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Where does (retro)virus replication take place?
When a virus replicates, it has to create several copies of its genome to the "daughter viruses"? Where in the cell does this replication of the viral genome take place? And how?
In my book, they use HIV-viruses as an example, which I've understood is a retrovirus. The first steps they describe are attachment, entry and uncoating, which I understand. Then, the next step is integration, which they say start with that the RNA translates to DNA and the new DNA strand works as a template to create a dsDNA. dsDNA is then integrated in the host cells genome, and then after that the transcription and translation of virus protein can start. What I don't understand is when the replication of RNA strands take place? After the synthesis of protein, there is the assembly, where the protein and RNA build up new viruses. Where does the RNA come from? Does the replication take place before the integration? Or when the DNA is integrated in the host cell genome, at the same time as the protein synthesis?
For other types of virus, they say that the genome replicates by a "rolling circle mechanism"? Where does that take place? In the cytoplasm? In those cases, isn't the viral genome integrated in the host cells genome at all? They just use the host cells polymerase, ribosomes etc.? Is retro viruses the only viruses that integrates in the genome?
This became kind of long, but to summarize my questions:

Retroviruses: Where and how does the replication of the RNA take place? Before or during integration of the host cell genome?
Where does the replication of genome of other viruses (that use the rolling circle mechanism) take place? In the cytoplasm?

Welcome to SE Biology.  I have no idea what your book is, but it has given you a limited and distorted view of viruses. There is a wide spectrum of viruses, with different sorts of genome — DNA, RNA, single and double-stranded, linear, circular and segmented. How and where they replicated differs accordingly. Retroviruses are a strange hybrid, and rolling-circle replication only applies to small circular viruses, so these seem an odd choice for a text. Read the general Wikipedia article and specific articles for viruses of interest…

…This should provide you with answers.  If there is a particular aspect you do not understand, then you need to show that you have done some research in crafting a question about that specific problem. At the moment your question is several questions based on false premises. And rather than just asking questions, try to think about and rationalize the problem. Ask whether a virus uses its own replicative enzyme or that of the host. If it uses the host DNA polymerase, it needs to be in the nucleus to replicate. If not, it may not — although other considerations come into play with retroviruses.

First Question:
Integration is essential for retroviruses, otherwise cDNA isn‘t transcribed efficiently into RNA (viral genome). Eucaryotic transcription requires multiple factors that are only present in the nucleus and work best when associated to genomic DNA (host). Retroviruses also lack an RNA-dependent RNA polymerase, which would replicate viral genome in the cytosol.
Craige & Bushman 2012:

Integration of a DNA copy of the viral genome into a host cell chromosome is an essential step in the retroviral replication cycle (Varmus et al. 1989; Coffin et al. 1997).

Textbook like reference Ref 1, Ref 2

The viral DNA is transported across the nucleus, where the HIV protein integrase integrates the HIV DNA into the host’s DNA. The host’s normal transcription machinery transcribes HIV DNA into multiple copies of new HIV RNA. Some of this RNA becomes the genome of a new virus, while the cell uses other copies of the RNA to make new HIV proteins.

For more details see Dutilleul et al. 2020

Once randomly integrated into the host cellular genome, HIV-1 gene expression is mainly regulated at the transcriptional level by hijacking the cellular RNA polymerase II (RNAPII) machinery. HIV-1 transcription initiates at the U3/R junction in the 5′-long terminal repeat (5′LTR) and is regulated by cellular transcription factors […]

So Replication happens after insertion of cDNA (complementary DNA, product of reverse transcription and second strand synthesis) into the host genome in the nucleus. Then transcription factors can bind the promoter and initiate elongation.
Second Question:
For DNA- viruses, some require integration into host genome, too. Interestingly, non-integrated viral DNA can populate the nucleus as dormant (circular) episomes (see viral latency, De Leo et al. 2020). Non-integrating DNA viruses often bring a DNA-dependent DNA polymerase and can replicate in the cytosol.
(If interested, see this review on viral polymerases that enable replication of viral genomes in the cytosol Choi 2016)
About Rolling Circle Replication:
Rolling circle replication is mainly found in procaryotic viruses (Phages). For eucaryotic viruses, rolling circle is pretty rare. The Geminivirus however, is one example of a non integrating DNA virus that replicates by rolling circle within the nuclei of plants. It seems that it relies heavily on nuclear factors for efficient DNA-Replication Castellano et al 1999

@markur - There are varying definitions of "schoolroom knowledge". To me, much of medicine is "schoolroom knowledge", and as a molecular biologist, much of biochemistry is "schoolroom knowledge". On this site, answers are expected to be supported regardless of your level of education, so that others may evaluate your answer on its merits, not simply on your say-so. There is no argument from authority (well, one can make a case for that from sources, but research is better.)

@anongoodnurse I've removed my comment. The answer still seems a bit misleading to me (e.g.: part 2 talks about DNA viruses only, but then quotes a passage that's broader than that) but I think that's mostly from the misdirection and multiplicity of questions in the original post, as pointed out by David in other comments.

@BryanKrause - I see. I edited that part on polymerases to appear more as a side-note. I think it‘s a cool review that helps understand viral lifecycles in general.


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Caudex vs Xylopodium difference
I live in Brazil and many plants from the brazilian grasslands/prairies exhibit an structure called, by the brazilian literature, "xylopodium" (or "xilopódio" in portuguese) - which are tickened, underground, lignified structures (root or stem) to store water and nutrients. I couldn't really find any work outside Brazil that mentions this kind of strucutre, and as far as I know, the structure known as "caudex" fits the very same definition. That being said, are these two terms synonyms?

The New York Botanic Garden gives the definition of xylopodium as:

An underground, woody, storage organ derived from stems or roots and common in cerrado vegetation.

And the definition of caudex as:

A short, vertical, usually woody and persistent stem at or just below the surface of the ground.

I think the main difference here is the focus on the xylopodium as a storage organ, as well as the fact that it is fully underground and can be derived from either the stem or root. A caudex doesn't necessarily primarily provide storage, and as a modified stem, is at or above the surface.

*There is also a definition of xylopodium meaning the type of fruit found in Anacardium (cashews).

source: Stack Exchange

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Conifer with red fruit
What kind of conifer is this?

Red fruit
Broad needles; not clusters
12 feet tall; north wall of apartment building
East of Toronto, Ontario
September 20, 2022
Hint: click the photos a couple of times to zoom in

Street view 2009:

Street View 2021:

You shouldn't eat anything that you've not identified with 150% certainty, which means this comment is technically not required. Still: the entire yew bush is poisonous.

Yew trees grow to 5000 years old and have been associated with cemetaries since pre-christian times. https://www.google.com/search?q=very+old+yew+tree&sxsrf=ALiCzsbCzlHolFTxlVLfuPM94rWqDyOrFg:1664074956444&source=lnms&tbm=isch&sa=X&ved=2ahUKEwjH-aGl-q76AhW-X_EDHZYJAsUQ_AUoAXoECAEQAw&biw=1366&bih=620&dpr=1.88

The basic appearance is consistent with the family Taxaceae, commonly known as the Yew family. Primary indicators are the relatively distinctive shape and color of the arils (the red fleshy bits around the cones, which are actually technically not fruit), the fact that it’s a shrub, the fact that it was seen in Ontario (correct climate for most Yew species), and the fact that it’s being used as a decorative plant (Yews are very popular as decorative shrubs in that region of North America).
We can eliminate most of the genera relatively quickly:

Pseudotaxus has only one species, which has white arils instead of red.
Austrotaxus has only one species, which has a rather distinctively different aril than what is seen in the picture.
Cephalotaxus species also have a rather distinctively different aril than what is seen in the picture.
Amentotaxus species have rather distinctively different leaves (they’re much larger, among other differences).

That just leaves us with the genera Toreya and Taxus, which account for most of the species of Yew globally. A Toreya species is not particularly likely, as they are not generally used much in that part of North America as decorative plants, which just leaves Taxus.
My first guess given the region and apparent lack of male cones would be Taxus canadensis (the Canadian Yew), but the stated height and growth habits seen by comparing the 2009 and 2021 pictures don’t quite agree with that (T. canadensis generally does not get much more than 2.5 meters (about 8-9 feet) tall, and tends to grow out much more than up.
More likely, it’s a hybrid of T. canadensis and T. cuspidata (the Japanese Yew), which is a relatively common variety used as a decorative plant in the Midwestern and North Eastern US, as well as South Eastern Canada.

As a side note, irrespective of what exact species this is, be careful around it. All parts of every species in the family Taxacae except for the arils are highly toxic to humans year round. Yew poisoning can easily be lethal, and currently has no known antidote (though in theory most of the symptoms are treatable).
Touching the plant is fine, but you should be careful handling any clippings or sawdust from cutting it, and definitely do not eat any part of it (the arils are theoretically fine to eat, but the seeds they surround are actually the most toxic part of the plant, so it’s generally not worth the risk).

We used to taste the arils (pericarp) quite commonly. They are safe. Some people also made a jam from them, but I would not recommend that.

I remember a funeral parlor surrounded by yew shrubs that my siblings and I passed on our way walking to and from school. I ate these berries by the literal handful every day they were available; my mother had told me it was fine as long as I was sure to spit out the seeds. I was never poisoned that I know of, so I think you might be overcautious. (I tended to listen to my mother.)

From what I've seen here, in Europa, this definitely looks like some kind of Taxus_baccata (Taxaceae family).
It most probably is a Taxus canadensis in Ontario. Also know as (local names): Canada yew, American yew, ground-hemlock, if du Canada, sapin trainard.
As it's always hard to tell based on photo that we didn't take ourselves, the best you can do is to compare its features with an identification key (either numerical/book).
The best online definition that I found for this species is:

Shrubs to 2 m, usually monoecious, low, diffusely branched, straggling, spreading to prostrate. Bark reddish, very thin. Branches spreading and ascending. Leaves 1--2.5 cm ´ 1--2.4 mm, pale green abaxially, mostly without cuticular papillae along stomatal bands, dark green to yellow-green adaxially, epidermal cells as viewed in cross section of leaf wider than tall or ± isodiametric. Seed somewhat flattened, 4--5 mm. 2 n = 24.
Provided by: [A].Flora of North America @ efloras.org
Straggling shrub with ascending or rarely erect stems to 2 m; lvs 1–2 cm × 1–2 mm, abruptly narrowed to a sharp point, attached by the shortly petiolar base to a decurrent sterigma on the twig; scales of winter-buds keeled, ± acute; fleshy seed ca 5 mm; 2n=24. Coniferous woods and bogs; Nf. and Lab. to Minn. and se. Man., s. to Va., Ky., and Io.
Provided by: [B].Manual of Vascular Plants of Northeastern US and Canada

Source: http://www.worldfloraonline.org/taxon/wfo-0000459412
See also:

http://www.efloras.org/florataxon.aspx?flora_id=1&taxon_id=233501254
http://sweetgum.nybg.org/science/vh/specimen-list/?SummaryData=taxus+canadensis
http://www.theplantlist.org/tpl1.1/record/kew-2521219

Source: Arbustrum Americanum : The American grove, or, An alphabetical catalogue of forest trees and shrubs, natives of the American United States, arranged according to the Linnaean system : containing, the particular distinguishing characters of each genus, with plain, simple and familiar descriptions of the manner of growth, appearance, &c. of their several species and varieties. : Also, some hints of their uses in medicine, dyes, and domestic oeconomy (Marshall, Humphry, 1722-1801) DOI: https://doi.org/10.5962/bhl.title.68506
Available at: https://www.biodiversitylibrary.org/bibliography/68506 or: https://collections.nlm.nih.gov/catalog/nlm:nlmuid-2562033R-bk

What is the principle difference to Taxus baccata? And I find the statement confusing. First saying that it is a kind of T. baccata and then that it is T. canadensis. Perhaps you meant Taxus baccata s.l. or agg.?

"Taxus baccata L., known as European or English yew, is a conifer native to Europe." > https://forest.jrc.ec.europa.eu/media/atlas/Taxus_baccata.pdf
I don't know enough its spread outside Europe to make an assertion about its presence in Ontario actually.

I do not think the natural spread is too relevant. The shrub is likely to be cultivated.  I only know the European one. But I was mainly pointing to the confusing statement in the first sentence.

authors: Vladimir F Героям слава

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Protein crystal X-ray diffraction at room temperature?
It seems essentially all protein X-ray diffraction structures are obtained with flash-cooled protein crystals (in a stream of very cold gas).  I’m curious if the diffraction pattern would be significantly different from the same crystal at room temperature (from thermal expansion, but not only - it may favor different conformations, and also flash cooling may disorder parts of the crystal).
What are some of the reasons that X-ray diffraction uses cooled crystals?  Is it possible to do the same experiment with a room temperature crystal?  Has this been done before, and what happens?

I don't know but I think it would have something to do with vibrations in the structure at room temp vs low temps. A la Brownian motion.

Please read the help on asking questions. You will see you are required to do some research before posting and show evidence of this in your question. A simple Google search ("why are crystals cooled for protein x-ray crystallography?") gives an immediate answer. And asking whether anyone has tried it at room temperature. Really!

@David Why not answer the question rather than try to police question quality?  I did do a number of searches; I just did it on pubmed, and the results were all about how to make crystals.  I also looked through recent structures on rcsb.org and they were all cooled.

Because it lowers the quality of the site. As an educator I try not to feed people with answers, but teach them how to answer questions themselves, even if they do not thank me for it.

see also Science (2018) Cooling Crystals is Great. Except When It Isn't.

While protein diffraction data is nowadays most often collected in cryogenic temperatures, the room temperature crystallography also exists and you can find thousands of datasets in the PDB that were collected in 300K.
The main reason for cryo-cooling is that it slows down radiation damage.
You can find in-depth discussion of both options in the literature. I just quickly googled it and found two review articles about advantages of cryo- and room temperature crystallography:
Cryo-cooling in macromolecular crystallography: advantages, disadvantages and optimization
Macromolecular room temperature crystallography


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What is this mushroom in Illinois?
I live in the Northwest suburbs of Illinois and we moved into this house last year. I noticed these mushrooms popping up in one corner of my yard and I’ve never seen this type before. They don’t seem to grow a typical stalk and cap shape and stay rather low to the ground. I’ve had to dig down under them a decent amount to get them out of the ground. We’re approaching Fall now so colder nights and hot humid days.

oh cool I also had one on my toe last week.

I might have figured it out. It looks to be a ganoderma sessile type fungi which is often associated with declining trees. It just so happens that this area of my yard is right next to a tree that isn’t doing too well from poor drainage. There were times where if I dug deep enough I’d end up hitting a tree root, so that tracks well.

It's possible to click "Accept" on your own answer (if you're not bothered about waiting for other responses), so that the question appears as "answered" in the list.


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Determine acidification of milk (no-probe/contact/destruction)
For a project, I am trying to figure out if it is possible to determine the acidification of milk without probing, touching, destroying or opening the sample, thus leaving the sample inside the plastic, transparent sample container. I am fairly experienced with machine vision and sensors, but not even a little in biology. I read somewhere that "Milk spoils when bacteria convert the lactose into glucose and galactose, producing lactic acid." I was wondering if there is any way of detecting any of these changes using a special camera or special lighting. Any advice or help will be much appreciated.

The easiest way would be to use a colored indicator in the milk that changes color with acidity.

Thank you for your suggestion, but I am looking for a no-probe/contact/destruction way to achieve this goal. I will edit my question to clarify this better.

Thanks for the edit, but are we supposed to correct spelling in a quote?

Supposed is probably said too much. I would have suspected a typo and corrected it as well.

If you're going to be using (I assume) a flow cell to do spectroscopy, why not just have a pH meter in the flow?

@MattDMo Thank you for your suggestion, unfortunately there is no flow, there are only samples in containers, I edited my question to clarify this.

Speculation here.
The viscosity may slightly change. Perhaps detectable by vibrating the sample and checking the pattern of standing waves on the surface.
Note that acidification due to lactobacilli may well happen after spoilage due to other bacteria.


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How well do ants and other insects smell odors other than pheromones, or are they highly tuned to pheromones only?
I have a vague understanding that ants and moths use pheromones in a variety of ways, but recently after a heavy rain my office is being explored by a some small ants looking for food. They decided it was a potentially interesting area to explore after finding a drink lid that had left on my desk. That the ants left a pheromone trail for other ant's to follow I understand, and after removing the lid, the number of ants has gone down as expected.
However this morning I came in put my Starbuck's  (Mocha with an extra pump of chocolate) on my desk and after a couple of minutes saw what appears to be the last remaining little ant climbing up the side of the cup. So my question is:
a) Was the ant just very lucky? Wandering around anyway and encountered the cup?
b) Did the ant smell the Mocha/coffee and decided to investigate because it smelled like there was something good in the area?
This led me to wonder how much insects use their sense of smell to find food. I was generally aware that flowers are brightly colored and some patterned in the ultraviolet, and I guess it might be obvious that flowers also might smell good and flies are attracted to rotting flesh etc. I think I also read some time ago Luna Moth's find each other by airborne pheromones and the antenna are very sensitive and they can follow the gradient to find the moth to mate with.
So do ant's find food by smell? How much do non flying insects depend on smell to find food?
Thinking about it, it must be yes, but are there specific 'food' molecules ants are especially responsive to?

Insects are highly developed to respond to smell. The fruit fly, Drosophila melanogaster, has genes for over 50 odorant-binding proteins which can be found here and genes for over 120 chemoreceptors, which include both odorant receptors and gustatory receptors.
There is a link to the FlyBase entry for each gene where further information can be found.
There is less information about other insects, but indications are that each has a large repertoire, honed to its particular sources of food.

Interesting, I am guessing that flying insects would tend to develop more sophisticated smelling mechanisms, but have no evidence to support that.


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(Why) can't blood sugar spikes be countered by consuming fiber generally?
Excessive sugar consumption is a widely-acknowledged problem in the modern Western diet.
One of the specific problems often stated is that the quick consumption of highly sugar-laden foods leads to spikes in blood sugar, the corresponding burden placed on the pancreas to produce a sufficient amount of insulin, etc.
But these same warnings on the ills of sugar always give a pass to fruit, and the justification is usually that the fiber in fruit slows down the processing of the sugar in the blood, thereby avoiding the spikes in blood sugar levels.
This is just one example of an article articulating what I've summarized above about blood sugar spikes, fruit, and fiber, but the same has been described in an innumerable number of articles: https://www.johnson.k-state.edu/health-food-safety/agents-articles/should-you-avoid-sugars-in-fruit-and-milk-for-weight-loss.html
In my mind, this then raises the question: can the blood sugar spikes caused by all sugar consumption be avoided by consuming a compensatory amount of fiber?
E.g. can a person mitigate the blood sugar spikes from eating an ice cream or cheesecake by eating Metamucil, or some other such fiber supplement?
An obvious response might be: if it was that simple, everyone would do it, which implies that the short answer is "no" -- but if so, I'd like to learn why it isn't that simple: if blood sugar spikes from sugar in fruit is mitigated by its inherent fiber, why can't blood sugar spikes from added-sugar in human-made food be mitigated by consuming some "compensatory" amount of fiber?

Yes, adding fiber to diet can reduce the "spikes" in blood sugar. Just a couple references I found quickly, I have not reviewed them closely so I'm not sure of their quality and there may be better examples, just want to demonstrate that these things are commonly studied:
Cassidy, Y. M., McSorley, E. M., & Allsopp, P. J. (2018). Effect of soluble dietary fibre on postprandial blood glucose response and its potential as a functional food ingredient. Journal of Functional Foods, 46, 423-439.
Pastors, J. G., Blaisdell, P. W., Balm, T. K., Asplin, C. M., & Pohl, S. L. (1991). Psyllium fiber reduces rise in postprandial glucose and insulin concentrations in patients with non-insulin-dependent diabetes. The American journal of clinical nutrition, 53(6), 1431-1435.
Sharma, R. D. (1986). Effect of fenugreek seeds and leaves on blood glucose and serum insulin responses in human subjects. Nutrition Research, 6(12), 1353-1364.
Torsdottir, I., Alpsten, M., Holm, G., Sandberg, A. S., & Tölli, J. (1991). A small dose of soluble alginate-fiber affects postprandial glycemia and gastric emptying in humans with diabetes. The Journal of nutrition, 121(6), 795-799.
However, the proposed mechanisms are mostly based on impacts on the digestive system and how quickly sugars are taken up. This mechanism has an obvious ceiling in that slowing digestion indefinitely is not going to be a good feeling. So, while you could certainly extract the fiber of an apple and pair it with some apple-equivalent amount of sugar, you're going to get a result comparable (though quite a bit less convenient) to just eating an apple, but there's no algebraic "canceling" of sugar and fiber, just a modest delay in uptake. While adding fiber may always reduce blood glucose peaks compared to no fiber, that doesn't mean you can add more and more fiber to compensate for any amount of sugar.

Prof. Dr. Robert Lustig says that both soluble and insoluble fibers are needed to avoid sugar spikes. Excerpts:

The fiber in real food is of two kinds: soluble, which is globular (e.g. beta-glucan, pectin, inulin, etc.); and insoluble, which is stringy (e.g. psyllium, cellulose, chitin, etc.). You need both, as they do different jobs. The insoluble fiber forms a latticework (like a fishing net) in the duodenum, and the soluble fiber plugs the holes in that latticework.
Psyllium is an insoluble fiber. Alone It could form the latticework, but not plug the holes.

One can further assume that the mixing of the sugar into the soluble and insoluble fibers has to take place before consumption in a way that makes the sugar stick to the fiber. This is apparently not done immediately.

agreed the the fiber cannot slow the absorption of sugar much unless the sugar is mixed into the fiber before digestion.


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Function of SMAR in plasmids?
A few years ago, the Thought Emporium published a video (https://www.youtube.com/watch?v=aoczYXJeMY4) in which he refers to a study in which they mix plasmid DNA with Chitosan and feed it to mice to express LacZ gene so the mice's intestines could produce Lactase (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4717060/?fbclid=IwAR0K7C8GounA9DZwkIRm8qSGMSKuo_uHsl8-2qd2fGjnIgn5SkPXddcODsY).
Thought Emporium then shows a plasmid that could do the same for humans. In the plasmid (image below), there is this "SMAR" sequence. He says this acts like an ori but for mammalian cells.
I don't understand how SMAR functions like an ori. When I look up SMAR, it seems to be a protein structure in the nucleus rather than a gene. And the original paper doesn't mention SMAR at all.
What is SMAR? How does it function? Why does it act like an ori?

Sequence for plasmid here says that it is ncRNA. It is added as in the cassette with the Lactase, so will likely be as one RNA, possibly as a nuclear localization signal or something

S/MAR (nuclear scaffold/matrix attachment region) Is a DNA sequence pattern that recruits the nuclear protein hnRNP-U/SAF-A a multifunctional scaffold/matrix specific factor.
Jenke et al. 2002

Immunoprecipitation of the crosslinked DNA–protein complex demonstrates that pEPI-1 is bound to this protein [SAF-A] in vivo. These data provide the first experimental evidence for the binding of an artificial episome to a nuclear matrix protein in vivo and the basis for understanding the mitotic stability of this novel vector class.

Jenke et al. 2004 confirmed their previous finding and shows that a tetramer of a 155 bp region together with upstream transcriptional activity is sufficient for mitotic stability (mediated by SAF-A).
It seems to me that the sequence of SMAR is the binding surface for an adapter protein that elevates foreign DNA to a chromosome-like state. It was also shown that SMAR handles chromosome-associated processes like nuclear localization, S-Phase, etc. (Stehle et al. 2007


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Does children have a gender?
I heard that a male is a human which produces smaller gametes and a female produces bigger gametes (Hanna Kokko and Katja Bargum: Kutistuva turska ja muita evoluution ihmeitä, a Finnish nonfiction book). But if a child does not produce any gametes, does children have gender at all?

Gender? I think you may be confusing biological sex and gender.

Children do not produce gametes, not does a postmenopausal female. Of course they still have a gender.

A grand majority of all mammals have 2 sexes (with notable but rare exceptions with very particular considerations): male and female. Humans are mammals and the same applies to humans. Sex is determined pretty much in the zygote, immediately following fertilization and gamete fusion, and rarely escapes 'fixation' beyond this point.
Gender refers to the range of characteristics pertaining to someone's idiosyncratic (personal) ideas of femininity and masculinity. You may be aware that these terms are politicized.
Since you ask a biological question, we ought to limit ourselves to the term sex and acknowledge that sex(ual dimorphism) is a broad concept, genetically, developmentally, behaviorally, morphologically, etc. We can talk about sex-linked genes, which we associate with X and Y chromosomes, and not genital morphology or even gamete size. We can talk about gametes (sperm and eggs) without speaking about menstruation. We can talk about maternal inheritance of mitochondrial DNA without considering one's endocrinology. We can talk about motherliness or breastfeeding without considering X-inactivation.
You can also imagine real world scenarios that complicate our simple 2-category grouping, at some scale of consideration. For example:

Sex hormone insensitivity (just as diabetics can be insulin-insensitive, one can suffer testosterone or any other hormone insensitivity).
Chromosomal disorders such as trisomies (e.g. Klinefelter syndrome, characterized by an additional X chromosome, producing a karyotype of XXY for the sex chromosomes).
A lack of traits commonly associated with feminine or masculine groupings (e.g. secondary characteristics such as hair growth, genitals, behaviors such as courting and mate choice, etc.).

The list goes on. Sex is a broad concept, and the adjectives we have for it are simplified categorizations; nuances are crucial or insignificant depending on context. Sexual dimorphism exists on a spectrum and determinedly male organisms can be female-like and vice versa.
From a biological point of view, it's practical to use this simplification, especially because many animal lineages continue and tend to depend entirely on the fact that two disparate gametes undergo fusion. Not because the gametes are sized just so, or because  of genes that exist only on one sex chromosome, or another.
We can overthink a strict definition of what constitutes sex, but I think the crucial point - directly addressing your question - is that infertility of any kind does not re-classify one's sex, generally speaking. It may remove you from the sexual pool from an evolutionary point of view. But that's too unreasonably specific. If all the nucleated cells in your body lack a Y chromosome, and you are of genotype XX, you are sexually female by most accounts and considerations, and pragmatically one would refer to you as female, just like a nurse can "diagnose" one's sex at birth by glancing at the genitals. Karyotyping, or a nurse's glance, are not meaningless efforts to make distinctions. If you were to suddenly stop producing gametes, stop ovulating, or make a decision to never have children in your life, that would not automatically strip you of a sex designation. Sex designation is important for reasons other than offspring production - e.g. social or medical reasons; often related or associated or 'co-morbid' with sex.
Sex designation also has no bearing on one's self-perception or self-identification, or social perceptions of one's social roles. These are additional layers beyond the scope of a biology Q&A site.

See also https://biology.stackexchange.com/a/89513/25523

To be fair, "gender" used to be mainly used as a politer-sounding word for "sex" until fairly recently.  (And still appears as that in some dictionaries).  It's only since the idea of "gender identity" distinct from biological sex has become well-known that the idea of using "sex" and "gender" to mean different things has become widespread.  So it's an understandable mistake.  It does seem pretty usual now, though.  ( https://www.etymonline.com/word/gender , https://en.wikipedia.org/wiki/Gender#Etymology_and_usage  )


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Can gene mutations cause Down's syndrome in humans?
I am working on an A levels questions:

Which of the following statements about gene mutation is incorrect?
A. It can occur in both somatic and sex cells
B. It can cause Down's syndrome in humans
C. It can change a dominant allele into a recessive one.
D. It can be brought about by exposure to ionising radiation

The answer at the back of the book says the correct answer is C. Its explanation is

A gene mutation cannot cause a dominant allele to become recessive, but can disallow it from being expressed phenotypically.

But I think that it should be B. From what i understand, Down's syndrome is caused by an extra chromosome (21). And it is not possible to grow an extra chromosome just by gene mutations?
Is the answer from the back of the book wrong, or did i make a mistake? Thank you for helping me with my A levels.

Mutation is a very general term that defines „change of genetic material“ (not just sequence) and can include the loss or acquisition of complete chromosomes. So down syndrome can be caused by mutation. However, I don‘t know why mutations shouldn‘t be able to convert dominant alleles into recessive ones (E.g, a mutation that halfens an enzymes activity?). In general, this page is not meant to help you with your A-level without efforts from your side. If you have googled the issue, please show us which sources you already checked.

"And it is not possible to grow an extra chromosome just by gene mutations?" Did you google this question? What did you find?

C is not impossible. A mutation in Gene A can cause alleles x and y of Gene B to swap dominance. E.g. if gene A encodes a enzyme that changes the substrate of gene B so that it is first recognized by allele x instead of y. The word "can" quite surely includes theoretical possibilities.

Don't feel bad, that question is horribly worded.
Gene mutation is a confusing choice of words, it is not a specific thing.
First, down syndrome IS caused by a mutation, specifically a duplication. Trisomy itself is a mutation, but not caused by a mutation to a single gene, which could be what "gene mutation" is referring to. If so, it is just bad wording and the book answer is wrong. But trisomy itself can be caused by a mutation to a single gene so even then it is iffy.
The question is a "gotcha question" at best or just straight-up wrong at worst. "Which of the following statements about gene mutation is incorrect?" There is no right answer here: a mutation can cause all of these things, since we don't know what exactly is meant with "gene mutation".
At first is seems like all of the answers could be caused by mutations, but there is twisted logic to C being correct.
A mutation can change alleles, thus, it can change a dominate allele into a recessive and vice versa. What it can't do is change a dominate allele into a recessive one... wait that sounds insane, but it is technically true. It is a confusion of language; lets go a little deeper.
A mutation can turn one allele into another different allele...but, if you referring to the allele as in the defined allele and not the gene then a mutation cannot change it. A mutation can never make the blue eye allele as it is defined, recessive, it can however change the gene from blue eyes to brown eyes, thus making gene go from recessive to dominant and thus changing from a recessive allele to a dominate allele. Think of it this way, I can make steel change color by heating it but I can never change the color blue itself. So C could technically be incorrect but from a slightly different angle it is complexly possible, thus the questions is just bad.
Why textbooks often have sucky questions.
You run into this problem with textbooks a lot for two reason.
The people who write/edit textbooks rarely understand the subject and even when they kinda do, they often reuse and shuffle questions often changing key terms without understanding how it changes the question. this is done to create a new "edition" which they can sell again when they drop online support for the old edition.

I think you've identified the most reasonable unreasonable way to consider option C the correct answer here, though it makes their "explanation" even worse than the question itself.

Honestly, I'm not sure what exactly is meant by "changing a dominant allele to a recessive one".  But if you have a mutation which breaks a gene, that mutation certainly could be recessive as compared to the original, functional allele.
Down syndrome is clearly not a mere "gene mutation", and I think high schoolers are meant to know that.  I think you book is just wrong; maybe there was a typo claiming the answer was C, and someone made up a justification for that that doesn't make a lot of sense.

Duplication is considered a type of mutation. It's a bit weird to describe a whole extra chromosome that way, but it's likely technically correct according to the textbook definitions given in a course. I agree that C doesn't make much sense, though.

I would think that part, if not the whole point of the question is "do you know know the general kind of genetic differences that causes Down Syndrome?  "

Perhaps, but if that was the goal they could have just asked about Down Syndrome. Instead, they may be trying to communicate the scope of changes that are included when someone says "mutation" and that "mutation" when used in evolutionary terms should not be confused with "point mutation"/substitution. E.g. the Wikipedia page on Mutation includes a section "large-scale mutations" that covers chromosome-level changes.

I think that's an area that is especially confused by anti-evolution arguments that fail to consider the importance of duplications of entire genes and larger and instead make silly arguments about the improbability of some combination of point mutations, and I'd think it's an apt target for exams assessing science literacy.

down syndrome is caused by a mutation, trisomy is by definition, a mutation. it is not is a point mutation but it is a mutation.


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Why does low redox potential mean less oxygen?
I often see statements about adding reducing agents like cysteine to anaerobic medium to decrease the amount of the dissolved oxygen.
However, I am not sure why.
I am wondering if it is because under the low redox potential conditions, dissolved molecular oxygen is easily reduced, is that correct?
If so, what is the oxygen reduced to? H2O?
For example, I am not sure of the rationale for the following statement?

The higher the redox potential is, the higher the oxygen dissolved in the media will be.

https://biology.stackexchange.com/a/52439/72932

Thank you very much for your comments. I did not quite understand the original purpose of adding reducing agents (to lower the redox potential) and the concomitant results (to reduce the contaminated oxygen).

@Beginner - I think that lot of people have applied different amounts of reducing agents to their culture and have found the best concentration enabling best viability simply by trial and error. One can speculate why certain concentrations are toxic while others support growth, however most of the time, culturing conditions are configured empirically. Usually people are simply happy that it just works for once. Here, we did lay out somewhat of a basis that there might be a "redox-sweet-spot" that is capable of reducing O2 in culture medium while minimizing H2O2 production.

You‘re partially correct. Adding reducing agents will cause $O_2$ to be converted to $H_2O_2$, as thiol groups are turning from $SH$ to $S$-$S$ (forming dimers). In a second reaction, further thiols may reduce $H_2O_2$ to $H_2O$, (but H2O2 also may react with $SH$ to form toxic byproducts like thiooxides $SO$).
Intermediates (like $H_2O_2$ or $O_2^-$) might get reduced to $H_2O$ by subsequent reactions with thiol groups, Enzymes or spontaneous dismutation (Kiley & Stolz 2004, Aires et al. 2008)

$O_2$ + 2 $SH$ -> $H_2O_2$ + $S$-$S$

$H_2O_2$ + 2 $SH$ -> 2 $H_2O$ + $S$-$S$  (see NG et al. 2007, DTT Assay Wang et al. 2018)

However, while the first reaction is very probable, the second reaction is less probable (some even argue that it is too unlikely to have an effect)
The second reaction might depend on concentration. Usually cell culturing protocols are designed by trial and error. So it’s based on testing multiple concentrations to find out the amount that yields the highest culture viability. I can only speculate that e.g. the right concentration hits a sweet-spot. That sweet-spot might lie between production of toxic thiooxide ($SO$) and oxygen reduction. But that depends on a lot of factors like organism and other culturing conditions.
Cell Cultures are in Generally too Oxidative; Reducing Agents might Help no Matter the Exact Reaction Path
Oxygen is a general problem in many cell cultures (Jagannathan et al. 2017). Even for human cell cultures, 20% $O_2$ is not physiological and introduces a background of oxidative stress (it even increases mutation rate).
To describe aggressive oxidative features of oxygen, it's useful to use the more generalized term „reactive oxygen species“ (ROS) instead of "oxygen", since redox potential doesn‘t care which exact compound acts as an electron donor. By referring to ROS, it‘s not necessary to keep track of exact oxygen-compounds.
The main point is that in the end, some biomolecule gets damaged by oxidation and the probability for that increases with high $O_2$ -levels. Hence, reducing agents could increase viability by scavenging any kind of oxidative species from the medium. And it makes sense to assume that one of the end products might be $H_2O$.

„the higher the potential, the higher the dissolved oxygen in medium“.

I think the wording is misleading, since high redox potential is a consequence of oxygen being present, not the other way around (as that would imply something like high redox potential attracting atmospheric oxygen into water). I speculate that the author meant that dissolved (organic) compounds tend to release $O_2$ (or rather any reactive oxygen species (ROS)) more often in an oxidative milieu.

I added "ultimately" in the first line to imply a possible reaction chain. Also, I don't think that sophisticated biochemistry is necessary, since in the presence of excessive thiol groups each oxygen-intermediate should be reduced subsequently by further thiol groups. It's not stated explicitly in the literature, but in my own experience,  adding DTT to reverse transcription reactions is good practice to protect RNA from oxidation damage. No other biochemistry needed.

first: O2 + 2 SH -> H2O2 +S2, second: H2O2 + 2 SH -> 2 H2O +S2 ... Where's the problem?

@user338907 -  how probable is H2O2 + 2 SH leading to -SOH compared to 2 H2O +S2? In fact, thiol groups do remove hydrogen peroxide NG et al. 2007  ... I think you might have gotten sidetracked here...

Yes I am claiming just that, and so do all scientist using the DTT assay to determine oxidative potentials Ref: H2O2 removes DTT. Ref2. No enzymes need. Again, in the context of this question reducing agents are added in excess, so the occasional formation of thiooxides does not prevent overall reduction of little Oxygen. I could ask a question on SE chemistry though, if enzymes are required for thiols to reduce H2O2

Ok, so 4 mM cysteine is too much, since it causes toxic side reactions. So you claim the ONLY product of thiols is H2O2?  So why do people add cysteine to their media? Could it be that less cysteine (than 4 mM) is actually favorable, since thiol oxidation is rarer than H2O2 reduction, and (like everything in chemistry) is dependent on concentration..?

Ok I changed my answer. Congrats, it‘s ugly and unconcise now. Please note that OP asked for reducing agents in general and what scientists aim to turn O2 into. (With emphasis on AIM. If what you‘re saying is correct, thousands of scientists are using a  wrong protocol). You‘re way too focused on thiol details which confuses the main message.

Thank you very much for your detailed explanation and discussions!

No problem. Remember to accept your favorite answer, if it answered your question.

Of course, I accepted your great answer!

However, I am still unsure how the concentration determines the probability of the second reaction.
"so 4 mM cysteine is too much, since it causes toxic side reactions."
I do not think 4 mM cysteine is harmful to bacteria (I lost its reference) because about 0.5g/L L-cysteine (about 3mM) is usually added to medium (an example is Whitaker et al. 2017).
Moreover, Karunatilaka et al. 2013 added 8mM L-cysteine. ("The 8 mM L-cysteine in the minimal media compensates for slow leakage of oxygen over time.")

@user338907 - Thanks for combining both praise and critique, it helps me get most of your input! — I‘m having trouble extracting the core message of your info. Could you summarize a bit? I mean, it‘s clear that 20% oxygen atmosphere IS a problem for ALL cell cultures. We in our lab solve that by adding selenocysteine (common culture protocols actually exclude Selenium, which is bad since it‘s needed to deal with oxidative stress in eukaryotes; I could look up the reference if you wish). Maybe there‘s no need to fully exclude oxygen, but just to reduce it a little to increase culture viability?

I‘ve edited the answer to focus on reducing agents to be something like a scavenger to remove oxidative species in general, not just H2O2. It could be misleading to isolate exact reaction paths. I mean we are talking about culture medium, a mixture of amino acids, glucose, growth factors, maybe even serum. Oxygen will definitely react not just with thiols but produce multiple different uncharacterized (hence no literature reference) oxidized molecules, inactivating their function or react as an oxidant themselves. These random intermediates could be countered by adding reducing agents, no?


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What is the species of this small bird in Germany?
I've recently (Steptember 2022) found this little guy in Frankfurt (Germany) in the morning. It could have fitted in my hand. It was staying very clam on the ground so I could go really close and take this photo with my smartphone.
I want to put it on Wikipedia. Can somebody help me to identify it?

I tried google image search and I think it might be Regulus ignicapilla (image / other image) or Regulus regulus?
edit: In case somebody is curious:

https://commons.wikimedia.org/wiki/File:Regulus-ignicapilla-top.jpg
https://commons.wikimedia.org/wiki/File:Regulus-ignicapilla-side-left.jpg
https://commons.wikimedia.org/wiki/File:Regulus-ignicapilla-side-right.jpg

Smallest bird along with Goldcrest. Reckon thats Firecrest

This is a common firecrest (Regulus ignicapilla) because of it's "three" black lines* on the head, especially the one that is passing on the eyes and its pale (almost white) and well marked eyebrow.
*In french, we call it "Roitelet à triple bandeau" because of that. Its german name is Sommergoldhähnchen.

Facts
The Common Firecrest only occurs in the western Palaearctic. It is a lightweight like the Goldcrest which, however, unlike ist more robust twin species, mostly leaves Switzerland in the winter. It is less bound to spruce forests than the Goldcrest and in addition to coniferous trees also uses deciduous ones. Where forests are damaged, the birds soon have problems: The thinned out branches no longer provide sufficient shelter and the food supply is severely restricted.

Source: https://www.vogelwarte.ch/en/birds/birds-of-switzerland/common-firecrest
Also available in German:  https://www.vogelwarte.ch/de/voegel/voegel-der-schweiz/sommergoldhaehnchen

You can also try to differentiate his call from Regulus regulus; it's very subtle but there is one.
Both species appreciate the dark environment of coniferous. Because of their very small weight (5-7g!) they spent most of their time searching for food (mainly insects), especially in winter. It's also this characteristic which actually determines the maximum latitude they can reach; too far north, nights become too long and days too short for them to feed enough during the winter season. (oral communication, Museum of Natural History, city of Geneva).

European distribution of both regulus regulus and regulus ignicapilla.
Source: Le Guide ornitho, 2015. Ed. Delachaux et Niestlé. By Lars Svensson Killian, Mullarneym Dan, Zetterstrom. ISBN 9782603023938.
Meaning of the colors:

purple: all year presence,
light blue: winter presence,
orange: summer presence,
pale yellow: during migrations periods.

If you are searching for a nice guide, you can checkout this one: "Collins Bird Guide: The Most Complete Guide to the Birds of Britain and Europe".
By: Lars Svensson (Author), Killian Mullarney (Illustrator), Dan Zetterström (Illustrator), Peter J Grant (Contributor). ISBN: 9780008547455 Edition: 3, Hardback Nov 2022"


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Purple caterpillar found in Peru rainforest
Caterpillar fron Peru rainforest with purple body and orange or reddish tips. From Manu National Park

That's a very striking caterpillar. Unfortunately a lot of caterpillars in those regions haven't been matched to an adult butterfly, so it might be very difficult to get an answer.


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Snake Identification in India
Location: Kharagpur, West Bengal, India.
Time: Near the end of September at around 1:00 pm.
This snake was spotted in a drain near my hostel in Kharagpur, West Bengal, India. Can somebody help me identify this species or at least tell me if it is venomous or not? It is hard for me as I can not distinguish its head from the piece of "trash" in the drain.
After a bit of research, I now believe that this is "Striped Keelback". However, I would like someone to confirm this.

The trash might just be its lunch, a rodent perhaps.

@JiminyCricket. Yes, I was thinking the same thing.


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"mutant" codon translations?
AFAIK codon->protein translation is pretty much universal (very few exceptions). I've seen people explaining this means every living organism descends from the same ancestral.
That's certainly a possibility, but perhaps any other translation would be extremely unlikely to evolve (chemically) and/or would end up evolving to the current one because it requires less energy (I'm speculating, but the tRNA could be simpler for example).
Are there evidences that it's possible to have a very different translation table? For example, an experiment in which the encoding of a couple of codons is swapped? I'm guessing this wouldn't work if genes are encoding more than one protein - but even if it did work, perhaps it would be too dangerous to have a lab leak of this mutant?

consider that many codons code for the exact same thing.

While the basis of the genetic code are highly conserved there are several variations that can actually be quite frequent. For example the mitochondria in your body use an encoding that is a little different from the cell nucleus.
As you stated, the most likely explanation for these small variations is evolution from an ancestral version.
Other encodings are clearly possible since all 64 possible triplets are used. Swapping the encoding can be achieved by modifying the enzymes that bring together t-RNAs and amino acids (so called t-RNA synthetases). This is quite complex and mainly done to enable the incorporation of new amino acids into proteins.
Not all potential codes would work equally well and might for example slow down translation. One possibility to completely alter the code without major problems would be to swap the first and second positions in each triplet.
And for your last question, an organism with a highly altered genetic encoding would actually be more save. This is because it would be impossible for this organism to exchange genetic information with its environment. Bacteria frequently obtain antibiotics resistances by gene transfer from other bacteria. The modified organism would not be able to make sense of a resistance gene obtained through this way.


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How common are boy, girl twins?
In the human population, if you meet someone how likely are they to be a twin with someone of opposite sex?
That includes non-twins, not just people who are twins.

Tried Googling but just came up with probability of boy/girl twins vs other twins

The answer will vary a lot by time and location because of changes in the use of fertility treatments, which increase the proportion of twins enormously, and changes in maternal age: from 1980 to 2009 "[twinning] rates [in the US] doubled among non-Hispanic white mothers, rose by about one-half among non-Hispanic black mothers, and by one-third among Hispanic mothers"(US CDC). Globally, "Researchers analysed records from more than 100 countries and found a substantial rise in twin birthrates since the 1980s, with one in 42 people now born a twin, equivalent to 1.6 million children a year. According to the study, the global twin birthrate has risen by one-third, on average, over the past 40 years." (Guardian, Monden et al 2021).
A twinning rate of 15/1000 looks like a reasonable global average.

Taking this information as true: given 15 pairs of twins and 985 single births, (2 × 15/(985 + 2 × 15)) ~ 3% of babies born are twins. Identical (monozygotic) twins are always same-sex, but are at least 10x less common than dizygotic twins, so we can ignore them for a rough estimate. Given a 50/50 sex ratio (I think this is true/close enough for dizygotic twins), 1/2 of twins have an opposite-sex twin, so 1.5% of people are part of an opposite-sex twin pair.
So about 1 out of every 68 people is a member of a male-female twin pair.
Monden, Christiaan, Gilles Pison, and Jeroen Smits. 2021. “Twin Peaks: More Twinning in Humans than Ever Before.” Human Reproduction 36 (6): 1666–73. https://doi.org/10.1093/humrep/deab029.

Of every 30 births, there will be 31 babies if 1 in 30 is a twin gestation. You also ignore the fact that this number reflects fertility treatments and IVF which is more common in higher income brackets of wealthier nations. Many of the more successful fertility treatments were not available, say, 40 years ago, so the age of the individual matters. Taking that into account, it depends on a lot more than one or two numbers. It depends on where the individual is from, their economic background, their age, and more.

I feel like I've accounted for your first sentence (I said that 2/31 babies were twins). I know that this number will vary a lot, but I don't expect that it's really possible to get more than an approximate answer to this question anyway ...

I've updated. (I don't understand where the 1/30 number came from - I looked at the original source, but it seems out of sync with the Monden paper - maybe a twins vs births confusion somewhere along the line)

I didn't see the calculation that you made in either of your sources. "...but I don't expect that it's really possible to get more than an approximate answer to this question anyway..." Neither do I, but you did anyway: "So about 1 out of every 68 people is a member of a male-female twin pair." The better answer is, it depends on too many factors to say with any degree of even speculation.


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Identification by tail feather
I saw the remains of a bird today I did not recognize, and it was pretty mangled so it was hard to describe it. It was about the size of a robin. However, it had a dark brown mottled body like nothing I have ever seen. I have included below a tail feather from the bird which is 5 inches long. I am sure it is not a thrush or a woodcock or a kestrel. So what was it?
Location is Great Bay, Portsmouth, New Hampshire, United States.

Alas, I can't answer the question, but I can suggest you check at this link: https://www.fws.gov/lab/featheratlas/index.php

I believe this is a tail feather (or retrix) from an adult male eastern whip-poor-will (Antrostomus vociferus). See right image below (click to zoom):
.
 Source: USFWS Forensics Laboratory
Details:

The brown, mottled appearance and the size (~12 cm) match that of the OP's specimen.

A great resource for exploring bird feathers: https://www.fws.gov/lab/featheratlas/

The whip-poor-will's breeding grounds include the OP's location (i.e., New Hampshire), and according to All About Birds this species could still be present even late in the year ("they seem to leave between early September and late November.").

 Orange is breeding. Source: All About Birds.

The whip-poor-will is a medium sized bird and similar in size to an American robin.

Whip-poor-will: 22-26 cm ;  Robin: 20-28 cm

 Eastern whip-poor-will, (c) Paul Cools, source: inaturalist


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database of Animals/insects which would contain their queriable geographic location?
Is there a database of Animals/insects which would contain their queriable geographic location?
I would need to perform a rather simple query, such as Animals of <Location>, where Location is some well-defined geographic area such as Elephant Nature Park - Thailand.
So far I have found multiple lists on Wikipedia and other webpages, however they seem to be quite incomplete as their intersect is quite small. Moreover, I have found EOL (Encyclopedia of Life) collections but they appear to struggle the same way.


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Do lipids have a monomer or not?
My biology class and I have been on the topic of macromolecules for quite some time now. Chapter 2.3 of the Foundations to Biology Textbook says that lipids are not polymers, so they do not have monomers. It is also stated in our Macromolecules powerpoint.
Now here is what confused me. We did a macromolecules review assignment to prepare for our upcoming biology test. We had to match each macromolecule with its monomer, but that is when I noticed that "No monomer" wasn't an answer; glycerol and fatty acids were the only choices for the monomer of lipids.
This really had me baffled, I thought it must've been a typo on the assignment. So I decided to search it up. I searched for "What is the monomer of Lipids", and google said exactly: Lipids - polymers called diglycerides, and triglycerides; monomers are glycerol and fatty acids.
I still didn't believe what I was reading so instead I searched "What macromolecule doesn't have a monomer?", and google said exactly: Lipids are not true macromolecules because the monomers are not covalently bonded together. Simple lipids are composed of subunits made of fatty acids covalently bonded to a triose sugar – glycerol.
This really confused me because it was saying that Lipids aren't a true macromolecule. I did more research and found that Lipids are polymers, but that is not what we've been learning.
We've learned that Lipids aren't a polymer and that they have no monomer, but google is saying otherwise.
So what is it? Do they have monomers or not? Are Lipids actually considered a polymer?

I fear for your education for several reasons, but the most pertinent is that the term lipid has no precise structural chemical meaning, and refers to a group with similar physical properties that includes steroids such as cholesterol. Presumably the ignoramus who set this educational abomination — MCQ — was thinking of triglycerides, but wanted to hide the “tri” portion because of his absurd answer. No modern biochemist has the slightest interest in the application of chemical terminology such as polymer, but  it seems to me fatty acids themselves justify that description.

No, classic lipids are not considered polymers. Organic chemists have specific names for aliphatic chains of specific sizes, so there‘s no need for polymer terminology.
For example, fatty acids are kept at specific lengths and cells generally don’t elongate them to large sizes. (They can be connected by glycerol. And glycerol can carry only three fatty acids. But that‘s it)
Fatty acids themselves might be called a polymer (repetition of CH2) if one really wishes, but that‘s like calling propane  (C3H8) „polymethylene“ or „trimethylene“, treating it like a polymer of three monomers. But no one does that. Also, fatty acids of different sizes have their own specific names (e.g. oleic acid), while polymer naming systems are usually blind to size.
Polymers are generally composed of roughly >100 monomers (Be aware that everyone sets their own threshold at which size something‘s a polymer). With fewer than that they‘re also called oligomers (oligo means few, poly means many)
lipids aggregate together forming membranes and droplets. But that‘s just lipid molecules sticking together like water molecules do. And water also is no polymer.

You are confusing lipids with triglycerides and pulling numbers out of a hat. If you think about the structure and synthesis of fatty acids they are clearly polymers — they result from the repeated addition of malonyl moieties resulting in multiple CH2 groups. Much more similar to chemical polymers than proteins, nucleic acids or polysaccharides.

Yup, that 100 is definitely a hat-derived number. But most chemists will agree with me that they „feel“ that number when talking polymer (you may dig up some definition from your favorite literature, if you wish). And yeah, you can call the aliphatic chains of fatty acids polymers of CH2. Just like you can call water dihydrogen-monoxide. But you‘re gonna be the only one who does that.

@markur  lipids absolutely do polymerize, lipids as David said lipids formed of many CH2 groups just like polyethylene. If lipids are not polymers, most plastics are not polymers. Also don't confuse "lipids" with triglycerides, lipids come in a huge variety, many drastically exceed 100 subunits. And you need a source for a claim like polymers need to be longer than 100 subunits, because that excludes a lot of biological polymers not just lipids.

Please explain why a biology beginner should know about lipids with the size of 100 carbons.

Edited my answer to prevent misinterpretation. Also explaining why calling e.g. „oleic acid“  a „polymer“ is overkill.


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What is a "marker-matched" plasmid?
I see this term used a lot in papers and have trouble understanding it. From what I have gleaned it seems they are used during control experiments, perhaps with the goal of making the control plasmids as similar as possible to the experimental ones to limit confounding variables?
Here is an example from I paper I've been trying to understand.
"Cells containing an ARS1 plasmid, or a marker-matched ARS-CEN plasmid, were subjected to life span analysis." - David Sinclair & Lenny Guarente, 1997
Let me know if you need more info. Thanks!

It is where a control plasmid is used - this is usually an empty vector or a non-target vector with the same "marker" on the plasmid.
The marker is often one that is either used for purification of a resulting protein (e.g. His, GST etc) or immuno-detection (FLAG, HA etc (these can also be used for purification, as can His and GST for immuno-detection)) or fluorescent (GFP etc).
In addition and as per comment from @MaximillianPress markers can also be selectable, so used to ensure that the plasmid is maintained in the cells and that all cells contain the plasmid. This is often done through expression of a marker that confers resistance to an antibiotic such as ampicillin for bacteria or geneticin for mammalian cells. In yeast nutrient deficient media can be used and the yeast will only grow if they contain a plasmid that allows metabolism or production of an essential compound (e.g URA gene for Uracil production).

I would actually expect that the marker be a yeast selectable marker, such as an auxotrophy marker like the URA3 / KANMX, that can be used to select the plasmid on dropout or antibiotic plates.

@MaximilianPress good point - I don't use selective markers very often, so I forgot about them. I'll edit that in.


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Genotype vs Alleles - What's the difference?
I have searched through various websites, however, I am still rather confused with the difference between 'genotype' and 'alleles' since each site seems to be contradicting another site.
I would be much grateful if someone could please give me a concise and clear differentiation between 'genotype' and 'alleles'.

This question is duplicated a lot on this page (e.g. this), but since this is a re-occuring issue and I didn't find a reasonable AND concise  answer on this site (or at least concise enough for my taste :P), I'm just gonna answer it here.

Please note that opinions on the exact wording of the following can differ a lot. You will have to find one for yourself that works best for you.
Gene = An element within the DNA/Genome with function(s)
Allele = A subtype of a gene with (or without) altered function(s) (due to function-changing mutation(s))

Every individual has two homologous versions (not exact copies) of every gene. 1 version on each chromosome (don't confuse with sister chromatids). This allows two versions (alleles) of the same gene to be present at the same time.
1 allele is from mama, 1 allele is from papa. Both alleles often have a similar known functions, although they're rarely exact copies (unless your parents are siblings).
If two alleles have the same function, they may or may not be summarized as the same allele, depending on the aim of the study or how well the function of each mutation is characterized. Most textbook examples work with alleles with very defined functions ("wildtype vs. white").
A whole population of individuals has the same exact numbers of genes as a single individual (A human has just as many genes as the species humans). But the population has a multitude of alleles for each gene, while a single individual can have max two alleles per gene.

Genotype = A summary of genes and/or alleles per gene of an individual.

"Small differences among alleles of the same gene contribute to each person’s unique characteristics." (from thoughtco)

Phenotype = The observable functions/properties of an individual that are determined by its genotype

An allele is a variant of a gene, while a genotype is an (arbitrarily) specified combination of alleles, mostly stating the homo- or heterocygous presence or absence of certain mutation(s) in a certain gene or combination of genes. E.g. Genotype A: Gene A (wild-type allele | mutant allele), gene B (wild-type allele | wild-type allele).

According to a format guide,  https://samtools.github.io/hts-specs/VCFv4.1.pdf:

Allele is representing single genetic haplotypes

Genotype is an assignment of alleles for each chromosome of a single named sample at a particular locus.

(A haplotype is a group of genes within an organism that was inherited together from a single parent. The word "haplotype" is derived from the word "haploid," which describes cells with only one set of chromosomes, and from the word "genotype," which refers to the genetic makeup of an organism. A haplotype can describe a pair of genes inherited together from one parent on one chromosome, or it can describe all of the genes on a chromosome that were inherited together from a single parent. This group of genes was inherited together because of genetic linkage)
(For human genome,  a haplotype is defined as the combination of alleles for different polymorphisms that occur on the same chromosome, and for any given stretch of chromosomal DNA an individual will have two haplotypes, although at a population level there may be numerous haplotypes for any given stretch of chromosomal DNA.)


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What percentage of introns are spliced in polyadenylated mRNAs?
I am asking a variation of a previously asked question: What percentage of RNA splicing happens during transcription?
I am planning mRNA purification using poly(A) antisense-oligo pull-down and, for subsequent purposes, would need to have an educated guess on what percentage of introns I should expect to be spliced out. An easier alternative question, mitigating the complication of mRNA turnover, would be the percentage of introns that are spliced until completion of polyadenylation.
Maybe someone knows more recent papers on this?

I mean the an answer for an average mRNA independent of concentrations. I will self-answer once I find a good estimate.

Might depend somewhat on the organism, whether the retained introns are part of "mature" alternative mRNAs vs. incompletely spliced mRNAs, whether cell compartment matter, etc. For example, Arabidopsis has lots of unspliced introns in polyadenylated nuclear transcripts that are absent from cytoplasm, with a report of >50% of introns being removed post-transcriptionally (apparently some of these are spliced before polyadenylation).

Introns are usually very huge compared to exons. If unspliced introns are worrying you, you could use size exclusion columns or PAGE to purify your RNA, if that helps.


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What does the term "centromere linkage" mean in genetics?
I am currently learning about tetrad/linkage analysis in yeast. I have read two statements similar to this:

If two genes are unlinked, but linked to the centromere the distribution will be 50 parental ditype (PD) and 50% non-parental ditype (NPD).
If two genes are unlinked, and unlinked to the centromere the distribution will be 1:1:4 in PD:NPD:TT

But I don't quite understand what the term linked to centromere means. I understand that two genes can be linked to each other if they are close together on the same chromosome.
So near the centromere no crossing-over occurs, so does "linked to centromere" just mean that there is no recombination taking place, as it is the case with the first statement?


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Does an ORF need a stop codon?
I try to read ORFs from a gene sequence but I am not sure how to interpret a sequence with a start codon but no stop codon. Imagining I have a gene sequence like the following:
atggcagaagaaga
The gene sequence contains a start codon (atg at the beginning) but no stop codon.
Does this count as ORF or not?

Generally speaking, every single ATG..... is not an ORF. That would be a LOT of ORFs in the genome. Not even every ATG.....STOP is an ORF. An ORF has to be transcribed...and spliced into an mRNA. Just looking through an entire genome and finding ATGs is futile for understand gene density.
More practically speaking, a sequence generated from a reverse transcribed library (mRNA to coding DNA, or cDNA) is a good source for ORFs. But, you can still be fooled by the multiple possible reading frames within a cDNA. Using software to convert all 3 possible reading frames of the ORF is an excellent way to start and make predictions. The best way to find out what is really made is to consult the literature OR put the cDNA in an expression vector and translate it in vitro. This tells you the general size of the actual protein and you can compare that kDa value to the expected weight of your ORF. Then, antibodies can be directed against portions of the protein sequence to study it in vivo.

It's actually for an assignment and the task is to read ORFs from DNA. In the assignment every start with stop codon is an ORF. With your answer I am just more unsure yet. Websites like https://web.expasy.org/translate/ also count a dna with no stop codon as ORF.

Darn. I hate it when biology gets confusing like this. Class assignments, depending on the level, can be almost too straightforward. Stick with the straight answer...ATG to STOP codon to find your ORFs. The Web.expasy.org/translate app is pretty weak and just meant to take sequence and find ATGs. Just like I mentioned before...futile. You could get the same answer by taking the sequence into MS Word and using the Find function to search for ATG. The only thing the app gives you is all the additional translation which doesn't mean anything if it's not a real ORF.

Okay. ATG to STOP codon means that ATG without a following STOP codon is no ORF?

Before I definitively say yes, tell me the size of the sequences you are being given to find an ORF. If they are really short, your instructor may just be trying to get you to find an ATG. But if they are long and some ATGs do have an in-frame stop codon and others don't, I'd say the instructor is wanting you to identify an actual ORF...ATG to STOP.

Also, remember that instructors' favorite trick question is find the ORF in an mRNA sequence: A) augccg....stop or B) atgccg...stop...Tricky...tricky


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DNA as a data storage medium: how many GB can a human genome store?
DNA molecules may be the digital storage medium of the future. I was looking at how much data you could fit if you would synthesize a DNA molecule the size of a human genome.
So DNA base molecules are represented by A, C, T, G and they are always found in pairs (so A connected to T and C connected to G). One such pair is called a basepair. The human genome contains ~3 billion of those basepairs (i.e. 6 billion bases). Now you mostly read about assigning two bits to every base, so A = 00, C = 01, G=10, T = 11. Then you could say a basepair stores 4 bits e.g. AT = 0011. BUT there are only 4 possible basepairs: AT and CG and the reverse, so TA and GC. This AT,TA,GC,CG system could then again be represented by only 2 bits for every pair.
Assuming the latter, a human genome contains 2 bits/basepair*3 billion basepairs = 6 billion bits. Divide by 8 billion to convert to GB, so a human genome could store 0.75 GB.
Now in case of digital DNA storage a part of the molecules needs to be used for error correction, indexing, etc. To account for this ‘overhead’ you can conservatively assume that only 50% of the total storage can be used for the data storage, which would result in 0.375GB.
Now in the whitepaper of the ‘DNA data storage alliance’ backed by Twist, Microsoft, etc. (https://dnastoragealliance.org/dev/wp-content/uploads/2021/06/DNA-Data-Storage-Alliance-An-Introduction-to-DNA-Data-Storage.pdf Page 20) they come to a different result: they assume 2 bits per base, but as 50% is needed for overhead, they say every base stores 1 bit, so 2 bits per basepair AFTER accounting for overhead (above I concluded 2 bits per basepair before accounting for overhead). The total storage then becomes 2 bits/basepair *  3 billion basepairs = 6 billion bits. Divide by 8 billion and we get 0.75GB can be stored in the human genome after we account for overhead. According to this line of thought the full human genome would have a size of 1.5GB (?). General consensus on the internet seems to be that the full human genome stores 0.75GB.
Who’s right??

Thanks! I used 50% overhead because they mention it in the paper. So know Im thinking the following: every base in a sequence stores 2 bits. We ignore the complementary strand as it basically stores the same information but ‘reversed’ but it does help in molecular structure. Then there only 3B 2 bit bases in the 3B basepairs that are or interest for storage. So 6B bits * 0.8% overhead = 0.6GB . If I use 50% overhear I get to 375MB again. Idk if this makes sense at all? Is it true the complementary strand doesn’t add info per se? (Srry this is not my field)

I removed my comments and posted an answer with the same information.

different but related: DNA as a digital storage medium; sequences algorithmically avoided for safety reasons (or should be)?

You are confusing the sequences with the pairs. AC is a completely possible sequence, and it will connect to a sequence of TG on the other strand of the double helix. Basically, everything in one strand is repeated with the complementary base pairs in the other one. This is why they say you have 50% overhead - the double helix requires everything to be represented twice.
The 50% you are already paying also provides the physical robustness of the double helix molecular structure, so you can probably get by with less overhead than with other solutions, since this already provides some resilience against single-bit errors.
Both sources agree that the capacity is 0.75GB and then whatever you need for additional error checking or other overhead you need to subtract from that.
As a benchmark, network transmissions under good conditions add about 20% overhead (so approx 10 bits per byte for parity checks, occasional retries, etc) but I would hesitate to come up with a concrete number without empirical experimentation. Off the cuff, maybe 10% redundancy would be good for reconstructing the occasional damaged sequence (look at Hamming codes etc). But the question is then what reliability you are hoping to achieve. Again, the raw storage capacity is 0.75 GB, and you use it as you see fit for your specific application.
Furthermore, it's unclear why you use the human genome as a yardstick for anything. You can't replace information in a human's genes with random information you want to store and still end up with a human cell. And as a carrier of information, a human is rather inefficient; quick Duck Duck Going gives me a number of 30 trillion cells per human, all carrying the same information in their DNA. The genome of the rice plant contains many more base pairs, anyway. But as the paper you link to emphasizes, you do not need living organisms to carry the DNA you want to store information in (nor could you, realistically).

Thanks for the answer/following up on my comment! To touch on your last comment; I was also looking at sequencing costs of DNA storage, and commonly you find the human genome is the benchmark (e.g. 600$ to sequence the full genome) - I wanted to convert this to $/GB

The much more expensive operation (I assume) would be getting the bits there in the first place, though of course, the cost of reading them will be a factor, too.

The 0.75 GB (assuming 2 bits per nucleotide) is correct as far as I know. But I think I can add some additional context. Typically, I point people to this Nature Review from 2019 for a nice overview of the field.
In theory the genome could store that amount of information. But it doesn't make sense to consider aspects such as error correction because it is not currently possible to encode digital data into nucleic acids on that scale in vivo. Typically, in vivo data storage applications are typically in the form of either cellular recording or use CRISPR–Cas to insert short nucleic acid sequences.
Conversely, in vitro data storage has been considered the most practical form of encoding digital data into DNA. In Table 1 you can see some of the most notable demonstrations of in vitro DNA data storage. You can see the strand lengths are limited to less than 200 nucleotides, which is about the current limits of synthetic capacity. The sequencing (read) technologies are maturing faster than the synthesis (write) costs which is among the current bottlenecks. Larger datasets need to be synthesized independently in strand segments and reconstructed from mixed data pools.
If you wanted to come up with $/GB value for the sequencing of the human genome as a fun thought experiment, you could make the simplifying assumptions (2 bits per nt) and call it a day. But to calculate a more realistic number for arbitrary storage of nucleic acid data on the order of the human genome would be much more complex. The experiment itself would also not be trivial or cheap.
Though to be honest I didn't read through your whitepaper, and it looks to be more recent from 2021. Maybe progress has been made I'm not aware of since it's not my area of expertise.
Hopefully that adds something worthwhile to the discussion.


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What is human body's overhead when storing calories into fat, and when retrieving calories from previously stored fat?
Questions:

Suppose that someone ate an excess of 1000 kcal.  How much of this 1000 kcal will become fat?
Suppose that someone had a deficit of 1000 kcal.  How many grams of fat will be lost in order to generate the 1000 kcal?

What I've done so far
I found that each gram of fat contains 9 kcal. So, a naive solution would be:

An excess of 1000 kcal will become 1000/9 = 111.11... g of fat.
A deficit of 1000 kcal will cause the loss of 1000/9 = 111.11... g of fat.

This is naive, because it ignores that the body itself requires some calories for simply converting excess calories to fats, or for converting fats back to calories.
In Quora, I found someone claiming that such conversion has a 20% overhead for each direction.  So, if I understand his answer, the better answer is:

An excess of 1000 kcal will spend 1000*.2 = 200 kcal as calorie-to-fat conversion overhead, leaving us with 1000-200=800 kcal that is going to be stored as fat.  Since each fat gram contains 9 kcal, we will eventually store 800/9 = 88.88... g of fat from the 1000 kcal excess.
Likewise, a deficit of 1000 kcal will also have a 20% overhead.  So, to get 1000 kcal, the body will have to burn enough fat that gives 1000 * 1.2 = 1200 kcal, which is 1200 / 9 = 133.33... g of fat.

But, the problem with this answer is two folds:

It assumes that the overhead is 20%.  I couldn't find a study for this.
It assumes that the overhead is symmetrical so that calorie-to-fat's overhead equals fat-to-calorie's overhead.  I couldn't find a study to claim this symmetry.


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What exactly is bound by the control line on COVID19 antigen tests?
Clearly the test line binds some component of the coronavirus, I believe most commonly the nucleocapsid protein (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8049777/). However, despite extensive googling (and Google is doing a lousy job of understanding my question) I have not been able to figure out what is being bound by the control line. Probably it differs by test manufacturer, but I'm sure there are some relatively common antibodies that are used in the control line?
My best guess is that it should test for some common mucin or collagen or elastin but this is based on nothing.
The reason I'm asking is that I want to understand if the "control" line being present is a good indicator of the test having been done properly. Let's say some person:

rubs the swab on a different body part than the nasal mucosa
or doesn't touch the body at all with it
or swabs the nasal mucosa very briefly
or only inserts the swab into the buffer solution extremely briefly

would the control line still show up?
I'm not simply trying this myself at home because it's annoying and expensive to get lots of tests simply to waste them to test their limits.

Related: https://biology.stackexchange.com/questions/101767/whats-happening-in-the-c-and-t-stripes-of-a-covid-test-kit/101777#101777

According to biotrend (SARS-CoV-2 (Covid-19): Rapid Antigen Test for Diagnosis), the control line has an immobilised Goat anti-chicken antibody. There, a chicken-IgY gets stuck which was carried from a conjugate pad by the sample fluid.
So even pure buffer solution would yield a positive signal at the control line. It seems that the control only tests for proper reactivity of the antibodies contained in the conjugate pad, and not for proper usage by the user:

A colored band in the control region serves as a procedural control, indicating that the appropriate sample volume has been added and the membrane is functioning.

This manual (health.govt.nz) reports that whole blood and Mucin do not interfere with the test (including control?). It sounds as if biological fluids are meant to be ignored by the test in general.

Indeed, this is why the control line is so stupidly designed. It should check not only for proper functioning of the test but also that the user did not just put pure buffer solution! Otherwise a negative test is not convincing even if supervised.

@user21820 No, this is not stupid because you need a control that shows that your test is valid which is independent of the sample. Having a positive control would sometimes be nice but makes the interpretation more complicated. Not to speak of the need to have a control that under no circumstances will produce a false positive result.

@Chris: You claim "you need". I disagree. What we need from the test is a way to distinguish between covid infected and non-infected. The way the tests have been designed is inferior for that purpose. For what I suggested, there is no complicated interpretation at all. (1) No control line ⇒ Test invalid. (2) Control line ∧ Test line ⇒ Infected. (3) Control line ∧ No test line ⇒ Likely uninfected.

@user21820: yes, in theory that sounds good. However, using a user dependent positive control introduces another variable, where the test may fail (making the test look worse compared to others). Also, it wouldn‘t ensure proper usage, since it does not prevent a user from applying an older/someone else‘s healthy sample. Supervision or Conduction by professionals is the only solution. I think it‘s smart.

@user21820 Believe me, you need this. What do you do with tests where the positive control is absent but the test band is present? Also: How do you control if the test is working at all? Antibodies are stable, but still storing conditions are important to ensure a result.

@markur Test line obviously means you have COVID. Control line missing obviously indicates you did something wrong with  the sample. Intuitive conclusion: you did something wrong, but COVID was detected anyway; if that bothers you, take another test.

@user253751 - I know, I‘ve been there, like everyone else. My point was that a user dependent positive control doesn‘t prevent fraud, hence it‘s worth can be debated. (For me I‘d feel more comfortable with sth like a Mucin control, but it‘s really not that necessary, given that these tests are expensive enough)

@Chris: What user253751 said... No control line ∧ Test line ⇒ Probably infected but you should get another test done because you botched the first one. If you keep botching tests unlike everyone else, then go to a hospital or clinic.

@markur: This isn't just about malicious testing. Even an honest person can't be sure that they have swabbed enough if the control line doesn't give them any feedback.

@user253751: Test line appearing but no control line does not mean you have COVID. It means something went wrong that caused colloid to deposit at the test stripe, but not at the control stripe. You can say in that situation that the test is unreliable, but not more. The control is meant to guard against false negatives due to errors in the manufacturing process or due to storage conditions.

@user21820: sure "non-contact swabbing" will cause false negatives. But: even proper swabbing (taking up sufficient mucin) is subject to sampling error due to spatial heterogeneity. And there is indication that this is a substantial source of error (I've seen some very early paper in 2020 looking at a series of PCR results from  back-of-the-throat swabs of the same individual, and roughly a quarter of those was negative. The rapid test sampling procedures like nasal swab are considered to have sufficient sensitivity in practice compared to that standard. The question is: compared to that, ...

... would an additional mucin control line be worth while? In particular, since a doubt about sufficient swabbing (e.g. by someone overseeing the test) can be resolved by doing another test (from the same lot). But a manufacturing or storage problem is likely to affect all kits of the lot or the boxes at hand.

For the FlowFlex brand, apparently substitute "mouse" for "chicken".  Are these likely to be in-vitro manufactured antibodies/antigens, or is someone extracting them from actual goats/chickens/mice?

@cbeleitesunhappywithSX: I didn't say you must have covid. That's why I used the word "probably". The likelihood of a manufacturing error is much lower (<0.1%) than the likelihood that the test line shows up positive but the person does not have covid. Yes, an entire batch may be faulty, and that's why I said "should get another test done".

@user21820: no, that was user253751, to whom also my comment went. Still, you're not doing the comparison we need here. In particular, we'd need the (posterior) probability of the SAR S-CoV2 line of the test being correctly positive given that the control line did not show up. Your < 0.1 % for manufacturing error is only the the prior (BTW do you happen to have a reference on this - this is not to raise doubt on the number in case it's a guesstimate, it's that I'm professionally interested in any such ref), but the data (control not showing up) is actually very strong evidence here...

(prior of manufacturing/storage error: I didn't see that many test kits, all in all ≈100, but there were some in there which were obviously short on extraction buffer). For the practice of covid testing, the 2 € for a test kit makes the discussion moot, since the practical answer will always be throw it away and do another one. But we're on biology.sx here where other lab tests are discussed as well, and I'm analytical chemist: it is an important point to me that an invalid test is invalid and it is wrong to use it for anything else than possibly digging into fault modes.

@DanielHatton these are most likely to be recombinant anti-species antibodies, as their performance is much more similar lot-to-lot than animal-derived polyclonal antibodies.

@cbeleitesunhappywithSX: There's clearly a difference in our goals. In my view, the purpose of using the ART is not to get a near-zero false-positive rate, nor to get reliable statistics of covid infection. Rather, it is to provide confidence that you do not have covid based on the ART result! If you have that goal in mind, then you will understand why I say that my suggested version is better, and why we do not need the conditional probability of infection given no control line but a positive test line.

If you follow my stated procedure (including getting another test done if the first one has a problem), then that probability is irrelevant. Rather, it is the probability of manufacturing error that is relevant, because that would give an upper bound on how likely there is a problem with the ART in the first place. You can't just treat this ART testing as a lab test. It is not, because its primary purpose is as a tool for dealing with the pandemic. Whenever I use the ART, I want to know ( likelihood of covid given negative ART result ), not ( likelihood of no covid given positive ART result )!

Thanks @MattDMo.  Same for the mouse/chicken antigen?

@DanielHatton yes, they're all recombinant. However, recombinant doesn't necessarily mean monoclonal - the final product could be a mix of two or more different clones to give the desired characteristics to the batch. I used to work at an antibody company that did this.


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What is the difference between antennae and pedipalps?
I know insects, myriapods, and crustaceans, have "feelers" that get called antennae, while spiders and many other types of arachnids have pedipalps which seem to serve the same functions. What is the difference?


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Which animals do bait hunting?
By bait hunting I mean some predator which first collects or finds some bait (food of its prey) and then uses the bait to lure and catch its prey. This question is inspired by this video showing an orca using a small fish to catch a bird.
To me this looks like it requires an amazing amount of intelligence from the orca to pull off. Note that the orca in the video is in captivity so I don't know whether this is something that wild orcas can do or whether this is a human trained behavior. More generally, is this something that some smart predators can do?

Intelligence? Ehhhhh...insects can use bait hunting too. I seem to recall I once saw in a book when I was a child that some assassin bugs wave around dead ant corpses to attract more ants (though most Google searches only end up with assassin bugs covering their body with dead ants which is not what I had in mind). Assassin bugs also pluck spider web strings to simulate caught  insects to lure the spider out.

Well,  Crocodylus palustris do this using sticks that birds want for nesting.

(Photo from below article, copyright)
Behind a paywall is:
Crocodilians use tools for hunting.
V. Dinets, J.C. Brueggen & J.D. Brueggen
Published online: 29 Nov 2013
https://doi.org/10.1080/03949370.2013.858276
It is also known that Crocodylus porosus caches uneaten food; and unproven suspicions that they use the cached food to bait-hunt aquatic animals.


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Is Mallow toxic to livestock or is it only Parviflora that is?
Thank you for your time.  I have a question about toxic plants.
Mallow plants.  Specifically, my horse (while up in North Central Arizona for the Summer) had access to (and ate, unsure how much), Malva Neglecta (identified in a fb plant identification group from photos).  I have found plenty of evidence of Malva Parviflora being toxic to livestock, depending on quantity consumed. There is a write up about several horses in Australia that died from ingestion and others got rapid onset laminitis.  Link: https://pubmed.ncbi.nlm.nih.gov/27341541/#:~:text=Reason%20for%20performing%20the%20study,euthanasia%20after%20ingesting%20the%20plant.
Should I assume both plants are toxic since they are from the same family, or is it possible only the parviflora is toxic and the malva benign?
The reason for my question, is that my horse has developed some hoof soreness issues over the Summer, and I am wondering if the mallow plants could have been an additional factor, along with too much toe sole being removed when trimmed, a very rocky pen, and a particularly wet monsoon season this year.
I posted in a vet group, but got no answer.  I think many of them just don't know.

According to Livestock Poisoning plants of Oregon (1969!) it "should be regarded with suspicion".  To quote: "Another species of cheeseweed or mallow occurring in our area is Malva neglecta Wallr. (Fig. 57), and it, too, should be regarded with suspicion". But, I suppose, that in itself is not very informative.


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Are DNA molecules negatively charged at low pH values?
We know, that for each monomer of DNA, phosphate groups are having -1 charge because one of the oxygen is negatively charged (2nd oxygen participates in the phosphodiester covalent bond), but isn't it really depends on PH level? and if it does, for some PH level of X, for every N base pairs of DNA, how many phosphate groups are charged?
To better interpret what I mean, let me draw this scenario: If the solution contains too many protons (so PH is very low), would DNA still will be charged? why the negatively charged oxygens would not take these hydrogen ions, and makes them bond as hydrogens by sharing additional electron?

You are right. At a ph<5 which is where the PI of DNA breaks down, the phosphate group will bind protons, while the nitrogenous bases will become positively charged owing to the acidic environment.