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What sort of social structure might *Homo floresiensis* have had?
I've found limited info on how they may have lived.
Physically, we've deduced the so-called "hobbits" used stone tools and hunted dwarf elephants in the Liang Bua cave, in hilly terrain 600 m/2000 ft. 50-100 years ago the region saw grasslands expand but rain forest persisted, maybe around the cave.
Physically they were small with long arms, short legs, and long feet and stood upright but they might have been partly arboreal. Very small brains suggest limited intelligence but they made tools etc.
Homo luzonensis, a possible sister species, was active in the Philippines in the same era, and also left remains in a cave alongside game it may have hunted with stone tools. Its curved fingers suggest it was more arboreal.
Both may have descended from H. erectus in the region and undergone island dwarfing. But to reach their respective islands both would have had to cross deep ocean straits, whether by accident on natural rafts of debris, by boat technology, or some other method, and many islands and long distances lay in between.
H. sapiens and chimpanzees have fission-fusion societies. Different baboon species vary. Orangutans are more solitary, bonobos more gregarious and peaceful.
Are there any clues, hypotheses, etc. to suggest if how the social structure or hobbits might have been?
Can you suggest a better forum?

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. Please note we expect some evidence of you having done some homework - simply saying you haven't found anything isn't enough - tell us where you looked and what you know already. Small brain size doesn't correlate with intelligence - it's due to the folds on the brain, which can be seen in the shape of the skull when scanned. H. floresiensis has these folds and was likely quite intelligent.

Most anthropologists will tell you that it's incredibly difficult to know anything about social structures so far into the past. We can, at this time, only make limited inferences based on evidence that survives (typically more hardy materials).

Almost universally, there is little evidence for the social structures of early hominids. Such things simply do not survive in the fossil record.
You may be able to glean some idea of homo floresiensis social structure by researching the societies of hunter gather people who still exist today and have histories going back tens of thousands of years. They tend to live in groups of families, and have relationships with other groups, some friendly, some adversarial, who's territories border on theirs. Those borders they protect.
For example Australia’s original inhabitants:
The leaders of society are the elders – the most senior men and women who are respected by others. Important decisions are made by a council of elders, which include clan leaders and the most respected elders of the tribe. Australian tribes were not ruled by chiefs, but they had senior men who might be regarded as the best warrior, the best spear-maker, a medicine man, or being particularly wise.
Aboriginal society has separate names for up to seventy family relationship terms in some tribes. That is, far more than the European terms “father/mother”, “grandfather/grandmother”, “uncle/aunt” etc. Under their family and society rules, people have obligations towards certain relatives, and these obligations are reciprocated.extract from
Or the bushmen of the Kalahari (San)
Traditionally, the San were an egalitarian society. Although they had hereditary chiefs, their authority was limited. The San made decisions among themselves by consensus, with women treated as relative equals in decision making. San economy was a gift economy, based on giving each other gifts regularly rather than on trading or purchasing goods and services.
Most San are monogamous, but if a hunter is able to obtain enough food, he can afford to have a second wife as well. wikipedia
As you suggest in your question, the social structures of chimpanzees and other apes may give some indications of how these people lived. Jane Goodall says that chimpanzee behavior is very similar to human, even to the extent of having wars.
From Jane Goodall’s expositions on the life of chimpanzees:
Much of a chimpanzee’s life, especially male chimpanzees, is dedicated to climbing up or being knocked down the chimpanzee social ladder. Those on top need to fight to stay at the top, and those at the bottom need to find a way to improve their lot if they want a chance at fathering offspring and access to the best resources. This, however, is only one component of the complexity of chimpanzee behavior, as they also demonstrate altruism, share resources and knowledge with one another, and build strong friendships. It seems there is always more to learn about these perplexing primates! Goodall
Or here for a rigorous mathematical approach :
Chimpanzees organize their social relationships like humans  Nature
It can be seen from the last two references that chimpanzee social relationship echo that of humans and so may be a good indicator of some of the basic relationships that might have existed among homo floresiensis.


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Can anyone identify this bug please
We had just gotten a new kitten from a not great home. It was her second night here, and she was laying on my chest when I noticed that where she had been lying on me was really really itchy. When I looked down I thought I was looking at dust, but it was moving and there must have been like 5 or 6 of them. I can barely see it, they just looked like little brown spots and I'm hoping to god its not bed bugs.
It looks like it has antennae and 6 legs maybe I'm really sorry about how blurry the photos are. The YouTube video is easier to see here (youtube video). I'm not good at identifying insects so please help me.
Thank you!

[

Do they live huge big pimples on you ?
Put the cloth your cat has been on in the freezer overnight first. You can get some "diatoms earth" (I am not sure what the name is in English) as a way to kill a few on your cat before resorting to hardcore chemicals.

Very hard to say definitively from your photos and video. To help with ID, a location in the world, and some indication of the environment where you got your kitten - urban, rural etc, would be helpful. Bed bugs don't tend to remain on the host animal, so I suspect something more like a tick or a mite.

Shes only been here for two days, i got welts after the bugs were on my chest and i found a dead adult in the blanket she came home in, im going through the process of heating and freezing every fabric thing i own because im overly paranoid. We live in a smaller town in the north of Vancouver island and its common here, she also came from an apartment which i know had a problem with bugs and rodents etc.

Not a bed bug. Really grainy video; can't be absolutely sure of anything. If you have any specimens, try to get a higher quality picture. Freeze or put in ethanol one if necessary.

what you have is most likely some type of tick,the best way to get rid of them is to treat your cat using one of the tic repelling products out there,ask your cat`s vet what the recomended treatment are.some of the products can be used to get rid of fleas,ticks and mites at the same time.

May be rat mite - https://en.wikipedia.org/wiki/Ornithonyssus_bacoti
When the tropical rat mite bites its host, it causes an inflammatory reaction to its saliva and then pruritic nonspecific dermatitis, known as rat mite dermatitis.

I agree they look like mites, but a better (more enlarged) photo would help there.  Definitely not ticks and probably not bedbugs, though.

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What were the three dinosaur evolutions and do they imply that bipedalism could have evolved multiple times in hominins?
At this pop-sci article transcribing an interview with Jeremy DeSilva, they state:

"If we’ve learned anything about evolutionary trends, it’s that good
ideas evolve over and over again. For instance, the evolution of
feathers and dinosaurs independently evolved three times. You could
get the independent evolution of bipedalism multiple times."

I have two questions:

What are those three events of the independent evolution of dinosaurs? Also, are there other such events that are suspected but are not as well understood?

Is he correct in using these independent dinosaur evolution events as reason to imply that bipedalism in hominins could have evolved multiple times? That is, are there nuances/details regarding the dinosaur evolution events that constitute important differences compared to the case of bipedalism in hominins?

Note: I used the word hominin here because that is what Jeremy DeSilva used in the cited interview, but I understand that may affect the answer to my question as chimps are also bipedal, but feel free to inform me!

"Dinosaur", when used properly, refers to a clade. There's no way for a clade to evolve multiple times, or even to really evolve at all as something that happens; it's just a name for a group of descendants sharing a common ancestor.
I'm guessing instead that it's an incorrect transcription of "feathers in dinosaurs", since in and and sound quite similar out of context; that is, that something structured like a feather evolved three times in the dinosaur lineage.
I know little to nothing about this area, but Wikipedia's article on feathered dinosaurs suggests that this is a bit unresolved:

It is not known with certainty at what point in archosaur phylogeny the earliest simple "protofeathers" arose, or whether they arose once or independently multiple times.

There are feathers observed in multiple lineages of dinosaurs, but it seems most plausible that they all came from the same origin rather than independently. For the intervening species it may be that either they lost the feathered phenotype or that there is simply not fossil evidence of feathers for those species.
As for bipedalism, well, we don't really need any feathers to reason that a trait could evolve more than once. Flight itself is a simple example: there are flying insects, flying birds, and flying mammals (bats), all who evolved flight from previously flightless ancestors.
The most direct example, though, is bipedalism itself: there are many bipedal dinosaurs, including modern birds. Human bipedalism evolved separately from non-bipedal mammals. Arguing whether it's happened multiple times among the apes is another story, that has little to do with any examples from other clades or other traits except analogy. Certainly, other apes locomote on two legs at times, but none of them walk quite the way humans do. If you want to argue that feather evolution involved an earlier "protofeather" that then separately evolved into a full-fledged (hehe) version multiple times, then maybe that would relate to a "proto-bipedalism" (as observed in apes) that could result in multiple "truly bipedal" lineages, but one would need further evidence to support that.

I'd add that there's a good chance that bipedalism in dinosauria as a whole, while it might have evolved separately, there were vast expanses of time (conservative short 166 million years) between the beginning and end of dinosaurs... something Apes haven't had (yet - 25 million years)

And don't forget flying pterosaurs :-)

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Plant ID - PNW, E Cascades

Trying to identify a plant I found recently. May 4, 2024; approx. alt. 3000ft on eastern side of Cascades (ponderosa everywhere).
I was at an NFS camping area near Ellensburg, WA, walking up the road. Lots of red-brown mud. Along the sides of the road are the usual wash outs where water streams down during storms. There's a lot of rocks and a select few green plants in those stream beds, but I noticed a splash of yellow-brown. I have been looking for an example of candystick, so I can say that what I did find looks a bit like that kind of parasitic plant.
The stalks are perhaps 1cm wide and 10-15cm tall, white-yellow with streaks of muted red, and have no obvious greenery to speak of. There are little, blanched (almost green) leaves toward the bottom, which are close to the stalk, short, and seem less developed. The dominant feature which caught my attention are the yellow, serrated leaves on branches toward the top. These leaves are shell-shaped and occur in opposing pairs, with a single leaf at the branch's tip.
I found only two examples of this plant - less than 20ft apart - and I can't find any images like them in my reference books or on the Google. If anyone can identify this, then I'd be thrilled.

Welcome to the Biology Stack Exchange. A pity the photo is out of focus on the plant - you seem to have captured the rock in the background as the focus point. Do you have any other photos of it? I've embedded the image so no need to visit off-site. Uses the format: ![name of image](link to image)

Cross-posted (with a different identity) on our great outdoors site - we ask that you don't do that so as to avoid cluttering the network with duplicate posts. If you wish to consolidate or merge your identities, then please use the "contact us" button on any page at the bottom to ask staff to help out.

I reckon if you went back in a week or two, those yellows will be bright green and probably instantly recognizable. I didn't spot anything on iNaturalist that looked similar at this point, but hard to narrow to the right region.


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I found this fuzzy spider type pest in alberta canada. I cannot find it online. Can anyone help identify it?
Tiny fuzz like critter on
My bathroom wall. Appears to have some blue on it. The rest is white. It seems to have a lot of legs , almost tentacle like?

Welcome Erin. Did you mean to post a picture? You can use the [edit] button to add one now.


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Why isn’t the food of captive pandas supplemented with cellulase?
Pandas spend a lot of time eating due to their low efficiency in digesting cellulose from bamboo. Adding cellulase to their food, or feeding cellulase in between meals, could surely make the process more efficient. Why isn’t that done?
According to this study conducted in India, lactase supplements in humans have decreased indicators of lactose intolerance in lactose-intolerant individuals.
While this does not suggest a direct link with the main question, one may see how a similar cellulase supplement may allow captive pandas to better digest cellulose and thus, devote their time to other tasks.
Ref:

Baijal R, Tandon RK. Effect of lactase on symptoms and hydrogen breath levels in lactose intolerance: A crossover placebo-controlled study. JGH Open. 2020 Dec 1;5(1):143-148. doi: 10.1002/jgh3.12463. PMID: 33490624; PMCID: PMC7812489.

Do you know if adding lactase to milk works? If it doesn't, would that make you rethink the benefit of adding cellulase to a panda's diet?

As I imagine nobody on this list is involved in feeding pandas, I think the use of “We” is unfortunate. I realize that it is a style of popular scientific writing, but I think the passive is preferable, even if it is more difficult for non-native speakers of English. I have done this for you.

@anongoodnurse Lactase certainly seemed to help my children when very young - an almost overnight change in feces consistency, gas production etc. Part of the problem is that a lot of people conflate a dairy allergy (i.e. to what is presumably cow allergens of some sort) with lactose intolerance. The response in people who cut out dairy while breast feeding proves for many the response is not due to lactose because it won't make it out of the gut into the breast milk anyway and human milk naturally has more lactose than cow.

@bob1 - Johns Hopkins might disagree. There are ways to approach lactose intolerance, but lactase has never been shown by studies to improve symptoms. YMMV, obviously.

@anongoodnurse Yeah, that's why I put "seemed" Could have been developmental stage - they are fine with milk now, level of intolerance, all sort of factors come into it. I wonder if pediatric studies have been done... off to PubMed I go...

@anongoodnurse Not to muddy the waters, but perhaps what my kids had was lactase deficiency, not full intolerance - explains the symptoms and resolution. American Academy of Pediatrics committee on nutrition recommends lactase supplementation (at least in 2006 they did). Looks like no decent clinical trials and inconclusive results rather than no effect. Anyway, sidetracked conversation here...

@anongoodnurse Interesting, I think the fact that it doesn't work is more surprising because, in pandas, the gut microbiome breaks down most of the bamboo. Do you have some insight on why lactase might not work in humans? Also, perplexity.ai fetched me this: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812489/

@anongoodnurse My guess is that stomach acid, similar to how bromelin works, deactivates lactase somehow. Then again, pandas don't have the same digestive system as humans (I would assume), so perhaps enzyme supplementation in pandas may work differently from humans.

@David Same as the lab reports, I guess? Thank you for the edit!

@anongoodnurse Ah, I see the nuance. I guess I should have asked why pandas aren't fed cellulase between meals, not why panda meals aren't fortified with cellulase, my mistake. Should I close the question?

@YoungJunLee - You're right that pandas have a pretty different gut microbiome, and that they do digest cellulose as well, but not completely.  Today I learned a few things... hmm. No, I think the question should stay open, and if you add what you learned about lactase with the link, your question will meet out request for research. :) Thanks! Interesting thread.

@bob1 - That's good to know (that inconclusive/no rigorous studies does not equal ineffective)! I was thinking lactase deficiency, too. But, I was too close-minded about lactase supplementation. Reading the same thing in a couple of papers seemed to stop my thinking about it, so thanks. Yeah, when I was in practice, I used to recommend it, but not once I moved into the ED. No need for it myself; if I did, I might not have opined so definitively!

Most mammalian herbivores have digestive tracts that are highly specialized for digesting cellulose. For example, ruminants (including cattle) have a special stomach (rumen) that harbors microbes that can break down the cellulose in the cell walls of their food. This way, these herbivores can get a lot of energy out of the cell walls of the plants in their diet.
Giant pandas are different. They're evolved from weasel-like carnivorous animals, and therefore have digestive systems that resemble those of carnivorous mammals more than those of other herbivores. They don't have enough microbial activity in their guts to break down cellulose appreciably. Since they get very little energy from the cells walls of the plants in their diet, they instead get most of their nutrition from the cell contents of the plants. They have several adaptations1 that allow them to be able to get enough nutrition from just the cell contents:

They have very strong jaws and spend a lot of time chewing their food, which exposes the cell contents.
They eat a ridiculous amount of bamboo, so even though they can only digest a small portion of their food, they still get sufficient nutrition overall.
To be able to eat so much, bamboo has a very short residence time in their digestive system (~8 hours).

Because of these adaptations, giant pandas can get all the nutrition they need from bamboo without cellulase supplements.
And even if it were possible to reduce the time a captive panda spent eating bamboo, what would be the point? In captivity, there's not a whole lot else they have to do than eat.
And there might be risks involved with cellulase supplementation. It could result in large increase in the amount of glucose and oligosaccharides in the digestive tract and that the panda is absorbing, which we don't know the effects of. Running a study on that would be difficult (there aren't a whole lot of giant pandas around, and getting permission to manipulate individuals of endangered species is difficult), so without a compelling reason to pursue it, it hasn't happened.

1 Dierenfeld ES, Hintz HF, Robertson JB, Van Soest PJ, Oftedal OT. Utilization of bamboo by the giant panda. J Nutr. 1982 Apr;112(4):636-41. doi: 10.1093/jn/112.4.636. PMID: 6279804.

Thank you for the response. In captivity, breeding will be encouraged in their spare time. In addition, going along the line of efficiency, perhaps it could be possible to allow pandas to survive while eating less bamboo than they currently do. I agree with the need for such studies, and hope that other more established scientists can ask similar questions as I have.

That being said, I would summarize your response as follows: herbivore mammals can digest cellulose well, pandas can't, they adjusted using XYZ adaptions, cellulase supplementation is ostensibly not needed and has not been tested yet. Are there reasons other than it being difficult to test upon pandas, that such cellulase supplementation has not been attempted?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6184034/ I have only skimmed through this article, but similar experiments as proposed have been done on chickens. The effect was positive, allowing higher nutrient absorption from relatively low nutritional value grains. One may see how a similar experiment on pandas can be done with ample scientific purpose, most notably to decrease panda consumption of bamboo so that their maintenance cost can be decreased and to allow panda survival even in a season of bamboo paucity.

@YoungJunLee Feed for industrial chicken farming is designed to maximize chicken growth with little regard for the health or wellbeing of the animals. Presumably, that's not what we want for giant pandas in captivity. Also, chickens aren't really adapted to eat a diet of mostly grain, which is what industrial farms feed them. Pandas are adapted to eat a diet of mostly bamboo.

@YoungJunLee It's also possible that the answer to your original question is that no one has thought of it. You'd have to ask someone actually involved with keeping giant pandas to get the exact reason. I just gave some reasons why it might not be necessary or safe based on what I know of nutrition and zoology.

Given NileRed's two videos regarding cellulose conversions to glucose, I am sure that this is widespread knowledge in the biochemistry community and I am sure if it has not been applied to pandas yet, there must be some good reason. However, in my limited worldview, I am unable to find any such reasons yet.

Perhaps if pandas are unable to control their eating, supplementing enzymes will just result in obese pandas? And yet, I cannot be sure because articles I read state the panda eats so much, so long mainly for survival purposes, and that most animals have mechanisms to tell if they are full or not, whose hormonal mechanisms I presume are based on the amount of nutrients the panda is able to uptake.


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Identification of cells containing the gene of interest at a double strand break instead of undergoing recombination
If I tried to knock in a gene for example KANMX and want to swap it with say some gene "x", but, since, there can be double strand break in the DNA and KANMX may get inserted within the ds break instead of undergoing homologous recombination with gene x, in that case how can we identify the colonies which can be a mixture of the following :-
A.) Undergoing proper recombination and now having KANMX but not gene x
B.) Having both gene X and KANMX (how can we specifically identify these?)
C.) Undergoing no homologous recombination (one way is using G418 sulphate).
This question was asked in my class, one possible reasoning given was that we can make forward primers upstream of gene x, which won't work for KANMX and only reverse primer will work.
But I was thinking how we will screen so many colonies and can we use probes instead of primers or even a simple thing as gel electrophoresis to see size differences?
I will be very thankful if anyone can clear up this doubt!
I was troubleshooting the question with designing probes upstream of gene x and also only specifically for kanmx to differentiate the two or even observing size differences through AGE.


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Table is confusing: Discovery of tRNA publication
I'm a student and kinda new to reading papers; currently trying to read A SOLUBLE RIBONUCLEIC ACID INTERMEDIATE IN PROTEIN SYNTHESIS!
Everything else I can parse together given what we now know about tRNA role in translation. However, Table II (Table 2) confuses me.
If they start with the same amount of prelabeled C14, why do we see different total counts in each row?
My biggest question is that we see radioactivity transfer to the protein fraction in the "complete system minus generating system" conditions, but not under "complete system minus generating system with 5xGTP" ?? Wouldn't that undermine the idea that GTP is necessary for translation?
Image attached below!

Welcome Cytos. It would be helpful if you transcribed your notes next to the table so that it is more readable.

As you are probably aware, Hoagland has written a detailed and readable account of his role, and that of the Zamecnik lab,  in the discovery of tRNA (Celebrating complementarity), together with a renowned autobiographical account (Toward the Habit of Truth – A Life in Science)


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Enigmatic picture of an axon
An image from Terrence Sejnowski's lab is around since at least 2015 when it appeared in an article about hippocampal spine head sizes and only recently (May 2024) in an article about synaptic information storage capacity:

Visualization of a pair of spines (an SDSA pair) (with gray necks) from
the same dendrite (yellow) and the postsynaptic density (PSD) associated area
(red, indicated by white arrows) formed by the same axon (black stippling) with
presynaptic vesicles (white spheres)
What I wonder about in this image is the appearance of the axon. It is neither a regular tube with a somehow fixed diameter nor an obvious terminal. It has several junctions/synapses along its length, while I believed an axon forms synapses only at its ends. Can someone please clarify? Which part of an axon do I see, and how realistic is it supposed to be?

Your belief is wrong; axons form synapses along their lengths. I'm most familiar with these being referred to as en passant boutons. See for example this image and description from: https://synapseweb.clm.utexas.edu/axons

To clarify, though, this is something that would happen in the terminal field of an axon; in other places an axon is entirely an axon of passage making no synapses at all. The specific anatomy is going to depend on the exact type of neuron and it's origin and target(s).

Thanks, Bryan. Can it be said that along the axon of passage its diameter is roughly constant, and only in the terminal field its diameter is as irregular as the images display?

The swellings/boutons are specific structures just like post-synapses, they contain vesicles and all the presynaptic release machinery. All that will only be found where actual synapses are made. I'd presume the axon would be mostly constant diameter elsewhere and certainly anatomists use the presence of swellings to indicate synaptic contacts, but I don't know what the magnitude of diameter variance is outside of synapses.

Another point, although I don't think it applies to this particular axon, is that many axons are myelinated and thus vary in apparent diameter along their length.

I have only seen synaptic boutons in unmyelinated parts of an axon. In the neocortex and the hippocampus, en passant boutons are very common. As is seen in both images, their inter-bouton distance is roughly 1-2 μm. The axons in both images appear typical.

Interestingly enough - and probably not by chance - is Kristen Harris both co-author of Terry Sejnowski (and the two papers I have linked) and author of SynapseWeb (that Bryan has linked). By private communication she and Tom Bartol confirmed the correctness of Bryan's answer.


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How did the Zinder-Lederberg experiment on Transduction work?
In the paper that introduced TRANSDUCTION (J Bacteriol. 1952 Nov;64(5):679-699), Lederberg and his student Zinder reported that S. typhimurium

"LT-22 is lysogenic for a virus active on LT-2. This virus is capable
of inducing lysogeny in LT-2."

I read this line as: LT-22 carries a prophage that, upon induction, can infect LT-2.
They then used subsets of these strains: LA-2 (also known as SW-414), which required methionine and histidine; and LA-22, a collection of strains with different metabolic requirements.
Zinder and Lederberg commented that

Prototrophs appeared in the platings of LA-22 but not of LA-2. Sterile
filtrates of LA-2 broth cultures did not elicit prototrophs from
LA-22.
However, filtrates from mixed cultures of LA-2 and LA-22 elicited about one prototroph per million LA-22 cells.
Thus LA-2 produced a filtrable agent (FA), under stimulation from LA-22, that could elicit prototrophs from LA-22.
Filtrates of LA-22 cultures, containing substantial amounts of phage (PLT-22) active on LA-2, also stimulated FA production from
LA-2.

Thus, LA-2 produced a phage that infected LA-22 to produce a prototroph.
But if the phage was present in LA-22 (derived from LT-22), how could it infect LA-2 (derived from LT-2)?
Is there a detailed explanation of this experiment?
Thank you

Regarding the bolded sentence, it's not surprising that a prophage from one strain of salmonella would infect another salmonella strain. What part of the process needs explanation?

The fact that the phage moved from LA-22 to LA-2, took some genes from it and then re-infected LA-22 (which, being lysogenic for the phage, should have been immune to it)

There certainly are detailed explanations of the experiments. For this answer I'm using a 2016 retrospective in J. Bacteriology, the same journal that published the original paper. However those descriptions will tend to gloss over the points that concern you as described in your comment:

The fact that the phage moved from LA-22 to LA-2, took some genes from it and then re-infected LA-22 (which, being lysogenic for the phage, should have been immune to it)

Remember, these experiments took place in a very early time for biochemistry. The Hershey-Chase paper that established nucleic acid, not protein, as the carrier of genes was also published in 1952! The "how" of transduction wasn't worked out until later.
The Filterable Agent responsible for transduction between LT-2 and LT-22 is now known as phage P22. Its prophage tends to be integrated into the host genome. When it switches from lysogenic to lytic phase, it replicates its genome while still integrated into the host.

The headful mechanism fills the first capsid with part of the prophage genome and continues through the adjacent bacterial chromosome for up to seven or more successive capsid headfuls.

So, a significant fraction (about 2%) of the virus particles produced by lytic P22 contain host bacterial DNA and little to no phage DNA.
Why superinfection exclusion (SIE) fails in the LT-22 is an interesting question, but it turns out to not be surprising. P22 has four separate SIE systems, and one, sieA works by binding to and blocking the exit of P22's "ejection proteins", so it can stop transduction by preventing entry of any kind of DNA. However, it looks like this system doesn't perfectly prevent DNA injection. From a 1971 paper on P22 SIE:

The frequency of transduction of wild-type lysogens is reduced by a factor of 250, indicating that transducing particles are excluded by P22 prophage

So, if the concentration of P22 particles with bacterial DNA is high enough, a few will get through.
Incidentally, I found that LT-2 was first isolated in Sweden, and LT-22 in Chile, both in the 1940s.

Thank you, I also read that paper. Your answer gives a better understanding of the issue. Tx

I hav found more info in two more papers. In Microbiol Rev 1978;42:385 it is said: "P22 ... generalized transducing particles consist primarily of host DNA... the transductant carries the transducing material as long as the prophage is present". Thus, lysogeny is actually needed for transduction to occur.

In the same paper, P22 superinfection exclusion is described as follows. There are 3 mechanisms (1) "chemical modification of the cell surface component (the 0 antigen)" but " P22 lysogens still adsorb P22 virions, but less efficiently"; (2) "preventing entry of the DNA of superinfecting phages into the cell" but " The sieA exclusion system can be saturated by high multiplicities of infection"; (3) "sieB" which " does not act on wild-type P22". Thus, one can assume either that there were many viruses that saturated sieA or that Zinder used sieA mutants...

In both cases, the model is more complicated than that delineated by Zinder himself.

The second paper (doi: 10.1128/mbio.02169-23) indicates 4 mechanisms of P22 superinfection exclusion; which Zinder had to bypass to obtain transduction. The additional one is the C2 repressor, which assures the non-expression of lytic genes (but does not exclude the insertion of new prophages).


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Is there a functional model of the human retina for simulation of conversion of illuminance pattern to nerve signals?
I'm looking for a model that would take a pattern of spectral irradiance over the retina as a function of time and space and convert this into the signals propagating through the fibers of the optic nerve.
I know that there's a variation in distribution of different kinds of receptors over the retina among humans and even between two eyes of a single human, just as there's a variation in the interconnections between the receptors and the outgoing nerve fibers. But I'm interested in a "typical" arrangement that would let me study more general properties of the sensor side of human vision, such as finding different illuminance patterns that yield the same signals after a period of adaptation, or studying how photopic vs scotopic level of illuminance of a scene affects the output signals.
Basically, I'm looking for a black box that would function just as a human retina in terms of input and output.
Is there such a simulator available? If not, has the function of the retina been studied thoroughly enough that I could find a book with enough information to create such a simulator?


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Why is Cannabis sativa considered a distinct form of Cannabis?
My understanding is that the word Sativa is Latin and means "cultivated." See here: https://en.wikipedia.org/wiki/Sativum
Since all cannabis consumed by people is cultivated and grown from seed, shouldn't all Cannabis be called Cannabis sativa? And so isn't Cannabis indica also Cannabis sativa?
If taking a cutting of a plant grown from seed and rooting it means that "clone" isn't considered to have been grown from seed then maybe those plants shouldn't be called Sativa, although this would still seem to qualify as cultivation. But either way I fail to see what bearing it has on phenotype or alkaloid profile. How has it come to mean having thin leaves and high THC content?

A ver energetic recent document from 2016 demonstrates that no scientists have used the recent genetics technology to see which are the oldest populations of cannabis and if they diverged 5,000 years ago or 50,000 years ago. indeed in Mexico and Russia there are varieties 1 foot tall and in Thailand 20 foot tall, which suggests there may be differences 50,000 or 5000 years old, a future PhD or Research group can find out. https://www.frontiersin.org/articles/10.3389/fpls.2016.01113/full

Be careful with over-interpreting etymology, especially in the context of biological terminology. There are hundreds of cultivated plants, very few of which have any reference to 'cultivation' in their names. This would be like complaining that someone named their child Amber and she grew up to have blonde hair, and then further arguing that everyone else with brown hair should have been named Amber. The distinction between indica and sativa strains is an interesting one, but it has nothing to do with etymology.

@BryanKrause ok, so I should not expect scientific names to have any concrete relationship to the plants they are naming?

Just recognize that names are names. They typically are based in something, but they need not follow a consistent system nor be entirely accurate nor are names describing a trait indicative that the trait is not shared with other species.

@BryanKrause i see. It seems strange to me that science, which normally values consistency and accuracy for obvious reasons, would not value either of those things when it comes to naming plants. I guess it probably is pretty difficult in this area tho, what with there being so many plants and so many subtle differences and new information being added all the time. Still, it sounds like real science has been influenced by stoner science rather than the other way around. Anyway, thanks for the information!

@dev_willis A name of a plant is just a name, that's it: it's a reference so we can all talk about the same plant. Each plant has too many characteristics to describe them all in a two-word name. Sometimes names come when other information is missing: you might name a plant based on where it is first discovered, and then find out it is more widespread than you first realized. You might name a plant based on a feature that is so far unique to it compared to similar relatives (maybe a different color?), and then find other relatives that also have that feature.

C. sativa was originally named by Linnaeus in 1753, long before the plant was commonly used for recreation (in Europe, at least), so the name probably reflects the fact that that species was cultivated for fiber (hemp), just as many plants have the Latin name Officinalis or officinale, meaning that they were used in medicine.  Later botanists considered other varieties to be sufficiently different to be different species or subspecies. (Including some interesting reasons based in the laws of the 1970s: https://en.wikipedia.org/wiki/Cannabis#Taxonomy )
It's also not true that all Cannabis is cultivated.  It can be found growing wild, either native or as a introduced plant, in many parts of the world.

Thanks for the link. So it sounds like it was named this way to make a distinction between wild plants and plants cultivated for industrial use and later when Westerners discovered it being grown in India they felt like it was different enough to need a distinct name? And from there the vagaries of language enabled the words to drift away from their original meanings to the totally unrelated meanings we have today?
BTW, I'm aware that it grows wild. Everything does, or did. But few if any people are consuming those plants. All I said was that the plants people consume are cultivated.

@dev_willis: No, I don't think Linnaeus was really making a distinction.  Nor do the Latin names given to plants (or animals) always (or even frequently) have an exact, literal meaning.  Consider all the species, or even entire genera (like Fuschia or Wisteria), that are named after people, for instance.  One of my favorites is Dichelostemma ida-maia: https://www.wildflower.org/plants/result.php?id_plant=DIID


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Why would it be impossible for gram-positive bacteria to store sulfur as gram-negative sulfur-oxidizing chemolithotrophs can?
I have a question that I am not sure what is the correct answer on <<Brock's Biology of Microorganisms>>
When the book introduces "Cell Inclusions", there was a mini-quiz that contained a question asking "Why would it be impossible for gram-positive bacteria to store sulfur as gram-negative sulfur-oxidizing chemolithotrophs can?"
I understand that gram-positive bacteria have a thick proteoglycan (consisted of a net of glucosamine and amino acids bonds together covalently) cell wall whereas gram-negative bacteria only has some lipid membrane.
I also understand that sulfur cell inclusions are usually elemental sulfur wrapped up in PHA (poly-beta-hydroxyalkanoate) polymer.
I just cannot put the two facts together to answer the quiz question?
Thank you in advance for your generous hint!

I also understand that sulfur cell inclusions are usually elemental sulfur wrapped up in PHA (poly-beta-hydroxy alkanoates) polymer.

This is not correct! It is true that most PHA producers generally belong to the Gram-negative group of bacteria. However, PHA is not used to store sulfur. PHA is there to store excess carbon and energy. Though, this energy can come from sulfur metabolism!
From Brock Biology of Microorganisms 14h edition I cite:
"The oxidation of sulfide is linked to the need for electrons to drive either reaction of energy metabolism (chemolithotrophy) or CO2 fixation (autotrophy). In either case, elemental sulfur from the oxidation of sulfide may accumulate in the cell in microscopically visible granules [...] Interestingly, although sulfur globules appear to reside in the cytoplasm, they are actually
present in the periplasm [...]"

"Why would it be impossible for Gram-positive bacteria to store sulfur
as gram-negative sulfur-oxidizing chemolithotrophs can?"

The as here is very important. Because some Gram-positive bacteria are perfectly capable of storing sulfur but not in the same way as Gram-negative bacteria. As we know, in Gram-positive bacteria the periplasmic space is found between the inner membrane and the peptidoglycan layer which – I assume so – is not suited to "hold" or produce these granules in a similar fashion.
To give a bit more context:
Sulfur oxidation and sulfur reduction are two different processes that involve the transformation of sulfur compounds. Certain Gram-negative as well as Gram-positive bacteria (e.g. Desulfotomaculum) are able to do so. Some strains are even able to do both reduction and oxidation! In either case, for both types of bacteria, there are strains with sulfur metabolism involving the storage and usage of sulfur for energy production, just in different manners.

Sir, is it because only gram-negative bacteria have periplasm, so only gram-negative can accommodate end products of sulfur oxidation?


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Evolution of Anoles
For context, I am currently looking at this virtual lab of Lizard Evolution by HHMI biointeractive.
Trunk anoles from an island called Iron Cay were placed in a few experimental islands filled with small bushes and grass.Over four years, the researchers measured the length of the hindlimbs of the anoles. After four years, they found that the average hindlimb length of the anoles in the experimental islands was shorter than that of those on Iron Cay.
I was wondering if the anoles from the experimental island were brought back to Iron Cay, would the anoles still mate with each other?
Thank you!

On the face of it, this seems to be a question regarding the behaviour of artificial constructs in a computer program and not a biology one. I gather it's an educational program, but I'm not familiar how it's programmed or how it can be adjusted to behave. Perhaps you should just try it and see. If you've an actual biology question about the scenario in real life, (about speciation) then please ask it, but the question as it is now seems to me to be off-topic. Please take our [tour] and read up in the [help], noting the [ask] section.

This is also definitely a homework question... note our homework policy

I'd recommend reading up on the different mechanisms of reproductive isolation. It's possible that changes in hindlimb length or morphology could be a source of behavioral or mechanical isolation, though post-mating barriers to reproductive compatibility would be unlikely on such short timescales

to clarify the two lizard populations have only been separated for 4 years right?  There's no reason to expect too much evolution to occur in 4 years.  If the surviving lizards have longer legs then I'd argue that all that happened is just the short legged lizards died.  While that is evolution, since the lizards are the exact same individuals taken to the island 4 years earlier, there's no reason to expect they'll have changed their mate choice behavior.


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Intensity of UVA needed to damage skin and cause ageing
Using a UVA/B measuring device, I was able to determine that approximately $\pu{10 μW/cm^2}$ penetrates a window even when not in direct sunlight. For reference, the intensity of direct sunlight without any glass is approximately $\pu{6000 μW/cm^2}$ UVA (this UV component represents ~6% of all solar energy from direct sunlight that reaches the ground on a clear day) and $\pu{50 μW/cm^2}$ of UVA penetrates the double pane glass window in direct sunlight.
If a person were to sit in front of this window most of the day (about 8 hours). Assuming indirect sunlight, is this $\pu{10 μW/cm^2}$ dose hitting their face going to cause significant skin damage over time?

Welcome to the Biology Stack. Please take a [tour] and visit the [help] for more information on this stack and how we work. Please note that personal medical advice is off-topic here, which this post leans towards (as in we'd need to know your race and other personal information to make an informed answer; so that would be a clear breach of rules). Having said that, I can see a good question here, that isn't medical advice if you depersonalize it.

@bob1 You're right I hadn't taken into consideration different races would have different skin types and different susceptibility to skin damage. Though an expert in this field should be able to provide generalized thresholds for different skin types. Hopefully...

I've depersonalized it and added some specifics - like duration of exposure, without which this is unanswerable. If you disagree with the changes feel free to edit some more or revert, but be aware it might get closed for medical advice.


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Are restriction sites added on to the ends of a DNA fragment or are they just conveniently there?
For a DNA fragment to be inserted, it must have two restriction sites on either end. My textbook makes it seem that this is naturally occurring but it seems a little too convenient, are they added in instead? And also, are promoter and terminator regions already present in the fragment or is the restriction site separated and reattached in order to insert them?

Depends on what you're trying to do, what materials you have to work with. What are you trying to do? What textbook are you using? What websites have you looked at?

I’m an A level student, using an aqa textbook. I’ve tried looking it up but the answers are over my head. I’m just trying to understand whether the restriction sites on the DNA fragments are added in sometimes rather than always naturally occurring.

Welcome to the site. Please visit the [help] and take a [tour]. In particular pay attention to the homework page. For these we require evidence that you have put some effort into working out the answer yourself.

I suggest you look up plasmids and have a play with the maps and sequence. Try Addgene for this.

That depends a bit on the method you are using, but mainly you are right, it is rather unlikely that a piece of DNA contains the right restriction site on both ends, let alone even two different ones for site directed cloning.
A common technique used to insert the restriction sites of choice is to amplify your DNA with PCR and special primers. These primers contain your wanted restriction sites next to the recognition sites and produce an overhang (at least in the beginning of the amplification reaction) which contains the restriction site. See the image (from here) on how this technology works.

Regarding promoter and terminator regions, I assume that you clone something into a DNA expression vector. Then these sequences are typically part of the vector and optimized for the cells to work with (bacterial or eukariotic).

thank you! that makes sense


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Intelligence of nervous system vs other human intelligence?
Viral proteins are shown to be used in intelligence such as for memory: https://www.sciencedaily.com/releases/2018/01/180111141450.htm
I wondered since proteins able to form prions are the most logical thing directly controlled by the soul, how intelligent is the nervous system compared with other systems the body uses for intelligence like viral proteins? Has anyone calculated the difference in computing power of them?

What are you implying by the phrase "intelligence like viral proteins"? Could you please elaborate your thoughts on it?

@ANandiΨ Viral proteins are shown to be used in intelligence such as for memory https://www.sciencedaily.com/releases/2018/01/180111141450.htm#:~:text=The%20protein%2C%20called%20Arc%2C%20is,like%20a%20protein%20from%20viruses.&text=A%20protein%20involved%20in%20cognition,like%20a%20protein%20from%20viruses.

@ANandiΨ I wonder how the non-nervous intelligence compares to nervous intelligence

"Arc" is the Activity-regulated cytoskeleton-associated protein. It's one of the "immediate early genes", which are genes whose expression changes very quickly in response to certain neuronal activity. They are thought to be important in mediating the changes in expression of other proteins that accompany learning and memory in neurons.
This is not talking about any other "intelligence" or memory besides what happens in the nervous system. It's about the mechanisms by which the nervous system operates. The paper (Pastuzyn et al 2018) suggests that this protein originally came to the animal genome from a virus rather than evolving from other animal genes, and that it behaves in a virus-like fashion to transfer genetic material from one cell to a neighboring cell. That's definitely interesting from an evolutionary and molecular biology perspective, but it does not mean the body "uses viral proteins for intelligence".
In an animal, these aren't "viral proteins" any more, they are animal proteins, built from DNA in animal cells and evolved alongside those animal cells. The paper is about Arc in fruit flies, though Arc is also found in vertebrates but seemingly from a different lineage; therefore the authors suggest that this has happened at least twice. It's certainly fascinating that such a rare event would happen more than once; I'm not sure if there is additional literature on this because it seems hard to believe, but I suppose it's one more element to how all the genetic variation in modern species evolved.

Pastuzyn, E. D., Day, C. E., Kearns, R. B., Kyrke-Smith, M., Taibi, A. V., McCormick, J., ... & Shepherd, J. D. (2018). The neuronal gene arc encodes a repurposed retrotransposon gag protein that mediates intercellular RNA transfer. Cell, 172(1-2), 275-288.


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Pulse pressure, vascular physiology
I always though compliance of a vessel is a thing that prevents systolic pressure to goes up a lot and also prevents the diastolic pressure to goes down a lot, and that works because in arteriosclerosis we see that because of low compliance the systolic pressure goes up and diastolic pressure goes down therefore pulse pressure increases,

but I see a graph that shows systolic and diastolic pressure changes with age, we say with aging the compliance of vessels come down,but as you see in the below graph, both diastolic and systolic pressure goes up(I also find this sentence in the textbooks), why does diastolic pressure go up? Why it doesn’t go down like with arteriosclerosis? And also pulse pressure goes up with aging.

Both of the graphs are from Guyton, also I have this problem: What factors affect systolic and diastolic pressure? I search a lot but didn’t find anything.

The first figure does not show diastolic pressure going down with arteriosclerosis, does it?

I don’t see too, I just write what I’ve heard  in the class. unfortunately there is nothing about it in guyton.

Welcome to the site. Please take a [tour] and visit the [help] for what makes a good question/answer on this site. This site values questions that show some evidence of previous research, of which there is plenty into blood pressure and arteriosclerosis etc. I'm not sure on your question here. The top graphs are point measurements of actual pressure over a single pulse-wave, but the second is average pressure with age. Why wouldn't the overall pressure increase with arteriosclerosis/age?

It would help if you were to focus down to a single question. At the moment it seems you want a complete rundown of all conditions that affect every aspect of blood pressure, that's too broad for this site's format. Please narrow to a single question, then ask any follow-up questions in their own threads.


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How to distinguish hornbeam from hophornbeam?
The town where I live plants both hornbeam trees (Carpinus betulus) and hophornbeans (Ostrya carpinifolia) as street trees. How can they be reliably distinguished, especially when there is no fruit on the tree? The fruit is different but the leaves are very similar.
To be clear, this question is about the European-native species, not American ones.

There is a German-language article on the topic: https://www.zobodat.at/pdf/Fl-Austr-Novit_4_0032-0040.pdf

Both plants like similar mesic conditions and so can be found in similar locations. However, these plants are actually very easy to tell apart using only a few easily observable characteristics*.
Bark:

Ostrya is peely/shreddy brown

Carpinus is smooth and grey. The bark almost looks sinewy, leading to its much better common name: muscle wood.

Leaves are both doubly serrate and similar in size. However, leaf texture is different:

Ostrya is finely hairy. Best to feel with lips (more sensitive) when 1st getting used to difference.

Carpinus is smooth (glabrous) and even somewhat papery like Fagus.

now, if I could only remember which one had the hop in its name! (this is why I stick to scientific names :p)

I'll update with sources soon.

I took the time to find an Ostrya where I could reach the leaves so I could examine one close up. You are right that it feels hairy, although some Carpinus leaves I got for comparison also feel slightly hairy (if not as much). However, the Carpinus seams to be hairy only on the underside and only along the veins, while the Ostrya is also hairy on the top and inbetween veins. Under a magnifying glass, the Ostrya hairs are shorter than the Carpinus hairs, and this seems to be confirmed by the German article I linked (as far as I can tell, my German is not good).

Two more interesting differences are: The tertiary veins clearly stand out on the Ostrya (like on big-leaf linden), but not so much on the Carpinus (which is more like little-lead linden). This is also confirmed by the German article. Finally, some of the secondary veins branch out on the Ostrya, but not on any of the Carpinus I looked at. This is the easiest to see difference. Do you know if it is a reliable way to distinguish them?

Picture of two Carpinus with Ostrya in the middle


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What is the origin of mammals X/Y sex determination system and what/when was the last common ancestor to possess these chromosomes?
I know many animals use an X/Y sex determination system, but not all of these animals use the same X/Y genes.  That is to say the X/Y sex determination system has convergently evolved in many species, and they often use different chromosomes as their X and Y than humans do.
I'm interested specifically in the variant of the X/Y genes that humans and most mammals use and their origin.  (side note, is there a better term for referring specifically to therian x/y genes vs the X/Y genes of say snakes or insects?)
I'm frankly curious what we know about how the sex chromosomes we use now evolved and when it happened.  For example do we know of any non-therian mammals that have autosomal chromosomes that look similar to our sex chromosomes that presumably suggest where our sex chromosomes split off from?
I'm aware that monotremes have their own odd variant of X/Y sex determination system, but it looks like neither the platypus, nor the Echidna X/Y chromosomes are similar to our own.  So clearly our sex determination system came after we split from monotremes, but are there any therian mammals that don't share a last common ancestor with us that used our X/Y genes for sex determination?
Not sure if this is asking for more then we can know, but if the monotremes' similarity to Z/W chromosomes in birds suggests pre-mammal ancestors used z/w sex determination system then how come we now have only one non-autosomal chromosome now?  How would a theoretical pre-mammal z/w sex chromosomes have become autosomal?

As I am sure you know by now, the Stack Exchange format works best with one question per question. I count 3 related questions in yours. You could split them up into 3 questions or re-word to make what you actually want to know clearer.

try googling "vertebrate sex chromosome evolution": https://www.nature.com/articles/nrg.2015.2


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Did or do these gigantic spiders really exist in Finland and/or Northern Europe?
In the year 2000, the newspapers in a small coastal town of Finland ("Hanko"; current population: ~8k) had some very disturbing reports of a couple who had just moved into a new rental apartment/house in the central part of the town, and there encountered these monstrous spiders that look like they come straight out of a horror movie. In fact, apparently, they are literally the kind of spiders used in the classic spider horror movie "Arachnophobia"...
Digging through old things recently, I encountered the saved newspaper pages and was shocked by just how large and disgusting they look. I must have repressed this whole thing for the last 21 years, since I first heard about it when it was current. From the oddly-worded Swedish-language report (clearly not written by somebody with perfect Swedish skills), it's not made clear whether the couple was "just" working on fixing the place up, or if they actually had already moved in and saw these monsters while they were there to sleep. But the basic point is that the spiders allegedly existed at all, and may well still exist...
The article also notes that these spiders were "common" in Denmark in the beginning of the 1900s, further creeping me out. My initial assumption and hope was that these spiders had miraculously survived in their undisturbed habitat for 50 years (the article also mentions that they were "last spotted" in the 1950s), and that they were not native to Europe at all, but simply had been accidentally shipped in a crate with exotic fruits or something from some tropical island somewhere back in the day, and had not spread but simply hung around in their little basement in a place which, somehow, just happened to not have any humans going there for all these years.
The article further mentions that some kind of professor had determined them to be Tegenari Atrica spiders. However, looking them up on Wikipedia, I got redirected to the disturbingly named article "giant house spider", where it's mentioned that these are:

among the largest spiders of Central and Northern Europe.

And:

original habitat consists mostly of caves, or dry forests where it is found under rocks, but it is a common spider in people's homes.

Source: https://en.wikipedia.org/wiki/Giant_house_spider
The map on that page suggests that they are all over Northern Europe... But if I ever saw such a spider, I could never again live in or visit that house and would need to have it burned to the ground and then salt spread all over the ground in the extended area so that nothing can ever grow or live there again. Not exaggerating.
I actually tried to contact the newspaper about this but haven't heard anything back so far. Hopefully, it was all completely fake and made up due to a shortage of "exciting" news, but if real, I'm not able to ever revisit that place (the town in general) out of fear of encountering further such spiders.
I'm having very serious trouble believing that people ever had these huge spiders "commonly" inside their living places, let alone these days. And I wonder what "common" means in the context; to me, it means that you regularly spot them on walls or walking across the street, etc. The Wikipedia article even mentions that they have started being spotted in some Eastern European countries in "the last few years", which is very bad news for me, and really makes me wonder what could possibly explain that.
I had to dig up the old scanner and scan the newspaper pages for this question:
Scan #1 (Swedish-language article with a photo): https://i.ibb.co/yy00H2b/1.jpg  (link broken)
Scan #2 (Swedish-language article, continued): https://i.ibb.co/DWfN3W1/2.jpg (link broken)
Scan #3 (Finnish-language article with the scariest photo): https://i.ibb.co/pW6gZMx/3.jpg (link broken)
I have not manipulated those photos in any way, but hopefully, the newspaper did... Maybe somebody wanted to show off their skills with Photoshop, the year being 2000? This is a place where I spent a lot of my childhood and we slept in all kinds of old houses there. I don't recall any monster spiders, but my skin starts crawling just thinking about the fact that I was sleeping quite near the area where the spiders were allegedly found... Although the exact street/address is frustratingly not mentioned in either article.
I almost get the feeling that this whole thing has been "hushed away" in order to not scare away tourists, rather than sensationalized. I would be very interested in hearing serious theories or even hard facts regarding this.

Re "hushing away", quite the contrary.  Promote a "Giant Spider Festival" to attract arachnophile tourists, as Scotland has done with Loch Ness.

@jamesqf I certainly hope that there are no arachnophiles...

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details on what is expected on this site and [edit] your post accordingly. In particular, please focus on a single biological question and eliminate the anti-spider ranting. You shouldn't expect a lot of sympathy for this irrational hatred here — spiders are an essential part of ecosystems and help control real pests like cockroaches (as well as being very interesting in their own right). I  suggest you find psychological help for your phobia (e.g. search for exposure therapy). Thanks!

@tyersome And I, in turn, suggest that you "find psychological help" for your insane love for these physical manifestations of pure evil.

@Dimitar: Alas, your hope is doomed to go unfulfilled, There's at least one web forum devoted to them: https://arachnoboards.com/  And while I'm not an actual arachnophile myself, I certainly like them for being the interesting and useful critters that they are.

I apologize if my comment came across as dismissive or insulting. As someone with more than my share of psychological issues, I have some understanding of how terrible a strong phobia can be. Unless you are massively exaggerating your feelings about spiders I imagine this must be a huge burden for you. My suggestion about looking into exposure therapy is not meant to belittle, but instead is done with the hope that you can find a way to make your life less stressful.

This is their size and demeanor (non-aggressive). And, yes, they are common and they tend to keep to themselves in their own spun funnel-webs: https://www.youtube.com/watch?v=Vy66QUsflKk

No and yes.
No - the articles are fear-mongering. I can see that without even being able to read a word of Suomi (Finnish) or Swedish.
In particular the Finnish article with the couple holding a picture of the spider. In this case the picture is a close-up picture of the spider that has then been expanded onto a largish photo (I would guess about 12 in/30 cm by 8 in/20 cm). In this picture you can see the texture of the cloth the spider is sitting on (seeing the texture would be unusual for a life-size photo) and a coin in the top left of the photo. I can't make out the coin denomination, but I doubt that they have a currency with approximately 8 cm (3 in) diameter coins - indeed the largest Finnish Makka was just over 3 cm (1.2 in), but this was only used between 1928 and 1939 (according to the linked Wikipedia page), so the coin is not likely to be that large. As you can see if you look at the photo, the diameter of the coin is about the length of the body, so at most the body will be about 1 inch, and the legs about twice that.
In the top-right of the same article is a photo that is much more realistic size - compared to the hand you can see that the body of the spider is about 1-finger width, so 1-2 cm or slightly less than 1 inch. If you then refer to the description part of the Wikipedia article you linked on the Giant House Spider (Eratigena atrica), you can see that the dimensions of the spider indicate body length of 18 mm (0.73 in) and a typical leg span of 45 mm (1.8 in) - so the hand picture is more realistic. They can have larger leg spans of up to 70 mm (3 in) apparently, but I have no idea how common this is.
However, the yes part is that: Yes, this type of spider does exist. They are widespread in Europe and parts of North America (introduced, but there are native Eratigena species in NA). They are mostly harmless and very unlikely to bite unless attacked. If they do bite, it will likely to only cause local pain with very little envenomation.
You are only likely to find them inside when it starts to get cold outside; as is the case for many animals, they try to find somewhere warm to live.
Note the spiders used in Arachnophobia were Avondale spiders (Delena cancerides) a harmless, but ugly looking, member of the Huntsman spider family, and a Tarantula species (I don't know which one, but there are quite a few species). Avondale spiders are from Australia and were introduced to Avondale in New Zealand, where they got their name, as they are apparently uncommon in Australia. Neither the Tarantula nor Avondale spiders are found natively in Europe.

After reading your answer, it makes perfect sense. I didn't even notice that the round thing in the corner was a coin, and indeed much larger than any coin used then (or now). It does indeed look like a scaled-up photo now. But even the "small" spider shown on the hand photo is still large enough to be quite horrible to me, although infinitely less so than the monster spider I imagined from that photo. I do feel a bit better now. Thanks (seriously).


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larvae in my balcony
yesterday I found lots of larvae on my balcony floor.  I couldn't find out where they came from. I put some in a jar to search for them and today they started turning into pupae.
Can anyone tell me what the insect is and how to get rid of it?

Welcome to the site. Take a [tour] and visit the [help] for details on how to ask a good question. For identification questions we also need a location (to local area, don't need your street address), what's in the environment (e.g. nearby plants, animals etc) and preferably size or some sort of scale to refer to. As another point you are asking for an identification of a pupa - this is entomology (insects etc), not botany.

keep the pupae in a jar so we can identify the adult later

Oh, I know those things.  I've seen the empty pupa cases, and I've seen the larvae.  I did not know the pupa cases were from those particular larvae, so you've already found uot more than I knew!


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In plasmid-based transient transfection of mesenchymal stem cells, do I have to select for transfected cells and verify GOI expression via a reporter?
I am transiently transfecting mesenchymal stem cells with a mammalian plasmid-based expression vector that does not contain any mammalian selection marker and also the gene of interest will be cloned into the plasmid without co-expression of any reporter fusion gene.
I would like to know if selection or expression testing is good practice and mainstream in plasmid-based transient transfection of mammalian cells.
As you know, in bacterial transformation selection against non-transformed bacterial cells is mandatory so that transformed bacterial cells could be enriched for. I wonder whether this is also mandatory in plasmid-based transient transfection of mammalian cells. If not, then  would not non-transfected cells outgrow transfected ones and affect downstream cell-based functional assays? Also, do I have to measure transfection efficiency beforehand? Also, how long can a mammalian cell retain a plasmid without a mammalian selection marker? Thank you.

Welcome to the site. This is not a tutorial site to explain every aspect of a given paper, concept, or idea. I strongly suggest you take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question. Please try to narrow down your question to one specific question instead of trying to get a tutorial on transfection as a whole.

You will need to verify the quality and extent of your transfection reaction after 24-48 hours, depending on the cell line and the promotor. The most common methods in situations where you don't have any reporters are Western blot, immunofluorescence staining, and flow cytometry. The best way to do this is to have a good antibody to the target. If you don't, make sure your construct includes an N- or C-terminal epitope tag like Myc, FLAG, HA, or something similar so that you can detect your protein of interest.

No and Yes, respectively.
No, you don't need to select for and generally you can't unless you use something like FACS to sort and capture cells expressing your marker/GOI.
Transient transfections are generally not selected for, if they are it is to make a more stable line, and either requires integration of the marker site into the genome (most common) or in some cases use of a plasmid and cell system that supports propagation of the plasmid.
With transient transfection it is normally a good idea, at least for the first few times, if not every time, to confirm that the plasmid is expressing as you expect. You can do this by immunological methods, most commonly western blotting (WB) or immunocytochemistry (ICC). ICC will give you a percentage transfection, which can be useful in assessing how well you would expect an overall population to respond to a stimulus and how well you can see that effect - what if only 10% of your cells transfected compared to 50% or 90%, but it can't tell you how much protein is being expressed. ICC can also tell you how cytotoxic your transfection is - commonly used methods like the Lipofectamine family of reagents are often in the 20-50% cell-death range. WB on the other hand gives you how strong your expression is - how much protein is there, but it can't tell you how many cells were transfected or how much cell-death there is.
In theory at least FACS can do both number and strength, but it would require calibration of your antibody by both western and ICC.
You can also look at RNA expressed off the plasmid, but this may not bear a direct relationship to how much protein is produced.


text:
Why is there no wavelength change in the hyperchromic shift in DNA?
From Wikipedia article on hyperchromicity (emphasis my own):

"When the bases become unstacked, the wavelength of maximum absorbance
does not change, but the amount absorbed increases by 37%."

However, theoretically speaking, any electron delocalization (in this case π-stacking) always lowers the overall energy of the system, hence the wavelength of maximum absorbance should be greater.
Why is this not the case in the hyperchromic effect?

Could you add the link to the wiki article in question?

Sure, here it is:
https://en.wikipedia.org/wiki/Hyperchromicity

We are dealing here with the quantities differing by (at least) two orders of magnitude:

energy corresponding to 260nm radiation is about 110 kcal/mol (here is a converter)
stacking energies of DNA double helix are of the order of 1 kcal/mol

The change in the absorption energy due to electron delocalization when unstacking is thus smaller than 1 kcal mol, and constitutes a negligible correction of less than 1% to the absorption energy.
Update
It is necessary to point out that:

The absorption at 260nm does not correspond to a specific electronic transition, but rather to the average of the transition frequencies of different bases (240-270nm) . Thus, the actual position of the peak of absorption is not necessarily at this wave length, but varies depending on the DNA base composition. Moreover, the peak is broader than the stacking energy.
The cited Wikipedia article (more precisely its English version) is the only source that I have seen so far, where it is claimed that the position of the absorption peak does not change. In fact, 260nm is not the position of the peak, but the standard wavelength where the absorption is measured and calibrated. In fact, the change in the absorption is so big, that a small shift of the absolute peak does not matter.

A quick Google search on stacking energy led me to this article (pubmed.ncbi.nlm.nih.gov/9199773), where it says, "the stacking energies in canonical B-DNA base-pair steps vary from -9.5 kcal/mol (GG) to -13.2 kcal/mol (GC)". And according to the converter, this would result in a quite noticeable shift to around 285-290 nm. Am I missing something?

@Rusty these values are very different from those that one finds in other sources.

@Rusty my initial answer was a bit simplistic. I have expanded it to include other aspects.

thank you so much, though I'm still uncertain as to the magnitude of the energies (still couldn’t find another reliable source), your updated answer is rather exhaustive!


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Optimal bacterial vegetative cell inactivation method(s) after subtilis spores germinated under pressure
I am writing a PhD research proposal and being a newbie in the field I am lost a little bit in the bacterial vegetative cell inactivation methods in foods.
I should propose two main methods to my future reseach team. The strategy is to germinate B. subtilis spores applying the high pressure, and then select one mild method to inactivate them.
My problem is to select max two most appropriate methods between:

Microwaves (MW)
Ozone (O3)
Pulsed electric fields (PEF)
Cold plasma (CP)
Ohmic heating (OH)
Ultrasound (US)
Ultraviolet (UV)
High/Low-energy Electron Beam (H/LEEB)
Chlorine dioxide (ClO2)
CO2 (HPCD, scCO2)

I need to select two methods..., I need to select only mild ones, to preserve the food taste - so I think the temperature should be <60° or max 70°... but what other criteria to take into consideration, being a newbie in this field?
Let's consider one of the method for dry foods, and another for liquids (juices, milk etc).

Are the spores in a food substance?

Yes, I edited the op

First thing to consider for a PhD proposal is the literature. Has someone already done this research, or something similar? Other criteria I would consider: What is the nature of the food substrate in question (solid, porous, wet, dry, cooked, raw, plant or animal based, etc.)? Could anything in a given food product interfear with or prevent any of these methods from working? Is subtilis the only spoilage organism of concern? What's the optimal stage in processing to apply your treatments? Just to name a few.

@MikeyC, there is no more details but I already gave. Let's select one method for liquids and another one for dry foods.


text:
What does the point in the middle between two numbers mean?

[...] cells were removed to a cover glass and treated with plasma for 2 min, then returned to TS broth and centrifuged for 10 min. Cells were harvested and washed twice with PBS, then mixed with tryptic soy agar. The agar block was fixed with 2·5% glutaraldehyde in 0·1 mol l−1 PBS. Samples were postfixed in 1% (w/v) OsO4 in 0·1 mol l−1 PBS for 2 h at room temperature, washed once with the same buffer, dehydrated in a graded ethanol series and embedded in low‐viscosity medium. Thin sections of the specimens were double‐stained with uranyl acetate and lead citrate...

What does mean this bolded point? Is it a decimal separator, or has other scientific meaning?
If this is decimal point, why is vertically middle aligned?
Source: a recent Korea researchers team article

Short answer
It's a decimal point.
Longer answer
A point in the 'middle' of the neighboring characters is called an interpunct, and was the standard in UK typography for marking a decimal at one point in time (possibly elsewhere as well). You're most likely to encounter it in older issues in UK and UK-inspired journals, and no doubt some have lagged behind the trends for reasons of tradition/stubbornness or whatever else and still use it.
Note that you will also encounter countries that use the comma as a decimal separator; Wikipedia has a list that includes most of mainland Europe and South America, for example.

I live in a country where the comma is decimal separator, this is common in Europe :) Thank you to clarifying that English Men habit )

This is even more strange cause encountered in a recent Korean article )) http://www.surfxtechnologies.com/fileaway-directory/full/067.%20Sterilization%20effect%20of%20atmospheric%20plasma%20on%20Escherichia%20coli%20and%20Bacillus%20subtilis%20endospores.pdf

ah, ok, the article was edited in an UK Journal ) https://sfamjournals.onlinelibrary.wiley.com/


text:
Why do viruses cause different symptoms?
If the sole purpose of a virus is to hijack the nucleus of a cell to replicate, why do we have different symptoms for different viruses?
I can think of the following coming into play:

immune response of the body
destroying tissue of type A is different than destroying tissue of type B
the rate of the destruction --- some (virus, cell) combination are causing more harm than others

Reference:

Why Do Viruses Cause Different Symptoms In Different People? --- talks about how we can have different symptoms for the same virus.

Welcome to SE Biology. Although we accept medically-related questions, you will see from the Tour that we prefer them to be about "the biological mechanisms behind medical conditions". As your question concerns the whole organism, I feel that it would be a better fit for Medical Sciences Stack Exchange.

every virus having differ differ spike proteins so they make infection  a particular type of cell ( just like HIV that only bind with CD4 type of receptor) and make effect. another fact is that every virus have different genomic marital so that have different codon and these different codon make different protein and that different proteins make different effect on host cell metabolism that's why different virus having different symptoms.

Welcome. This doesn't seem to target the question. Rather, your answer looks like a textbook description of the general makeup of a virus.


text:
Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut?
Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut?
For instance, how likely is it that the hazelnuts pictured below contain Aflotoxin?
P.S.: these hazelnuts were fried before packaging in a vacuum sealed plastic bag. ( I am not sure whether the color change in the middle part comes from fungal activity (e.g., aflotoxins) or from the frying process?)

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular note that personal medical questions are not appropriate for this site. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

This is not a personal medical question, sir, to put it in other words: Can aflotoxin presence be inferred from the mild discolorotion at the middle parts of a hazelnut? I was gonna edit the question but I could not see an edit option.

@NerdyNerdie Your question is fine except for the question "is it safe to eat?". This very much is a question that falls under the umbrella of asking for advice that may impact your health. Please see here. As such, your post will likely be voted closed unless you remove that portion of your post. You can [edit] your post by clicking on [edit] at the bottom of your question.

Reformed the question accordingly.

related (how to test it cheaply?) https://biology.stackexchange.com/questions/104505/how-to-reduce-the-quantity-of-carcinogenic-mycotoxins-in-oatmeal/105022#105022

Depends on who you bought them from and how you stored them.
Molds can grow in nuts and nutmeats and produce mycotoxins (from toxin-producing strains such as aflatoxins by Aspergillus flavus). The mold is usually visible and below is picture of Aspergillus flavus growing on a nut product. Source

The amount of aflatoxin produced by the mold is dependent on weather conditions and storage. We can only account for or control the storage conditions. When food substances are not well preserved, fungal growth may occur, leading to the production of mycotoxins.
The pictures presented could also just be an improper storage (with no health risks). There's indication that storage of wet nuts in poorly ventilated silos increases the potential for developing kernel brown centers. Source
If these nuts were stored in improper conditions from farm to store and the farm has been associated with a breakout of Aspergillus flavus then there's chance, but slim. QA/QC and aflatoxin levels are regulated. Codex Standard 193-1995 mentions the maximum levels of aflatoxins and sampling plans.
If the nuts had mold on them and they were washed to get rid of the surface mold, they could have spores from Aspergillus flavus capable of producing alfatoxin. Aspergillus fungi can case discoloration of  certain grains (rice), but that implies that you're able to see them on the product (the mold growth). The nuts in the picture seem quite clear.
In terms of where you bought the product, street vendors are at higher risk of having their products present alfatoxin problems rather than commercial enterprises, because of the location the product is sold at. Source


text:
Identity little brown lady bugs taking shelter in my home
Can someone please identify this little creature for me. They are appearing more frequently in my room. What are they doing here? Could it be those basic needs and requirements?
The size is about 2 x 1 millimetre. My location is the Netherlands. I am on the 20th floor of a flat. The season is now heading towards end of spring.

Could you please edit your question to include the size of the insect as well as your location and season?

Thanks for the tip, description updated. Getting all biological now hehe


text:
Understand and reproduce withdrawn publication method - Blastp - covid19
I try to reproduce the method of this withdrawn paper. I know this paper has been debunked and withdrawn. I am curious to understand the details of the method used on it. I am a programmer and I don't work on the field of Biology.
I have some questions about "The identified amino acid and nucleotide sequence" with
MultAlign software:
I have trouble to understand how those supposed "inserts" were selected:

"Insert 1": The selection is where there are dashes and dots on the second and third lines because the sequence is not present in SARS-GZ02
"Insert 2": The beginning of the "insert" start with these dash and dots but why is it stopped at 155 ?
"Insert 3": The end at 261 is at a dash for the second line but why does it starts at 256?
"Insert 4": why these start and end of selection?

Later on the paper they used these selected regions with Blast and on the "motif alignement" column these letters are used which are a little different:

"Insert 1": TNGTKR (first letter "G" removed)
"Insert 2": HKNNKS ("YY" removed)
"Insert 3": RSYL-TPGDSSSG (4 letters at 250 added)
"Insert 4": QTNS-PRRA

Why are some different from the selection ?
Even for the first "insert", I can't find those alignement with Blast using for example GTNGTKR or TNGTKR. If someone could indicate me the good parameters in Blast to find these alignements it would be awesome.
Sorry if it sounds too ingenuous, thank you for your time reading all this.


text:
Can below-threshold potential changes of neurons convey information?
In neuroscience we learn that when the membrane potential of a neuron reaches a threshold (typically around -55mV) it "spikes": That is, it actively propagates a signal. I have two related questions with this respect:

The spike initiation zone is typically (e.g. for mammals) at the axon hillock - from there the action potential is actively (opening of ion channels..) propagated through the axon. But what happens then at and after the (chemical) synapse? Is the propagation after the synapse to the postsynaptic cell passive?

Newer imaging techniques (e.g. calcium imaging) can capture sub-threshold changes in the membrane potential. How are these sub-threshold potentials relevant for information processing? Are they propagated to postsynaptic cells, albeit again only in a passive manner?

For an interesting reversal, check out C. elegans neuroscience. In C. elegans most communication occurs by sub-threshold potentials, and detection of action potentials is rare 2008, 2018 and controversial. Not my field, but it might be worth checking out C. elegans neuro-transmitter release absent action potentials.

This type of passive conduction (sub-threshold) is called electrotonic conduction. When an action potential reaches the axon terminal (pre-synaptic knob) it induces Post-Synaptic Potential (PSP), through chemical or electrical synapse. Now if there is EPSP (i.e. excitatory) generation, then in the post-synaptic neuron there will be electrotonic potential, that will move towards 'axon hillock'.
Upto the axon hillock, the conduction is mostly electrotonic and hence we need this type of conduction to actually generate Action Potential.

In theoretical neuroscience this electrotonic conduction along dendrites is computed by using Cable Theory. It will eventually die out with distance as$-$
$V(x)={V_o}\, e^{-\frac{x}{\sqrt{r_m/r_i}}}$ ; standard notations used.

ref article:
https://www.sciencedirect.com/science/article/pii/B9780123971791000178

Hence we can conclude that for information transmission, sub-threshold potentials are extremely important.

If these are subthreshold, does that theoretically also means that they can travel both way (as closed ion channels do not prohibit that)?

Theoretically yes. If there is potential gradient it will flow.

All voltage perturbations can propagate in both directions. Usually, they are called orthodromic and antidromic if propagation is from dendrites to axon or viceversa respectively.

@heracho what then actually hinders the current flow in the dendrites, stemming from an action potential, do reverse direction? In axons we know that channels close to hinder exactly that - but how about dendrites?

@TestGuest As I understand, the voltage perturbation propagates passively through the dendrites. This is because they don't have the Sodium channels (or another) necessary to actively propagate the signal. To be more precise in your comment, it's Sodium channel inactivation (not just closing) the mechanism that hinders the action potential to propagate antidromically in the axon.

Electrical synapses (Gap junctions) can generate current to other cells without the emission of a spike. This sub-threshold interaction is proven to have functional implications in neural activity (eg. Retina).

Thank you, that is good to know, though I was also interested in this property wrt chemical synapses.


text:
Can antibiotic resistance cause problems for the microorganisms producing them?
My understanding is that antibiotics are naturally produced by microorganisms as a defensive measure against certain kinds of bacteria. For example, some Penicillium molds produce penicillin.
Clearly, antibiotic resistance has direct negative effects for humans because it makes certain infections more difficult to treat. But could this resistance also lead to problems for the microorganisms that produce antibiotics in the first place?
If this were the case then could there be additional negative "second order" effects for humans?

Does this answer your question? Will all bacteria become resistant against all antibiotics in the long term? Specifically, see the first paragraph of my answer.

I depends on what you mean by "problems." Antibiotic resistance mechanisms have probably existed in the wild for nearly as long as naturally occurring antibiotics. It's certainly possible for an antibiotic resistant organism to have an antagonistic effect on an antibiotic-producing organism, for example by competing for key nutrients or niche space. It's also possible for positive interactions to occur where one or both organisms benefits from symbiosis with the other.  Also not sure what kinds of second order effects for humans you have in mind.


text:
Sediment Size and Mayfly (Explanation + Literature)
I am doing investigation into association of sediment size with the movement of mayfly nymphs in a choice chamber, sampling the organisms from a stream. I will be doing a chi square test to determine statistical association. I have three species of mayfly to choose from - swimming, burrowing, and flattened and I will investigate two. My question is this: biologically speaking, either from your knowledge or from the literature etc., where and why would you expect there the different mayfly nymphs to migrate towards, in terms of size of rock/sediment (e.g. categorically speaking, small, medium and large which I will categorise in the field). I'm really looking for for a biological reason for why there might be an association - any at all!
Thank you in advance.
UPDATE: I'm now also looking for sources of secondary data/published papers in journals/literature which might talk about this topic/have similar data/anything at all that I might be able to use. A google search of 'sediment size distribution swimming mayfly nymph' for example hasn't yielded very much so far, but I'm hoping an expert might be able to find such research more quickly.

What is your goal in doing the experiment?

@BenBolker - to find an association between these two variables to see if the type of sediment in a river will affect the distribution of these invertebrates. NB - It is only a introductory undergraduate based project.

@Rushi - an interesting question. I will see what I can find. Don't give up - the community will eventually come to your aid!

@vugpt - any luck?

@BenBolker - any luck?


text:
VPg priming of the replication of RNA viruses
I'm doing a presentation on the replication of SARS-CoV-2 for my chemistry class, and I found that to replicate its RNA, the virus uses RNA-dependent RNA polymerase, which is primed by a VPg primer. Since the presentation is for a chemistry class, not a molecular biology class, I would like to know the chemistry behind the way that primers work.
I've tried searching the information on the internet, but could not locate the information I need.

Can you clarify what it is that you are looking for? What is it that you need that resources like the Wikipedia page on base pairing do not provide?

Welcome to Biology.SE! We expect you to do research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. This wikipedia page may be a helpful starting point. ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I have edited your title so that it is clear you are talking about the specific VPg primer for the replication of RNA viruses like coronoviruses. It would helpful if you could tell what you know about the chemistry of RNA polymerase already so that I (as an ex-chemist) can an answer your question appropriately from a chemical standpoint.

Search for Subissi papers on the CoV RdRp, he did several in-vitro experiments, mixing directly some nucleosides, oligos, nsp7,8 and 12 in a test tube and looking at what was synthesized. https://pubmed.ncbi.nlm.nih.gov/25197083/

Although this question should probably be ruled off-topic as unresearched homework, I fancy that not all readers will be familiar with the VPg primer for viral RNA replication. I shall therefore suggest some of the chemical aspects of this process that might be include in a presentation, and comment on the process itself.
Some Chemical features of VPg-primed viral RNA replication

The chemical reaction. This is no different from many other reactions involving an RNA polymerase. It involves the reaction of an NTP with the 3’OH of the ribose on a growing RNA chain, forming a phosphodiester bond, thus extending the chain. The growing RNA chain is termed a primer because it is required to start the addition in many cases, however in the case of many single-stranded RNA viruses the actual initiation of a new strand uses a primer composed of a small peptide to which to U residues have been attached. Simple diagrams of this process are generally presented for DNA-dependant DNA polymerase and can be found in standard texts, e.g. Berg et al. Figure 5.22
The reaction mechanism.  This reaction is catalysed by an enzyme which participates in the reaction. The mechanism of catalysis is summarized on the EBI facility (where diagrams can be found) as:

RNA polymerases catalyse the nucleophilic attack of a bound nucleoside
  5′-triphosphate by the 3′-hydroxyl of an RNA primer, resulting in the
  incorporation of a nucleoside monophosphate into RNA and the release
  of pyrophosphate. This is thought to occur using two-metal catalysis.
  In RNA polymerase II, two magnesium ions are coordinated by four
  aspartates (3′OH of RNA also proposed to weakly coordinate to Mg2+A).
  Mg2+A is proposed to lower the pKa around the attacking hydroxyl while
  Mg2+B is there to stabilise the negative charges during transition
  state…

The thermodynamics of the reaction. The breaking of one phosphodiester bond and the formation of another means that the reaction is more or less at equilibrium (no change in Gibbs Free Energy). One reason that it is thought not to reverse is because the pyrophosphate produced is hydrolysed in the cell to orthophosphate, which is irreversible as the free energy change in this reaction is lost as heat.
Hydrogen Bonding to the template.  The reaction involves copying a template strand, and the basis of this specificity is Watson–Crick hydrogen bonding between template base and incoming NTP. However, specifically for the VPg primer, there is hydrogen bonding of the two U residues to the end of the template strand. (Diagrams of AU hydrogen bonding should be easy to find.)
The chemical linkage of the VPgUU primer. The uridylic acid residues are added to the VPg peptide at the hydroxyl group of a tyrosine residue in a reaction that is catalysed by the viral RNA polymerase. It is worth noting that although many amino acid residues of proteins are chemically inert, the hydroxy amino acids have reactive potential, most notably in being phosphorylated.

A broader point for reflection
One question that this raises is why the need for a protein — VPg — as adjunct to a nucleic acid primer. Reading further on the subject will reveal this protein actually interacts with different parts of the viral RNA in the course of acquiring the Uridylate residues and selecting the AA where it should bind. The chemical interactions with RNA and other proteins here are the weak non-covalent interactions — hydrogen bonds, van der Walls interactions and some ionic interactions — that are typical of proteins. Rather than their weakness being a reason for considering them unimportant, such interactions are crucial to the chemistry of life because their very weakness means that they can be both broken as well as made. The interactions are reversible, leading to the very dynamic property that typifies life. They are worthy of a chemist’s attention.

Nucleic acid synthesys can occur two ways, with a template or without. In most biological systems the template synthesis is the one that occurs since it is the only way to replicate genomic information. For template based nucleic acid synthesis in biological systems (being of DNA or RNA) the enzymes performing the reactions can use single stranded material (in the case of virus ssDNA or ssRNA virus) however they still need a small region of double stranded nucleic acid to bind and start polymerizing, otherwise synthesis could start anywhere in the template strand which wouldn't be particulartly useful, hence the primers, the polymerases bind to the double stranded region and start polymerizing always adding new nucleotides to the 3' end of the primer strand that are complementary to the nucleotide in the template strand. Usually in living cells the synthesis of new RNA molecules won't occur with an RNA template (there is usually no RNA dependent RNA polymerase, there are exceptions but they are usually result of previous viral infections), but only with a DNA template to procuce messenger/transfer/ribossomal RNAs. In the case of COVID and othe + strand RNA virus, the virus has to encode the RNA polymerase and also produce a primer that will create a double stranded region that will allow RNA synthesis to occur.

Hello @lint, and welcome to Biology.SE!  Yours is a good explanation of the reasons for using primers and their importance in guiding polymerase amplification.  You clearly explain the molecular biology of PCR, but OP is explicitly looking for a chemistry perspective -- perhaps one that includes a discussion of the hydrogen bonding involved in primer specificity and the catalysis of DNA polymerization.

I don't think there are any biochemical reasons for the requirement of primers. The need for a primer in the synthesis relates to the requirement ofhaving a double stranded region that guides where in the sequence the process starts, otherwise you would have an entire population of molecules with different sizes and start sites. There are cases where primers are not needed for nucleic acid synthesis from template like RNA transcription and DNA replication start, in this case the specificity of the start is  given by the recognition of specific sequences by the machinery.

@lint — The need for a primer is tied up with ensuring the ends of a linear genome get replicated. Easier than for a double-stranded chromosome, but still an important consideration. It's not that there will be a population with different sizes of RNA that is important, it's that the genome would get shorter and shorter.