head and jaws seem too small and weak to be an ant. The heads of ants are usually more shiny also.

@PolypipeWrangler It might be a male ant. "Male ants ... can be identified by their smaller heads and longer antennae." (https://www.naturalresources.sa.gov.au/files/sharedassets/adelaide_and_mt_lofty_ranges/nrm_education/amlr-native-ants-teacher-pack-gen.pdf). Or "males ... have smaller heads with bigger eyes and straighter antennae." (https://askabiologist.asu.edu/explore/ant-anatomy). According to https://antark.net/ant-life/the-ant-family/drone-alate-ant/ "Drones ... look more like wasps than ants." See the silhouette-style pictures at https://antark.net/ant-life/the-ant-family/ .

To clarify: I currently think it is almost certainly a winged male ant (drone).


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Why Can't Muscles Push When They Return To Their Original Length?
I understand that muscles can only contract and shorten and thus can only pull, but why can't a muscle push when it relaxes and returns to its initial length?

Try to push something with a piece of string :-)  To push with something, it needs to be rigid.  Muscles aren't.

In effect, the "Push" does happen automatically when the muscle relaxes.
The muscle itself does not push and cannot push, but it sets off the connected bones from the adjoining joint/s after its contraction.
It's the same as firing a gun or a catapult or a rubber band - create big tension in the contraction or pull, and let go suddenly, and there is the Push, achieved on relaxation.

You are now answering a lot of old (and sometimes downvoted) questions. There is nothing bad on this per se, but please do not use the answer box to simply write a small comment below the question. If you have to add something, please add it but write real answer which explain something and add references. Since you are a new user, I also recommend you take a look into the help section on what is expected from answers here.This avoids deletion of your answers.


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Why is the current flow shown to be flowing from the negative area towards the positive area?
When I was studying the ECG chapter in the book "Guyton and Hall Textbook of Medical Physiology", I noticed something odd in one of the pictures:

As you can see the current is shown to be flowing from the area with a more negative potential towards the area with a more positive potential.
Also here's the part of the text that alludes to the image:

This process provides electronegativity on the insides of the ventricles and electropositivity on the outer walls of the ventricles, with electrical current flowing through the fluids surrounding the ventricles along elliptical paths, as demonstrated by the curving arrows in the figure.

How is this possible? Isn't the current supposed to flow from an area with a higher potential towards an area with a lower potential?

By convention, positive current is assumed to be the direction of flow of positive charges. The trouble is that in many common situations (like this one), the current is actually carried by electrons which are negatively charged.
It can be confusing. Blame it on Benjamin Franklin. The convention for current flow was based on his work, before anyone knew about electrons, protons, and ions.

So basically what is shown in the image is the direction of the flow of the electrons and not the flow of the current, correct?

Not literally electrons, the flow is mostly Chloride ions that direction, and Sodium, Potassium and Calcium ions the other way.


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Eukaryotic cell lysate-based protein expression efficiency
What is average efficiency of eukaryotic cell lysate-based protein expression systems in terms of (mg of protein expressed) / (mg of lysate) ?

This is nothing what you can determine that easy. The question is from what cells your lysate is prepared, how does your protein sequence look like (long or short and so on) and other parameters. You can have a look into commercial kits, which may give you a yield estimate, but this might not be true. Also: Functional protein or just total protein?

Total protein .


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The fastest vaccine developed is a mumps vaccine, which took 4 years. Where is the hope that we will find a COVID vaccine in less time?
I understand that doctors and scientists are working hard to find a vaccine, but is there a reasonable chance that we will find one in the time that scientists and politicians are suggesting?
I also understand that we have no choice but to socially distance and bithe our time to find a vaccine if COVID is anything like the flu, but what if it proves to be as hard as finding a vaccine for HIV? The first HIV outbreak occurred in the 1980s, and if I'm correct we still don't have a vaccine for it yet (even though we do have treatment for it so people could just live their life with it).
So my question is with all this in mind, how could there be a chance that we will find a COVID vaccine in less time? Is it just optimism, or is there actually reason to believe the vaccine will be produced say by the beginning of 2022.

@David With all due respect, I don't agree. The tour that you linked me to does not suggest this question is off topic. In fact, this question first came to mind when I saw a Biology.SE question asking why a COVID vaccine wasn't quick and simple. I wouldn't understand why vaccine development wouldn't be considered "general questions about biological concepts" as described by the help center. I also have an inkling that you misunderstood the question as musings of future success for the vaccine candidates. Instead, I was asking why a COVID vaccine could possibly take less than four years.

A question about a biological concept is of the type "what does the spleen do?", "How do eagles fly so high?", "How does insulin regulate metabolism?", "How does coronavirus enter cells?", "What determines an IgG v. an IgA response?"  Your question is about commercial drug development, presumably in a regulatory context as I imagine you are aware that vaccines are already in use in China and Russia. It might or might not be on topic in SE Medical Sciences, although they may question the preparation for the question given the widespread coverage of the topic in serious news media.

Expectations for accelerated vaccine development are based on two main points.

Groups have been working on vaccines for SARS-CoV-1 since 2003, and much of that work is applicable to SARS-CoV-2 (the COVID-19 virus). Here is a review article discussing work on SARS-2 vaccines based on work on SARS and MERS. One example, transgenic mice are available that express the human version of ACE2, the host receptor protein that allows SARS coronaviruses to enter a cell. These mice allow vaccine testing that is much more informative than cell culture tests, and weren't developed until 2006-2007. SARS was eliminated in 2004, so we can estimate it would take at least two years to develop an animal model for COVID if it wasn't already available.

Here is a diagram from the linked review showing timelines for traditional vaccine development and the accelerated SARS-CoV-2 vaccine development:

Several pharma companies have developed "plug and play" vaccine platforms which allow rapid manufacture of vaccine candidates once a molecular target is known. In this case, the target is the 'S' glycoprotein. Once the sequence that encodes for this target is known, it can be inserted into the platform and produced quickly.

Here is another diagram from the same review describing some of these platforms:

EDIT - I wanted to emphasize a third point: If you notice the "Production (at risk)" text in the accelerated development diagram, it means that pharma companies are producing large amounts of their vaccine candidate before testing is complete, and therefore running the risk that their warehouses full of product will be rendered worthless by bad outcomes in the clinical trials. Moderna had started production of their mRNA vaccine candidate by July 15 2020, so this gives them a several month head start if the trials turn out well.

Thank you! Your response was concise and answered my question.


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What does allelomorph mean?
Is there any difference between allele and allelomorph since most websites call them the same.
If they are same then why two different term?

Welcome to Biology.SE! Thank you for taking the [tour], but please also go through the [help] pages starting with [Ask] questions effectively on this site. In particular asking why synonyms exist is about language not biology. Also note that for "homework" questions, you are required to use the "homework" tag. (Note that "homework" can apply to questions even if they are not assigned as homework — in this case you question "addresses a basic biology concept that may seem trivial to biology professionals".) Thanks!

Ok , thanks would consider your points

Allele, allelomorphs - the common word in both is "Allele" - When Multiple genes code for a contrasting or similar traits/ or multiple genes in the same locus on homologous chromosomes can be qualified as an allele.
Now let's look at second word "Morph" - Adjective MORPHOLOGICAL meaning that - relating to the form or structure of things. Now I'm going to mix this word MORPH with another word POLY which gives "Polymorphic" (Meaning Many Shapes/Forms) - Polymorphism is the ability of an object to take on many forms. This is the same behavior that we could see in an allele. Let me put this polymorphism more specific to our topic.
Gene-Polymorphism -

A gene is said to be polymorphic if more than one allele of a gene exists within a population.

In addition to having more than one allele at a specific locus, each allele must also occur in the population at a rate of at least 1% to generally be considered polymorphic. - Wiki definition

Now comparing the definition of allele with this second point of Gene Polymorphism, we get Allelomorphs - Meaning that a single Allele taking different forms/ multiple occurrences within a given population.
Here is an example for easier understanding,
Eye Color is a Trait,
Let us say that eye color is controlled by a single gene, for simplicity (this is generally not true in nature).

Blue Eye gene variant is an Allele,
Red Eye gene variant is an Allele,
Yellow Eye gene variant is an Allele,

Your eye color is then controlled by which of these alleles you have for the eye color gene.
Here eye color allele takes different forms. Thus making it polymorphic, Putting all these forms together we get Allelomorph(s) (plural), each individual one is as an allele/allelomorph (singular)

I edited to remove some unclear statements and make it easier to understand. (I think that this is a case where diagrams would really help.)


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What are the interaction energies/chemical potential values for the cytoplasm - protein interactions within the cytoplasm?
I'm trying to simulate phase separation in a biological based system using a Cahn Hilliard model. I have 3 components, they are 2 theoretical enzymes and the cytoplasm. I have found plenty of sources describing the interaction energies/chemical potential/free energy for protein-protein interactions, however, I cannot seem to find any of these values for cytoplasm interaction with proteins. Any help would be appreciated. Please let me know if I am not being specific enough. Thank you!


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Why is the SARS-CoV-2 target receptor ACE2 not endocytosed when bound physiologically?
The COVID-19 coronavirus SARS-CoV-2 enters cells by receptor-mediated endocytosis.
See, e.g.  here.
Why doesn’t the enzyme ACE2 — SARS-CoV-2’s target receptor — undergo endocytosis when bound by its physiological ligand, angiotensin II? If ACE2 triggers endocytosis on binding SARS-CoV-2, why doesn’t it trigger endocytosis on binding its physiological ligand?
For instance, from
https://www.nature.com/articles/cr200815
I know what receptor-mediated endocytosis is. However, I just cannot imagine just the opposite, in my wording:  non-receptor mediated (endocytosis). My guess is that the virus contacts a receptor and gets endocytosed, however I imagine the receptor as being left behind, on the membrane, where it remains, it's just some anchor. In other words: does there exist some mechanism that uses a receptor for attaching the virus like a  rod to get - not  the spike  but - the virus membrane  close to the membrane of the cell so fusion of   membranes might happen. Would that be endocytosis, fusion of membranes?
Some idea to get into it deeper, so to speak: ACE2 is special as it's an enzyme - and it does not have, alternatively: does not need any communication channel behind the membrane as it does not trigger anything inside the cell. Thus, ACE2 does not appear as a receptor leading to signaling, and tentatively I suggest that  signaling might lie in the endocytosis of the receptor, in a broader sense of signaling (maybe earlier staged in evolution: no G-proteins, no cascade...)  and in contrast to just blindly harbouring  an enzmye on the membrane. Edited, see comments: it's not blindly that ACE2 has been "expressed", I realized that  the very expression of proteins - be it on surface or not or not at all -  can be seen as signaling.
Interestingly, especially Sars-Cov-2's spike is known to be cleaved by other enzymes on the cell's membrane (furine). Edited: Another exciting perspective: ACE2 which is a cleaving enzyme isn't used by the virus in its cleaving function, it looks like some exchange of "enzyme", not receptor. This is interesting in the context of CoV-2 mutations which add to specifity. Compare newer comment below: what normal interaction is "perturbed" by binding of CoV-2 to ACE2? My point is that there is no signaling cascade after ACE2 which could be perturbed - however, there is "competitive binding", as it is known with any other receptor, so a new way to look at CoV-ACE2 is to see a longer lasting state of blocking the receptor, shielding it away from its natural ligand (sorry, edited: such kind of poetrick is very familiar "competitive binding") Angiotensin II, and I couldn't tell if such kind of non use might trigger endocytosis, haven't heard of any "De-Overexpression", i.e. endocytosis of receptors that are not bound or used physiologically - which makes sense, as competive binding molecules are homologues, identical, how could one cell tell the difference? Aha, it's the "intrinsic effect" (you call it?) in contrast to just blocking - which in case of ACEII does not exist! Nothing behind ACE2 as some follow up cascade.) To me it's a possibility that the getting used of Furine triggers endocytosis of ACE2 (I don't think it does, End of editing).
That should bring up some other question - importance of receptor expression (that is discussed in the context of blood pressure medication, i.e. ACE antagonists as medication). Now, in context of this question, the expression as such just as the opposite, the endocytosis (which physiologically does not seem to be undertaken)  might be seen as a way of  regulation. So, why is ACE2 endocytosed, and why isn't it...
Also see
https://science.sciencemag.org/content/early/2020/10/19/science.abd2985

...however, it is also possible that SARS-CoV-2 can enter cells independently of ACE2 when viral loads are high.

This might be explained by SARS-CoV-2 not searching for a receptor that is  endocytosed to facilitate entry by receptor-mediated endocytoses  but attaches to any antigen that fits its spike, which speaks in favour of my assumption that it is the closeness of membranes. This is quite exciting as it's on the side of the victim - as I postulated - if ACE2 is prone or not to be endocytosed as the opposite of overexpression i.e. diminishing ACE2 is the way (to go away the way to go :-))
Edited, found https://pubmed.ncbi.nlm.nih.gov/15897343/
Confer at figure 4. Endocytosis of receptor not necessary(?)

I have reframed your question in a more scientifically formal manner to make your argument clearer. You will see I have made explicit an implicit assumption in your argument. I suggest that before posting this question it might have been reasonable to read about endocytosis.

I've also corrected your terminology. The disease COVID-19 is caused by infection with a member of the coronavirus family known as SARS-CoV-2. There is no such thing as "CoV-19."

Thank you. To David: you might be right in your reproach, as I am still a beginner, I have read a whole lot of stuff and learnt about endocytosis - clathrins and all that. I'm bringing up because it seems seems such an easy and basic question - but I just can't answer it but know I ought to. Please help...

To David again: by the way, I liked "to trigger", I do not like the "it", though :-) It's free speech anyway, so why use those - äh, I guess you call them - citation marks. "Did I make myself understood" (just kiddin'). Thank you. I'll consult the guidelines as a newbie around, as I guess al this is from the land of the free speakers, To be serious and true: I cannot really assume that, here at stackexchange, it's not up to the author, to have the "the last word". I wouldn't want to feel like a worker for a newspaper. Talking of non author editing which means non authorized editing to me.

To whom it may concern: I' m excited as I believe I have found some anwer, it's within my editing. ACE2 is an enzyme - some implication added here, please forgive me: the very proneness to Covid-disease might be some tendency - coming from within the host cell - to endocytose that ACE2-enzyme so that it does not exist any more as it is not needed. So, receptor-mediated endocytosis in that sense is just the opposite of so called expression, of over-expression of receptors.

If you wish to answer your own question that is permitted and would be infinitely preferable to the additions you have made that, quite frankly, nobody will read and are unsuitable in a question.

To David. Thank you! I will take the tour - it's permitted to use the answer format to answer one's own question... So I declare my further amending as "suggestions for possible answer" as I'm not sure yet if it does make sense what I think the answer could be.

To add to the noise -- a good answer would reframe the question.  How is SARS-CoV-2 endocytosed when it binds ACE2?  After all, if we assume that the normal state of the system is the absence of endocytosis when ACE2 interacts with its ligand, then it is more useful to ask how that normal interaction is perturbed to induce endocytosis when the virus is introduced.

...a good answer - I mean mine, of course, see above - did reframe the question? We assume the normal state is the working of ACE2 with its substrate - so what we see is some non-"cleaving" of e.g. the spike protein. Normal state would be just to cut the spike (least, not the virus) into two pieces (cp. insuline, and in this case Angiotensin II as the physiological ligand which is cleaved to AT1-7). I will think about "normal interaction" - there is no normal interaction "perturbed" (just competitive binding)  - I would say there is some new interaction "we do not know of yet".

To acvill:  your refer to the wording of my question? I thought about it, the other way round. For the time being one could answer: "why should it be" (endocytosed, as ACE2 just isn't). A more convenient wording would be: why is ACE2 endocytosed when bound by the virus. Indeed, my way to put the question is the very "edding to noise".

@acvill This paper discusses clathrin-mediated endocytosis and suggests that the first event initiating endocytosis is not well understood. Also many papers say that in cells with ACE2 and TMPRSS2 the virus doesn't really enter into the endocytosis vesicles and does the entry in a more active way (the S2' cleavage does release the fusion peptide, when such transmembrane serine protease is lacking the virus may wait to be endocytosed and the cleavage achieved latter by cathepsin, activated by the acidified endosome)

To @acvill: exiciting news to me, dont' be irritated by the way I framed the question, and put that up as an answer? Question was why ligand ATII is  - now: - never :- endocytosed. The receptor without the substrate may well be as I just see. Wow, you made me see: it's the receptor "with or without" the "u" as just the opponent of the cleft that's can or is not be endocytosed. This means... why does CoV-2 seem to fake  a non usage of receptor (given assumption  that endocytosis in case of non-landing, non-usage by ligand ATII).

To @acvill: also, "with ACE2 and TMPRSS2" it should be in the paper cited if the cleaving by TMPRSS2 differs from cleaving by Furin (and there is even cathepsin - all three cleaves cleave the same way, "I am not a believer". Once again, an open unused receptor should be recycled and endocytosed one day, physiologically. How can the spike hasten that time by suspension? Maybe by some conformational change that resembles oxidation or degradtion that comes wiht time or environment and lets recycling start; endocytoses then just doesn't realize that "there is something on".

So, the question is

Why doesn’t the enzyme ACE2 — SARS-CoV-2’s target receptor — undergo endocytosis when bound by its physiological ligand, angiotensin II?

(Clarithin-mediated) endocytosis of "intended" ligands only occurs mediated by ligand-specific cargo adaptor proteins or by AP2 itself (which is a sort of "universal glue", but AP2 only binds specific motifs.)

As cargo is selected and bound
by AP2 or by cargo-specific adaptor proteins, the
clathrin coat has to be assembled.

The presence of different
cargo adaptor proteins, including the ubiquitous
protein AP2 and many accessory cargo adaptor proteins,
ensures that specific receptors are recruited to
the protein interaction network. For example, ARH is a specific adaptor for low-density lipoprotein receptors
(LDLRs), Numb binds Notch, stonin binds synaptotagmin, HRB binds SNARE proteins, and
ß-arrestin and Dishevelled bind G protein-coupled receptors (GPCRs). These accessory cargo adaptor proteins bind directly to the core AP2 adaptor appendage domains and therefore do not compete with direct cargo binding. They may be expressed by distinct cell
types to confer tissue specificity; for example, stonins are found in neurons and thereby help to recruit the calcium sensor synaptotagmin specifically into synaptic vesicles. Other tissues, such as the liver, have cargo adaptor proteins, such as ARH, that bind to LDLR to allow its incorporation into clathrin-coated vesicles. Furthermore, different accessory adaptor proteins can be expressed in different tissues, thus allowing a whole
range of proteins to be recruited into a clathrin-coated vesicle. In addition to conferring specificity, the presence of distinct cargo adaptor proteins ensures that,
when one receptor (for example, TfR) is present in high levels on the membrane, this does not block the uptake of non-cognate cargo (in this case, EGF or LDL).
Therefore, even if a receptor is present on the membrane
with low representation, it can still be endocytosed.

There is basically no such cargo adaptor protein for angiotensin II (that was identified). Nor is it clear why there should be one since ACE2 acts as a "knife" cleaving angiotensin II. Also, clathrin-coated vesicles take on the order of minutes to form (see previous ref), while the catalytic cleavage that ACE2 does almost certainly takes a lot less time; although I could not find a precise figure for the latter, it's probably on the order of milliseconds given how other reactions in that class take.
If you wonder how viruses manage to get themselves endocytosed... that's a long story, which I won't try to fully cover here, especially since it's rather poorly studied (Fields Virology 6th ed. manages to completely gloss over it), but the basic idea is that they are much bigger than a usual physiological ligand, which turns the process into a different game:

Although well-known endocytic receptors such as transferrin and LDL receptors occur in the list, the majority of virus receptors are not directly involved in the uptake of physiological ligands. By inducing clustering, viruses can generate a receptor-rich membrane microdomain that differs from the rest of the plasma membrane in protein and lipid composition (English and Hammer 2005; Lozach et al. 2011b).

I couldn't even find a detailed mechanism study for this on (any) enveloped viruses, but there is one on adenovirus (which is nonenveloped) on how it might trigger endocytosis, basically by providing its own polymerization promoters on its capsid, as summarized in a review:

Nemerow and coworkers demonstrated that the interaction between adenovirus pentons (protein complexes which together with the hexons make up the adenovirus capsid) and integrins activates phosphatidylinositol 3-kinase (PI(3)K), which in turn activates Rac and Cdc42, resulting in the polymerization of actin- and clathrin-mediated endocytosis of the virus. Activation of many different signaling pathways has since been described with the involvement of a variety of factors, including serine/threonine, tyrosine, and PI kinases; phosphatases; and a variety of small GTPases (including Arf, Rab, and Rho family members) (Greber, 2002, Pelkmans et al., 2005).

It's not really clear if all viruses come with polymerization promoters like that because even inorganic nanoparticles seem to be internalized; e.g.

Analogous to viruses, colloidal nanoparticles have been shown to be internalized through different cellular pathways in a size-dependent manner. For spherical nanoparticles, Rejman et al. related particle size and internalization pathways in the absence of specific cell receptor interactions: particles smaller than 200 nm in diameter are generally internalized by CME while particles larger than 500 nm enter cells via caveolae-mediated structures. For polystyrene particles in particular, a size of 100 nm is more efficiently internalized by CME in comparison to 50 or >200 nm. Interestingly, for gold nanoparticles, the preferred diameter for clathrin internalization is 50 nm. For both viruses and nanoparticles, the molecular and biophysical determinants driving these size-dependent entry mechanisms are still uncertain. This gap of knowledge is mainly related to the lack of a method to study virus-cell early interactions, which are highly unpredictable events that take place in a extremely narrow time-window (1–2 min).

But surely promoters would speed up the process. Furthermore, it was shown that at least for the reovirus (which is also
nonevenloped), inhibiting its usual binding to its target receptor did little to change its ability to recruit clathrin-mediated endocytosis, if the virus was otherwise pressed against the cell:

JAM-A is a critical receptor for reovirus infection. [...] Nevertheless, the number of clathrin recruitment events colocalizing with virus particles was similar in untreated cells compared to cells treated with the JAM-A neutralizing antibody. [...] these results strongly suggest that the recurrent recruitment of clathrin on immobilized viruses is JAM-A receptor independent.

Furthermore, SARS-CoV-2 doesn't actually bind to the catalytic domain of ACE2 (i.e. the part that cleaves angiotensin II) but somewhere above it, as crudely illustrated in this diagram:

Finally, regarding SARS-CoV-2 entry, the most recent research I found suggests that TMPRSS2 is the main pathway by which SARS-CoV-2 releases its payload into the cells it usually infects at plasma membrane level, with endocytosis being a secondary mechanism. (This actually explains why hydroxychloroquine [alone] works poorly in vivo in treating Covid-19.) It is a a bit unusual for coronaviruses to prefer release at the cell membrane, but not completely unheard of, e.g. Fields Virology mentions that several strains of the  mouse hepatitis virus also do this and even that:

For one strain of MHV (MHV-4), as few as three amino acid
changes in the heptad repeat region of S2 switches the virus
from plasma membrane fusion to acid pH-dependent fusion [i.e. to prefer endocytosis].

And if that's not enough, the same coronavirus can use multiple endocytic pathways, e.g. PEDV has been studied in that regard:

To clarify the specific endocytic pathways, systematic research methods were used and showed that PEDV enters cells via the clathrin- and caveolae-mediated endocytosis pathways [...]. In addition, lipid raft extraction assay showed that PEDV can also enter cells through lipid raft-mediated endocytosis  [...] but the utilization efficiency of each endocytic pathway varied depending on the different [virus] genotypes and types of cells.


text:
Why are chickens passive when their eggs are taken?
Most species don't seem enthusiastic when their eggs are taken, yet on farms with domesticated hens, they seem more passive when their eggs are harvested. Why does this occur?

You might ask a similar question about cows and milk.  I suspect that at least part of the answer is that chickens that showed the most resistance to having eggs taken became roast chicken or (if they were old and tough) chicken soup.  Thus over thousands of generations, the "protect your eggs at all costs" was selected against, and chickens were domesticated.

That is certainly one possibility, but I do not know of anything that strongly supports it. –

Preferential breeding so you don't get attacked every morning at the hen house supports it. If you've ever worked on a farm or raised chickens you'll know that some breeds are more aggressive than others, but those "heirloom" breeds are typically found only on small family farms where the hens have a lot more room. Factory farming has provided incentive to breed any kind of violence or aggression out of their layers, because you can have thousands (or more) chickens living together, especially if they're "free range" with no barriers, and you would want them to be as docile as possible.

Okay, that makes more sense. How long did this process take exactly for hens to become docile through selective breeding?

@jamesqf - I had a saying on my farm: if it draws blood, it's dinner. Exactly as you stated. Young=meat, old=broth. Selective pressure in action. The chickens and roosters who were aggressive didn't get to breed for long.


text:
neural genes expressed in nasopharyngeal specimens
Is it possible in a nasopharyngeal specimen genes of neural system to be expressed? For example, genes about neural differentiation?

Can you please add some more details? Of course there can be some genes that are expressed in two different tissues. If you provide a background to your question then it would be a bit more clear.

I mean if it is possible to find genes that are specific for neural development and differientation in pharyngeal cells.

This paper mentions using a cytology brush (not the usual NP swab) to obtain cells from the olfactory epithelium. They obtained and cultured neural precursor cells. Have a look.
Trends in molecular medicine.
"The Olfactory Neural Epithelium as a Tool in Neuroscience"
Joëlle Lavoie, Patricia Gassó Astorga, [...], and Koko Ishizuka
from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5399677/


text:
Biological Neural Network Modification to Unlearn Understandings
Lets assume that a person grows up thinking that religion X is true religion. So he builds up a profile in ones head and when notion of religion X appears the neurons that is related are fired, giving sensation of God and related stuff.
Lets us also assume that later in life he learns that religion X was not correct, then does "realization" of this fact happens by modifying old neural networks or a new profile is created for religion X and old profile gets deleted?
In other words do neurons associated with sensation that religion X was true religion "modified" or a new network is created giving a new sensation that religion X was not true religion along!
In my general understanding modification of old network could be challenging assuming that they are surrounded by other neurons associated with other stuff, a certain modification by having more or less neurons would result in borrowing neighboring neurons and wiring them to create a modification or loosing some connections to create a modification, which doesn't seem efficient.

I am not sure how is this question "opinion based"? I have asked a concrete question with a general example.

i'd suggest putting this on psychology and neuroscience instead, I don't know if you're going to get a good answer here: https://psychology.stackexchange.com/

I will, do you think its not related to biology?

Why was this close as opinion-based?

@BiologyEnthusiast Since there is a SE site specifically pointed towards neuroscience and cognition, that is likely a much better place to get informed commentary. Moreover, I personally can't tell if there is enough information to answer the question but I suspect there might not be (for example, there are no linked sources); this suggests to me that an expert would need to look at it to decide whether it can be answered. That expert would be a psychologist or a neuroscientist; and such specialists have their own site.

This has now been cross-posted at Psych&Neuro. I don't necessarily agree that it should have been closed here, but I think now that it's been posted there it shouldn't be reopened here.


text:
Bats observed hunting insect prey - any evidence of "handedness" (laterality) in circular flight pattern?
Whilst watching a bat hunting on the wing at dusk (most likely was a species common to my urban UK location, e.g. pipistrelle) its flight pattern around the garden comprised circles, several metres in diameter, but I'm reasonably sure going in the same direction - in this case it seemed always to be turning to its left. (The circular flight pattern is something I've observed many times.) Is there any evidence in bats of a preferred direction of circular "sweep" whilst hunting? More generally, are bats known to exhibit left/right- handedness (or laterality in technical-speak) and does/could this manifest itself in flight patterns?
What I've already tried to answer my question:
Searched this site for related questions/answers + tried Internet searches with variations on circular flight for bats- results included a 2013 Nature paper, Bandyopadhyay, P., Leinhos, H. & Hellum, A. Handedness helps homing in swimming and flying animals. Sci Rep 3, 1128 (2013). https://doi.org/10.1038/srep01128 - fascinating stuff re. handedness and advantages for homing, but the brown bat featured was trained and observed under controlled lab conditions. Hoped that someone here with knowledge of the subject could provide a research paper/book ref., etc. I posted this question out of simple curiosity - I'm not a biologist and so don't have institutional access to many papers (just the Abstracts).

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, we expect you to demonstrate that you have done some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— In this case, editing your question to include a summary of and reference (plus a functional link) to the paper you mentioned would make this much better. Thanks!

@Jimbo, welcome to Bio.SE! I've edited your post to include the info from your comment -- thanks for the update! Could you please update the link to your Nature paper? It's broken. A citation would also be good to include to avoid broken links in the future. Interesting question -- thanks for asking.

This article shows a lefthanded bias for climbing and eating, with one bat species:
Paolo Zucca, Alessandra Palladini, Luigi Baciadonna, Dino Scaravelli.
"Handedness in the echolocating Schreiber's Long-Fingered Bat (Miniopterus schreibersii)"
Behavioural Processes,
Volume 84, Issue 3,
2010,
Pages 693-695,
ISSN 0376-6357,
https://doi.org/10.1016/j.beproc.2010.04.006.

Paywalled - only the abstract is visible.

Found using Google Scholar with search terms: handedness, microchiroptera

You could mention sci-hub as a way to bypass paywall.

I hadn't seen this site before. I will have to seek advice as to where I stand legally.


text:
What makes boric acid so toxic to roaches and not so much to any other insect?
When I look up boric acid on the net there are various ads for it to kill roaches but no explanation of why it is effective on roaches. I am in East TX , roach central. When my house was built I put pounds of boric acid in between the studs before drywall went up . For 25 years  I don't think I saw a dozen roaches in the house. But starting this spring ,I have killed a few roaches every night . As if they became immune to the boric acid ( as much as I put in ,it could not be gone). We have pets so I am reluctant to use insecticide in the house.

boric acid plus sugar is a common ant control home remedy as well. The belief is that it crystalizes inside the insect and blocks their digestive tract


text:
What does FETCO2(end-tidal fraction CO2 concentration) represent?
What is end-tidal fractional CO2 concentration? I have searched online and found little actually explaining what this measurement is. Thanks again.

I'm not sure if you're asking about the procedure or the underlying concepts of CO2 concentration or how a capnometer works.  But in brief, it is measured at the end of an exhaled breath, which is least 'contaminated' by inhaled but unused air from the conduction zone (trachea, etc.).  The measurement is done by looking at the blockage of light from an infrared light to a sensor by the CO2 - exactly the same mechanism by which global warming works.  And the way it's reported is, in this case, as a fraction from 0 to 1.  It could be reported as a percentage by multiplying by 100, or as a partial pressure by multiplying by the total atmospheric pressure (often 760 torr at sea level).


text:
Development of radial symmetry in starfishes and other animals
How does nearly perfect radial symmetry arise in an animal like the starfish? My confusion lies in the fact that cells are fluid & amorphous, & that these characteristics seem to make it difficult to form symmetric structures. Many of the sources I've read describe the formation of the blastula but not the development of the five arms following that. Also, at one point in the development it is bilaterally symmetric. Furthermore, some species of starfish can regrow from a single arm.
What process mediates the formation of radial symmetry in a developing organism? Is it that arms grow individually & there are cascades of cellular signaling that mediate the production of new arms until the desired amount is reached or is it something else? How do the arms of the starfish remain evenly spaced?

The morphogenesis of symmetry is an enigma in biochemistry, especially for echinoderms. Biologists can't agree totally and tell you a specific reason. here's all I can find(2018) "Over the last 20 years, an answer for how vertebrate embryos can tell their left from right has emerged. This model involves midline-located L-R organizers (LROs) – the node in mice. " https://dev.biologists.org/content/141/8/1603 some wiki info: https://en.wikipedia.org/wiki/NODAL wiki says that echinoderms also have the Nodal development gene.

That is the field of developmental biology which deals with organizers. Cell organizers are processes, genes and signalling proteins cells use to communicate / send and receive information from their neighbors, so that their spacial distribution in the body regulates their development.
The cells also have gradients of signaling proteins inside the cytoplasm, and cell polarity, so the cells know which way round they are:
"A spatially distributed signalling cascade can create step-like activation profiles, which decay at successive distances from the cell surface, assigning digital positional information to different regions in the cell. Feedback and feedforward network motifs control activity patterns, allowing signalling networks to serve as cellular devices for spatial computations."
All metazoans use the same types of organizers to develop different patterns of cells, so starfish use the same genes as mice to organize their axes. They are early metazoan genes/ Precambrian. Here is an in depth answer to your question: www.ncbi.nlm.nih.gov/pmc/articles/PMC5307799/
The cells know where they are, because they are receiving multiple signalling proteins from further away in the animal. Here is a picture of Bicoid morphogen in fruitflies:
The signalling proteins are received from cells far away, and that signals to other cells to make different kinds of signalling proteins to organize the local neighbors.

Given the complexity of metazoan morphogenesis, there are very many organizers and we only know a few of them. The axis formation is related to the Nodal gene which uses some kind of axial/mid-line located organizers to control symmetry, there are documentd about LRO: left right organisers, in starfish its the same chemistry in a different geometry. The Nodal biochemistry: https://youtu.be/kO8k9aiQJsQ?t=189


text:
Source for Specific Models of Birds' Habitat Suitability
This source gives a very detailed analysis of what habitats are best suited for many different species. However, this is a government funded project and, to the best of my knowledge, not published in a peer-reviewed paper. In addition, this project has officially been depreciated for 18 years.
There are 2 features of this project that are very attractive to my own project. First, each habitat is ranked as a value between 0 and 1. Second, it ranks 31 habitats, each with very precise differences (e.g. a conifer palustrine forest habitat is ranked separately from a deciduous palustrine forest). Compare this to other sources, such as the IUCN Red List which only says 'Yes' or 'No' to whether a species has been observed in a habitat and only tracks 18 habitats that are very broad groups (e.g. all forests are ranked together).
Can anyone direct me to a more modern and/or peer-reviewed source that has one or both of these benefits?

A quick google reveals several databases of bird habitats, which appear to be at least somewhat more recent.
I believe that the one closest to what you describe is here (there may not be a single publication but they do have a lot of associated publications on their site). But this climate change geospatial database (with a newer version here) and this more local database may also be helpful.

Thanks. I think I missed those when searching because I always included terms like "dataset" or "database".


text:
Can Cas13 edit DNA
Can Cas13 be used to edit DNA or is it only for RNA?
I have tried looking at literature and my understanding is that it can only edit RNA.

The Cas13 protein targets/edits RNA specifically and not DNA. That said, as you probably know, the Cas9 protein is famously used to edit DNA and was the inspiration that led the Zhang Lab to seek out the Cas13 protein for editing RNA.
If you're interested, you can read here for some additional detail on how Cas13 targets RNA and why it's RNA-specific.

The question asks "Can Cas13 edit DNA" - why is your answer about Cas9?

Maybe I didn't make it clearly but I was just trying to make the point there is something that edits DNA, but it's not Cas13. Will edit to make it clearer.

Then you probably shouldn't start with "yes" :)

Done, yes was intended to reply to "is it only RNA" but you're right that that was not very clear :).

No, Cas13 can't be used to edit DNA. Cas13 does not contain nuclease domains RuvC and HNH  domains responsible for DNA cleavage, so they cannot directly edit the genome. For that Cas9 and Cas12a is used.


text:
How do viruses provide selective advantage
I've heard in many talks as a passing, well-known fact that viruses(e.g. pathogenic HPV strains) offer selective advantage for the infected cell to multiply. But I'm not able to quite wrap my head around this.
I assume this has something do with episomal qualities of viruses, but how exactly does that does translate to selective advantage.
My intuition says that if there is an uneven segregation of the viral genomes to the daughter cells, than that heterogeneity can cause give selective advantage. But given no preface of the heterogeneity of a virus during cell division, how is one able to claim that viruses offer selective advantage?
Background: I am not a biology person, but rather computational scientist who works with biologists.
one example source

See the instances of "selective advantage / pressure" from the source provided by Jonathan, emphasis mine:

Persistent infection with HPV leads to an environment of genomic instability and local immune suppression, which can lead to both the accumulation of genomic alterations in the host cell, as well as to the integration of the viral genome into the host genome. When these additional alterations provide a selective growth advantage to the cell, carcinogenesis may ensue.

Furthermore, the integrated viral transcripts confer stronger transforming capacity than those derived from episomes, due to longer half-life of transcripts (32). This promotes immortalization and transformation of these cells and provides a selective growth advantage (3, 8, 30, 33). Integration may, however, confer a selective growth advantage to the host cells not only through its effects on the viral genome (i.e., enhanced/deregulated expression of viral oncoproteins), but also through its effects on the host genome (i.e., by affecting key cellular genes).

Several mechanisms by which HPV integration may confer a selective advantage have been described (Fig. 3).

This environment is also amenable to accumulation of genetic alterations and viral integration, and subsequent tumor formation. Integration affects both the viral genome and the host genome, likely conferring additional neoplastic selective pressure, by one or more of the following mechanisms: (i) enhanced expression of viral oncoproteins, (ii) alteration of critical cellular genes (leading to increased expression of oncogenic proteins, decreased expression of tumor suppressor proteins, altered DNA repair mechanisms, or modulation of the immune system), and (iii) changes in global promoter methylation and transcription.

In biology, "selection" often refers to natural selection -- in short, genetic diversity in a population manifests as different traits in individuals, which result in differences in relative fitness in a given environment that, through time, result in evolution.  The quoted excerpts refer not to the environment acting on different traits but rather to the (potential) enhanced growth characteristics of HPV-infected cells, relative to non-infected cells.  So, the use of "selective" here is misleading.  Yes, viral integration may lead to enhanced growth of a cell population by disruption of certain cell cycle checkpoint genes, but the organism on the whole will certainly be less fit when that unrestricted growth leads to cancer.
In my opinion, the text could read "growth advantage" or "enhanced growth" in all instances and do away with "selective" entirely.

I believe they use the term "selective" in reference to experiments where infected and non-infected cells are co-cultured. Over time, infected cells become a larger fraction of the population due to increased replication/survival of those cells, so they can say that in the culture environment (where cells are acting more like individual single-cell organisms than like members of a multicellular animal) there is a selective advantage to being infected with HPV. I agree with you, though, that the word is not particularly important and could be omitted.


text:
If sexuality is genetic, how did asexuality evolve?
If sexuality is genetic, then it stands to reason that evolution would strongly favor people who have children. In other words, heterosexuality & bisexuality should be favored, while homosexuality and asexuality should be disfavored and in fact eliminated by evolution. Why hasn't that happened?
I can find plenty of resources via Google for the evolution of homosexuality, such as this one, but not for the evolution of asexuality. Asexuality seems to pose a bigger challenge as well, since the lack of sexual attraction entirely should make it even less likely for asexual people to have children. Some of the explanations for the evolution of homosexuality can conceivably apply to asexuality too (such as "the genes for asexuality do other things"); still, I would like an authoritative paper/reference if there is one.

can you point to a reference that suggests that sexuality is in fact substantially genetic? i'm not disputing that you can find some signature of heritability, but for this variation to be selected upon, there should likely be a fairly strong genetic signal. furthermore, can you demonstrate that asexual/homosexual people have fewer children? this is less obvious than you seem to think it is, and it is also a necessary prerequisite

@MaximilianPress there's this that addresses both points for homosexual people. I have no sources for asexual people - it just seems natural, given what applies for homosexuals.

If 1% of a population is asexual, but can have children when they want to, or when a well positioned male wants to, perhaps that has a negligible or a positive effect on group success and evolution. https://external-preview.redd.it/Y28QUOGsV7qbq2YCfjF7u10-4BpujEdAXTetnKoR0xs.png?auto=webp&s=111feab8fe6d218ab006b83740a23744ce7ff259 For some reason, I think that Freddy Mercury was on the far right of that graph.

@aliential I don't understand - homosexual people can also have children if/when they want to, but they still have fewer children than the rest of the population. Presumably the same would also apply for asexual people.

Does this answer your question? Why do some bad traits evolve, and good ones don't?

Update:
See @Bryan Krause comment. Just because something exists (or equally, doesn't exist) does not mean that it was selected for or has any evolutionary relevance. Imputing selection to any particular state of affairs is usually bad reasoning without a lot of evidence.
I didn't do a good job of coming out and saying this in my answer.
My answer is best understood as answering the question: how could asexuality evolve under selection?
It does not at all address the question: DID asexuality evolve under selection (in humans)?
This second question is one for which the answer is probably "no". Without more evidence, we cannot say whether asexuality has any evolutionary/selective relevance at all.
Original answer:
I would suggest looking more into the evolution of social animals for which large proportions of the population is non-reproductive (or sterile). There are many such examples, with insects as the obvious case:

Contrary to widespread belief based on heuristic arguments of genetic relatedness, non-reproductive workers can easily evolve in polyandrous species. The crucial quantity is the functional relationship between a colony’s reproductive rate and the fraction of non-reproductive workers present in that colony.

I would suggest looking more into that paper and citations therein. The question to answer is whether an individual's labor can be more important than their gonads to the continuation of their genes.
As suggested in the wikipedia article on homosexuality that you link to in your own comment, there is a positive effect on female fertility from having homosexual family members ("kin selection"). Granted, what causal mechanism is behind this is likely difficult to sort out.
It's quite plausible that asexuality behaves similarly to homosexuality in this regard. Those authors want it to be a genetic factor driving both sexuality and fertility. But to me it seems a bit more parsimonious to posit that it's good to have more warm adult bodies around to care for/support children.
From a practical perspective, if grandparents with non-functional gonads can help raise kids (i.e. increase effective fertility of kin), why not asexual relatives too?

There is also https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont Not to say there is anything wrong about asexuality, but to say that the existence of a trait does not mean that the trait was selected for, and similarly, just because a trait does not exist does not mean that the trait was selected against, even if the trait is entirely genetic.

@BryanKrause that is an excellent point that I did not explicitly address. I'll edit.


text:
Collagen, are fibrils arranged in overlapping fashion too just like tropocollagen?
Collagen molecules (tropocollagen) are interlinked into fibrils, with a banded structure showing the spaces ("lacunae") between the molecules. Do fibrils in turn also interlink in a similar way, or, do fibrils run from end to end in the fibers?


text:
What are the stretch of amino acids?
I found the words "stretch of amino acids" in a newspaper article.

"This lipopeptide matches the stretch of amino acids in the spike protein of SARS-CoV-2 exactly."

What is the "stretch of amino acids"? Is this different from "amino acid sequence"?
I looked for a definition of the word but could not find it.
From the usage, I guess it means something similar to "sequence", am I right?

Yes, stretch means sequence.  "This lipopeptide matches the stretch of amino acids in the spike protein of SARS-CoV-2 exactly."

Thank you for your answer.　I'm also not sure what the word "match" means in that quote.
Does it mean that the primary structure of spike protein and lipopeptide are the same? Or is it to be a "key and keyhole" relationship with spike protein?

@acvill you can expand your comment and make it a proper answer

I think this question should be closed because it is scientifically trivial and would seem more to relate to a restricted experience of English language usage, for which there are many aids on the internet. As far as Stack Exchange is concerned, English Language Learners might be appropriate.

Unless ones know more or less chemistry, you may not understand the concept of "amino acid sequence" itself. For the non-native speaker of English, making up two or three technical terms that have exactly the same thing is the cause of the confusion, I think.

Yes, stretch means sequence in this context.  See definition #5 for stretch (noun) on Wiktionary:

A segment or length of material.

So, the "stretch of amino acids" in the article refers to the peptide sequence portion of the lipopeptide prophylactic.

I was confused, guessing that there was some point in changing the terms. Thanks to you, my confusion was cleared up. I'll read the paper to see how these inhibit the infection process using the same sequence of peptides. I imagine it's similar to competitive inhibition, though.

English speakers might also say "That stretch of road has a lot of potholes".  It might even be used more loosely, like "a stretch of time".  It's not an exclusively scientific term.

The lipoprotein has a 36 amino acid sequence that is the same (matches) as part of a protein from SARS-Cov-2.
The newspaper article refers to this paper below.
"Intranasal fusion inhibitory lipopeptide prevents direct contact SARS- CoV-2 transmission in ferrets"
Rory D. de Vries1@, Katharina S. Schmitz1@, Francesca T. Bovier#2,3,4@, Danny Noack1, Bart L. Haagmans1, Sudipta Biswas5, Barry Rockx1, Samuel H. Gellman6, Christopher A. Alabi5, Rik L. de Swart1, Anne Moscona2,3,7,8, Matteo Porotto2,3,4
available at:
https://www.biorxiv.org/content/10.1101/2020.11.04.361154v1.full.pdf

Thanks for your answer. Your explanation really helped to understand the followings; The "matches" in the article means that ”part of the primary structure of the spike and part of the amino acid sequence of the lipoprotein are identical".


text:
Popliteal artery for a heart bypass
My father undergone surgery 10 years ago to get 3 bypasses close to the heart. Surgeons did a very long cut on his leg to get the material to make the bypasses they would later put on his chest.
What I understood at that time, is that they took three sections of the popliteal artery to obtain the material to make those bypasses, and that they fixed the cuts again to restore such artery. The reason why that artery was chosen is because it is very elastic and surgeons can extract a section and stick it together again.
My father is convinced they removed the whole popliteal artery from that leg and chopped it down to make the material they would use for the bypasses.
I am trying to find information about this procedure to find out who is wrong. The problem is that we both are completely illiterate in medical stuff, so we are lost in the mist. What I found is that the popliteal artery is important and blockage could be problematic.

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I'm not a physician, but I suspect the popliteal artery may not have been the vessel used.  The popliteal artery has a very important role in supplying the leg with blood, and maintaining the blood supply from it to the lower (distal) leg is sometimes reason for harvesting other vessels.
You described a very long cut, which sounds like what you would see for harvesting the great saphenous vein.  The great saphenous vein is the longest vein in the body, and dominates recent scientific publications in response to a query of ''coronary bypass harvesting''.  (There are publications in that batch evaluating newer endoscopic techniques in which the long cut can be avoided)  Wikipedia reviews the use of this vein reasonably well.

This is the correct answer.

I believe you are right, it must have been the saphenous vein. What I am not clear yet, if it is removed completely or just removed a section and the cut ends joint again.

@val It isn't stitched back together if that's what you ask. The reason a superficial vein is used is because collateral circulation is sufficient. The saphenous vein is not necessary.

See, generally for coronary bypass surgery to relieve ischaemia of heart, a segment of 'Great Saphenous Vein' is removed and used for aorto-coronary grafting to bypass an arterial obstruction. Due to the opposite direction of venous valves (Veins in lower limb allow blood to move upward), it should be reversed in direction before ligating.
Now you are telling that popliteal artery was used for the bypass, but I doubt it.
Although there is an arterial anastomosis around knee joint that allows slightly compensated blood flow even after Popliteal artery obstruction. So, if the great saphenous vein was not in a condition to be used for a bypass, the surgeons might have used popliteal artery.

I think the doctor will definitely clarify everything to you & he/she won't do any harm to your dad.


text:
Can a non-response to a vaccine be tested?
The BioNTech/Pfizer vaccine against SARS-CoV-2 is said to be 90% effective.
Is there a test to establish the (degree of) success in individuals of a vaccine at provoking the desired immune response? Or will we all have to hope for the best?

Some measure like this are listed as secondary or exploratory endpoints in the Pfizer protocol. It's a bit technical, but with some careful reading and googling, you should find what you're looking for in the protocol here

I suppose the follow up question is: is per-person efficacy verification likely to be standard protocol in a vaccination program of such a scale?

You can test for antibody titers (and also connected memory) for the persons who got the vaccine and then decide, if these antibody levels are protective or not. Problem with this method is, that it is not clear, what levels are protective. There is still no experience with it for SARS-CoV-2, this is routinely done for other diseases.
According to clinicaltrials.gov, the study design is a placebo controlled trial triple blinded (Participant, Care Provider, Investigator) which enables the direct comparision of the vaccine arm with the placebo arm. Here you analyze the difference between these arms. If the vaccine delivers a sufficient protection, less (or ideally no) people in the vaccine arm get sick - which is exactly what was observed.
A last possibility would be to challenge people, who received the test vaccine with the virus and see, if they develop the disease. However, this approach is highly unethical since you possibly infect a large number of people with a potentially deadly virus, when the vaccine does not work. I doubt that a researcher who wants to do this will get clearance for these experiments by the internal review boards involved in these trials.
This is done in earlier stages in animal experiments, to challenge the immune response.


text:
What is the impact of selection on orthologous and paralogous genes? How would this impact differ in different regions of protein coding genes?
Since paralogs increase the size of the genome and provide more opportunity for the evolution of novel characteristics, would they be more prone to selection?

Exactly .
Paralogs and orthologs , both go under natural selection. But harmful mutations tend to have a less fatal effect if they happen to paralogs as there would  be a backup for the malfunctioning protein. In paralogs, if a bad mutation happens to a protein, the paralogous protein will compensate and help the organism maintain its function but in orthologs one mistake is enough to do harm because there are no other proteins to perform the function of the wild protein.

All the different members of the tubulin family of genes (and
proteins) are sufficiently similar in sequence to suggest a common
ancestral sequence. Thus all these sequences are considered to be
homologous. More specifically, sequences that presumably diverged as a
result of gene duplication (e.g., the α- and β-tubulin sequences) are
described as paralogous. Sequences that arose because of speciation
(e.g., the α-tubulin genes in different species) are described as
orthologous

Reference : Molecular Cell Biology of Lodish et al 8th edition page 325
Also see Campbell Biology 9th edition chapter 26 section 26-4

this is a good answer, but it would be helpful to include a source or citation.

@sam, thanks for the great answer! I am just wondering though how the impact of selection would differ in protein coding regions.... I know it would be more impactful in this region as opposed to non coding, but im not sure how the impact differs between protein coding regions.. or why? thanks!

@Manon Valiquette , natural selection effects the whole gene.  (Beneficial) selection in protein coding regions includes 1.Active sites / binding sites for complexes  2.Allosteric domains 3.Structural/Less important sections. In 1 , any change leads to a large scale of "FUNCTION" and  the "AFFINITY" to ligand of the protein/enzyme.  In 2 alternation of sequence leads to changes in "AFFINITY" for the ligand and more importantly "RATE OF CATALYSIS", while changes in 3 tend to have a less impact on the protein. Plus selection can also occur in non coding regions which mainly result in ---

--- "Gene expressing patterns and timing and amount of transcription" . for example a selection in promoter sequence can increase the rate of trancription of a specific gene , leading to overexpression of it which sometimes may be beneficial. I hope that I've understood your question correctly.


text:
Does the magnitude of gene-expression changes decrease the more downstream a gene is from the origin of change?
If I have a decrease or increase in expression in one gene, will the decrease/increase in expression in the downstream genes always be of a magnitude lower than the previous ones, or can they be higher?
I’m thinking in terms of signal propagation in a network. If I, for example, knockdown gene $X$ to 40% of its basal level, and it influences genes $Y$ and $Z$ in the following manner:
$$X → Y → Z,$$
Will I expect genes $Y$ and $Z$ to suffer lower decreases/increases than the previous gene, for example:
$$X: 40\% ~⇒~ Y: 60\% ~⇒~ Z: 80\%$$
Or could I have a scenario where a small change in one gene’s expression can lead to higher magnitude changes in downstream ones, for example:
$$X: 40\% ~⇒~ Y: 20\% ~⇒~ Z: 10\%$$
I suppose that in some networks the signal will always decrease in magnitude the farther it is from the source, but I’m wondering if, in a biological network, that will also happen and consistently in each step. I read papers with knockdowns all the time, but I never stopped to analyse if knockdowns always create lower magnitude changes in downstream genes or not. So I was wondering if this intuitive notion holds empirically or not.

It's going to vary depending on the gene. Some genes exhibit dose dependence, others don't.

@MattDMo I know some genes are dose dependent and some not, but I'm not sure that's the problem. Dose dependence would change downstream genes in acordance with the dose of the source of change, but that doesn't tell me if the magnitude will always be lower, or not. So if 40%X -> 60%Y and 20%X -> 40%Y, that's dose dependent, but will the magnitude always be lower like in this example?

@David well, I work with molecular biology and bioinformatics. And I don't see how that is making a simplistic mathematical assumption about biology. Biology is not simple, and cannot be reduced to simple assumptions sometimes. But other times it demonstrates very well conserved patterns. I'm making no assumption. I'm merely trying to discuss to see if there is a pattern here. It might not have. But if one cannot make very objective questions about whether some pattern exists or not in biological systems, then we should close all systems biology departments, because they would be pointless.

Gene expression can be very well described by Hill functions, i.e.:
$$c_Y(c_X) = \frac{c_X^n}{1+c_X^n}$$
when $X$ activates $Y$ and
$$c_Y(c_X) = \frac{1}{1+c_X^n}$$
when $X$ represses $Y$ (omitting units and all sorts of constants for simplicity). For the common case that $n>1$, these functions look like this:

As you can see, they are far from linear, but sigmoids. For $n→∞$, these become perfect step functions.
As a result, gene regulation mostly works like a switch:
As long as you are not close to the critical concentration ($1$ in the above example), changes in the regulator have a less than proportional effect.
For instance in the above example, it doesn’t matter whether the concentration of your activator is $2$ or $10$, the protein production is pretty much $1$.
Therefore, “signals” in gene-regulation networks get stabilised instead of diluted.
There are also some other self-regulation effects contributing to this such as genes that self-regulate, the availability of amino acids, and the limits of the translation apparatus.
Note that without these sigmoidal relationships, you would also have big influences of the inevitable fluctuations of the regulator.
As a result, it would be impossible to keep the metabolism in some stable state – the only stable state in a linear system is death.
Simply put, you would have to keep a very precise and regular diet, lest your body stops working.

Great answer, and exactly the kind of answer I was looking for. I remember reading about the Hill equations in Uri Alon's book many years ago in the begining of my masters in biochemistry. But I had other things in mind and ended up not finishing it, and forgot most, except the network patterns. Guess I should go back to it now. But just some questions: do we know the range and frequency of Hill coefficients in nature? Because it is going to be linear somewhere around n=1.5, right? But I guess the question is whether n=1.5 is a value that exists in practice.

Also, this switch behavior does make sense in terms of stabilizing the signal, but we can clearly observe some dose dependency when inhibiting genes in the lab. So, at the very least, it's not a binary switch, but one with many states (or steps), unless all the dose dependency we are observing is in the linear phase, in which case the functions are far from perfect steps. Is there some literature on that? And third, just stretching a bit, is there some general pattern of how much the expression changes after the "switch" is on?

@LizardMan: 1) I would have to search for a source on the distribution of Hill coefficients myself, but IIRC they are often considerably larger than 1. Of course there also are some cases, where you (or evolution) want the Hill coefficient to be small. 2) Sure, it’s not a binary switch, but for many practical purposes, it’s sufficiently close. Remember that in any cascade, it suffices if you are not in the intermediate region for one expression step. 3) I am not sure, what you wish to know here. The general pattern is that you have no expression if the switch is on and otherwise, it depends.

Ok, I'll try to look for this later. Thanks. 2) I meant binary in the sense of having only one step (two states), but I get it anyway. Just out of curiosity, are you aware of any gene for which all expression steps have been characterized? Something like, gene X goes through one step when it's TF is at concentration A, through another step at concentration B, and so on.

I meant something like this: gene X has a basal level (will not be zero for many); it's TF rises sufficiently to make it go through one step; after the step, X's expression is N fold in relation to it's basal level. Is N some kind of constant (either for each gene per step, or in general for all genes)?

2) I am not aware of any mechanism that would cause multiple steps. Beware that this is all a thermodynamic process which smoothens things like cooperative gene regulation (and are in fact responsible for $n>1$). 3) I don’t think so. The basal level depends on different things (how well does the transcription apparatus work despite lack of activation) than the activated level (how does the activation work).

Just to expand on @Wrzlprmft's great answer with a concrete example:
Sticking to your simple gene circuit with $X$, $Y$, and $Z$, now consider the possibility that $Y$ also activates its own expression via a positive feedback loop:
$X \to \underset{\circlearrowright}Y \to Z$
Here activation of $Y$ will be only minimally dependent on $X$. Once $Y$ is activated, the following self-activation makes $Y$ practically independent of further $X$ activity, causing $Y$ to drive its own activation until saturation.
If by decreasing $X$ to 50%, its levels are still above the minimum level required for activating $Y$, this would have practically no effect on the final (steady state) levels of $Y$. Conversely, if a 50% decrease brings $X$ below the $Y$ activation level, it would lead to a complete shutdown of $Y$.

Note that you need an additional ingredient for a positive feedback loop to act as a robust bistable switch which isn’t switched on by the slightest noise: Either $Y$’s self activation doesn’t suffice for a self-amplifying effect at low concentrations of $Y$ or you have something like “$Y$ suppresses $W$ suppresses $Y$”.

Indeed, good clarification! I was thinking of giving some examples of positive feedback in biology (cell cycle and lac operon, for example) where such "protective mechanisms" indeed exist, but didn't want to go too off-topic.


text:
Do SILK fibres let light pass through it?
The reason given by Wikipedia for silk fibres being lustrous is that:

Silk fibres have triangular prism-like structure, which allows them to refract the incoming light at different angles.

By my understanding, refraction takes place only when light enters another medium. (This is only for reference)
My question is: Do silk fibres allow light to pass through them?

If the question is not suitable for this site, I would like it to be transferred to the another site. Thanks!

Nobody bothers to reply.....

Patience, many of us are asleep or at work.

How is this about animal husbandry?

@MattDMo I beg your pardon, but you all are making fun of someone who is not as experienced and knowledgeable like you.

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] or delete your question accordingly. MattDMo was pointing out a mistake in your post — constructive criticism is encouraged on this site. ——— Also, note that as written this question doesn't appear to be about biology, but instead about the optical properties (physics) of a biological material and so would seem to be off-topic for this site. Please consult the above links and [meta] for details.Thanks!

@user100323 you tagged the question animal-husbandry and I simply inquired how this question and that tag were related. You are a member on enough other Stack Exchange sites that you must surely know how the tagging system works, so your plea of ignorance doesn't hold any water. The other comment was in reply to your complaining about no one commenting on or answering your post yet - not making fun at all. Here's a hint: when joining a new community, educate yourself about how it works instead of complaining about everything.

@user100323 as for your actual question, if the reason for silk fibers' being lustrous is that they diffract light, then of course light can pass through them. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please see our homework policy for more information. Additionally, as indicated above, this is not even about biology, it's about physics. Please read the [help] to learn more about this site.

Yes, silk allows light through.
I did a google scholar search using terms:
optics of silk
Lots of articles, the article below measures a refractive index of about 1.54
Paywalled except abstract and figures.
Bucciarelli, V. Mulloni, D. Maniglio, R.K. Pal, V.K. Yadavalli, A. Motta, A. Quaranta,
A comparative study of the refractive index of silk protein thin films towards biomaterial based optical devices,
Optical Materials,
Volume 78,
2018,
Pages 407-414,
ISSN 0925-3467,
https://doi.org/10.1016/j.optmat.2018.02.058.
Found at:
https://www.sciencedirect.com/science/article/abs/pii/S0925346718301241


text:
Is there a taxonomy of species with emergence and extinction dates?
I know the NCBI has a list of each species and their place in the evolutionary tree. But do they have the dates that these species existed? Does any such database (partial or complete) exist anywhere?
For example, Adelobasileus on Wikipedia says "about 225mya", so that would be one example date. Obviously they aren't super exact, but it would be cool if this has already been collected somewhere.

for the vast majority of species those will just be question marks.