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what is the ancestral relationship between dogs and cats and bears?
or Mr. person who may  have my answer,
     I would like to know the answer of my question so I can make a craft out of it and show my dog. I know it may sound silly, but biology is one of the very few things in science I'm good at, I would really like to know my answer when ever it is efficient with you.

Welcome to Biology.SE! Please take the tour. Your question needs some improvement to increase its chances of attracting a good answer. For instance, you should show that you've made an attempt at finding the answer yourself (for instance by Googling 'dog cat bear phylogeny' first and reading some of the links), and we don't need to know anything about your dog or your crafting intentions to answer the question :)

The same which is between you and your cat, and your dog and bear :P

@another'Homosapien' dogs, cats and bears are all Carnivora while humans are primates. So dogs and cats are more closely related than cats and humans are.

@Remi.b I ain't that good at classification. I just wanted to say that this would be the answer if you ask here without any research effort.

There are online resources such as tolweb.org or onezoom.org that allows you to visualize the tree of life.
Cats, dogs and bears are all Carnivora. The Most Recent Common Ancestor (MRCA) between dogs and bears lived about 44.9 Million years ago. The MRCA between the lineage giving rise to both dogs and bears and the lineage giving rise to cats lived about 51.4 millions years ago. You can find this ancestor here on onezoom.org.
Depending on your understanding of of phylogeny, you might want to have a look at Understanding Evolution > History of life, a short introductory series of slides, to understand the diversity of life and understand how to interpret phylogenies.


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Fixing the cell with 4%PFA and staining with PI to observe cell cycle?
I am wondering whether we can replace 70% ethanol to fix and perm the cells with 4% PFA to observe the cell cycle. Do I understand correctly that 4% PFA can permeate the cells, thus the PI will intercalate DNA?

PFA can also cross-link DNA, interfering with intercalation.

Thanks, I will search more details.

source: Stack Exchange

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

sort: votes


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

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

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

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

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

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

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

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


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Does SARS-COV-2 produce toxins?
I wonder whether toxins are produced only by bacteria and fungi and not by viruses. Looking at the paper below, I read that several toxic proteins are produced by SARS-COV-2. Can these proteins be considered toxins?
Reference:
Lee, JG., Huang, W., Lee, H. et al. Characterization of SARS-CoV-2 proteins reveals Orf6 pathogenicity, subcellular localization, host interactions and attenuation by Selinexor. Cell Biosci 11, 58 (2021). https://doi.org/10.1186/s13578-021-00568-7

Please define what you understand by the word “toxin”. (And if you do that you will presumably be able to answer the question yourself.) As far as I am aware, the words has no unique scientific meaning, outside, perhaps, the specialism of bacteriology. It is enough that viruses infect and often destroy cells without getting into semantic arguments about toxicity.

It seems that the key here is the definition of "toxin" in a biology context. The best definition I have found is this one from Merriam-Webster:

Definition of toxin
: a poisonous substance that is a specific product of the metabolic
activities of a living organism and is usually very unstable, notably
toxic when introduced into the tissues, and typically capable of
inducing antibody formation.

Key aspects of this definition include that it is "a specific product of the metabolic activities of a living organism " (so e.g. cyanide or even HCl would not be considered toxins) and that it is "notably toxic". It's the latter characteristic that the SARS-CoV-2 proteins fail, as your article link shows at most roughly 50% cell mortality when the various ORFs are overexpressed in target cells.
Basically, those proteins are nowhere near toxic enough to be considered "toxins".
A WHO publication on biosafety (Lab biosecurity guidelines, Sept, 2006 WHO/CDS/EPR/2006.6) includes the description:

Toxins  are  poisonous  substances  produced  by  living cells or
organisms.

And you go to an English dictionary to find the meaning of a supposedly scientific word?

As I said, it's the best definition I could find. I think the "specific product of a living organism" and "notably toxic" aspects are key. I did not check dictionaries in other languages, but as you imply, those may provide additional useful information :)

I am not interested in dictionaries in any language unless I wish to find the first recorded usage of a term. For scientific meaning I would either consult a document on standards or nomenclature in the area or research usage in scientific publications.

Thanks. I was going on my own usage as a practitioner and finding a pre-existing definition that matched that.


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Were the Francevillian biota real?
The announced discovery of macrofossils suggestive of large multicellular organisms 2.1 Ga ago is now over ten years old.
Is there by now a scientific consensus whether these constitute real fossils of an abortive early evolution of complex life, or real fossils ancestral to extant life, or simply pseudofossils just looking like complex life?

Interesting question, you might be better off posting it to the Earth Science SE site for this one. All the papers discussing these fossils were all from the same authors, so I can't say one-way or the other.

Yes they are real.
it is a a collection fossils that are different enough from modern forms it is difficult to say exactly what they are but they definitely exist. Occasionally someone proposes a specific individual fossil might be Pseudofossils but so far they have held up to a great deal of scrutiny. Some are too regular to even be disputed. much like the Ediacaran they are just forms very different from anything we are used too.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0099438

I'm also a believer in them, but I'm interested to find out on what basis you found that the scientific community put them under a lot of scrutiny? All I could find were papers published by the same group, admittedly largely in well respected journals, but nothing showing any form of debate - which may in itself be telling of acceptance.

don't expect to find a lot of authors of papers from different places for fossils. Funding, physical access, ad the lack of paleontologists  tend to mean only those very interested publish papers especially on invertebrates.

Thanks. That makes sense, I had wondered if the situation were something like that - I don't imagine a whole bunch of people outside of geographically close countries get to Gabon in general.


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Do all stem cells have a full number of chromosomes?
Do all or only some stem cells have a full number of chromosomes?

Are you attempting to distinguish between totipotent and pluripotent stem cells here?

Not really, but is that one of the differences between totipotent and pluripotent stem cells? (one has a full number of chromosomes and the other has half the full number of chromosomes)

I guess I'm just confused by your question. What causes you to think stem cells wouldn't have a full set of chromosomes, since by definition they're the cells that can differentiate into many different types of cells, which means they generally need all that genetic information.  People have created artificial haploid stem cells, but I don't know if that's what you're trying to get at. And how would you count something like a muscle cell, that has many nuclei?

Yes, you're right. I also thought that it would make sense for them to have a full set of chromosomes, but I just read it somewhere (that stem cells don't have a full set of chromosomes) and so I thought maybe only some had half the full set and some didn't so I decided to ask to make sure. Well, thanks for the help. I guess they were (somehow) referring to the artificial haploid stem cells. It seems like I don't know enough about this topic so I'll just read about it more.


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Is circular DNA the same as plasmids?
Chloroplasts have circular DNA, but would it be right to say that they have plasmids? Are plasmids and circular DNA even the same thing?
Thank you in advance.

A plasmid is a length of circular or linear double stranded DNA that exists independent of chromosomal DNA with a cell (i.e. extra-chromosomal DNA) and often confers a selective advantage to an organism such as antibiotic resistance.  Plasmids have been identified in archaea, prokaryotes, and eukaryotes and allow horizontal gene transfer within a population, in processes such as conjugation, which proliferates the selective advantage contained within, if any exists.
Bacteria contain genomic DNA in chromosomes while a plasmid in the same bacteria contains non-genomic DNA such as genes that provide AR, virulence, pathogenicity, etc.. Bacteria may survive without plasmids depending on environment but without the chromosomal DNA survival is not possible.
Circular plasmids are often utilized in genetic engineering to transfect a target species with a desired gene for various reasons such as to enhance the performance of the organism, to understand the function of the gene, etc..
Not all plasmids are circular but all plasmids contain extra-chromosomal DNA.  Chloroplast DNA is contained within a chromosome and is not a plasmid.  Symbiotic theory of eukaryotic origin asserts that chloroplasts were once independent bacteria and this will perhaps allow you to develop an intuition as to why chloroplasts DNA is chromosomal rather than a plasmid.  The chloroplast could not survive without the DNA contained within the chloroplast chromosome so it is not categorized as a plasmid.

Your answer would be much better if you started with an actual definition of the term “plasmid”, based either on its original introduction or textbook or journal usage. Only then is listing of attributes really meaningful. (And the singular is bacterium.)

Hi thanks David, this is my first answer to give so I appreciate the feedback.  I can see you're reputation points and found your suggestion to be insightful to help me be more clear.  I've given a revision to my answer and would welcome further  suggestions.

I'd like to hear about "membranes" in that context: chloroplasts if in  membranes should thus make a difference.


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Do the quantum mechanical properties of the particles that make up DNA affect mutations in the genome?
Do quantum mechanical properties of particles, such as uncertainty, probability, tunneling, and so on, affect mutations in the genome?

Not that anyone has ever noticed, but it's not the sort of thing biologists look for as 1. They generally don't have the physics, and 2. There are plenty of macroscopic factors that affect mutations. It is interesting in a more general respect that the celebrated Max Delbrück, a physicist who made early contributions to molecular biology, did so without, as he had hoped, applying any of the new ideas of physics to biology. The supposition that explaining life would involve applying these was incorrect (or at least never realized).

@David Are you saying that quantum mechanics has no effect on life? But what about quantum biology?

I am only saying that the mechanisms in genetics are explicable in terms of general chemistry. Quantum biology, as far as I am aware, is mainly concerned with the energetics in systems like photosynthesis, which, although involving biological molecules, are essentially problems in their chemistry. Delbrück did not do quantum biology. However others may be aware of things I am not.

@David My question was about the processes and mechanisms in genetics that can be explained by quantum mechanics.

Did you google that question [processes and mechanisms in genetics that can be explained by quantum mechanics]? Because the answer is yes, they affect mutations, on the very first hit (of my search.) Third: Why does DNA spontaneously mutate? Quantum physics might explain.. [emphasis mine] So you probably knew the answer already, asking such a very specific yet detail-less question. Oh, and yeah, tunneling and waves and stuff.

@anongoodnurse I think David's point is that the quantum part is only necessary for understanding the physics of the chemical reactions, not things we ordinarily care about at the level of cells and organisms. Much like how relativity affects every physical interaction, yet if you want to know how long it takes for a ball you drop to hit the floor, Newton is entirely sufficient up to a very small rounding error.

@anongoodnurse I think these things raise some hackles because there's a tendency for people working in the quantum world to over-extend the value of their work into criticizing those who work with a simpler model or claiming their model is important because it's more accurate or is a "real" explanation or something, and it sounds cool because "quantum" is such a buzz word, yet offers no added real predictive value to models at a higher level that explain the world just fine. It's like if every time a physics TA writes F = ma on the board, a student in the back screams THAT EQUATION IS WRONG

@BryanKrause - "Not that anyone ever noticed" is a really broad (and possibly discouraging) statement. I'm not usually into physics (including quantum mechanics) much beyond the level you gave an example of. But I am curious by nature, and when someone asks something that takes me by surprise, I usually want to know something about it. Maybe because I don't know very much, especially about boundary pushing by quantum physicists, my hackles didn't get raised. And I find the question suspect. But thanks for the alternative way to look at this.

@BryanKrause But the question was quite specific: are there mechanisms and processes associated with mutations that can be explained only by quantum mechanics?

@АрманГаспарян I think what David is trying to get you to think about is what does it mean to be explained "only by quantum mechanics"? Given some chemicals that react in some way, you can measure all sorts of useful things like forward and backward reaction rates, equilibrium concentrations, you can model the effects of temperature and pH, all without knowing a single thing about quantum mechanics. Those numbers, though, do come from some physics. Does that physics matter?

If you want to understand the physics behind the chemistry, sure, maybe it does. But it doesn't matter to the typical biologist who just needs to know that the chemistry happens and in what conditions/how fast/to what extent, etc.

@BryanKrause I understand what you mean. However, not all processes in nature can be explained by ordinary chemistry (if it is not quantum chemistry).

@АрманГаспарян Well, electron transport is one area in biology where quantum chemistry is often invoked (as far as I know; this is really outside my area, except that people make bold, unsupported statements about quantum this and quantum that in my area as well :) ), and indeed, it seems like it may be important to understanding how exactly electron transport happens, but it certainly isn't necessary to understand the biology of electron transport, since you can write the end result in a simple chemical equation and go from there.

This issue in the philosophy of science is called "reductionism".

@BryanKrause I'll try to give an example. Quantum tunneling is a purely quantum effect that is not present in classical physics and conventional chemistry. If there was a mutation mechanism that would be caused by quantum tunneling, that would be the answer to my question.

@АрманГаспарян In biology we very rarely care about the mechanism of a chemical reaction, so there is no distinction. You can easily represent a chemical reaction that occurs due to quantum tunneling without invoking anything quantum at all.

Yes. (I mean, that's the answer to your question. You didn't ask for specifics.)
From Quantum and classical effects in DNA point mutations: Watson–Crick tautomerism in AT and GC base pairs:

Proton transfer along the hydrogen bonds of DNA can lead to the creation of short-lived, but biologically relevant point mutations that can further lead to gene mutation and, potentially, cancer.

So that's proton tunneling at work in DNA.
This isn't really a new idea. I found one paper theorizing this from the 80's.

authors: Арман Гаспарян


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Chromosomal disorders
I was reading about chromosomal disorders and encountered a line stating that

'An individual may lack one of any one pair of chromosomes'

So does it mean that an individual cannot have monosomy of two different chromosome pairs? Or does it has some other meaning. Please Help.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Welcome to Biology.SE. This is not a forum or tutorial service; it is a Q&A site where specific questions relating to biology get specific answers. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to [ask] a good question. In particular, we can't "explain" random quotes — which will be opinion (and thus off-topic). Finally quotes must always include a source!

The only "complete" monosomy that is survivable in humans is Turner syndrome.
So your source is a bit silly.
http://en.wikipedia.org/wiki/Monosomy

Theoretically anything can happen, but you also have to take into account firstly, the probability of such an incident (which is particularly rare in this case) and secondly, if the creature can survive after or even until birth, to be counted as an organism with that kind of anomaly. For instance, the odds of trisomy 21 taking place in humans is not much greater than that of trisomy 11, but almost all fetuses with trisomy 11 would be aborted and never make it to this world.

Please add further details to expand on your answer, such as working code or documentation citations.


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Do breakthrough infections spread attenuated virus?
No vaccines are 100% effective, so it's possible that patient A catches Covid-19 even after receiving two doses of vaccine. I understand that the risk is low, and the symptoms will generally be mild.
Now, patient A infects patient B who is not vaccinated.
Will patient B experience mild symptoms, or will their chances of hospitalization, ICU and death be the same as they were at the beginning of the pandemic?

Why should B show mild symptoms?

@Chris, I read that a virus is often attenuated by introducing it into a species in which it does not replicate well (https://www.sciencedirect.com/topics/neuroscience/attenuated-vaccine). I thought that the virus does not replicate well in a vaccinated person either; then I felt that I was jumping to conclusions and I thought I'd better ask here.

Attenuating viruses is a long process and nothing you can achieve with one infected person. This virus replicates pretty well in humans, so this is not a factor.

I would bet that, if it's replicating well enough to become transmissible, it's probably not going to attenuate. But that's just my handwaving explanation without having a closer look at the literature.

There's no way to know what effect passage through one vaccinated individual would have on an unvaccinated individual. The relationship between a virus's fitness in a particular host and the severity of disease it causes in that host is not straightforward, but generally we would expect a virus variant that can infect a vaccinated host well enough to pass on to another to be MORE aggressive and therefore cause more severe illness. With SARS-2 specifically, there's a chance a vaccine-selected variant could be milder, if the way it evades immune response is by more selectively limiting infection to those cells in the lungs that are involved in forming respiratory droplets and aerosols. (here is a reference if you want to read about mucosal vs. systemic immunity in COVID) My gut feeling is that such a mutation is much more complicated and therefore less likely than mutations that increase immune evasion and replication speed; which would lead to more severe disease.
Passage through animals leads to attenuation because the cellular machinery and immune response are different. A virus optimized for cows is no longer optimized for humans. A vaccinated human is still a human though, the mutations that work in one will work in the other.
Here is a paper discussing how HIV adapts to the immune system of individual infected humans, and how those strains are 'pre-adapted' to closely related hosts. You may find it relevant.


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Why do different people perceive the colors of the Northern Lights (Aurora Borealis) differently?
A few days ago, I was in Norway with a group of about 20 people. We were fortunate enough to witness an impressive display of the Northern Lights that lasted several hours. The next day, we discovered that while some of us saw the Aurora as clearly green, others perceived it as white or grayish (the split was about 50/50).
Our cell phone photos showed bright greens and reds. I understand that the cameras used long exposure times (about 4 seconds), allowing their sensors to capture much more light than our eyes. However, I’m puzzled as to why different people saw different colors.
Here are a few things to note:

There was no obvious correlation between the colors seen and factors such as age or gender. For instance, I am 53 years old and saw distinct colors that others, both younger and older, could not see.
We were all in the same location, far from city lights or car headlights. We watched the sky for over an hour, so our eyes were likely as dark-adapted as possible.
None of us are color blind.
No one saw the red color that appeared as bright as the green in the pictures we took.

The only somewhat reasonable explanation for the different experiences was the difference in pupil diameter between individuals (a smaller diameter means that less light enters the eye, so scotopic vision may be prevalent). However, it seems that the pupillary light reflex is only a minor part of adaptation to ambient light.
So, what could be the main factor influencing the varied color perception of the Northern Lights?

Remember your cell phone has its own colour balancing too.


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Do same DNA sequences lead to the same proteins in all organisms?
I'm not a biologist, but I am curious about a particular question about DNA.
As I understand DNA encodes proteins using special sequences of nucleotides and cells decode these proteins from DNA during cell division. My question is whether all organisms on earth have the same "decoding scheme" for DNA? Meaning that given a particular nucleotide sequence, will all organisms produce the same protein or some organisms evolved a different "decoding apparatus" that will produce some different protein?

The decoding scheme that you refer to is called the Genetic Code. Your question is answered on this list here. Your understanding is incorrect in certain instances. It is mRNA — not DNA — that is decoded, and this occurs all the time, and not particularly at cell division. These latter aspects of your question are very basic, which is why you really need to read the relevant chapters on transcription and translation in a text book.

Aside from the genetic code itself, "post translational modification" can affect protein sequence and structure. Here's a brief overview: https://www.thermofisher.com/us/en/home/life-science/protein-biology/protein-biology-learning-center/protein-biology-resource-library/pierce-protein-methods/overview-post-translational-modification.html


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If a person does not have green cone cells, then will he see the colour purple as purple?
If a person does not have green cone cells, then will he see the colour purple as purple? Since by default he should see green.
I am asking this because our brain interprets light that has red component and blue component as purple but it ideally should interpret it as green. Since we already have cones to detect green light our brain interprets this light as purple.


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What are the current theories on what causes the sunflower sea star wasting disease?
There's a prion disease that has wiped out 97% of sunflower starfish, and the only thing I can find about it is there's a small subsection of the starfish who are genetically immune.

Well, if it's known to be a prion disease (is it? What is your source for that?) then that's kind of the "cause" in itself, what exactly do you mean by "cause"?

The Wikipedia page indicates cause unknown, thought to be multifactorial.

https://marine.ucsc.edu/data-products/sea-star-wasting/


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Can a male Ginkgo Biloba tree bear one fruit?
It is well known that Ginkgo Biloba trees have sexual difference. There are male trees and female ones. I've seen female trees in Japan in the proper season, which is about now, there are lots and lots of fruit that fall under them. They vaguely look like plums, but when crushed they stink like dog's poop.
Now today, in France, I saw a huge Ginkgo Biloba, 150 years old, in a public botanical garden. Since it is a rather remarkable tree, they have put a panel telling its age, its size and specifying it is male. And indeed, if it were female there would be scores and scores of fruit below it.
But I saw one thing below it, looking vaguely like a plum, quite clean on one side, and a bit crushed on the other side. I picked it up, the skin was smooth to the touch, and smelled the crushed side, it stank like dog's poop. So it was quite obviously a Ginkgo Biloba fruit.
Is it possible that the male tree had, exceptionally, at least one female flower, was self-pollinated (or perhaps, was pollinated by another, younger and smaller Gingko Biloba tree in the same public garden but about 100 meters away, also male since there were no fruit below it either) and produced a fruit ?

It is normally dioecious as the OP states, however there are occasional exceptions.

A male Ginkgo tree at Kami Yagisawa, Minobu-cho, Yamanashi Prefecture,
Japan, is  shown to possess a small, localized, branch that produces
ovules that mature into viable  seeds. This tree is recognized as an
Ohatsuki Icho because of the occasional production  of pollen sacs on
otherwise normal vegetative leaves, but most of the abundant male
cones that it produces are of normal morphology.

Full text to be found at Researchgate Sex Conversion in Ginkgo biloba (Ginkgoaceae)
Looking up Ohatsuki Icho, gives "Pollen sticks to leaves", so an indication of another rare condition in which some of the catkins/cones that are pollen producing parts are found emerging from some leaves. - Thanks to Andrew T..
It is speculated that they evolved from monoecious trees, and that at some point the old pattern reasserts itself in a small (unspecified) number of specimens.

Thanks. So I was right, just as the tree you mentioned in Japan, the one here in Paris must have somewhere a small part that bore at least one ovule. The fruit was really impossible to confuse from anything else.

Absolutely. Sex-change in some fish was familiar to me, but trees, a whole new area I'd not been aware of. I notice that the linked paper is only about 8 years old - there may be more research into this in the future. @Alfred

If anyone has a better translation of Ohatsuki Icho, then please feel free to edit the answer.

Looks like Ohatsuki Icho (オハツキイチョウ) refers to the species variant of Ginkgo biloba var. epiphylla Makino and it's from お葉付き, which roughly means "(pollen) sticks to leaves" (the quotation already explains the meaning).

I think that generally, this is called "sporting" and the unusual feature is a sport: "A plant or an animal, or part of a plant or animal, which has some peculiarity not usually seen in the species; an abnormal variety or growth...."

@Wastrel - A sport is new, something not before seen, caused by a genetic mutation and is often is able to be passed on to offspring or through grafting. What this part of the tree has experienced is sex conversion, which (as this answer points out) has been documented in gingkos. If it developed, say, yellow and green stripes on the same leaves at the same time which persisted with propagation, that would be a sport. (If it doesn't already exist; that I don't know.)


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Help with B Cell Assignments in Single Cell Data
I am trying to assign cell types to the B cell subset of the PBMC 8k dataset from 10x (https://www.10xgenomics.com/datasets/8-k-pbm-cs-from-a-healthy-donor-2-standard-2-1-0). Cell type assignment is tricky, with a lot of overlapping marker genes specified in the literature. I am a bioinformatician, not an immunologist, and though I have found some interesting trends across the subsets of B cells, I want to make sure I don't embarrass myself by using the wrong assignments. Any help would be appreciated. As of now, I think I would call cluster 4 "transitional" or "naive", and cluster 7 "activated" or "plasma". I was previously grouping 19 in with 7, but the presence of B2M and TRAC (which seems more common on T cells, though it has been reported on B cells) is confusing to me...Any advice would be greatly appreciated.


text:
Do PI-SceI and PI-PspI from NEB work in each other's buffers?
I'm considering a plasmid design strategy that would allow me to use restriction enzymes to exchange plasmid inserts among different backbones. In this case, the plasmids would first be made through MoClo assembly of pL1 inserts into different pL2 backbones. Then, ideally I could exchange the whole complete insert to another backbone at a later date without repeating the GG reaction.
To do this, I was thinking to use homing endonucleases, which have large footprints and are thus unlikely to show up in a given sequence. I already have I-SceI in the plasmids to use for linearization, so can't use that one. That would have been convenient because I-CeuI from NEB and I-SceI both are 100% active in CutSmart.
The other HE options from NEB are PI-SceI and PI-PspI. Neither work in any of the standard buffers, but use similar buffers as each other:
1X NEBuffer™ PI-SceI

10 mM MgCl2
1 mM DTT
10 mM Tris-HCl
100 mM KCl
(pH 8.6 @ 25°C)

1X NEBuffer™ PI-PspI

10 mM Tris-HCl
10 mM MgCl2
1 mM DTT
150 mM KCl
(pH 9.2 @ 25°C)

I'm wondering if anyone has tried using them at the same time in one or the other's buffer?
Alternatively, are there any other good HEs out there I should look into?
Finally, is this even worth it? Or should I just re-run the MoClo reactions into new backbones? Would that be more efficient and reduce hands-on effort?
Thanks for any input!

Have you looked into gateway cloning?

Welcome to Biology.SE. If you look carefully at the NEB site you will find that these enzymes require very different temperatures for activity (37°C vs. 65°C) ...

Oof you're right! PI-PspI only has 10% activity at 37°C. Bad idea....
Yeah Gateway is possible, though I try to avoid it if possible. Would be weird too because transferring in would cause PB to switch to RL or vice-versa. So I'd need BP and RL versions of each backbone depending on which way I wanted to switch. I think the simpler solution is to just replicate the Golden Gate into different backbones as needed. That's very efficient and not that time-consuming (esp with all calculations essentially pre-done).

If you have questions, you can always call NEB's tech support. You'll get to talk to a real person who actually understands the products and the science. (I used to work for a company that was spun out of NEB and has the same tech support model.)


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How can I accurately determine how much someone likes a sound?
I was thinking about this question the other day. My first instinct was to evaluate the dopamine levels before and after listening to a tune. I proposed this to my friend in the medical field, and she said that it might not be the best way to assess how much someone likes a sound, since dopamine is released when the body feels pleasure. However, she can't think of an alternative. Is there a good way to do this? Preferably something that is feasible to do on human subjects in a non-lab environment (although this might be a lot to ask). Thanks.

You've rejected "ask them"?

@swbarnes2 Of course that is a possibility, but I was thinking of something more accurate than good/bad.

Whether they've actually bought the CD/MP3? Or concert tickets &c?  And on the other side, how much they'd pay for earplugs if trapped in a (pick your genre/artist) concert?

@jamesqf I was thinking less of a song, more of a tune, but thanks anyway

@TheBestMagician: What's the difference between a song and a tune, though?  Unless you mean that a song is sung by human voices?  But even then, it's possible to enjoy that simply as music.  I certainly don't understand Gaelic or medieval French, and I struggle with Latin & even Middle English, but I enjoy songs sung in those languages.

The gold standard would have to be to ask. Any other physiological parameter would just be based on correlation with what people report.


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Are living cells electrically neutral?
I found random scientific table which had a comment attached:

the cells must be electrically neutral.

Per my knowledge whole intracellular solution contains more electrons than protons (definition of negative charge) when cell rests and extracellular space is more or less electrically neutral, means it contains same number of protons and electrons at any time.
Could someone tell me whether my understanding is wrong or this comment below this scientific table I shared?

There are two ways to think about the "charge" of a cell. One way is by looking at all the chemical species inside the cell and calculating their sum charge. If you do this, you're going to get a neutral solution up to many decimal points of rounding error. Therefore, we don't really care or bother to do this. You'll get the same for the extracellular space, and really anywhere else you measure outside of a physics experiment. Electrical forces are incredibly strong, and when you get even modest charge separation the result is lightning.
In a table like is presented at your link, you can sum up some of the "major" anions and cations but you won't get anywhere near neutral; the comment is just making sure you don't think that based on the table there are no other charges there, we just don't care about them that much for membrane potential, they're boring and static. The reason we don't care about all the other ions so much when we calculate membrane potential is easy to see from the equations that actually tell us about membrane potential. Take the Goldman equation:

In this equation, you'll see we don't sum all charges inside and outside the membrane. Instead, we look at the ratio of concentrations of ions multiplied by their permeabilities through the membrane; anything that isn't permeable gets multiplied by zero and we ignore it entirely. The reason for this is that the potential across a membrane we measure isn't because there are measurably more or fewer positive or negative charges on either side, but that there is an imbalance in permeability of ions relative to their charge and concentration. Without any electrical forces involved, ions will tend to diffuse until their concentrations are equal on both sides of a membrane. However, if there is charge involved, the net diffusion is influenced by electrical forces such that for each ion there is some voltage at which the net movement of that ion is zero even though the concentration is not equal: that's the reversal potential for that ion calculated by the Nernst equation. The Goldman equation gives the weighted sum of all of those ions that can transit the membrane to give the overall equilibrium potential when there is zero net flow of charged ions.
I'll recapitulate the reference I quoted from Alberts et al here:

For a typical cell, 1 microcoulomb of charge (6 × 10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly 1 V. This means, for example, that in a spherical cell of diameter 10 μm, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of K+ ions in the cytosol.

Extrapolating from that, if we really only had the ion species in Table 11-1, what would that mean? Intracellularly, that table shows about 140.5 mM of net positive charge inside the membrane. 10 um sphere * 140.5 mM * 6 * 10^23 ions/mol = about 3.5 x 10^11 positive ions to move over 1.3 x 10^-5 square cm of membrane. 3.5 x 10^11 / (1.3 x 10^-5) / (6 x 10^12) = about 4500 volts to get to neutral - there aren't any biological voltages anywhere near that range.
Back to the title question:

Are living cells electrically neutral?

Yes, if we think about the summed charges inside the solution of a cell. However, if you look across the plasma membrane of a cell, you will find there is a miniscule charge separation at rest, principally because membranes are permeable to potassium ions and there are more positively charged potassium ions inside cells than outside of them (for most cells and solutions). Because a few more potassium ions flow out of the cell than flow in, there would be a little more positive charge flowing out than in if the voltage were zero; this creates a voltage across the membrane until there is a balance between charge and concentration gradients, and we say that most cells are electrically negative (in a typical range of -50 to -100 mV for mammalian cells). However, this is just charge sitting across the membrane that acts like a capacitor, you'll find positive charges sitting against the outside of the membrane as they get pulled toward the negativity inside the cell.
Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). Ion channels and the electrical properties of membranes.

Thank you for clearing out these misconceptions. Now I've understood that resting potential (~-70mV) what is commonly suggested by many sources, is potential difference across membrane (so charge difference in regions near membrane), which does not mean that whole cell is negatively charged.
But, Could you elaborate more around why cell (let say at rest) is thought to be neutral at default? Why even small charge could not it have? Would it actually be similar to lighting phenomenon?

@LashaBukhnikashvili I don't really know what to say besides what I've already written in this answer. It's not perfectly neutral, but it's so close you might as well consider it as such. There's just no process to create any substantial level of charge separation, biologically or otherwise.


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How frequent are transposons in action?

A transposable element (TE, transposon, or jumping gene) is a DNA sequence that can change its position within a genome, sometimes creating or reversing mutations and altering the cell's genetic identity and genome size.

Almost 50% of the human genome contains transposable elements. I have several questions:

how rarely are they changing positions along the genome?
Are these events most likely to occur during Meiosis, Mitosis? Or they could come in an action in other parts of the cell life cycle?
Do humans nowadays contains almost the same genetic information (99,9%) including these elements? or does similarity occur only in the protein-coding region?

Generally, we ask that answer-seekers only include one question per post, or, at most, a few highly related questions. It could be argued that your first two questions (1. how often do transposition events occur? 2. during what point in the cell cycle does transposition occur?) are related, but your third question (3. do measurements of inter-person genetic distance account for TEs?) is distinct. Please edit your post to focus on one question, and, after doing some preliminary research, consider writing your other questions as separate posts.

To answer your first question and address the title of your post, see this review on active TEs in the human genome. Some excerpts:

Although a large proportion (44%) of the human genome is occupied by transposons and transposon-like repetitive elements, only a small proportion (<0.05%) of these elements remain active today.

Active human transposons have been estimated to generate about one new insertion per 10–100 live births.


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Question about the use of Var. in different species
I just recently started studying Taxonomy and seem that I am the only one that got such question in the Internet...so pardon if this is a silly question...and my silly grammar because it is not my first language.
After genus we have species, sometimes subspecies and variety. For example, the Full Red Albino Guppy breed is named Poecilia reticulata var. "Full Red Albino" because it is one of the variety of guppies. But I was soon confused when it comes to succulents and dogs/cats.

Echeveria elegans 'Alba' is one of the variety of Encheveria elegans, why it is named so with the '' marks instead of Echeveria elegans var. "Alba"?
Dalmatians/Maine Coon are a breed of dog/cat under Canis familiaris/Felis catus, so they are actually varieties of the subspecies/species but I never see anyone naming them as Canis lupus familiaris var. "Dalmatian"/Felis catus var. "Maine Coon"?

I know there is no point of naming them so but I am just curious about if this is scientifically correct or I got the wrong concept. Thanks for reading till here.


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What does the hornet do on the ivy blossoms?
We've got blooming ivy growing around a tree. Since several weeks lots of hornets have been whirring in the foliage and I wonder whether they want to feed on insects that are lured by the blossoms or whether they come for anything they get from the ivy plant.

Hornets, just like wasp in general, hunt insects to feed their larvae but feed themselves with carbohydrates like nectar (or lemonade). So it is quite probable that the hornets are feeding on the nectar of your ivy. wikipedia


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Could abiogenesis still be ocurring?
From my understanding, most biologists believe that under certain conditions life can form from inert chemicals. If the conditions for this to happen still apply, is it possible that in bodies of water single-cell organisms could still be forming?

From the latest I've heard or read, there is too much oxygen in the atmosphere and oceans... Maybe highly anoxic places might suffice... Semi-arid areas on early land with small pools of water and underwater vents are where most scientists believe life arose... Way too much toxic/reactive O2 there now....

Welcome to SE Biology. Please search the site before posting. Searching for "abiogenesis" shows several related questions, e.g. https://biology.stackexchange.com/questions/59892/is-abiogenesis-possible-today


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Does the body make alterations to fatty acids before their storage?
I was wondering if you would be at all able to help me with some questions I can’t find the answers to. I’m a first-year uni student doing some research for the fun of it but I’m really struggling to answer some of the questions I’ve thought up and would greatly appreciate any help!
I’m trying to research how the body stores the fat it consumes. I understand that fat is stored in adipocytes as triacyl glycerides (TAGs) but I’m trying to find some information on which fats the body stores.
For example, if you were to consume some olive oil (oleic acid), would the body synthesise TAGs from the oleic acid or would the body convert the oleic acid into another fatty acid before this step (like palmitic acid)? Does this have any impact on the body’s ability to store fat (or the energy density of the fat?)? Does the body have a preferential approach to the storage of saturated vs unsaturated fats and are these fats stored in different places preferentially?
I’ve read through 9th Edition Biochemistry by Berg, J et al. (2019) which is where I raised these questions from. I’ve also looked through 3rd edition Molecular Biology and I’ve read a few papers on Google Scholar but none of them had the answers I was looking for.
If anyone would be able to offer any help, I would be eternally grateful Thank you in advance!
Mason

The books you have consulted may be good for certain things, but not for mammalian energy metabolism. Older books such as Lehninger are more suitable. Looking at the really old literature (1965) some fatty acids will be oxidized to acetyl CoA, whereas others would appear to be utilized directly. If this is your research project you need to start with this older work (https://link.springer.com/content/pdf/10.1007/BF02636928.pdf) — use your university library to access it — and search for more sophisticated recent studies on Google Scholar using a query like "fate of dietary fatty acids".


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What is the solubility of rotenone in ethanol?
I’m trying to kill SH-SY5Y cells with rotenone, but the rotenone does not kill. I saw an article where rotenone is soluble at 5mM in ethanol. I dissolved 1.7 mg in 1 ml of ethanol to obtain a 1ml of 5mM solution. I also tried DMSO but it’s viscous when dissolved in DMEM. Is there something I am doing wrong?

How much DMSO are you adding to how much volume of media?

Also, your solution is only 4.3 mM, not 5. Please [edit] your question and add more details, including how old your rotenone stock is and how it's been stored, how old the solutions are and how they've been stored, the concentration you're using to kill the SH-SY5Y cells, how long after the addition of rotenone you're waiting before checking for cell death, and the manner in which you are looking for cell death.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

This sort of question, although related to practical biology, is not really suitable for this site, because it is, in effect, a question about the properties of a molecule that anyone can find by searching the web. And if you finish the [Tour] and read the Help on asking questions you will see that this is what we expect from posters. I know nothing about rotenone, am not familiar with organic chemistry databases, but was able to find that NCBI has a PubChem site documenting compounds. Look here: https://pubchem.ncbi.nlm.nih.gov/compound/Rotenone#section=NSC-Number .

Actually, as written, it looks more like a Chemistry.SE question.


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What is right below skin?
I was skinning a gopher so my cat can eat it (it was a pest and we didn't want to waste it). I thought its organs would fall out and make a mess, but that didn't happen. There was this sticky, transparent substance that surrounded its insides. What is this casing called? My dad said it was mucus but that isn't specific enough since there is mucus inside the stomach so I don't think they are the same.
I think this casing is found in all multicellular animals but I couldn't be sure.

Based on your reference to organs falling out and the overall description, I presume you're thinking of the abdominal cavity primarily, so there you'd be looking at the peritoneum or possibly the serous membranes of other organs (e.g., pleura, pericardium). These are membranous (in the general sense, not as a cell membrane) connective tissues covering the organs found in the abdomen and chest.
Other things you'll find underneath skin would include layers of fat, other connective tissues, muscle.
Here's a labeled image of a mouse dissection from Friedrich, L., Schuster, M., de Celis, M. F. R., Berger, I., Bornstein, S. R., & Steenblock, C. (2021). Isolation and in vitro cultivation of adrenal cells from mice. STAR protocols, 2(4), 100999.:

You might also look for dissections of fetal pigs or cats, which are commonly used in laboratory demonstrations for students (more often cats longer ago, more often fetal pigs these days).

Thank you for your great answer! I believe it is the peritoneum that I was observing.


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What coronaviruses have been identified in racoon dogs?
Christian Dorsten says in an (Apr 26) interview in the Guardian that racoon dogs as [intermediate] source of coronavirues have been overlooked (in China):

Q: What do we know about that intermediate host – is it the “poor pangolin”, as it’s come to be known?
A: I don’t see any reason to assume that the virus passed through pangolins on its way to humans. There is an interesting piece of information from the old Sars literature. That virus was found in civet cats, but also in raccoon dogs – something the media overlooked. Raccoon dogs are a massive industry in China, where they are bred on farms and caught in the wild for their fur. If somebody gave me a few hundred thousand bucks and free access to China to find the source of the virus, I would look in places where raccoon dogs are bred.

So what studies are there on coronavirues in racoon dogs up to now? (A quick search found a 1992 US paper that some coronavirus [unsurprisingly] infects racoons too. But I can't find much else. Is there more up-to-date survey? Also, duh, racoon dogs aren't even the same family [Canidae vs Procyonidae].)

Here's an abstract for a paper from 2006: https://www.ncbi.nlm.nih.gov/pubmed/16450706

An RT-nPCR assay was used for testing fecal samples of dogs, foxes, raccoon dogs and minks for the presence of canine coronavirus (CCV). The animals were raised in homes, dog schools or farms... Among 24 raccoon dogs samples, 22 were CCV type II-positive, and from those 16 were additionally type I positive.

Here's another paper from 2003: https://www.ncbi.nlm.nih.gov/pubmed/12958366

A novel coronavirus (SCoV) is the etiological agent of severe acute respiratory syndrome (SARS)... Evidence of virus infection was also detected in other animals (including a raccoon dog, Nyctereutes procyonoides) and in humans working at the same market.

So at least a couple types of canine coronavirus and other strains closely related (but not identical) to the coronavirus that causes SARS.

Racoon dog is almost like dog (only 10 million years, human and chimpanzee is 6)

So it seems obvious the canine betacoronavirus_1 (OC43 & BCoV related) CRCoV infects racoon dogs


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Is the SHC014 chimeric coronavirus "eerily similar" to Covid-19 in anything but a journalistic sense?
Gulf News writes:

In the virology community, their project is known as "chimeric coronavirus", eerily similar to COVID-19. This chimera is created in a petridish, reportedly with the "surface spike protein (S protein) of a coronavirus found in horseshoe bats, called SHC014, and the backbone of a SARS virus that could be grown in mice".
Here's the scary bit: In the lab (we don't know which one), this new coronavirus was found so potent it could infect and replicate in human airway cells naturally. It also infected mice lung cells. It's one of the experiments which prompted Prof Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris, to warn that such research is "misleading" and "irrational", stating thus: “The consequence of any accident would be anywhere from a handful of infections to a catastrophic pandemic.”

Is this SHC014 chimeric coronavirus "eerily similar to COVID-19" in a scientific (not just journalistic) sense? Have any scientific publications drawn a parallel between the two viruses?
(I know that SARS-CoV-2 is most closely similar to RaTG13 at whole genome level and at RBD level [most likely] to Pangolin-CoV. I'm asking what if any scientific relevance does SHC014 have to Covid-19.)

And I think this worth answering because people keep bringing up this SHC014 on skeptics, unfortunately just in the form of "nudge nudge wink wink" https://skeptics.stackexchange.com/questions/47429/were-zhengli-li-shis-and-ralph-s-barics-research-groups-the-only-groups-in-th ; https://skeptics.stackexchange.com/a/47378/29579 rather than any claims that could be directly answered. Likewise journalists like to bring it up as per above, but it's a again a wink-like statement. So, I can't use/challenge it as such on skeptics.

The lab is Baric lab at Chapel hill, North Carolina.

The "similarity" of this specific chimera was addressed in a recent paper concerning the lack of evidence that SARS-CoV-2 is lab-grown:

Another claim in Chinese social media points to a Nature Medicine paper published in 2015 [7], which reports the construction of a chimeric CoV with a bat CoV S gene (SHC014) in the backbone of a SARS CoV that has adapted to infect mice (MA15) and is capable of infecting human cells [8]. However, this claim lacks any scientific basis and must be discounted because of significant divergence in the genetic sequence of this construct with the new SARS-CoV-2 (>5,000 nucleotides).

Liu, S. L., Saif, L. J., Weiss, S. R., & Su, L. (2020). No credible evidence supporting claims of the laboratory engineering of SARS-CoV-2. Emerging Microbes & Infections, 9(1), 505-507.
The "eerily similar" nature seems at most to be something well recognized by virologists, particularly in the wake of SARS: coronaviruses circulating in bats could become dangerous to humans if mutations occur in key parts of their genome or recombinations occur with other coronaviruses in bats or intermediate hosts. That's more or less what happened with the first SARS and more or less what happened with SARS-CoV-2, as best as can be told right now.
I'd also take a bit of umbrage at the language used in that article:

this new coronavirus was found so potent it could infect and replicate in human airway cells naturally

seems like a bit of fear-mongering. Any virus that affects humans can "naturally replicate" in human cells: the author could have merely written that instead of calling it "so potent".

Coronavirus main lineages

alphacoronavirus : bats and many mammals including 229E and NL63 (ACE2), Feline-CoV, TGEV
betacoronavirus : bats and many mammals, 15% similarity to the previous, need to look at the RNA polymerase and the general structure to establish a phylogenetic relation

Mers (Camel) plus a bat lineage
MHV, OC43, HKU1, plus a rat and a bat lineage. Humanity probably had a great influence on this lineage
Sarbecovirus

SARS-CoV (ACE2) and SHC014 (ACE2, 93% similarity) and many non-(ACE2) bat viruses (90% similarity)
SARS-CoV-2 (ACE2) 80% similarity to the previous and 96% to RaTG13 (ACE2) and 92% to Pangolin (ACE2)

gammacovonavirus (avian, beluga)
deltacovonavirus (avian and swine)

As you see SARS-CoV-2 is very very close to the virus you are mentioning, even if there are enough difference (and bat and Pangolin viruses) to be 100% sure its emergence is totally unrelated to the SARS-CoV and SHC014 experiments. Until this year everybody would have considered SARS-CoV-2 as too distant to SARS to be a danger.
Wuhan's lab is specialized in ACE2 Sarbecoviruses. But the chimeric CoV and the controversy and condamnation of gain-of-function researches was about Baric lab in Chapel Hill, North Carolina, to which Wuhan participated by providing SHC014, the bat virus using ACE2 they found 2 years before. Note everything was published in Nature, there was nothing hidden. Also the chimeric study proved that SHC014 wasn't able to infect human cells, not because of its spike but its backbone, which was reassuring for a possible reemergence of SARS. On the Neertheland, USA and Japan side there was a similar story about H5N1 mutants and chimera.

Interestingly that last story mentions a funding pause for GOF research between 2014 and 2017. The Shi-Baric paper on SHC014 was published in 2015, but I guess the work was done in 2014 before the "freeze". Also Baric has published such papers before e.g. in 2008 without Shi being a co-author, which lends credence that (most of the) work was done at the NC lab.

Actually the 2015 paper even says "These studies were initiated before the US Government Deliberative Process Research Funding Pause on Selected Gain-of-Function Research Involving Influenza, MERS and SARS Viruses (http://www.phe.gov/s3/dualuse/Documents/gain-of-function.pdf). This paper has been reviewed by the funding agency, the NIH. Continuation of these studies was requested, and this has been approved by the NIH."


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What could independent investigators learn from the first (known) copies of the virus from Wuhan, if they had (physical?) access to these samples?
RFI reports:

"You have to remember -- these labs are still open inside of China these labs that contain complex pathogens that were being studied. It's not just the Wuhan Institute of Virology," Pompeo told reporters.
"It's important that those materials are being handled in a safe and secure way such that there isn't accidental release," Pompeo told reporters.
Pompeo cited the example of nuclear facilities, pointing to the rigorous global inspections to ensure safety.
He renewed concerns that China has not shared a sample of the initially detected virus, known scientifically as SARS-CoV-2.
"We still do not have a sample of the virus, nor has the world had access to the facilities or other locations where this virus may have originally originated inside of Wuhan," Pompeo said.

(China has now rejected this US call as being "politically motivated" but they weren't terribly specific beyond that.)
Would China [physically] sharing "a sample of the initially detected virus" (which of course begets the question which sample is that precisely--but let's assume they share all 40 or so initial samples they reported/discovered back in Jan) have any scientific value? E.g. is [physically] sharing those samples (more broadly) likely to shed any additional light on the virus' origins? (In that regard, have Western scientists asked for those [physical] samples, or said they are important for China to [physically] share them, independently/before the US political leadership's involvement in the matter?)
For more context, a Yale med page from January says:

Two weeks ago, we didn't even know what the nCOV2019 virus was. Today, thanks to China’s quick public release of the initial nCOV2019 virus genome [...] To go from unknown pathogen to diagnostic tests so quickly is incredible! The scientists at the Fudan University, China CDC, Chinese Academy of Medical Sciences, Chinese Academy of Sciences, Zhejiang Provincial CDC, and the Thai National Institute of Health should be highly praised for making their data rapidly available to the public.

A bit later, Chinese researchers published a paper on 10 genomes from the initial outbreak in Wuhan. The (FASTA) data for those seems publicly available, although behind a registration page.
So, per comments below, if Pompeo means something else by "sample of the virus" (not physical sample[s]), what is that?

You interpolate [physical(ly)] throughout - does that mean that you are asking about physical sharing only, as opposed (e.g.) to sharing complete genome sequences of all the samples?

@BenBolker: I'm willing to be corrected that Pompeo meant something else, as you suggest. (E.g. if non-Chinese experts said that such extra sequences would help.) I know China shared some genome sequences, do you think if they shared more that would elucidate the kind questions that Pompeo is interested in, like the origin of the virus?

@BenBolker: https://www.thelancet.com/article/S0140-6736(20)30251-8/abstract "We did next-generation sequencing of samples from bronchoalveolar lavage fluid and cultured isolates from nine inpatients, eight of whom had visited the Huanan seafood market in Wuhan. Complete and partial 2019-nCoV genome sequences were obtained from these individuals. [...] The ten genome sequences of 2019-nCoV obtained from the nine patients were extremely similar, exhibiting more than 99·98% sequence identity. "

@BenBolker: "These data have been deposited in the China National Microbiological Data Center (accession number NMDC10013002 and genome accession numbers NMDC60013002-01 to NMDC60013002-10) and the data from BGI have been deposited in the China National GeneBank (accession numbers CNA0007332–35). " And the data seems available on http://nmdc.cn/nCov/en although it seems to require a login to download the actual fasta files. (They have a registration page, alas the latter seems to only be in Chinese, and I haven't tried to use it.)

The premise of this question presupposes the veracity of a Trump agent, whose behavior is political, in the least.

@AlexReynolds: it doesn't presuppose it, I'm asking if there's some science base base/logic behind that demand. That last sub-q was because of Ben's (initial) comments which suggested that Pompeo wasn't asking for physical sample, although later in his answer Ben seems to have changed his mind about that.

Per related q here I see that asking for login in order to download full sequences is not uncommon even in some Western countries. And from the MIT article linked by iayork, it seems there are bioterrorism reasons to ask for logins.

I'll take a shot at this. It's my impression that most of this is political rather than scientifically grounded.  There are reasons to want physical samples of viruses (rather than just genomic sequences), e.g. if you want to do experimental (in vitro or in vivo) studies on a particular virus strain. (It might be theoretically possible to edit the genome or reconstruct the genome of an earlier strain, but it's much easier if you have the desired viral strain in hand.)
Based on this Financial Times article (which may or may not be accessible without a subscription/accepting cookies)

Mr Pompeo added the Chinese Communist party had still not shared virus samples with anyone outside China, impeding efforts to understand how it emerged.
A researcher at Wuhan Institute of Virology, who declined to be named, told the Financial Times earlier this month that China had not shared samples of the live virus with the WHO as the country “had already published plenty of information” such as the genetic code of coronavirus.

It does seem that almost all of the research on the origins of SARS-COV-2 is based on genome sequences rather than on phenotypic studies (i.e., in vitro and in vivo studies of actual viruses).
I don't think viral samples would actually be very useful (that's why I said at the beginning that I think most of this argument is political rather than scientific). In principle I guess you could use the viral samples from an early stage  do experimental infections in different animal species, but I don't know that any researchers actually want to do that, and I don't think there's been enough phenotypic evolution in the last few months that the early-epidemic viral samples would behave that differently from current samples ... it's also likely that researchers could study the effects of particular mutations (observed in genomic sequence) by modifying viral samples they had in hand.
To take an example from an earlier pandemic, researchers have done experimental studies in mice to show how particular mutations influenced the virulence of earlier flu strains. This is an example where it's useful to have an actual virus rather than just the genome - but in this case the virus was actually reconstructed from knowledge of the genome ("two isogenic recombinant chimeric viruses were created with an influenza A/WSN/33 virus background containing the PB1 segment from the HK/156/97").

Thanks for that clarification. So. as I suspected, the Chinese rejected the US request interpreted as a request for live virus samples because they though/said the genetic info they have published suffices. But besides validating my q to some extent, this isn't really answering it. Why are domestic live samples not enough? Why are live samples from China in particular necessary in the US?

More precisely, in re your last para, when have "phenotypic studies" elucidated the origin of an outbreak? Are there [past] examples?

Thanks for the update. (+1)

Ralph Baric already cloned the virus from Chinese sequence data. This is just politics.

@layork feel free to post your own answer, or edit my question (if I don't do it first)


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Arizona spider that I cannot identify - help?
I cannot seem to find a "duplicate" photo of this spider anywhere and am curious what it is. It came by to say hello on my back patio in Vail, Arizona so I snapped this shot.
Any input would be amazing so I have more info if I should encounter another.
Thanks!

Could well be Latrodectus sp. Known as "widow spiders" including  the famous "black widow" Compare with this photo, but I'll let someone more knowledgeable ID this one.

It's a subadult female Western Black Widow, Latrodectus hesperus.  The pattern on the back will fade to black when she molts into her final adult growth stage, but the red "hourglass" marking on the underside will be quite visible from an early stage.  Good photo!  You can nicely see the big "mecha" legs that make adult Widows stand out so much from related Theridiid (comb-footed) spiders.  Even young female Widows can deliver a serious (but usually not dangerous) bite, but not all bites deliver a full load of (or even any) venom.  Still, and even considering that these spiders are extremely inoffensive, I wouldn't care to handle one myself.  Accidents happen!
Here's a link and photo:
https://bugguide.net/node/view/1854758


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How do Gram + bacteria use a proton gradient for F-type ATPase?
Does anyone know of any papers showing how Gram positive Fermiculates or Actinobacteria use  a H+ gradient for an F-type ATPase, It seems impossible since there is no outer LPS membrane to maintain the protons in a periplasmic space. Is the use of ATPase for production of ATP exclusively a Gram negative thing?
I found this question "Production of ATP in Lactobacilli" but no answers:
https://biology.stackexchange.com/questions/14669/production-of-atp-in-lactobacilli

Don't have an answer, but it seems to me that given that the Gram negative outer membrane is stuffed full of porins, there is no barrier to proton loss in this case either.

@AlanBoyd Are porins permeable to hydronium ions as well as water?

found this on wiki: This cation is often used to represent the nature of the proton in aqueous solution, where the proton is highly solvated (bound to a solvent). The reality is far more complicated, as a proton is bound to several molecules of water, such that other descriptions such as H5O2+, H7O3+ and H9O4+ are increasingly accurate descriptions of the environment of a proton in water

Protons are pumped out of the bacterial cell by the electron tansport chain. This creates a protonmotive force with two components, one due to the difference in proton concentration, the other due to the membrane potential that is created. In bacteria and mitochondria it is the membrane potential component that provides most of the driving force to pull protons back in through the ATP synthase. Thus the fate of the protons outside the cell doesn't matter too much. Even if you were to buffer the exterior absolutely, the fact that charge had moved out would drive ATP synthesis.

"the fact that charge had moved out would drive ATP synthesis."
this is only true if the protons are going down a concentration gradient, if they work against the gradient ATP is being used not synthesized...

unless there is chlorophyl involved (ex. chlorophyl G in Heliobacteria) and then there's some oxidoredux work dunno by which electron carrier...

but what if a bunch of fermiculates are in a small space and the fluid isn't buffered, it could work as a community...

In response to your first comment, protons would move up a proton concentration gradient if the membrane potential was favourable, until the chemical and electrical potentials were balanced.

do you know of a good review article on electric gradients causing a substance to move against a chemical gradient in a biological context?

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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The Operation of tuning in the S1 layer of ventral model
According to my previous question in ventral Stream pathway and architecture, I want now to get a brief example about how the S1 layer is constructed. In other words, how all the simple units are tuned with the gaussian-Like tuning (for example). I am only interested to get such a cartoon example in step by step how this operation can be achieved in given of inputs (which inputs? and what we mean about these inputs?) in order to obtain the tuned simple units.
We all know that each simple unit is obtained after a tuning operation around their inputs (Subunits) in order to select an optimal output which corresponds to the preferred orientation for such a simple unit.
Moreover, I know that the S1 layer units perform a convolution on regions of the raw input image using gabor filters at different orientations and sizes. The entire population of S1 units represents a convolution map of Gabor filters of different sizes and orientations with the entire raw image (really I didn't understand this point) you can read the subsection 2.2 in this article
The image below contains the image to be recognized by the brain and some simple units obtained after the tuning operation. So what I want is to obtain a brief example which can include the details (step by step) of how the operation of tuning can be achieved.

i didn't understand well the concept. That's why i need a real example with a specific image which can contains all the steps described in my attached image (step by step) because i still don't understand what we mean about inputs x, etc.
So please if anyone can give me a real example with a specific image which can respond briefly to this attached image

I'm quite busy at the moment. Perhaps tonight I might have some time to answer this. :'(

ah don't worry :) thank you so much, anw i put an image in the answer below. But i didn't understand well the concept. That's why i need that you give me a real example with a specific image which can contains all the steps described in  my answer below (step by step) because i still don't understand what we mean about inputs x, etc.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Need help identifying this microbe

Sorry for the bad image, we don't have a camera hooked up to our culture room microscope yet. But Has anyone seen these kind of (what I'm assuming are) contaminating bacteria before? We see these from time to time in our transgenic A431D/MDA cell lines. They're not motile. They're not visible by eye so I'm assuming they're not fungi either. The media we maintain these cells in is supplemented with geneticin (G418) antibiotic for selecting the transgenic clones.
If you've come across these, could you also share how you dealt with them?

Have you searched the literature for geneticin resistant bacteria? Did you do a gram stain? I doubt anyone can identify the bacteria from that photograph. A wild guess might be possible (Acinetobacter?), but I don't see how that would really help you.

From a practical perspective, if you have contamination like that, the best course of action is to just dump the cells and start over. Go back to earlier passages in your frozen stock. If they're all contaminated, you may have to re-derive the cell line. It is extremely difficult to rid cells of contamination 100%. If even one viable cell remains, it can start multiplying again in culture. It's not impossible, it's just a lot of work.

What magnification are we looking at here? Many fungi (especially yeasts) are microscopic, and significantly smaller than your mammalian cells. If they are bacteria, you're not really going to narrow it down with much confidence by looking at microscope images alone. I'm seeing a couple of potential diplococcus pairs, but that doesn't get you much closer to a positive ID on it's own.

I'm assuming you are meaning the blob-like thing in the middle of the picture, below the senescent cell? If so, does it get bigger over time or you find a lot more of these with time? If not, then there's a good chance that it's not contamination, but something like an apoptotic cell or a lump of something from the FBS.

please update with 1) magnification of image, 2) which object your are asking about, 3) and other relevant information about media/culture/storage/etc.

@MattDMo - I agree with you completely. It would be nice to know what got in, though. There might be a clue as to how it got in.

@anongoodnurse but sometimes, you don't want to. I once worked for a pharma company doing QA investigations of environmental monitoring failures. In one case, they identified contamination in the air (in a non-critical area, fortunately) as Gardnerella vaginalis. No one had any desire to further investigate its source. We just called it "resulting from human presence in the area" and left it at that...

@MattDMo  - Oh my word, lol! That is a bit awkward...

Couldn't you draw  a circle around the microbe in question? Like, with whatever basic image software your computer  has.

I am assuming you are referring to the blob thing in the middle of the pictures. Very hard if not impossible to say what is it. If I was you I would do a PCR on the 16S rRNA gene and send it for Sanger sequencing. the results can then be blasted against nrNuc databases in NCBI, you will have then your answer.


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What is the oxygen concentration in the lumen of the small intestine?
I am researching how oxygen affects enzyme activity in the small intestine, and I need to know how much oxygen there is in the lumen. I understand that the average amount of O2 in the lumen is ~2% (<10 mmHg), however I am curious as to how the number changes from the beginning of the small intestine to the end. If you were to measure O2 concentration from the beginning to end, would it be a decreasing linear or exponential curve.

From a recent review by Konjar et al. (2021), see Figure 2 and associated text:

There is also a steep decrease in oxygen longitudinally from the small intestine towards the colon.

Longitudinally—from the small intestine to the colon—the oxygen level
drops (Figure 2) [15,16], and a negative gradient is also observed
from lamina propria towards the lumen. To illustrate this, in mice,
pO2 drops from 58 mmHg in the stomach to 32 mmHg in the duodenum,
through 11 mmHg in the ascending column and to 3 mmHg in the sigmoid
column (all values measured using electron paramagnetic resonance,
EPR) [16].

For your convenience, I link references 15 and 16, respectively.

Although this is helpful, the values are taken from experiments done on mice. I am interested in the human small intestine.


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Why do the components of PCR mixture need to be added in a specific order?
I have recently been told that the components of a PCR mixture need to be added in a specific order: primers, dNTP, and finally polymerase. May I know why this is the case?

Welcome to the Biology Stack. Please take a [tour] and visit the [help] for more information on what we do here. Please also note the homework policy, which requires questions to contain evidence that the asker has attempted to answer the question for themselves. On that note; what do you know about those components and why might you add polymerase last (what does it do, and what could it do if you add it earlier?)?

you may be able to find your awnser here: https://biology.stackexchange.com/questions/79024/why-is-dna-polymerase-added-at-the-end-of-pcr-reaction

Polymerase last: One reson is that pipetting conditions are vastly differing by person, I.e. a lot of people don't keep the reactions on ice. When no hot-start polymerase is used, pipetting it in too early in a room temp. reaction mix might lead to unintended reactions.


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How is melatonin production related to proteins produced by clock genes?
I am a high school student learning about feedback mechanisms. My teacher gave an example of how proteins produced by clock genes are related to melatonin production. However, I'm confused about the relationship between constant darkness, clock gene protein production, and melatonin production. My teacher said that constant darkness results in a drop in proteins produced by clock genes, but wouldn't melatonin production increase in constant darkness? Does this mean that the relationship between clock gene protein production and melatonin production is inverse? I would appreciate clarification on this topic.

I don't know much about this topic, in the absence of a real answer though, I'd suggest looking at a review paper on the topic: https://www.sciencedirect.com/science/article/pii/S0928425711000040?casa_token=VRcXQ1EiXEMAAAAA:1oQJp3oNyRn9cEIZqEhbU4RWHUoWDQDi3HSdYK5xsVixDhigc4gKMk_G8xmQdkf-jIE3WAHydus.


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Why are mallards ornately green despite lack of sexual selection?
Mallards reproduce by group sex, with multiple males mating with a female against its will. This means that the common explanation of ornate birds evolving due to sexual selection isn’t applicable to them, so I’m curious why else they would evolve their green heads. Could it be a vestigial trait or are there any other explanations?

Do you have a reference for the claim that mallards reproduce without female mate choice?

there are a lot of studies of rape in mallards, that doesn't mean that the female mallard doesn't choose a mate and avoid the others, and you can also read about mallard pair behaviour, here's a broad overview: https://www.newscientist.com/article/dn11764-female-ducks-fight-back-against-raping-males/

The simple answer, as suggested in the comments, is that mallards are generally monogamous, with extra-pair copulations occurring but not canceling out the pairing, and with the note that some extrapair copulations are initiated by the female, e.g. female mate choice:

Once females had paired, it was observed that there was a trend for females to have displayed only at higher ranking males than their eventual partner (Wilcoxon signed ranks test, T+ = 30, p =.07). Of 10 females, eight displayed at more than one male. Out of 97 pairing displays by these eight females, only two by the same female were directed at a lower ranking male. Both these occasions were when the female's partner had displayed with another female and were directed at the next highest ranking male.

"Ranking" was essentially how quickly a male got into a pair, and it was strongly associated to breeding plumage (Table 1 of the paper). The sample size is a bit low, admittedly, but I'm sure the references of this paper have more to say about pairing behavior.
However you feel about "ranking" males, which I personally have mixed feelings about, this seems like a pretty textbook case of sexual selection.


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Why do protanopes see yellow and not green?
Why can protanopes see yellow but not green when the relative absorbance of these two colour waves by the m cone can be identical?

What makes you think that "protanopes see yellow and not green"?

Only because the colour wheels that I see keep referring to shades of yellow for what they can see

How else should they display the color wheel so you can view it?

Are you saying that green could be substituted for yellow and that it doesn't matter? I was probably overthinking it because I know blue-green and red cones are involved in green colour vision, so I thought the brain would default to yellow because that only requires two cones or because the green cone can still "pick up" yellow waves.

Yellow makes some sense from the perspective of opponent-process theory of color determination, see e.g. this answer: https://biology.stackexchange.com/a/27486/27148 but really someone who is "red-green colorblind" sees all wavelengths, from red through blue, it's just that red and green can't be differentiated easily (especially in different shades).

Thanks, @BryanKrause, for your perspective. I will look deeper into what the resource you have linked to provides.


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Different hominid species or simply mutated humans?
I am not a biologist, however, I am curious as to how do evolutionary biologists classify a newly discovered hominid fossil as a separate species. If simply the bone structures are a criteria to classify a hominid specimen as a separate species, how do we know that the different bone structures are not a result of a genetic disorder or a terrible mutation in a human? From what I understand, DNA specimen do not survive that long for consideration. Can anyone provide me with a layman explanation of the process of classification which seemingly doesn't involve genetic data?

As a hint towards the homework aspect - you should look up comparative anatomy and understand what differs in a pathologic (i.e. mutant) vs normal state, and how anatomy might differ between humans and other species.

@bob1 How are we sure that what we consider anatomy of a different species is not a pathology in a human?

Ok then - how do you (as in you personally) tell that someone has dwarfism is human vs non-human? Now, look at the proportions of individual in this state in any animal and extrapolate to other populations and think a little about what we might commonly find as remains?

@bob1 Or rather how do we distinguish between a human toddler and a dwarf of similar height (or built?) based on purely skeletal remains? From what I understand there seems to be some level of guesswork and arbitrariness in how we decide and define a new hominid species which is kind of bothering me.

@bob1 And from what you are suggesting, there seems to be an involvement of extrapolation based on the current diversity of primate anatomy. I was under the impression for a while that there exists theoretical models that allowed biologists to predict the anatomy of our hominid ancestors which are later confirmed or refuted accordingly by discovery of new fossil evidence. But from what I searched on google there is no such methodology under implementation as such. Now I am kind of bothered about this whole thing.

That's where the comparative anatomy comes in - how do pathologists determine the age of bones of a body? (hint: plates) This tells us age. in addition pathologies such as dwarfism have characteristics - look for skeletal pictures for both normal and pseudoachondroplasia or even achondroplasia. This will get you a fair way along to an answer.

The extrapolation was that pathology is rare in populations generally. Bones we find are most likely from "normal" as they are much more abundant...

@bob1 Hmmm. Fair point.

Hey, quite tricky to correlate but good logic
When a fossil is being examined, carbon dating is one of the methods used to examine its age. Also, as time passes, organic components of bones are slowly decomposed and get absorbed in the surrounding (into soil) and the entire mass either collapses under pressure or, inorganic materials from its surroundings replace the empty spaces(rest of the body degrades very quickly). Thus if the fossil is determining exact skeletal structure, then it must have inorganic compounds which resemble to the surroundings. If not(it has inorganic materials that are as same as the inorganic materials of an actual bone), then the fossil is unfit for determining organismal structure, bcuz it had collapsed due to external pressure.
 Now coming to your question.... for mutation to take place, there is a certain time period with a certain percentage of accuracy. Which means that for such a change that causes gross phenotypic difference, it requires a certain number of generations and fixed progeny-coincidences. Thus we can compare the age of fossil and the approximate probability of a mutation, which caused phenotypic changes in a normal human to look like the one determined by the fossil. By this we can calculate the probability that whether the fossil is a legit "non sapien hominid" or just a mutated human.
And often these probabilities are are very low. So we finally identify the fossil to be of a certain hominid with a certain level of similarity to the modern day human.
Hope you understood the process.
References: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/fossil-hominid#:~:text=Most%20early%20fossil%20hominids%20appear,9.10).
https://byjus.com/physics/types-of-fossils/
And for further information on fossilisation and chemical nature of fossils, you can check out this pdf:
https://egyankosh.ac.in/bitstream/123456789/69611/1/Unit-9.pdf

Can you provide any references for this process?

References? Like you want to know in the form of examples or a deeper explanation of the methods and the process?

Yes. Any references or lecture notes perhaps will be helpful.

I've attached the links in another answer...

The oldest DNA from Africa is 15000 years old. From Europe it's 120,000 years, and from Siberia they have horse and mammoth DNA from molars that are [700,000 to 1,2 milliom years old][1]. It's feasible that they will find homo erectus and habilis DNA from cold regions.
The more bone and tooth fragments the better. Then a comparative anatomist can study the age and differences of the bone fragments and articulations to see if they have a lot of similarity with a currently known homo species.
If they can find enough differences in bones of a specimen, concensus can agree that it's a new species. It takes quite a lot of bone to decide that. a small shard isn't enough. Half a skull/leg is fairly vague evidence and half a skeleton can be generally convincing.
[1]: https://www.science.org/content/article/mammoth-molars-yield-oldest-dna-ever-sequenced#:~:text=1.2%2Dmillion%2Dyear%2Dold,record%2C%20reveals%20new%20mammoth%20lineage&text=A%20genetic%20analysis%20of%20long,the%20oldest%20DNA%20yet%20sequenced.


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Relationship between Km and IC50 in cellular uptake assay
I'm going to describe the scenario in general terms at first so as to try and get to the theoretical content of the problem, but I'll post a link to the paper which got me thinking about it at the bottom of the post.
The setup for the assay is as follows. There is a membrane transport protein $P$ which can transport multiple substrates, of which we'll focus only on two, call them $S_1$ and $S_2$. To measure transport via $P$, we have a radiolabeled version of $S_1$ which I'll label as $S^{rad}_1$. The assay protocol is to first incubate cells overexpressing $P$ with a mixture of $S_1$ and $S^{rad}_1$ as well as other molecules of interest, wash off any remaining radioactive substrate which has not been taken up, dissolve the cells, and measure the resulting radioactivity in each condition. We can directly observe the $K_m$ for $S_1$ by measuring the initial rates at which $P$ transports $S_1$ at varying concentrations of $S_1$. We'll further assume that the ratio of $S_1$ and $S^{rad}_1$ is constant. Because $S_1$ and $S_2$ can both be transported by $P$ (assume via identical mechanisms), $S_2$ will act as a competitive inhibitor to the transport of $S_1$ if we add it into the incubation solution during the assay. If we keep $S_1$ and $S^{rad}_1$ constant and then vary the concentration of $S_2$, we'll observe less uptake of $S^{rad}_1$ as $[S_2]$ increases due to $S_2$ out-competing the former. We can then get an $IC_{50}$ value for $S_2$ with regards to the transport of $S_1$. My question, then, is: how does the $IC_{50}$ of $S_2$ when it is inhibiting the transport of $S_1$ relate to the $K_m$ of $S_2$ when it is being transported by $P$? Does there even exist such a relationship or would we have to use a radiolabeled version of $S_2$ to observe any data about its $K_m$?
I believe this is an accurate generalized description of the scenario at hand, but please point out/correct any mistakes I have made! As I mentioned, this scenario was inspired by a published journal paper which you can find here:
https://jpet.aspetjournals.org/content/295/1/392.long
In this paper, succinate acts as $S_1$ and N-Acetylaspartate, aspartate, and glutamate independently take on the role of $S_2$. In Fig. 2, the authors provide inhibition curves for succinate transport as the concentration of NAA, aspartate, and glutamate vary. They are able to fit this data to get $IC_{50}$ values for the three molecules, but they then, in the abstract, extrapolate these $IC_{50}$ values to be identical to the Michaelis-Menten constants for the substrates. This is the primary source of my confusion, as intuitively I don't feel that it is a valid assumption that $K_m = IC_{50}$ when the competitive 'inhibitor' can also act as a substrate for the transport protein. However, I haven't been able to find any information about this topic online and it's certainly not my strength as a new researcher hence my asking here instead.
Thank you for reading and for any help you are able to provide!

Another clue that something is going awry here is that I don't believe the paper (or my generalized scenario) assume anything about how the 'inhibitors' interact with the protein. That is to say, even though the authors show that NAA does get transported, their fitting of the $IC_{50}$ and then extrapolating this to the Michaelis-Menten constant does not make any assumptions about the fate of the 'inhibitor'. Obviously, a competitive inhibitor which lodges itself in the active site and prevents transport has no $K_m$ yet you could apparently claim its $IC_{50}$ as such.


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Aerobic respiration takes place in the mitochondria; anaerobic respiration takes place in the cytoplasm. Is there a biochemical reason for this?
According to hyperphysics.edu, and my general knowledge, anaerobic respiration occurs in the cytoplasm. ("Anaerobic respiration (both glycolysis and fermentation) takes place in the fluid portion of the cytoplasm whereas the bulk of the energy yield of aerobic respiration takes place in the mitochondria".)  Is there a biochemical advantage to this, or do eukaryotic cells simply lack specialized anaerobic respiratory organelles? I could understand this; few cells use this form of respiration besides muscle cells. But even in muscle cells, it occurs in the cytoplasm. Why? Is it simply taking advantage of fortuitous chemical circumstances, or was it evolutionarily desirable to respire anaerobically in the cytoplasm and aerobically in the mitochondria? I am aware, also, of the endosymbiotic theory of mitochondria.

The statement "few use this form of respiration besides muscle cells" is incorrect, as explained in a recent answer of mine to another question. (Quite what the logic of the sentence is remains unclear to me.)

@BryanKrause in this case "we usually remove them eventually" was a rather short timescale in practice, less than 24h after the comment was made. Without access to my comment (it is not in my history either) I cannot easily polish it into an answer. So this approach seems heavy handed and dismissive of my effort, in the name of site policy. If you sincerely thought it should be an answer, you don't need to delete so aggressively.

@Ryan The deleted comments contained barely a single thought, there wasn't much there to preserve, just thought it'd be useful to explain the policy rather than silently removing them. The solution is to not put effort into answering in comments and to use the answer box instead, and use comments only as described in https://biology.stackexchange.com/help/privileges/comment

The problems here would seem to be (1) a misconception of the biochemistry of anaerobic respiration — strictly anaerobic glycolysis or fermentation (see this Wikipedia article for explanation of the term), (2) not considering the bacteria in which these processes evolved rather than eukaryotic cells, and (3) a failure to regard the lack of organelles as the default situation.
The majority of the reactions of anaerobic fermentation constitute glycolysis, and glycolysis was probably the way in which most bacteria obtained energy before the great oxygenation occurred. The ATP is generated ‘at the substrate level’ — i.e. in the actual reactions — and there is no biochemical reason to think the pathway would need to evolve anywhere other than the bacterial cytoplasm, where the ATP would be available to reactions that need it and the various metabolites could feed in or out to other pathways. The product (lactate in mammals, but also ethanol etc. in bacteria) could easily diffuse out of the cell.
Why on earth should one imagine “specialized anaerobic respiratory organelles”? They are just not required and, for example, would impose an energetic cost for shuttling of metabolites in and out of them, as is the case for mitochondria.
The pertinent biochemical question is not, I think, “Why do eukaryotic cells lack anaerobic respiratory organelles?”, but “Why do  the cells need an organelle — the mitochondrion — for aerobic respiration?”. There is a specific answer to this, which is not some vague concept of tidy subdivision of the cell.
This specific answer is, in brief, that aerobic respiration requires a compartmentalized system separated by a membrane so that a pH and charge gradient can be established, to be used subsequently to generate ATP. In Gram-negative bacteria it is the double membrane that provides this; and in eukaryotes it is the successor to the captured bacterium — the mitochondrion.
So there is a good reason for eukaryotic aerobic metabolism to require an organelle, and no reason that I can see for anaerobic metabolism to do so.

An exception to this is the glycosome, a membrane-bound organelle containing the glycolytic enzymes. This organelle is present in all kinetoplastidia, and has been very well characterized in (eukaryotic) Trypanosoma brucei (see here, for example).  One obvious advantage is that concentration of glycolytic intermediates and glycolytic enzymes are maintained at a higher concentration.  From an evolutionary point of view, it is though that glycosomes are descended from peroxisomes

@user338907 — Now you mention it I remember attending a seminar on Trypanasomes (there is a group that work on them in my Uni) with mention of some odd organelles. The key question is why they evolved in this particular organism — why does it need to concentrate its glycolytic enzymes and intermediates — and if you can shed further light on that I think it would make a valuable contribution as an additional answer.


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What kind of skull is this - fish?
Skull found near Merrimack River, West Newbury, MA frequented by Eagles, Hawks. Some kind of fish maybe? It's about the size of a hand

I'll leave answering to someone who can tell for certain, but it looks more pelvis-like than a skull to me.

that is not a skull, it is a weathered bird pelvis. but without scale and how heavily weathered it is picking an exact bird will be tricky. some bird pelvises for comparison https://ecuador.inaturalist.org/posts/27974-peacock-chicken-and-duck-pelvis-comparison

Wow! You guys are fantastic - I never would have thought pelvis. Thank you for the help. It's about the size of my hand, including the fingers. Probably duck since that's what's in the area. Thank you!


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Biological Key for Yard Weeds?
I'm tinkering with an idea for an app to identify yard weeds, just as a personal project. I've been looking for some sort of dichotomous key (ie, "Does it have fur?" "Does it have feathers?" sort of thing), but so far everything I've found is just a list of pictures (ie Top 10 Yard Weeds in Southern US). Is anyone aware of an existing resource I could use?

The folks at Gardening and Landscaping SE might be more likely to know :)

You should check out the Seek app--point your phone camera at an organism (insect, plant, animal, fungus) near you and it'll give you an ID! I've used it for a few years, it's really cool, and mostly correct in my experience

Firstly, I would recommend searching the following on your browser: 'plant species identification gov'.
Also here are some resources that you might find helpful: you can search for a common list of invasive plant species in your country (such lists are available on Wikipedia, here is an example), alternatively you could use a local government webpage to search and identify invasive plant species in your specific region.
Dichotomous keys can be found on botanical/herbarium/environmental government websites, here is an example.
Lastly, apps like iNaturalist can identify plant species for you.

As it turns out, changing what I searched helped. Thank you!