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Questions regarding the four pollination mechanisms of papilionaceous flowers
I want to understand the four mechanisms of pollination in papilionaceous flowers: pump/piston, explosive, valvular and brush.
The topic is lightly touched upon in this part of a Wikipedia article, but I find the explanations somewhat shallow and incomplete.
This study from the journal Plant Systematics and Evolution about the explosive mechanism mentions all mechanisms but only deals with the explosive. Regarding the explosive mechanism it mentions that the androecium and gynoecium are subjected to pressure from the keel. My interpretation is that when a pollinator presses upon the keel the reproductive column "snaps" up due to the released pressure. Taxa which I know utilize this mechanism are: C. scoparius, Medicago sativa and the three Desmodium species studied in aforementioned publication (D. incanum, D. subsericium and D. uncinatum) but due to my location I have not been able to study the explosive mechanism in the field. If my interpretation is correct, then how is the pollination transferred to the pollinator after the column is released? In the previously mentioned Wikipedia article it is said that the column hits the banner (standard), but it does not tell whether this "collision" with the banner is what causes the pollen to be released. Does the collision with the banner release the pollen in a "cloud" which envelops the pollinator? Or does the reproductive column hit the pollinator along the trajectory it travels from keel to banner?
The pump/piston mechanism I have on the other hand been able to study quite easily due to the great amount of Lupinus polyphyllus growing in my area which inhibit this technique of pollination.
This study published in The Scientific World Journal explains the valvular mechanism as follows:

In the valvular mechanism, the upper rim of the keel is unsealed; it opens along its total length when the keel is moved downwards by the pollinator and closes when the insect leaves the flower. In this case pollen can be released repeatedly to numerous visitors.

and the brush mechanism in this way:

In the brush mechanism, as the pistil is longer than the stamens, the stigma extends beyond the anthers, avoiding self-pollination; the upper part of the style develops erect trichomes acting as a pollen brush. When sufficient pressure is exerted on the standard and wing petals, the pistil protrudes from the keel tip: the stigma comes first into contact with the insect receiving (if present) external pollen and the style brushes the pollen on the visitor. When pressure is released, style and stigma return to their former position inside the keel.

As for this last explanation of the brush mechanism I do not entirely understand how the spread of pollen occurs. The publication says that the stigma extends further than the anthers and that the "style brushes the pollen on the [pollinator]". What do they mean by this? Does it have to do with the trichomes on the style? If so, how do they play into the transfer of pollen?

The formulation of this question suggests that it is homework of some sort, which would definitely require you to show the research you had done to solve it yourself (a general expectation in any case). Furthermore it seems to ask several questions or a general review, whereas this site exists to answer specific questions. Please re-read the [Tour] and the Help on Asking Good Questions.


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Resources for understanding the basics of cell signaling, gene expression and cell fate determination, for a physics student?
I'm a physics student who will join a theoretical biology/applied mathematics research group this September. I'll link some papers at the end for further context.
The main problem I have is that my last biology class was in 10th grade. While the mathematical part isn't that harsh, the biological side of things really does get me. I don't understand half the terms thrown around, or the general context of what is being studied. So what resources would you recommend?
Chemical Reaction Network Theory elucidates
sources of multistability in interferon signaling
Transient hysteresis and inherent stochasticity
in gene regulatory networks

Welcome to the Biology.SE. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and [ask] a good question. In particular, this seems far too open-ended and is also likely to generate opinions rather than factual answers, both of which make this off-topic on this site. This makes it likely your question will be closed (I see one vote to do so and will reluctantly be adding one of my own). ...

... I have personally found when learning about a new area that starting with a relatively accessible and reliable source like Khan Academy is very helpful. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI. ——— Wikipedia can also be a good starting point if you check the references.

I would recommend talking to the principal investigator of the lab and asking him/her for some good introductory reviews. You can then chase down references from there, and do searches for terms/ideas you don't understand. Also, just talk to people in the lab! Many scientists are more than willing to explain their work in excruciating detail.

@MattDMo — This is good advice, but depending on their background (and wisdom) the PI may have little or idea how to effectively advise someone with the poster's lack of background knowledge. It also sounds like the OP has talked to people, but they are using a lot of unfamiliar terminology. While many of us are willing to explain, not as many can explain cutting edge research at a 10th grade level (and even fewer will be willing to do so) ...

@tyersome true, but you'd be surprised at the number of people who haven't even pursued those simple steps. I used to work in tech support for an antibody company, and my colleagues and I would get calls/emails all the time asking for us to interpret the results of Westerns, ELISAs, etc., b/c the person for whatever reason hadn't approached other people in the lab first. I see this a lot on Stack Overflow as well. People seem to be much more willing to ask strangers on the internet for help than the person at the desk right next to them.

Time to hit the library,  caveat: my suggestions may be ~20 years out of date - pick up a general biology textbook, perhaps something like Campbell's "Biology"  if you need real basics. For genetics - try Lewin "Genes". Immunology - try "Janeway's Immunbiology".

@MattDMo — You might be surprised at how unsurprised I am ;-) ——— I am painfully aware of the large number of people afflicted with significant social anxiety (with some "positive" feedback due to a non-trivial amount of arrogant assholes) ...

@tyersome I didn't even think of the social anxiety part. Thanks for reminding me.

I could tell you to buy "Stryer: Biochemistry". It has many chapters that you need, which are:

Gene regulation (Regulation on DNA, RNA, Protein level, etc.)
Signaltransduction (JAK/STAT pathway & general concepts)
Regulatory strategies (Product inhibition etc.)
Stem cell differentiation (French Flag model, specification vs determination)

Stryer also explains the biochemical machinery behind that, which is interesting. Your other paper mentions interferon signalling, which is part of the immune system. So you could buy "Janeway: Immunology" for that. You also mentioned cell fate determination, for that the best book imo is "Scott F Gilbert: Developmental Biology".
They are awesome books, with tons of awesome pictures and are simply very very fun to read!
HOWEVER, these books are huge and contain many chapters that you will never need. So I might also tell you to just google stuff. For biology purposes my goto strategy is hammering this query into the search bar:
"pubmed review <biologic term I don't understand>"
For example when I google "genetic regulation network pubmed review" I get this pubmed link. Then you press "full text links". Then you realize there's a paywall. I would never recommend visiting a certain page (starts with sci and ends with hub) to circumvent that paywall.
So I keep searching and find another review from 2012. However it lacks those biological terms that you need. I tried finding some comprehensive reviews online about biological topics, however this kind of literature often focuses on flashy state-of-the-art topics that go into too much detail. So you might want to consider buying "Stryer Biochemistry", after all!
Or just ask your supervisor to buy those books and keep them in your research group. They are definitely worth it. And these books definitely know a lot more than anyone in a physical research group (including your PI). Yes, it will take you some time to look up those topics and read them, but I promise, they're written in the best and most understandable way possible (no background knowledge is necessary, unlike published papers!) and might save you and your whole research group a trip to the library or a lot of time and frustration trying to google terms that no one taught them.
It doesn't have to be the Stryer, maybe there are books that specialize on regulatory strategies in living beings. But it's a good start.

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Is there are theoretical limit to the number of proteins possible and their respective structure?
I saw an article saying that DeepMinds AI has catatogued every protein known to science. I guess "known to science" and what is the theoretical limit is not exactly the same thing but the only way one can claim "known to science" at least as I can figure out is to have some idea what the highest value can be in the first place.
On the other hand it may be all the proteins known from every living object on the planet but I don't see how anyone could claim that when most species on the planet are not even know.
So that is why I ask is there is some theoretical limit.
As for example there is a theoretical limit for the highest possible element past the transuranics based on nuclear chemistry. I believe at some point the number of protons would not be able to stay bound long enough to get past the electrostatic repulsion. I think the number is 200 something. But that is an example and not my question. In this question I am interested in knowing how a computer algorithm could predict all protein structures if there was not a theoretical limit imposed in the first place.
I have never posted here before so if the question is inappropriate for this stackexchange my apologies

They just mean known proteins, the simplest interpretation of the statement.

yes amazing still but that would solve my problem. You are probably right on. Thank you

Not even all known proteins! There are many proteins that exist in multiple isoforms, and they used only one isoform per protein coding gene. For a reddit q/a on this, see here.

All depends what you mean by protein - basically take a single amino acid and add another .... on to very high number. Largest known is titin I think, at about 35,000 residues, but no reason that there couldn't be 35,001 or 70,000 or 100,000 etc.

You can certainly estimate a theoretical limit, given some assumptions.
Let's say you do not care about any post-transcriptional modifications, you are interested only in the primary sequence. There are (more or less) 20 proteinogenic amino acids, so there are $20^N$ possible proteins (amino acid sequences) with length $N$.
An "average" protein has about 400 amino acids. Therefore, there are theoretically $20^{400} \approx 2.6\times 10^{520}$ possible proteins with 400 amino acids.
But proteins can also be larger. Let's enumerate all possible protein sequences up to length 1000:
$$ \sum_{N=1}^{1000} 20^N \approx 10^{1301}. $$
All of this is only a lower limit. We did not take into account any non-standard amino acids, none of the post-transcriptional modifications, or the ability of proteins to have multiple different stable conformations.

Note that there are only about $10^{82}$ atoms in the visible universe.

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What insect is this? Found in a dying tree
I recently found this insect near where I live, where my childs play always! Is it dangerous ??. What insect is this ?
Is it poisonous?
Its about 3cm
Picture:

I live in Montreal, Quebec, Canada

Welcome to Biology.SE. Can you [edit] what the 3 cm is measuring into your post? (e.g.s: head to tip of abdomen vs. tips of antennae to tip of the ovipositor, which is the "drill" sticking into the wood). If you can specify the type of tree that you found it on that could also help. ——— This wasp is likely only dangerous to the wood boring larvae she is trying to lay eggs in, but we can't give health advice on this site. At any rate if you (and your children) don't harass her, she'll most likely pay you no attention at all.

Looks like some kind of https://en.wikipedia.org/wiki/Parasitoid_wasp Maybe even the species in the first example picture

Yes that's exactly what I saw ! Thanks for the response!

Does this answer your question? Is this a hornet?

From Gil Wizen's page, it's a wasp.

Giant ichneumon wasps (genus Megarhyssa) are some of the biggest North American wasps thanks to the females’ long (10cm) ovipositor, which is longer than the wasp’s own body. These wasps might look fierce but they are actually shy and harmless insects. They are parasitoids: their larvae develop as parasites living inside the body of other insects. The female’s ovipositor is therefore not a stinger, but an organ used to inject eggs into the larva’s host. (emphasis mine)

Here is one of his amazing photographs or the wasp laying eggs (into a dead tree).


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What precisely is the pairwise Fst calculated in GenAlEx 6.5?
A professor of population genetics informed me that there is not a unique notion of pairwise Fst scores in the literature. This information has made me more cautious about what may be implemented by a given software package.
I am considering the GenAlEx Excel plugin (Peakall & Smouse 2005, Peakall & Smouse 2012) for computing pairwise Fst scores. The documentation states

Pairwise Fst : Outputs the pairwise Fst values between populations.

Output Pairwise Matrix: Outputs pairwise population statistics as a triangular Matrix.
Output is to worksheet [NeiP] for Nei’s Genetic Distance, to [uNeiP] for Nei’s
Unbiased Genetic Distance and to [FstP] for Pairwise Fst. This is in GenAlEx format
for further analyses if required.
Output Labeled Pairwise Matrix: Outputs pairwise population statistics as a labeled
triangular Matrix. Output is to worksheet [NeiL] for Nei’s Genetic Distance, to [uNeiL]
for Nei’s Unbiased Genetic Distance and to [FstL] for Pairwise Fst.
Output Pairwise Matrix as Table: Outputs pairwise population statistics as a table.
Output is to worksheet [NeiT] for Nei’s Genetic Distance, to [uNeiT] for Nei’s
Unbiased Genetic Distance and to [FstT] for Pairwise Fst.

I gather from this that [NeiP] is for a function called Nei's genetic distance, but the Wikipedia page on genetic distance suggests that there are multiple distance functions named after Nei. This also confuses me because I thought that these functions named after Nei were distinct from fixation indices, and yet they are mentioned under this Pairwise Fst section in the documentation. I am similarly confused about the inclusion of [uNeiL] and [NeiT].
And then there is the mentioning of [FstP], [FstL], and [FstT]. Clearly the P, L, and T correspond to whether the function returns a matrix, labeled pairwise matrix, or the same but as a table.
I've probably misunderstood the documentation, but I didn't understand why Nei's distance was mentioned. But in any case, what is GenAlEx 6.5 actually calculating (i.e. formula/model) if I use any of [FstP], [FstL], and [FstT]?

I have emailed the authors of the GenAlEx6.5 package. I'll post an update if I get a response.

Nei's original genetic distance was described in 1972 (paywall). He described the unbiased calculation in 1978.


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Do moose usually browse woody foilage approximately perpendicular to the long axis of the branch?
I am trying to improve my understanding of moose browsing behavior. One basic question is whether browsing on woody vegetation can tell us anything about the orientation of the moose's head. The following are videos I have watched that feature moose browsing on woody vegetation.

moose eating trees
Moose Eating Tree
Moose Browsing in Winter
moosing eating tree
Alaskan moose cow and calf browse on budding tree branches
Moose fences to protect ... trees?
Bull Moose browsing tree branches in Maine
Albino moose getting drunk on apples and fighting the local lawnmower to the death! (just at the beginning)
Bull Moose browsing in meadow at 11,000 feet.
Moose Browsing in Platte River Wilderness
North Platte River Adventure (at t=39s)

From these videos I have made some inferences.

For really short trees and brush a moose is might feed on buds from above.
Depending on the height and thickness of the central stem of a bush or tree, a moose might bite on it sideways to bend/break it into a horizontal orientation.
For branches off the side of larger trees I see that often the moose's head comes from roughly perpendicular to the branch rather than straight-on.

Is it more generally known that moose tend to browse from the side (i.e. roughly perpendicular) to branches on (larger) woody plants rather than straight on?

Note that this other question is about teeth marks on bark, whereas this question is about how moose browse on branches.


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Do Pharaoh ants eat sealant?
My high-rise apartment has had pharaoh ants for the past 3 years (maybe more).  It is being handled by a pest control company.  I am not looking for countermeasures.
One of the countermeasures advised by the pest control technician is to seal the opening through which my water pipes travel.  The apartment management sprayed a sealant that looks like whipped cream, but had a distinct chemical smell (images below).
The ant sightings are usually on the kitchen counter top, mostly around the perimeter of the sink.  I try to wipe the counter often, and keep the area dry.  The sightings were getting kind of low just before the hole was sealed, sometimes going for days without a sighting.  Since that day, however, the sightings have been on the upswing.  Quite a coincidence.
I wondered whether the pharaoh ants are attracted to the chemical sealant as a source of food.  Googling doesn't turn anything up for pharaoh-ant-eat-sealant.  Does anyone know about the plausibility of this?

It's possible,. The sealant is an expanding polyurethane foam, marketed in the US as "Great Stuff", among other brands from a number of different companies. Basically, it's plastic. Ants or other pests could chew through it by removing small pieces, but I doubt they're eating it, as it has no nutritional value.

If it has no nutritional value, then it seems that the plastic foam isn't attracting the ants.  There must be another explanation for their sudden increase, coincidentally starting on the day that the foam was applied.

Just a thought, but - instead of sealing them out - might you have sealed them in?

It might be possible that at the same time the pest control company sprayed something in the basement and other parts of the building that forced out the ants.

@Jiminy Cricket: I've been told over the years that the number of an sightings in my unit is way too low for me to be hosting the colony.  So if I trapped a few scouts in my apartment (which I likely did), then why would the number of sightings steadily increase since the day the opening was sealed?

@FluidCode: It was the apartment building staff who sealed the the opening, not the pest control company.  Of course, that just leaves fewer avenues into my unit, not zero avenues.  It is possible something elsewhere caused more ants to be closer to my unit, and more ants to enter.  The timing of the increase is quite a coincidence, so I think it is not likely, but still possible.

@user2153235 Why don't you leave for few days some flypaper in some strategic points. In this way you could find out where they come from.

@FluidCode: Huh.  Never thought of that.  It's like troublehooting a technical problem.  Thanks, I'll have to mull on some locations at which to start.

It doesn't need to have nutritional value, if there's something on the other side that's attracting them. Have you looked at the foam to see if anything has been chewing on it or penetrated it? This could also be a good location to leave some of your flypaper.

It's hard to get up and close to inspect, and my vision isn't that good.  But the photo's show underside of the sink.  There's nothing there.  The outside is whatever is on the other side of the wall with the hole that was sealed.  The contents of the inside and outside did not change when opening was sealed, so that doesn't explain the presence of more ants.  I should clarify that the greater sightings are on the counter top, around the perimeter of the sink.  I try to wipe down often, and that hasn't changed.

@MattDMo: Would you care to post your comment as an answer?

@user2153235 sure. What country are you in, so I can localize my answer?

@MattDMo: Canada.

The sealant in question is a self-curing expanding urethane foam, marketed under numerous brands and formulations in the US and Canada such as DuPont Great Stuff, Loctite Tite Foam, and DAP Touch 'n Foam. It is widely available at hardware stores and home centers.
After curing it forms a hard cross-linked polyurethane mass - essentially a plastic foam. While it has no nutritional value and is solid enough to be marketed in a pest control application, it could theoretically be chewed through by a determined-enough ant colony, as the marketing material for that particular product doesn't say anything about insect repellant properties, only mice. Non-rodent-repellant formulations are known to be susceptible to eventual "chew-through" and inhabitation by both mice/rats and insects such as carpenter ants. Great Stuff markets a Pest Block formulation that supposedly is formulated to prevent chewing, but its claims regarding insects are a little vague. You'd have to ask your building management if they used a pest-blocking foam.
You say that the sightings started to swing up again a day after the sealant was applied. I would imagine that it would take some weeks for a colony to chew through the amount of foam pictured (even longer if an insect-repelling product was used), and they would need a rather compelling reason to keep at it, as the foam itself is not a food for them. It's likely that you're seeing ants that were already in your apartment when the "escape routes" were sealed, and they're simply foraging in a more visible manner now because they don't have other sources of food. On the other hand, the fact that you think you're seeing more ants now after the pipe openings were sealed could simply be a coincidence. Remember, correlation does not mean causation.

Thank you! Some time after I posted my original question, I added details, such as the fact that the sightings increased on the very day that the sealant was applied. Wiping with bleach seems to bring down sightings again. I hope that this surge is temporary due to trapped scouting ants, because I dislike the residue of bleach on the kitchen counter. The vapours aren't healthy, either. On a related note, there is no change in the food source on my side of the wall, and since the other side is just pipe space, I don't expect whatever passes as food on that side has changed either.

@user2153235 sorry, I didn't read the edited question closely enough regarding the timeline. I changed my wording a bit. Based on that, I'm pretty sure that you're seeing trapped scouts, not new ants.

Thanks!  That's a very encouraging outlook!

It has been a week since the sealant was applied, and the number of ant sightings seem to be staying at their heightened levels.  Sigh........

@user2153235 Interesting. Do you have ant traps in your apartment? Depending on their kind, they should be having some sort of effect by now, assuming my theory is correct...

The professional pest control company has laid down bait of various types and in various forms (directly dropping goop on various places versus the less messy plastic containers of bait).  The "stuff" has varied through the years.  At the beginning, I also got my own.  Each new chemical brought about a temporary lull.  The ants seem to be adapting before they are wiped out (a problem with Pharaoh ants, whose colonies can easily split). Completely wiping them out is hard in a high-rise, especially with the warming weather.

My bleach solution seems ill-advised, both because of the fumes and the adverse effects on laminate countertops.  It looks as if I will have to get comfortable again with ants on my food preparation surface.


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Is this a Kestrel?
Apologies for the poor pictures, they are a crop of a tiny part of a picture taken with max zoom.

A nature reserve in Bulgaria, I often see those birds while I hike there. They let people come quite close, but they always care to stay between your eyes and the sun. Only this time I managed to see their back in full daylight, but it happened because they were very far. I searched some information online and I understood that the most commons birds of prey in the area are the Kestrel and the Buzzard, I think the one in the pictures is a Kestrel. But when I tried to search online to confirm the identification I could not find a picture of the back, it seems I am not the only one who can only see them against the sun.

Is there any other information you can give us? An estimate of the size would be very helpful (hard to do by eye, but maybe you've seen it near another bird you can identify). Behavioral information would also be very helpful. How did it fly? Soaring vs. frequent flapping? Level direct flight vs. spiraling vs. a rising and falling  pattern or something else? Did it interact with any other birds? Calls?

@tyersome I am not very good at estimating the size. I could say that it was a bit smaller than a urban crow. As for the behaviour what I usually notice is when they stand still mid air or flap the wings without moving for several minutes and then suddenly dive. But actually the moment I took the picture it was just flying  in a saddle between two peaks.

Well, it does have the characteristic pointy wings of a falcon, so that narrows the choices.  I wouldn't worry about the back - most birds have a fair amount of variability in plumage as it is, and with young birds flying around this time of year, that adds to the fun.  I'd focus on the tail, which is likely to be far more useful.
That black band at the end of the tail seems to be a good fieldmark for Kestrel, but I'm not sure about the white border.  Perhaps it's a young bird and the white border will wear off (as so often happens with young birds' plumage).  Or perhaps it's simply an artifact of the photograph/enlargement process.
Edited To Add:
In the attached links, the various illustrations show both the black terminal band and the white border to that band, as well as the brownish back as we can see from your photo.  I'd lean toward the Eurasian Kestrel rather than Least Kestrel, but I'm not experienced with European birds, so you might want to take that for what it's worth.
https://identify.whatbird.com/obj/469/_/eurasian_kestrel.aspx
https://ebird.org/species/eurkes

Thank you. In the second link, the picture labelled "Immature" seems a good match, at least for the wing and tail tips.


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Is this poison ivy?

Location: Sunny, dry, well-drained yard. East of Toronto, Ontario.
Date: August 2, 2022
Description: Three leaves, new leaves are oily and reddish, woody stem, vine crawls along ground
Hint: It's possible to zoom in on the photos by clicking on them a couple of times

The question is about the larger 3-leaved plant in the center of the photos. Not the smaller, more serrated 3-leaved plants in the background which are alpine strawberries. (I'm extremely familiar with strawberries -- there's no question there.)

This appears to be poison ivy (Toxicodendron radicans).

Descriptions (Univerity of Michigan):

Distinguished by alternate compound leaves composed of three leaflets, the middle leaflet petiolule longer than the other two.  The leaves of this woody plant are usually shiny, especially when new.  Leaf margin varies greatly: smooth, toothed and lobed are all been observed.  Leaf shape also varies: some leaves elliptic and others much more round in shape.  Leaf color changes with season and age; young leaves in the spring often have a reddish tint, while mature leaves turn dark green, while leaves might change to orange yellow and red before falling in the fall. Toxicodendron radicans can grow as a vine, shrub, or sprawling plant; sometimes vine stems have a hairy appearance due to aerial roots that emerge from climbing stems

 Long answer
As can be seen from the range maps in BONAP's North American Plant Atlas*, three species of Toxicodendron have been found in Ontario: T. radicans ([eastern] poison ivy), T. rydbergii (western poison ivy), and T. vernix (poison sumac). Well-known (by name) [Atlantic] poison oak (T. pubescens) does not occur above 40oN Latitude (i.e., North of the "Mason-Dixon Line") so can be ruled out.  Of the three species present in eastern Canada, only the two species of poison ivy are trifoliate (i.e., having 3 leaflets). T. vernix is also grows as a tree so can be doubly ruled out.

*Note: USDA PLANTS Database shows greater range spread of all species (e.g., see here and here), but the species indicated to be found in Ontario does not change.
How to tell the difference between eastern and western poison ivy?
Different sources use different criteria. Let's explore:

Rhoads & Block (2000) "The Plants of Pennsylvania"
 A. vines or erect shrubs; leaves trifoliate
  - aerial roots usually present; leaflets not folded....................... T. radicans
  - aerial roots not present; leaflets somewhat folded along the midrib..... T. rydbergii

 Left: Aerial roots on climbing vine of T. radicans [Source] ; Right: folded leaflets of T. rydbergii [Source]

To be fair, I've definitely seen T. radicans appear to have slightly folded leaves under certain circumstances, so I think this aspect of the key is suboptimal.

Weakley (2015) "Flora of the Southern and Mid-Atlantic States"
 1 Leaflets 3, toothed, lobed, or entire; shrub or vine.
   2 Fruits pubescent or papillose; leaflets entire, coarsely toothed, undulate, or round-lobed; lower surfaces of leaflets either velvety puberulent, sometimes becoming glabrate in age (T. pubescens) or glabrous (glabrescent or rarely pilose beneath) but with prominent tufts of tannish hairs present in the vein axils (T. radicans var. radicans).
     3 Leaves sparsely pubescent (rarely pilose beneath), the apex and the lobes (if present) generally acute to acuminate; drupes papillose, scabrous or puberulent; plant a high-climbing vine or stoloniferous shrub; [of mesic, swampy, or dry habitats].......... T. radicans var. radicans
     3 Leaves velvety puberulent (sometimes becoming glabrate in age), the apex and the lobes (if present) generally obtuse to broadly acute; drupes pubescent (becoming glabrate); plant a stoloniferous shrub; [of dry habitats, especially sandhills] ............. T. pubescens
   2 Fruits glabrous (or very sparsely pubescent); leaflets coarsely toothed or notched (rarely entire); lower surfaces of leaflets glabrous to pubescent, but without tufts of tannish hairs in the vein axils.
     4 Leaves densely pilose and velvety on the lower surface; leaves pubescent on the upper surface; pubescence of the leaves erect ................................................................................................................................. T. radicans var. pubens
     4 Leaves glabrous to sparsely strigose on the lower surface; leaves glabrous on the upper surface; pubescence of the leaves appressed.
       5 Leaflets suborbicular or broadly ovate, nearly as wide as long; petiole glabrous (rarely glabrescent); plant a shrub, the stems upright, entirely lacking aerial roots, not vining; fruits (3-) 4-7 mm in diameter .......................................... T. rydbergii
       5 Leaflets ovate to lanceolate; petiole puberulent to densely pubescent; plant a shrub or vine, the stems upright or twining; fruits 2.5-5.5 mm in diameter ................................................................................................... T. radicans var. negundo

Clearly, Weakley goes into much more detail and includes lots of less well-known botanical terms as well as various varieties (subspecies) of T. radicans. A look at USDA PLANTS Database suggests of the varieties of T. radicans listed, only var. radicans and var. negundo are found in Ontario.

Of note, if we could see tan-colored tufts of hairs in the corners (axils) of the leaf veins on the underside of the leaves or fuzzy (pubescent) fruits, we could definitively rule in favor of T. radicans var. radicans. Or, if we could see aerial roots on the vines we could rule out T. rydbergii.

T. radicans can have either glabrous (not hairy) or sparingly hairy petioles, which doesn't help us decide between T. radicans and T. rybergii (not that we can easily see that detail in your images anyway.

I find leaf shape and border (margin) to be quite variable for all species listed (as Weakley hints at), so stopping at leaf shape alone always makes me feel like I'm giving an underwhelming answer. Despite this, T. rydbergii will almost always have coarse teeth/notches, which your image does not. (The ovate/lanceolate shape of T. radicans var. negundo would itself stand out as unique from the others, and again your specimens lack this leaf shape).

If I zoom into your image, I can see evidence of leaf hairiness (look around the border so that the contrast of the darker background enables you to see the hairs). This rules in favor of T. radicans var. radicans

Other common trifoliate plants or poison-ivy look-alikes:

Parthenocissus quinquefolia (Virginia Creeper) -- has 5 palmately-compound leaflets

Rhus aromatica (Fragrant sumac) -- terminal leaflet lacks petiole

Acer negundo (Boxelder) -- grows as tree. Leaves are oppositely arranged.

Rubus spp. (Raspberries, blackberries) -- presence of prickles

Yes, this is very likely to be poison ivy. It has all the right hallmarks (trifoliate leaves, long petiole, ovate leaflets with few teeth, shiny blades, and slightly elongated central petiolule), in an appropriate location, and there's little else in the area it's likely to be confused with.
Two species of poison ivy are possible in this area, Toxicodendron radicans (poison ivy, or eastern poison ivy) and T. rydbergii (western poison ivy). I think I can see that the petioles (connection from the group of three leaflets to the stem) here are pubescent (hairy), which would indicate T. radicans. If any nearby is climbing, that would also point to T. radicans. Otherwise, if it's only low-growing and has glabrous (non-hairy) petioles, then it's likely T. rydbergii.


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Why do people say that blue light is damaging to the eyes?
It's easy to find claims that blue light (e.g., from computer screens) is damaging to the eyes. For example, here is some discussion of the topic. Is there any physical mechanism by which blue (not violet or UV) can damage eyes?

Not an answer, but I can't help but notice that that's a commercial concern which sells blue-light blocking wearables.

At the bottom of the article are links to the relevant research article.


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Hepatic lobules and hepatocytes

"The hepatic lobules are the structural and functional units of the liver containing hepatic cells arranged in the form of cords. "

My textbook says that the hepatic lobule is the structural and functional unit of the liver. I'm confused as to why don't call hepatocytes the structural and functional unit of the liver instead, as they are the actual units secreting phospholipids, bilirubin and other components of the bile juice.
I framed this answer based on my understanding, please verify if I'm right or not and do suggest improvements-
"Properties of the hepatic lobule are not present in hepatocytes, they arise due to the interaction of hepatocytes. Therefore, hepatocytes on their own, cannot be termed as a functional and structural unit of the liver"

Who is "it"? What are the functions of the liver? There is more than one.

"It" refers to my books and teachers. They say that a single hepatic lobule is capable of performing all the designated functions of a liver. But that doesn't make sense to me, aren't hepatocytes capable of doing all of them in the first place??

My question about "It" was meant to prod you into citing your source. A bit of research on your part is expected. No, a hepatocyte can't perform all the functions of the liver. Why would I ask that question if you were correct?

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

Related question: https://biology.stackexchange.com/questions/89056/functional-unit

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What is it about bleach that keeps Pharaoh ants away even after drying?
My apartment high-rise has been afflicted with ants in the past few years.  The pest control technician says that it has become a common problem due to warming weather.  Various things have been tried, and I am leaving this in their expert hands (or rather, the apartment management is).  This question is not asking for further countermeasures.
When I find a place or pathway with many ants, I find that simply wiping with a damp cloth or vinegar doesn't keep them away for long.  Wiping is supposed to disrupt their pheromone trails, but I only find somewhat lasting effects if I wipe with undiluted household bleach.  I am pleasantly surprised that they stay away even after the bleach has dried.  After some internet research, I found that bleach leaves behind a salt residue when dried.  Is it the salt residue that keeps the ants away when wiping otherwise doesn't have lasting effect?
I've had another corroborative experience that leads me to suspect that salt residue has a repulsive effect on pharaoh ants.  I keep a large beer glass of very salty water on hand because of the dental benefits of salt water rinse.  I probably use too strong a solution, which likely has drawbacks (something I have yet to research).  It is kept on top of the fridge.  Around the glass is salt water staining.  I never see ants around it, even though ants like water.  I admit that this corroboration is not very strong, as I generally do not see ants on top of the fridge anyway

Although not familiar with the requirements set by biology SE this strikes me as being a suitable question for this site, since it is more about the sensorial perception and behavioral response of the ants, where the chemistry is important but relatively straightforward (and well addressed by the current answer).

My bleach solution seems ill-advised, both because of the fumes and the adverse effects on laminate countertops.  It looks as if I will have to get comfortable again with ants on my food preparation surface.

It's likely that the bleach (hypochlorite), which is a strong oxidizer, is destroying the trails more effectively than the vinegar. The mechanism of action here is the organic pheromone molecules, known as monomorine-1 and faranal are broken down into smaller organic molecules through oxidation. This chemically disrupts the trail and it takes some time for the ants to re-establish it.
I'm no organic chemist, but the acetic acid in vinegar may be a good smell masker for us, but I don't think it will have any chemical effect on the pheromones.

Thanks!  I upvoted the answer.  I have no idea how I can determine if it is the right answer.  Maybe a biological chemist can weigh in with a more authoritative assessment?

@user2153235 You might get a better response if you request migration to the Chemistry SE, though there are some good biochemists on here too, who might be able to answer authoritatively.

I will try that.  Er....I was just about to cross-post. I then googled how to migrate. From what I read here and here, I suspect that I have to flag the question for closure and specify a migration as the reason. Unfortunately, I can't find a Close link/button.  Maybe because I am the OP?

@user2153235 there should be a "Flag" link at the bottom of the text. I think that'll let you request migration, though I've never tried.

Done.  Thanks, Bob1!

Another answer that is fairly speculative (though quite plausible, in my view) results from the fact that I am using undiluted household bleach.  It leaves such a heavy salt residue.  Information online is mixed as to whether and how much ants dislike salt.  In my case, however, it may be that the salt simply provides a physical barrier against ants travelling up to the countertop from the seam between the sink and the countertop.  I actually see white crustiness forming at the seams after jamming the bleach soaked rag along the seam.


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Bolete (?) mushroom identification
I'm attempting to identify a gorgeous set of mushrooms.  I'm not anything resembling a mycologist, and I have no intention on consuming these... But for my own curiosity, I'm trying to identify these striking mushrooms.
Some notes:

These mushrooms were found directly under a red oak tree, in central New Hampshire, near Lake Winnipesaukee
The mushrooms were found this morning, on August 2nd
The largest cap was about 6 inches in diameter
The pore surface bruised rapidly (10s of seconds) to a blackish blue, even when lightly bruised.  Harder pressure bruised nearly instantly.
The cap flesh, though, did not.  You can see a slightly more-yellow streak where I rubbed the cap pretty hard.  Even after several minutes, no bruising appeared.
The stipe similarly did not bruise.  In fact, it was quite solid.
When cut in half, no bruising was apparent, even after several minutes (when the picture was taken)

Digging around, I thought maybe it was B. Bicolor, but the cracked appearance of the cap doesn't match basically any photos I can find.  It's not as bruisable as B. sensibilus.
Can anyone help me identify this?  I can run further tests as well.

For even more precision, make a spore print overnight and photograph.


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PEGylation safety and hybridomas
PEGylation is the covalent attachment of PEG (PolyEthylene Glycol) to molecules (e.g. proteins). It states in wikipedia   ("PEGylation"):

The covalent attachment of PEG to a drug or therapeutic protein can
"mask" the agent from the host's immune system (reducing
immunogenicity and antigenicity), and increase its hydrodynamic size
(size in solution), which prolongs its circulatory time by reducing
renal clearance

It seems  to be a widely used method in phrmacology.
(Other medical uses for peg PEG - as a laxative- macrogol, and as an excipient in some drugs.)
However, there is another use for PEG which is to fuse B cells with immortalised myeloma cells in order to produce hybridoma cells for the production of antibodies. That means, PEG have the ability to fuse two cells together.
How then, it's considered safe to use it as a drug? How come it doesn't fuse cells inside the body (when taken orally or intravenously)? Under which conditions is this property (cell fusion)  of PEG observable?

Can you provide a citation for the cell fusion function of PEG? Bear in mind also that PEG is a polymer; molecules of different MW will have different activities, and those bound to another molecule will be different from PEG in free solution, etc.

wikipedia "Hybridoma technology".:  Once splenocytes are isolated from the mammal's spleen, the B cells are fused with immortalised myeloma cells. The fusion of the B cells with myeloma cells can be done using electrofusion. Electrofusion causes the B cells and myeloma cells to align and fuse with the application of an electric field. Alternatively, the B-cells and myelomas can be made to fuse by chemical protocols, most often using polyethylene glycol.

Looking at the indicated protocols, they specify the myeloma cells should be split the day before fusion so they will be in "log phase" that is, constantly dividing. Normal cells don't do this in the body so that may be a factor.


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Marine invertebrate San Juan Islands, WA, USA
I noticed a green-colored marine arthropod in harbor in the US San Juan Islands (early July 2022, around noon), specifically Haro Strait, and took several pictures from the dock.
The bug was approximately 1 centimeter in length. I am guessing that it is algivorous (or algivore-vorous) based on the green color. It was in constant motion in sunlight, possibly hunting though it wasn't clear what it was going after (though the area was very algae-rich).
Apologies for the low quality images, some of these are stills from a movie (I had issues focusing because it was underwater and it was swimming around quite quickly).
Google image search was not very helpful, and neither was iNaturalist.


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Why and who: named some fish "bashers" (African electrofish taxon "stonebasher")
Folklore question for itinerant elephantfish/electrofish experts happening to see this:Is any stonebasher fish named for a behavior related to bashing...
something or some part of its anatomy against some stone, somewhere? Nonbiologist (so far) or certainly not grad level, so I don't know what mailing list archives or other sites are out there here in English-Interwebs-land.
20 minutes of wikipedia, goog, bing etc yields nothing, but maybe one of the tree-of-life type phylogenome-DB sites has a "history, indigenous and non-scientific names, etc." field? I found none on the sites I looked at (2-3 sites) via footnotes on eng.wikipedia.com references.
Probable possible source might be a print publication from around the period of first characterization of whichever one was named first.
Best imaginable answer would be who saw what on what day when, with an excerpt from field notes, but any reference helps!
Thanks for the welcome! I'm off to read the new member's tour

Welcome to the site. Please visit the [help] and take a [tour] for more information about the site. In particular one of the requirements here is that askers make some attempt to answer a question for themselves. Having said that; common names often don't have a source, unlike scientific names which do have an origin/attribution associated with them. Stonebashers seem to be a informal group from a few genera within one family. None of the scientific names have to do with stone.

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

Sorry, and thanks. Just falling in love with this "place" via the Mathematics exchanges, and dived in to add sites without taking individual stacks' tours. Now I know to do that first. (unfortunately un-)common courtesy for the win!

l should have mentioned several general Google searches, which I will now repeat with bing, and any bio/zoölogy or hopefully ichth specific search engines or preprint-server searchlinks those of you who happen to see this may chance to recommend.  I know this is only likely to be easy in places where people who know "folklore" of taxonomic adventurers past, tho'!


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Shrub in open gravel field

Location: Gravelly open field. East of Toronto.
Date: August 4, 2022
Description: Shrub; alternating leaves; 8 feet tall; trunk is 1.5 inches wide at the base.
Tip: It's possible to zoom in on the photos by clicking them a couple of times

Almost certainly Hawthorn (Crataegus) genus. This is a fairly common genus of flowering and fruiting shrubs to small trees that produce white flowers in the spring and small red apple-shaped (pome) fruit in autumn. Species are found wild all over the Northern Hemisphere and are invasive in a number of countries in the Southern Hemisphere.
They are characteristically quite thorny (as you can see in your photos 2 and 3), with the spikes being actually short stems. Leaves arise from the short spurs off stems and several species have deeply lobed and/or serrated leaves (leaves have both in your photos).
There are quite a few species, but which one this is, I don't know.


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What specific molecules cause the difference in spectral sensitivity in the cones?

What causes the difference in their spectral sensitivity of the S, M and L cones. I'm guessing that the opsin or photopigments are different, but haven't been able figure out conclusively from my web searches. Would you happen to know what opsins or photopigments each of cones have?

In Protanopia, the L cones are absent, or their spectral sensitivity has shifted. In the latter case, is it that the molecular structure of the opsin in this cone is different than normally expected, or is it that the opsin is using a different photopigment than normally expected?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] to a single question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

When we talk about spectral sensitivity, we talk about the spectral sensitivity of light-responsive complexes which are composed of

non-protein chromophore moieties that combine with
photosensitive chromoproteins.

In cones, you find a specific kind of opsin (photopsin) which combines with a non-protein photopigment that reacts to light via photoisomerization or photoreduction. Long story short: with light, you change the shape of the protein, and this initiates or boosts signal transduction cascades.
This study on Drosophila photoreceptors and spectral sensitivity-modulating factors is a great place to start, with supporting empirical data.
You'll find that both protein component and chromophore affect spectral sensitivity. For instance, difference between Rh1 and Rh2 opsin are responsible for different spectral sensitivities, as well as differences between the same opsin (say, where amino acid subsititutions are made to recapitulate other photoreceptors' structures and sensitivities, see this example). Likewise, the chromophore affects the overall sensitivity to light spectrum too:

The apparent lack of reduction in sensitivity of the UV-sensitive Rh3 and Rh4 rescue flies may be explained by the simultaneous reduction in UV-sensitising pigment associated with Rh1, which strongly absorbs UV wavelengths in the outer receptors.

This answers your title question.
Protanopia is characterized by missing or malfunctioning L-cone (red) cells. The cells are absent/malfunctioning, so the pigment genes specific to the L-cone have no 'place' to function, or are themselves absent from the retina (no expression).


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Is this bear excreta on trees?
We were hiking lately in Canadian Rockies (the Kananaskis country) and kept encountering branches of conifers near ground covered in brown substance similar to mud or excreta.

It didn't have any strong smell but it also was mostly dry and looked quite old. There were many occurrences mostly, but not only, along trails.
One of the hiking books we have here calls this a "rarely seen bear toilet paper".

However, for us this definitely wasn't "rarely seen" and I also doubt it to be bear's poo as there was just so much of it everywhere. What is this? And if it's a bear's poo why do bears do this?
EDIT: After asking on Facebook some people suggested it's a kind of fungal infection. Though they weren't able point out the species. What kind of fungi may this be?

In your photograph, it looks like the crown of a small conifer. Unless a bear reached up to swing the top down to assist in the force applied to its behind, it's unlikely that a bear's poop would be on the top of a tree. So, not bear poop.
The saying is, "Trees grow from the top up and die from the top down." That deterioration is called crown decline or crown dieback and happens to branches sometimes as well. Seeing this in multiple trees, not rarely, and near the trail, indicates that these trees are experiencing significant stress. That it's happening along hiking trails may be because there is compacting of soil or some other human activity affecting the tree's roots, and therefore its vigor.
When we were in the planning stages of building our house on wooded land, the builder warned us that heavy equipment compacting the soil would kill trees as far as 15 feet away or more from the tree (it was a fairly mature forest.) He wisely told us to pick the trees most important to us in planning our driveway and building site. These trees were marked, and tape was put up along the route of the future driveway and the house. It saved us from the nasty surprise many homebuilders face a few years after their home is finished. God bless conscientious builders!

Thanks for your thoughts. I'm still seeking an exact answer to what that substance is. It's definitely not the tree "just dying" as there is this brown thing on top of the branches. After asking on facebook some people suggested it's some kind of fungal infection. Though they weren't able point out the species.

Also, although the photo depicts a crown of the three the three was still small enough for a bear to reach up there with his bum. .)

@Jen - You'd need a lab analysis to determine the exact nature of the substance. Most likely it's composed of multiple communities of microorganisms present on dead organic matter. When the organic matter no longer nourishes these communities, the whole thing tends to dry up like dry gangrene. So you won't get a definitive answer here. :)


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What is meant by "Common descent"?
"Common descent is a concept in evolutionary biology applicable when one species is the ancestor of two or more species later in time." (Wikipedia)

[Credit:https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_Introductory_Biology_(CK-12)/05%3A_Evolution/5.12%3A_Phylogenetic_Classification (I added the letters to the common ancestor nodes)]
Does this mean that Species 1 and 2 have a common descent which is (A), but Species 1 and 3 do not, even though they share a common ancestor which is (B)?
I was thinking that "common descent" means the immediate previous ancestor. After all, it's a relative matter and there will be a common ancestor at some point. There has to be a term for that other than "just previous common ancestor".

Welcome to Biology.SE. You've done a good job with laying out a clear question, but the question itself seems quite naïve. In addition, the way you've worded this odd — common descent isn't an individual it is a relationship! (Please fix this.)  I also encourage you to check out some of the online resources available for learning more about evolution. For example, this a useful introduction to evolutionary theory from UC Berkeley. ——— I'm going to edit your post, but please check and make more changes as needed.

The Wikipedia definition is suitable to say that species 1 and 3 share common descent.

Common descent is a concept in evolutionary biology applicable when one species is the ancestor of two or more species later in time.

Any node in a (fully bifurcating) tree that is an ancestor to more than two tips will necessarily contain tips that are also descended from some other node.
OP is correct that "there is a common ancestor at some point," and there is strong evidence that all cellular life arose by common descent from our most recent common ancestor.
In practice, the term is usually limited by context. For example, many more relevant comparisons can be made between roses and apples, than between roses and dogs, even though the ancestor of animals and plants did once exist. In a conversation about energy procurement it wouldn't make sense to reference the common descent between roses and dogs; but in a conversation about, say mitosis, it might.
The term "related" suffers similar ambiguity.
As the figure shows, two species can share many "common ancestors," so it may be necessary to specify the "most recent common ancestor." In the figure, both A and B are common ancestors of 1 and 2, but A is their most recent common ancestor.
B is the most recent common ancestor of 1,3, 2,3, and 1,2,3.
The thick black line coming down from B in the figure represents the connection to B's ancestors. All of those ancestors are common ancestors of 1,2,3, but none are the most recent common ancestor of 1,2,3.
The most recent common ancestor of cellular life is the last universal common ancestor.
OP may want to review the term clade for a slightly more precise way to talk about related species. A clade is a group composed of an ancestor plus all and only its descendants.
In the figure:

1 and 2 form a clade with A.
1, 2, 3, A, and B form a clade.
1 and 3 (excluding 2) do not form a clade.

Indeed, I think it's easiest to think about using family relatedness as an analogy; you're related both to your parents and to your 8th cousins four times removed. In the context of life on earth, it's relevant that people are related to fruit flies; in the context of social behaviors it may only be relevant to consider primate relatives.

Thanks for your help, in "clade" wiki page, i found this "last common ancestor". Please edit your answer to include how last common ancestor can be applied to the figure in my example. Is it true to say that Species 1 and 2 have the same last common ancestor but Species 1 and 3 do not have the same last common ancestor

https://en.wikipedia.org/wiki/Most_recent_common_ancestor

This is good, but I think it would be helpful if you addressed the OPs misuse/misunderstanding of "common descent". They seem to think this term refers to an individual species (i.e. that it is synonymous with some type of ancestor) rather than referring to relationship or process ...

I figured it out my self from the answer, that all these terms: "common descent", "common ancestor" and "last common ancenstor" are being used in some abstract way or relative way, rather than to specify  a single one.

@Bowel "Common descent" is a bit abstract; "last common ancestor" a little less so, but the important word there is common. Your last common ancestor with a sibling is your parent. Your last common ancestor with a cousin is a grandparent. Etc. Something similar works with species.

B is the ancestor of 1,2 and 3.  Why do you think that is not an example of common descent between 1 and 3?

I was thinking that "common descent" means the just previous ancestor. After all, it's relative matter and there is a common ancestor at some point. There has to be a term for that "just previous common ancestor".

@Bowel Species are not well defined, especially in time, so "just previous common ancestor" is not a useful category and can't really be identified.


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Identification of insect casing
Photo of specimen with a US quarter (~24 mm diameter) for size reference. Please help identify what left behind this casing. It was found in middle of the yard, approximately 25 feet from nearest tree but was near a lumber pile if that is relevant. Located in south Central Colorado. Appears to be a winged beetle of some kind

Welcome to Biology.SE. This could be a California root borer (Prionus californicus), but since the antennae are broken off I think it may be difficult to get a good id ...

Note: I'm no expert and not even from North America, so take this with a grain of salt.
I think this is a May Beetle (Phyllophaga genus) or possibly a Junebug from the widespread scarab family of beetles. The adults range in size from about 12-25 mm (0.5-1.0"). A distinguishing characteristic of the scarabs is the linear ridges along the wing-casings and the beautiful stippling of the elytra (wing casings). Unfortunately you seem to have lost the antennae, which, if they are scarabs, have an enlarged club-shaped tip. It has an exposed scutellum and straight edges to the elytra, which are also features of the May beetle/Junebug family (Melolonthinae)
The Scarab family are a common pest of grass-lands and trees world-wide, and this genus is no exception - the name literally translates as "leaf-eater" (phyllo - leaf, phaga = eater).


text:
Do cells not grow during mitotic S phase (synthesis phase of interphase of the cell cycle)?
Both these links mention cell growth during G1 and G2 phase, but not during synthesis phase (only DNA replication is mentioned). Is replication all that happens and is there no cell growth during S phase?
https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/interphase
https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_General_Biology_(Boundless)/10%3A_Cell_Reproduction/10.02%3A_The_Cell_Cycle/10.2A%3A_Interphase

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. This will help you ask good questions and avoid some of the pitfalls that new users can experience using this site.

Also note that each post should only have one question, so I've focused on the question of "growth" as that seems the most central to what you are asking. There are of course many other processes that occur throughout the cell cycle, but that is beyond the scope of a single question (or this site in general) so I've removed those.

By growth I'm assuming you mean something like an increase in cell mass/volume.
This can likely vary depending on the organism and cell type (biology is riddled with exceptions), but in budding yeast (Saccharomyces cerevisiae) cell mass increases during mitotic S phase1.
The following is a quote from the introduction to reference 1:

Typical pie chart representation of the cell cycle (Figure 1A) stresses the discontinuous events that have to take place only once per cell cycle (i.e., S and M phases), but fails to show that proliferating somatic cells are continuously increasing in their mass throughout the cell cycle (Figure 1B). As pointed out as early as 1971 by Mitchinson2, the “continuous events of the growth cycle” (i.e., increase in cell mass) and the “discontinuous events of the DNA division cycle” (i.e., DNA replication, mitosis, and cell division) need to be tightly coordinated in order to maintain cell size homeostasis.

Main Events That Occur during the Yeast Cell Cycle
(A) General representation of the cell cycle showing the discontinuous events that have to take place only once per cell cycle, namely the S phase and the M phase, spaced with G1 and G2 phases that allow increase of the cell size before DNA replication and cell division, respectively.
(B) During the dynamics of the cell cycle, RNA and proteins increase exponentially, while the DNA content show a typical doubling amount until the cell divides to generate a newborn daughter. From G1 to M phases, the cell increases continuously in mass.

References:

Barberis, M., Klipp, E., Vanoni, M., & Alberghina, L. (2007). Cell size at S phase initiation: an emergent property of the G1/S network. PLoS computational biology, 3(4), e64.
Mitchison, J. M. (1971). Biology of the cell cycle.

thank you very much

You're very welcome! If this addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. Once you have ≥15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.


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Is this a Sunflower? Well over 10 ft tall
Huge stem but not the broad heart-shaped leaves like I have seen in pictures of sunflowers. Leaves look more like those of Helianthus. Stem is a good 6 inches around and smooth not hairy. The red branches are also throwing me off. No flower yet. . This is an Elementary School garden in Clermont, (central) Florida. We planted sunflower seeds, which is why, when they began growing that is what I thought they were. After much research I couldn't find any pictures that look like these plants. I have tomatoes and pepper plants in the same raised bed and it gets misters every 12 hrs for 3 hrs. Full, hot, Florida sun. If they are not sunflowers nor vegetable, we didn't plant it on purpose.

The trunk's glabrous whereas in sunflowers it would be hairy. As to Identification - is it developing a flower head of any sort anywhere? That might help pin it down if you can post a photo of that.

Welcome to Biology.SE. For identification questions please [edit] your post to include the location (e.g. country and region — the more specific the better) where you observed this plant. The location can be an essential clue for identifications. Clear, closeup photos of a leaf from above could also be helpful. Such questions should also use the species-identification tag. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

I've made a few (what I hope are) improvements to your post — please check and make sure I've not misstated anything. In particular, I'm not sure what the red lateral structures are — I think they are branches rather than petioles (leaf stalks), but please change that if I am incorrect. ——— Also, this looks like it might be a school garden — do you have any way of finding out if these were planted intentionally or whether they are "volunteers"?

Could be pokeweed, though I associate that with reddish stems. Can you please edit with photos of the leaf blade

Pokeweed is a good guess. Whatever it is, it's definitely not a sunflower. Did you plant a maximillian sunflower by accident? Doesn't strongly resemble that, either, though.


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Does ellagic acid dissolved in DMSO react with Brain Heart Infusion media?
I dissolved 2mg of Ellagic acid in 500 microliter of DMSO. I used 100 microliters of this solution to test for antimicrobial susceptibility against E.faecalis by adding it to 100 microliters of BHI media. After incubation for 24 hours in 96 well plate, I noticed precipitate at the bottom of the first row in the wells, which was confirmed not to be microbial growth . Another observation I made is that there was a distinct change in color(brownish) in the well. I tested other antimicrobial compounds as well but I had no issues. I repeated the experiment but got the same results, which lead to high optical density values.  I maintained the ideal pH range mentioned for the media.
My question is what caused the formation of precipitate? Is there a reaction that takes between ellagic acid and the media?
EDIT: Ellagic acid is poorly soluble in water(0.82 g/L) hence DMSO(dimethyl sulfoxide) solvent is used. The media requires pH  7.4 ± 0.2 for its properties to be stable. The reason I posted this question here is I am not sure if there is any reaction taking place, or if any other factor is responsible for the formation of precipitate and also because it is about antimicrobial susceptibility testing.

Please [edit] the following information into your question: 1) What is BHI media? 2) What is the solubility of Ellagic acid in water? 3) Is Ellagic acid's solubility dependent on pH and if so how does this relate to the pH of your media? Have you tried mixing equal volumes of Ellagic acid and your media? How about with just water? ——— Finally, if this is a reaction with the media, then this would be better moved to [Chemistry.SE] — either delete from here before reposting or request migration because cross-posting is impolite.

Hint : look at the structure of Ellagic acid. Is it like tannins? How do tannins react with proteins? All in Wikipedia.


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Examples of passive membrane transport proteins that only transport in one direction and their mechanism
I would like to know about those transporters with alternating-access-type mechanism, that can only efficiently shuttle molecules in one direction but the other direction is severely kinetically inhibited. From this question I know that they exist, but Google searches are futile in finding examples. Wikipedia is not much help, either. I also skimmed the seventh chapter of the Campbell biology book, about the structure and function of the cell membrane, but there was no clue.
More generally, I have found examples of enzymes that is inhibited only in one direction, such as F1-ATPase (even without the inhibitory epsilon subunit) with its mechanism of ADP inhibition, which primarily affect ATP hydrolysis and not ATP synthesis. I just have not found examples of this in passive transporters specifically.
Furthermore, is the mechanism of unidirectional inhibition inherent to the transporter domain itself, or does it require a separate domain, as in the case of the voltage-gated ion channels, to sense the gradient flowing in the other direction and then inhibit the transporter domain?
Is there even an universal mechanism?
My guess for an universal mechanism would be the former, as I am aware of the basic kinetics of the active ABC transporters, in that they preferentially open to one side of the membrane.

“Google searches”? Have you tried Wikipedia, or a text book, or  a Google Scholar search for reviews or looked on NCBI Bookshelf? We welcome you to SE Biology, but suggest that you finish reading the [Tour] and then look at the Help on Asking Good Questions. A single specific question expressed clearly and precisely — independent of the title — is what is required. Please do some more research and then focus. At the moment you start by asking for a list, and end by floating ideas on the evolution of transporters. Again, focus.

id be interested to know if there is such a review.  between archaea, eubacteria and the many many branches or eukaryota i doubt if this is entirely known.

Voltage-gated proton channels are passive transmembrane transport proteins that will only transport protons in one direction. These channels will be open when there is a lower pH in the cytoplasm, allowing protons to flow out of the cell, but will close when the pH is higher in the cytoplasm, not allowing protons into the cell. [1] In this case, the protein does not sense the direction of flow, but rather opens only in conditions where one direction of flow is possible.
Most voltage-gated proton channels have a separate voltage-sensing domain from their pore domain. However, HV1 does not have separate voltage-sensing and pore domains. [2] Therefore, neither combined nor separate regulatory and transport domains is universal. I am not aware of the mechanism in either case, or whether their are other proteins with different mechanisms.

DeCoursey, T. E. (2003). Voltage-gated proton channels and other proton transfer pathways. Physical Rev, 83, 475-579. https://doi.org/10.1152/physrev.00028.2002
DeCoursey, T. E., Morgan, D., Musset, B., & Cherney, V. V. (2016). Insights into the structure and function of HV1 from a meta-analysis of mutation studies. J Gen Physiol, 148(2), 97-118. https://doi.org/10.1085%2Fjgp.201611619

I'm fascinated by such questions @symmetrickittens so i'll just post a first pass here.
There are probably too many families which are not characterized right now to make a comprehensive answer.  This review estimates that 21% of prokaryote proteins are integral membrane proteins.  A large percentage of these are of unknown function, and there are many variants of each gene which may be functionally distinct.   This last reference just talks about the human proteome.  Each new genome sequenced has a substantial proportion 20-40% of protein products predicted with no clear function [anecdotal recollection from reading genome papers].
As such there are some nice reviews taking some fat slices of sequences which are really exciting to read (if you are a nerd like me). The above reference predicts 1700 structural membrane protein families.  This review of human membrane proteins discusses 89 transporter families but leaves 41% of membrane proteins uncharacterized.  Remembering that we diverged from eubacteria the better part of a billion years ago, there are probably well more than 89 protein transporter families!
A good fraction (majority?) of research is focused on human biology. If you can get used to the idea, then starting with the human transport protein proteome is not a bad place to start.  Here is a link to the Transporter Classification Database from the Saier Lab at UCSD.  They have proposed 1708 families of transporters.  I sincerely doubt they are promising not to discover more!

Uh... perhaps I was not clear enough. I asked for list/examples of a very specific kind of membrane transporter. I edited the question to reflect this. But you are somehow very informative, nonetheless.

TOM porins are an example.  https://en.wikipedia.org/wiki/Translocase_of_the_outer_membrane


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How does the central nervous system create the feeling of physical sensation in our consciousness?
I know sensory neurons that respond to light and physical sensations (pressure, temperature) exist throughout our body, giving us information about our surroundings.
For instance, when I push the tip of my finger onto the table. I feel the coolness of the table as well as the smooth and hard texture of the wood.
The pressure and temperature create action potentials in the sensory neurons at the tip of my finger. This action potential triggers the next in the cascade of neuronal firings that reach the somatosensory cortex the brain.
Now, this is where the crux of the question lies. Forgive me if it's a little unclear.
When one thinks of where oneself resides, one thinks they reside behind their eyes. Our consciousness and mind reside behind our eyes and in our brain. So when that signal from the tip of our finger reaches the somatosensory cortex in our brain, how does the action potential then recreate the experience of "hard", "cool", and "smooth" in the final neurons in the brain?
How do the chemical and physical changes in the affected neurons of the cortex equate to real, "felt" sensations in our consciousness?

This is a very broad question. The guideline is that if you need a book chapter (or a book) to explain it, it's too broad. Try focusing the question down if you can. It's just plain simple neurology (as if neurology is simple...) but quite a bit of it. There's nothing "mystical" about it, if that's where you're headed.

Certainly disagree with @anongoodnurse. Not really a 'broad' question; it is also as mystical as mystical gets in science. Historically it has been a deep, fascinating topic for millennia of philosophy, and surely no chapter will provide an 'answer', only fragmented insights. Just an old and so far unsolved, or perhaps unsolvable problem by empirical science. You are asking about how physiology instigates qualia, i.e. you ask about the hard problem of consciousness. I suggest you read the wiki entry and expand readings from there.

Anyway, voting to close as duplicate of these questions (one, two, three) which already have sufficient and insightful answers. OP, please consult these!

Comments are not for extended discussion; this conversation has been moved to chat.


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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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Sex in diploid cones in gymnosperms
Gymnosperms have male and female cones. If the cones are diploid, how can individual cones be male or female?

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

In addition, can you answer this if you replace gymnosperms with animals and cones with genitalia? If so, then do you really have a question?

Thanks. Yeah, you're right, I didn't think of it that way. I did many searches and thought about it a couple of days. But guess what -- no one explains patently obviously things. I was being silly, as you noted. I mean I still had a question and I'm glad I asked and your rude response makes me glad I also didn't make an account.

I'm sorry you found this rude, but perhaps you are being oversensitive? This site has standards that your question did not meet. You did not bother to take the (very short) tour to familiarize yourself with those standards and yet I took the time to let you know how you could do better and to give you (an apparently) useful hint as too where your thinking had gone wrong. If this level of feedback bothers you I suspect you will not be happy using Stack Exchange sites ...

Being diploid or haploid isn't really related to which sex organs are produced by a plant. As you say, many gymnosperms (and angiosperms) produce both male and female cones on a single plant.
Development of these cones would be caused by genes carried in all of the plant's cells, but expressed differently in different locations.
Some gymnosperms (and angiosperms) are dioecious, meaning they have different sex organs on different individuals (i.e., male and female individuals).

Here, still, the sex determination is not related to ploidy. The sex determination could be caused by several mechanisms, depending on the species, including a single gene, or a variety of sex chromosome combinations.


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Growing peaches from (supermarket) bought seeds
As a hobby I like to grow stuff from the seeds of fruits (or bascially everything) that I buy in grocery stores.
I have heared often that if the trees will eventually grow own fruits, they will not taste well, or maybe they do not even grow fruits.
What is the reason for this?
I know that normally the trees are 'grafted', but I do not see the reason why this causes bad taste by seed grown trees.
Can you explain?

Not sure about peaches but in apples the part you eat is made from the genes of the only the mother plant, but apples breed easier with very different strains of apples, and breeding is required to make fruit , so the fruit body  may be say honeycrisp but the seeds will be a hybrid of honeycrips and crab apple.

Having done this for peaches, the fruit was not as large it still good. This is usual.

@John Thank you for this comment. I didnt know this. Very interesting.

@PolypipeWrangler Thank you!

I'll admit I'm not super familiar with peaches specifically, but many agricultural strains are carefully selected hybrids of true-breeding plants.
That means that you take two breeding stocks that are crossed with themselves extensively to the point that we can consider them homozygous at all alleles, and then you breed two of those plants together. The resulting F1 generation is your primary agricultural production strain.
You can get more seeds by continuing to successively inbreed and cross-breed the parental strains, or by making grafts (clones) of the hybrid strain. Importantly, the F1 generation of two inbred strains will be genetically consistent.
Not every F1 generation is going to be the perfect plant, but if you carefully test and try out different parent strains, you can find combinations that give you a great offspring.
If you breed the F1 generation, you don't get a constant offspring but rather a whole mix of possible phenotypes. Some might be great, some not, but they're going to be much more unreliable.
See also https://en.wikipedia.org/wiki/Seedless_fruit

Very insightful. Thank you.


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A question on cell division rates
It seems that in the adult human body the rate of cell division should be approximately equal to the rate of cell death, but how is this reconciled from the developmental phase where a single germ cell becomes the many trillions of cells in the human body. Is there some change in the rate of cell division throughout lifespan?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

"Is there some change in the rate of cell division throughout lifespan?" Yes, there is. Is there something specific about this you want to know?


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What happens to the empty space ion pumps create?
Sodium-potassium pumps pump two potassium ions in and three sodium ions out. That means that it creates space for one more ion. Eventually, it's going to be filled. The concentration will be fine, as it would be 3 sodium out and 3 potassium in (because one potassium ion flowed in), or 2 potassium in and 2 sodium out (as three goes out and one comes in).
However, sodium-potassium pumps supposedly change the membrane potential by pumping more positive ions out than in. Wouldn't this be nullified if another ion comes in to take its place?

I’m voting to close this question because it: 1) contains multiple questions; 2) shows no evidence of prior research; 3) is unclear; and 4) appears to based on an assumption that seems to reveal a lack of basic understanding of chemistry — if so, this is best rectified by taking an chemistry course or an online equivalent (e.g. from Khan Academy).

There is no special "empty space" due to the action of these pumps. Ions are very, very small and even in liquid there are always gaps between molecules/ions/atoms. If you dissolve a bunch of salt in a glass of water, the volume doesn't change noticeably, but even if you measure carefully you find it actually decreases. That's because water molecules surround the ions and take up a bit less space than they would in a pure solution.
Additionally, sodium, potassium, other ions, water, etc. can all cross membranes by a variety of mechanisms. For charged ions, they cross the membrane primarily through ion channels though also through transports, some of which use ion concentration gradients to move other things (see https://en.wikipedia.org/wiki/Cotransporter).
Though flow through these channels is indeed somewhat random, in aggregate you can predict how much ions will move. It isn't as though a random ion will "replace" a sodium ion that has moved, rather, all ions will have net flow according to their concentration gradient and any electrical gradient across the membrane. You can determine the direction of net flow for given ion using the Nernst equation.

Well ... this does not apply to ammonium sulphate, and is one reason for the popularity of nomograms.  Try dissolving 50g ammonium sulphate in 100ml water, for example, or try dissolving 30 g SDS (sodium dodecyl sulphate) in 100 ml water: in both cases there is a very considerable increase in volume.  (In my experience, a very common mistake in biochem labs is to dissolve 30g SDS in 100 ml water, ignore volume changes, and assume this is 30% (w/v) solution: it isn't (the final volume is considerable greater than 100ml).

What I actually meant by "empty space" is how much ions can enter before before potassium flow and sodium flow equalize, and did not mean actual space (don't really know why I termed it that way). I can imagine a pump leaving one charge worth of "empty space (that is, one ion is needed until potassium and sodium flow equalize. This obviously isn't exact, but is true on average)", therefore slowing down potassium flow a tiny bit (less diffusional force), and allowing sodium to build up in the cell (one sodium ion on average), nullifying the pump's contribution to the membrane potential.

@SentientRays The pump's contribution to membrane potential is fairly minimal, a couple mV perhaps. If you want to use a water analogy, think about it as pushing some water to one end of the pool; there's nothing preventing it from flowing back, yet you can have slightly more water on that side indefinitely if you keep pushing. I've repeated this a few times to you now, but use the Nernst equation and Goldman equation; have a look at them and play around with possible values to input. These are the important things.

Related questions I've answered: https://biology.stackexchange.com/questions/88730/when-is-voltage-generated-across-a-membrane/88777#88777 https://biology.stackexchange.com/questions/81570/neuronal-membrane-resting-potential-for-large-cells/81571#81571 https://biology.stackexchange.com/questions/95192/why-do-ion-leak-channels-exist/95193#95193

Your question implies that proteins are like metal tubes (i.e., constant shape and form). This, however, is a bad assumption since there really is no "empty" space. Proteins have active sites and their movement is a highly chemical process; they often change shapes (e.g. hemoglobin) as well. Additionally, proteins are really "smart" (i.e., highly specific) and won't accept different ions. This "space" you refer to is very small, diagrams are misleading in that sense. You can look up 3D renders of proteins and quickly realize that they are difficult to understand. There is always the possibility of taking in different ions. This can definitely affect cell metabolism and function not because the cell cannot get rid of the unwanted material (homeostasis), but because when they do, they expel the material onto neighboring cells.
I am sure my answer is probably unsatisfying because you've asked too many questions under one post making it difficult to focus in on one topic. Try researching each question on your own first and if you do not find a satisfying answer, you can always ask a question in this forum :)


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Heat shock proteins in T cells of tumor microenvironment
Analyzing human tumor single-cell RNA sequencing (scRNA-seq) data, I found abundant expression of Heat shock protein (HSP) family genes in T cells. My literature review on "HSPs in T cells" brought a lot of papers. But all those papers are talking about how HSPs in cancer cells suppress anti-tumor immunity through different pathways. I do not particularly see much HSP expression in cancer cells though. Does that mean HSPs expression is not important on T cells or maybe it was not extensively studied from that point of view? Could somebody explain that from biological meaningfulness perspective, please?

Welcome to Biology.SE. I've made a few changes to your post, please check to make sure that I have not accidentally altered your intended meaning. In the future, please make sure you explain all acronyms and abbreviations the first time you use them — they are often ambiguous. Providing links that explain techniques and other relevant source material is also helpful. ——— In addition, can you tell us why your search didn't include "T-cell"? NB: if you are doing "Google" based searches then the "AROUND" operator can be very helpful e.g. "HSP" AROUND(3) T-cell tumor microenvironment ...

... Also, this site works best if you make sure that each post contains a single clear well-focused (narrowly scoped) question — you appear to have more than one question and the last question is both unclear (¶ What is the "that" you want biological meaning for?) and potentially too broad. ——— I encourage you to take the [tour] and consult the [help] starting with [ask] for details — this will help you get up to speed on this site's peculiarities and avoid pitfalls that can lead new users to have a poor experience here.

ok. thank you for the tips! should I ask a new question then?

You're welcome! It is best to [edit] this post so that is a single question and then move any additional questions into separate posts.


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How long does DNA last in wood?
I was wondering if it's possible to find out if the wood of the table I bought is from the same tree of the chair in the same set. Most likely not, but I was wondering if it's theoretically possible to get the DNA from both and compare them.
How long does DNA last in wood to the point that it's still useful for DNA comparisons? Are we talking about days, months, years, maybe longer?

I initially read the title as “a wood” and started wonder what crime was being covered up!

Even if you can get DNA, it might not be useful. I think in a lot of commercial situations trees are propagated by cuttings, which means two different trees could be genetic clones.

DNA can remain intact in wood, enough to perform useful identification, for centuries (this study had success with wood from ~1300 AD). However, successfully extracting DNA from the wood may be difficult, depending on the species, age, cut, and preservation.


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If guanosine transfer reaction in the RNA capping is reversible, should intermediate reactions be reversible as well?
Guanosine transfer is the second step of RNA capping. The enzyme (GTase) first displaces a pyrophosphate of a GTP molecule, forming an unstable covalent enzyme-GMP intermediate (E + Gppp ⇌ E-pG + PPi). Then the GMP moiety is transferred onto the diphosphate end of RNA (E-pG +ppRNA ⇌ GpppRNA + E) forming a triphosphate bridge. It’s obvious that this reaction is highly reversible, because the GMP moiety is transferred from a diphosphate to another diphosphate. As a result, the two intermediate reactions should be reversible as well. This is indeed the case according to this paper.

Recently a paper revealed that coronaviruses use a distinct reaction to make 5’ caps. The viral enzyme nsp9 reacts with the triphosphorylated RNA, forming an enzyme-pRNA intermediate (nsp9 + pppRNA ⇌ nsp9-pRNA + PPi). Then the pRNA is transferred onto a GDP molecule (nsp9-pRNA + Gpp ⇌ nsp9 + GpppRNA). This reaction is shared with nonsegmented negative sensed RNA viruses, and is likewise reversible (the L–pRNA intermediate is able to transfer pRNA to PPi to produce pppRNA, although less eﬃciently than to GDP to form GpppRNA). However, the paper claimed that “Interestingly, although inorganic pyrophosphate (PPi) was able to deAMPylate nsp9-AMP, it was unable to deRNAylate nsp9-pRNA”, “RNAylated nsp9 was not reversible in the presence of PPi”, which indicates that the first reaction is not reversible. This creates a problem. If the first reaction is irreversible, the covalent intermediate should be very stable and the reaction should be strongly thermodynamically favorable (large ΔG gain), which will make the second reaction strongly unfavorable. Although coronavirus nsp9 is different from the L proteins of negative sensed RNA viruses, the reaction thermodynamics should be irrespective of catalysts.


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Confused About Why Red Queen Hypothesis Wouldn't Apply to Deer's Color Vision
In this site,https://www.livescience.com/why-are-tigers-orange, it says ""But there seems to be no evolutionary pressure, particularly for deer, which are the main prey of the tiger, to become trichromatic. That's probably because the tiger doesn't know it's orange either because it, too, is a dichromat."
I am assuming the "evolutionary pressure" refers to the Red Queen Hypothesis. But then why would it matter if the tiger doesn't know its own color? Because it is hiding in the brush anyways, so wouldn't deer who can see red have an advantage over deer who couldn't?
Thank you

"That's probably because the tiger doesn't know it's orange either because it, too, is a dichromat." That phrase right there is garbage. You don't need to know your own weaknesses for someone else to exploit them nor do you need to know why something works for it to work.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In general, we expect 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). In particular, this question demonstrates the value of consulting multiple sources — the quoted statement is as you guessed nonsense. You may find this introduction to evolutionary theory from UC Berkeley useful.

@tyersome That was helpful indeed! Thanks! Also, could you explain how you got the link to the stack exchange link? Was it through a search engine query, saw-the-link before, etc.? Thank you

You're welcome. This type of question comes up quite often, which is why that post was created and why I was already aware that it existed. Due to it being a very general answer it isn't that easy to find when you have specific question like yours in mind, so don't feel bad about not finding it yourself.

what makes you think orange is bad camouflage. in many many environments orange is very good camouflage, no color pattern is good in every environment.