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Sexual dimorphism of the Amphimachairodus genus of saber-toothed cats
Amphimachairodus is an extinct genus of particularly large saber-toothed cats.
Per Alan Turner and Mauricio Antón's The Big Cats and Their Fossil Relatives: An Illustrated Guide to Their Evolution and Natural History (which I lack a copy of and cannot find an E-copy of), Amphimachairodus was "markedly" sexually dimorphic, "with males being much larger than females".
Before I get into sources, the overall question: does anyone know how sexually dimorphic Amphimachairodus was — specifically in terms of physical size? Was it like modern lions, where males weigh somewhere between 1½ to 2 times the females, or was it more or less pronounced than that? Google search results for this are few and far between.
Now, I found calculated sexual dimorphism indices for Machairodus aphanistus and Promegantereon ogygia (not to mention several modern species, such as the lion, serval, leopard, and jaguar, as well as Smilodon fatalis) in this article; said figures suggest M. aphanistus was between modern tigers and modern lions in terms of sexual dimorphism. But Machairodus is a wastebasket taxon out of which several species have been moved into Amphimachairodus, so I have no idea whether the figures for M. aphanistus are representative of Amphimachairodus as a whole.
This source can be cross-checked against the first source to slightly improve one's understanding of Amphimachairodus's overall size over what a Wikipedia article can tell you (specifically, compare tooth sizes), but has no information on sexual dimorphism. The best it gets:

The three available tali from Las Casiones show strong differences in
size, but comparable to those observed within the sample from
Crevillente-2 (Montoya,1994), supporting the existence of strong
sexual dimorphism in A. giganteus

Indeed, what I assume is mean mesiodistal length ("MDLMean") of the fourth premolar ("P4") of Amphimachairodus giganteus varies from 24.9 mm to 32 mm. However, I doubt comparing one type of tooth across a handful of specimens gives an accurate picture of A. giganteus size, let alone an accurate picture of dimorphism across all of Amphimachairodus. It also means you need to assume that the smallest teeth represent females and the largest ones males, which isn't necessarily true when it comes to big saber-tooths, as Smilodon demonstrates.
Basically: I'm asking for information specifically concerning this, if there is any. It would also be helpful to have more sources on the Amphimachairodus genus which aren't Wikipedia or books I can't get ahold of without buying them.
I believe Biology Stack Exchange is the best Stack Exchange for posting this question, as Earth Science Stack Exchange's "paleontology" tag states that:

Questions about the biological aspect of paleontology (such as
taxonomy and anatomy) are off-topic here and should be asked on
biology.stackexchange.com


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Why do animals excrete excess nitrogen instead of recycling it?
I am aware of the different ways animals excrete excess nitrogen (mainly ammonium, urea, uric acid). My question is: why do we excrete excess nitrogen instead of recycling it? How can we explain that there has been no selection for more nitrogen recycling in animals, as this would probably constitue a selective advantage?
I have read here that "In the quest for sufficient food energy to meet caloric requirements, animals ingest more nitrogen, largely as amino acids, than they require. Accordingly, the excess nitrogen ingested must be excreted in some form.". This is exemplified by this paper: a low protein diet comes with lower urea levels.

Herbivores and carnivores have vastly different nitrogen intakes, so it depends how much excess or paucity there is in the diet, i.e. ruminants recycle nitrogen more than carnivores. https://www.google.com/search?q=nitrogen+metabolism+in+mammals&oq=nitrogen+metabolism+in+mammals&aqs=chrome..69i57j0i22i30j0i390i650l3.7608j0j4&sourceid=chrome&ie=UTF-8 I would say they excrete it if they have a major excess, especially given the pH considerations of nitrogen, urea and ammonia.

An analogy with human recycling may be helpful: For millenia we've been tossing our garbage because it's easier than saving and recycling it. Recycling is hard, and we've only recently started recycling because we've been using some resources faster than we can replace them, and the environmental impact of tossing garbage has gotten exorbitant.

Helpful answer: https://biology.stackexchange.com/questions/111475/why-do-cartilaginous-fishes-not-excrete-ammonia/111477#111477

Recently asked: https://biology.stackexchange.com/q/111880/16927

I think your quote more or less explains it: what advantage is there is recycling nitrogen when you're ingesting more than required?
Additionally, we recycle nitrogen all the time, especially in amino acid form. Proteins are constantly broken down into their amino acid constituents and recycled into new proteins.
When you talk about waste nitrogen, that involves the excess (no need to recycle an excess - excess means there's already too much).
Further recycling may make some sense in conditions where nitrogen intake is not in excess, such as hibernation.

Since liver converts excess amino acids into glucose and subsequently glycogen. Won't it be better to store proteins as a reserve food material in form of muscles and other structures etc. ? That should be better than storing it up as fats which beyond a limit cause hundreds of health problems

@Aurelius Fat is more energy-dense than protein, and it costs energy to move that stored stuff around. Negative health impacts from fats are coming from over-storage that's only made possible by our extensive technological advancements over incredibly rapid time evolutionarily. And, in any case, storing nitrogenous materials as energy would hardly make a dent in the excess nitrogen in an adult human with a protein-rich diet.

I would add to the points made by @BryanKrause by stressing that the poster is misusing the word ‘recycling’. In metabolism you can only recycle something that was previously present, such as protein (as in turnover) or nucleic acid bases (for which there are salvage pathways).
The alternatives for dealing with dietary excess of a metabolite are either to reject (excrete) it or to store it for use in future conditions of deprivation. Presumably because the demands for energy are greater, more immediate and more crucial for life than that for protein precursors, animals have evolved to prioritize the storage of the carbohydrate portion of amino acids (as fat predominantly), rather than store both carbon and nitrogen as protein.
Indeed, when muscle protein ‘wastes’ in extreme starvation, this is to provide energy — and particularly glucose and ketone bodies for nervous tissue. The nitrogen portion cannot be utilized too, so that it also excreted under these conditions.
As with many questions of evolutionary rationale, the simplistic “this would probably constitute a selective advantage” is unsupported by actual evidence. In this case it is negated by a consideration of actual human starvation and the chemistry of the molecules involved.

Body builders have to take up a high protein diet. Because of exercise the excess nitrogen is used up in muscle making. Won't it be advantageous if it was done without exercising considering our body would rather die of obesity than excrete carbs or fats.?

While we are at it, why is the body so crazy about carbs and fat storage? Why does it store more fat than would be required to survive without food for months? And when it has all that extra fat why make us hungry for more.

@Aurelius my answer is to a specific question. The way that SE works is that if you have a different question or questions — which you clearly have — you should post it as an independent question (after careful preparation to provide clarity and context). This will enable others — who may know more than me about the topic — to contribute, and, above all, allow indexed access to those who share your concerns.

source: Stack Exchange

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

sort: votes


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How to calculate phage infection rate from decreased PFU counts?
Some experiments measured the effect of particular chemicals on the infectivity of lytic phages in terms of influence on the PFU/mL counts.
For example, the reduction of PFU/mL of exposed phages over controls might be 2 logs (let's say from 1000 PFU/mL in controls to 10 PFU/mL in exposed). If I knew the infection rate of the control phage (let's say 1), how can I calculate the infection rate of the exposed phages?
Thank you

I think you have a few problems here - first off would be that it should be PFU (plaque forming units); as CFU is for bacterial colony forming units. Second, assuming a standard concentration of bacteria, what do you think is measured by the PFU/ml?

Thank you, yes I have mistaken CFU with PFU, I have corrected the post.

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


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Indian snake ID
I saw this snake being attacked on the ground by a dog and it escaped up a tree with amazing rapidity. Can anyone help with the ID? It was maybe nearly a metre long. Seen in Rajasthan.

Quite hard to ID without being able to see the pattern on the dorsal side.


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Can citrate in semen be utilized as a source of energy by the sperm?
Prostatic secretions of semen include citrate as one of the component.
The role of citrate in motility has been suggested by some researches.
(Kavanagh JP. Isocitric and citric acid in human prostatic and seminal fluid: Implications for prostatic metabolism and secretion. Prostate. 1994;24:139–42).
Is there a possibility, that it can be utilized as an energy source, and enter the citric acid cycle of mitochondria of spermatozoa?

Many microbes can use citrate as a carbon source for catabolism or anabolism. Citrate however is not a dominant (if at all) energy source for human cells  because transport of citrate across the cell membrane is not as efficient as those of monosaccharides such as glucose and fructose. Semen has high levels of fructose compared to other fluids in the body, and glucose and fructose are the primary sources of energy for sperm 1. It is possible that citrate is important for sperm motility and viability through other mechanisms. If I can speculate, citrate could be a chelating agent in semen, but I do not have a source to back this up.


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Are there autoimmune disorders caused or mediated only by T cells?
I have frequently read that 'most' or 'the vast majority' of autoimmune disorders involving the adaptive immune system are caused by autoantibodies.
These comments imply that there are known disorders involving only rogue T- cells.
Does anyone know of specific examples?  Is there a list somewhere?

Can you provide a link for where you heard that from please?

There are several primarily T-cell driven autoimmune diseases like Rheumatoid arthritis, Type 1 diabetes, Inflammatory bowel disease, Multiple sclerosis [PMID: 29123529, 32457742].


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Lipid Bilayer composition
I am currently taking a course on introduction to biomolecules and the other day our professor showed us a photo describing the composition of lipid bilayers of various organelles in a eukaryotic cell. I just wanted to ask how would one go about to find these compositions? Me and my friends tried to think about it, one of them came up with an experiment in which you grow the eukaryotic cell in a medium where the only source of a particular lipid is "tagged". But the obvious mistake here is that the particular lipid you have tagged is present in all the organelle layers (how much so ever its percentage), so when you actually try to observe it, I would assume the cell will appear to be illuminated throughout. Any help would be appreciated.

The characterization of lipids in specific organelles would not be done in an intact cell, like you said, since the entire cell would light up with all the organelles spread around throughout the cytoplasm. They are separated, usually through subcellular and suborganellar fractionation so that each organelle can be characterized separately. Then, when the fractions containing each organelle or groups of organelles are separate, the lipids in each fraction can be further separated using a method like gas chromatography (essentially any good chemical separation technique will do) and then identified with mass spectrometry. One paper that describes this process in more detail is this one: https://www.jbc.org/article/S0021-9258(20)70077-3/fulltext


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

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

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

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

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

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

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


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Why are odd numbers of chromosomes (triploidy, pentaploidy) less common than even ones (tetraploidy, hexaploidy)?
Perhaps there is an obvious reason, and I know that most organisms that are either exclusively sexual or at least capable of sexual reproduction are diploid, but....
Is there a specific reason triploidy seems to be less common than tetraploidy?
It seems like a weird coincidence for a normally diploid organism to produce two rare gametes with extra chromosome(s) at the same time, or to do so at the same time a neighbor does so....

Sexual reproduction means taking chromosomes from two parents. Most commonly, that means that each parent gives just half their chromosomes to their gametes, such that the offspring will have a full complement.
As such, at some point you have to multiply h*2, where h is the number of chromosomes that one parent donates, the "haploid", and 2 is the number of parents. It's possible that 'h' could be some odd number, like if each parent contributes 3 copies in the haploid case, but multiplying by 2 parents always gives you an even number in the offspring.
From there, it's straightforward to either get an extra or lose a chromosome somewhere, but improbable for it to happen for all chromosomes at once.
The Wikipedia page on ploidy is a good place to read about these sorts of things.


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Why do Bactrian camels have two humps and dromedaries one?
Why has the Bactrian camel evolved to have two humps instead of the one that the dromedary has?
I searched on Google and I found nothing about it.
All I found was that the that humps store fat, that the fat can be converted into energy and water, that this lets them survive in deserts. As far as I know this is true also for dromedaries.
I also found that the Bactrian is smaller than the dromedary, that Bactrians are less numerous and they are at risk of extinction.
No site explains why Bactrian camels have two humps instead of one hump, as in the dromedaries.
Sources:
https://www.google.com/search?channel=fs&client=ubuntu-sn&q=why+do+bactrian+camels+have+two+humps#bsht=CgRmYnNtEgQIBDAB
https://en.wikipedia.org/wiki/Bactrian_camel
https://en.wikipedia.org/wiki/Dromedary

Why do you think there needs to be a reason as opposed to say genetic drift of two different lines?

@John Of course there was a genetic drift, but why dromedary was successful? I suspect that the fact that it's more small make it more adaptable to desert conditions. But I suppose this is another question.

First of all, it seems that the Bactrian is not smaller than the dromedary, and that dromedary and the Bactrian camel evolved from a common ancestor with two humps. So it seems it's the dromedary that evolved to have only one hump, and not the contrary.  I quote Wikipedia:

The modern dromedary probably evolved in the hotter, arid regions of western Asia from the Bactrian camel, which in turn was closely related to the earliest Old World camels.

It seems that the dromedary hump can store 80 pounds of fat:
https://www.nationalgeographic.com/animals/mammals/facts/arabian-camel
I failed to find how much fat a Bactrian hump can contain. A male Bactrian weights 590-1000 kg. Dromedary weights 400-690 kg.
So it seems a dromedary has only one hump because on average its weight is less than the Bactrian.
We can assume that the ancestor of the dromedary was a smaller camel with two humps. Over time, probably the second hump became smaller and smaller, until it disappeared. From Wikipedia:

the dromedary foetus has two humps, while in the adult male an anterior vestigial hump is present.

Be careful with conclusions. Does it only have one hump because its weight it lower or is its weight lower because it has one hump only? I tend to the second possibility.

@Chris good observation. I think you're right. I don't know if we have dromedary fossils, but I suppose a big camel with only one hump have smaller opportunity to survive than a smaller camel with two humps. I'll edit the answer.


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How do proteins 'know' where to go?
I've just found once again this famous animation I've been curious about for many years:
https://youtu.be/WFCvkkDSfIU?t=213
Here's a screenshot from the animation:

The green blobs (proteins, I believe) are moving from outside the scene to "the crowded area" (where unzipping happens). Then some of them (paler-green ones) are leaving in the same way as they came.
I am curious about how they are doing it!
I suspect that the "crowded area" emits some molecules (or perhaps ions), and "green blobs" might be literally electromagnetically attracted to the source due to density gradient of those ions. As for the "paler ones", they might be gaining on some other molecules (after contact), which probably disables their attraction to the "gradient". And the reason why they're so "determined" while leaving remains unclear, but I can guess that the same "gradient" molecules might be just pushing on them (as far as shown).
I would like to watch or read more about such details! And also about two-legged proteins from the end of that video — the ones that look like giant fighting robots from the Star Wars 1st trilogy.
Surely, these couple of things alone would take at least few month of studying.

As a fun bonus, that's somewhat close to the true speed of the process (about 50 base pairs per second).

Even though this animation is very well-known and the narrator says it is "... an accurate representation of the actual DNA replication machine ...", be very careful of its visual appeal. It is, after all, only a fancy animation for educational purposes. Some aspects of the process are shown correctly, but many are simplified, omitted or prettified, and can thus be misleading.
For example, a key ingredient not being shown in this animation (for obvious reasons) is water. DNA and the accompanying proteins do not float in free space, they are immersed in water. But not only that – intracellular molecular enivornments are far more crowded with other proteins than shown in the animation. See for example this whole-cell 3D model of a Mycoplasma bacterium.
Molecules don't know where to go. They move randomly1, bump into other molecules, and generally tend to disperse evenly across the solution. If you put a little drop of food color in a glass of water, it will eventually spread throughout the water. The same "force" drives macromolecules (such as enzymes shown in the animation) to move around. But when two molecules which are somehow "compatible" just happen to by chance come very very (!) close to each other2, molecular forces can help them position in the right way and stick them together. You can watch a simulation3 of molecular dynamics showing a small molecule finding its way into a large protein.
Although your hypothesis about some (mysterious) ions signalization and electromagnetic attraction is somehow reasonable, this is not the correct explanation for the process in animation4. First, electric forces in solution with ions are weak and short-ranged due to screening. Second, they could not be specific enough to attract only some molecules and not the others.
I put some keywords such as Brownian motion, diffusion, macromolecular crowding, molecular dynamics ... with links in my text which you can use to start exploring the topic of physical biology. Any textbook on cell biology or physical biology will be a good start, but the choice very much depends on your prior knowledge.
Oh, and the two-legged proteins are molecular motor proteins.

1 There is also a directed transport of substances inside of a cell, but this is a different phenomenon.
2 Macromolecular crowding actually hinders the movement (diffusion) of molecules around the solution (smaller diffusion coefficient), but it helps them stick together (larger binding constant).
3 Mondal et al. (2018)
4 Moving along a gradient of some chemical does happen, but it usually involves membranes or it happens at larger scales.

The motor protein animation is also misleading. He just gave everything a simple repeating walk cycle when in reality it's far more irregular. As far as I can tell he made these animations solo, they're not peer reviewed, and I can find no evidence he's ever done research in this area, so I wouldn't presume any aspect of the animations to be accurate.

This answer is specific to the "two-legged" proteins from the end of the video (motor proteins).
The animation shows identical proteins moving in perfect lockstep, but really there is wide variance in the time between steps, as seen in this graph of the motion of kinesin from M. J. Schnitzer and S. M. Block, Kinesin hydrolyses one ATP per 8-nm step, doi:10.1038/41111:

Here's a plot of the motion of myosin V from a different paper, showing a similar pattern.
This video shows what I think is a somewhat more accurate picture of the motion of kinesin, though it still shows all steps as taking a similar time.
The animations in the question were created by Drew Berry, who is also the presenter. My impression from his voiceover ("It's that mechanical. It's molecular clockwork. [...] This is all derived accurately from the science.") is that he didn't know that his depiction was inaccurate, though that was certainly known in the field at that time (the papers I linked were published years earlier). He doesn't seem to have ever done any biological research, and is primarily an artist. As such I would be suspicious of the accuracy of everything in his videos, but I'm not qualified to evaluate them.

There have been some suggestions that biological molecules may 'know where to go'.
Barry Honig's group at Columbia analyzed the electrical charge arrangements in protein and proposed that by placing charges throughout the protein in specific configurations that electrical fields could be focused and direct diffusion to accelerate the function of some proteins esp in finding their binding partners and reaction substrates.
An early paper for their electrical field analysis package DelPhi proposed that Super Oxide Dismutase had a strong electrical field that would strongly attract the negatively charged superoxide ion into its binding pocket.  In particular the hydrophobic core's electrical permittivity in contrast to the water around the protein has a pronounced effect on the electrical field around the protein.
This is still not common analysis because such models are often compromised compared to the realities at atomic scales but they are probably qualitatively valid.  Honig's work was most likely motivated by the regular measurements that diffusion in biology is faster than it has a right to be.  In particular Super Oxide Dismutase's reaction constant is orders of magnitude above diffusion.
I am looking for the original work above and will bring it in.  Another more relevant case to the question is that DNA binding proteins also [find their binding sites faster than diffusion would allow]3.  DNA is highly negatively charged (albeit with positively charged ions surrounding it in solution) certainly its reasonable to believe that the orientation of the protein to its intended binding must be important and that the cylindrical shape of the field around the DNA would explain some of these observations. Certainly the advantage of such an adaptation in the protein would be highly preferred in an evolutionary environment.
This topic is covered in the case of several molecules in this reference.  Here i've scraped a figure from the paper showing the positive charges around
PartII
I just got to attend a short conference and i have another interesting take on this.
The current thinking is that the ribosome and RNA polymerase both have a bubble of proteins that condense around them that are specifically involved in translation or transcription respectively.  These 'condensates' are not compartments in the cell but self assemble because of protein protein interactions.  This would make the functions in the cell partitioned because of protein self- assembly.  Evidence is still coming together but another example of how biology does not submit to Occam's Razor very well.
Reference : "Honig and Nicholls, "Classical Electrostatics in Biology and Chemistry" Science v268 p1114 (1995)

I'm not as familiar with the intricacies of e.g. protein synthesis, but for, say, vesicle release at synapses between neurons I feel like saying biology "knows where to go" is a bit magical; what actually happens is quite simple and intuitive: the various proteins involved are co-localized via associations with other structural proteins, which means that when, say, calcium ions enter through an ion channel, they aren't diffusing throughout the volume of the cell, they're diffusing a very short distance to a calcium sensor located right next to the channel.

sure - though that is a specific system among the many in the cell.  there are some cases like clathrate mediate endocytosis and the endoplasmic reticulum and mitochondria that are better studied than others. the question is pretty broad and perhaps focused on individual proteins specifically. would love to see a good question on synaptic vesicles.  there are visualizations of these processes available too which are pretty specific.


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What puts a lower bound on the size of warm-blooded animals?
The smallest known vertebrates are frogs that range down to 0.01 grams.  I would take that as evidence that at smaller sizes an endoskeleton is more of a liability than an asset.
1-2 grams is a lower limit of what has evolved across all phyla of warm-blooded animals.  Are there physical reasons that this would be the case?
One I can imagine is that any smaller and the surface-area/volume ratio makes it too expensive to regulate body temperature, but that's just a broad guess.

This is a guess, not a proper, sourced answer, but my bet is that below ~2 grams is where a warm-blooded organism has so much body surface area relative to internal volume that it can't eat quickly enough to make up for body heat loss. It's why shrews eat several times their body mass daily.

@KEY_ABRADE so that would be a sort of surface/volume constraint, but on digestive-system processing capacity rather than heat regulation.  Sounds plausible, given that (AFAIK) hummingbirds consume almost pure sugar, which I assume is the most efficient/concentrated means of getting bio-available energy.

Is there any reason to believe that the current smallest known vertebrates actually represent the lower bounds? We know that the current upper bounds are not the largest ever (for terrestrial mammals at keast).


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Fisher's principle in humans
Some research suggests that men have historically had far less reproductive success than women, even given the approximately 1:1 sex ratio in humans. However, doesn't Fisher's principle suggest that the sex ratio should adjust to the point where neither sex has a reproductive advantage over the other? In this case, shouldn't the equilibrium sex ratio for humans have more females than males?

The duplicate used a cat example, but it's the same principle regardless of the species: just replace cat with human. Half the genetic material of each offspring comes from a male. It may be "riskier" to be male in a world where few males reproduce, but the payout is better for one that survives.

Welcome to Biology StackExchange! I am not an expert, but I think you might be misunderstanding the Fisher's principle. "Fisher's principle states that natural selection favours an equal number of male and female births at the population level ..." (source) and "Fisher, in 1930, famously provided an explanation for why most animal species, including humans, produce approximately equal numbers of males and females." (source)

Ahh ok, I implicitly assumed the objective was on the extensive margin (i.e. whether one reproduced or not) as opposed to the intensive margin (number of descendants). Under risk neutrality and the latter objective, the 1:1 ratio makes sense.


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Is this a deathstalker

I want to know is this a death stalker ?

What are its dimensions? How long is the body, and how long to the tip of the tail? Where and in what sort of environment did you find it? Please [edit] your question and add as many details as possible to assist in identification. On the surface it looks like a deathstalker scorpion, but we can't tell for sure without more information.

Where did you see this? Looks interesting.


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Why is it essential to uproot a plant just before flowering in order to see nodules?
In my textbook it was written - Uproot any plant from common pulses just before flowering and you will see near spherical outgrowths on the roots .

It isn't necessary to pull them just before flowering. It is merely that the optimal time to check for effective nodulation is about 10-12 weeks post emergence, which also happens to be about the same time as flowering in many species.
Root nodules for the nitrogen fixing legumes develop throughout the life span of the plant. The nodules contain bacteria from the genus Rhizobium which are attracted to the root by release of certain flavenoids. The root hair tip then curls around the bacteria and forms a symbiotic relationship between the plant and the bacteria.
As the nodule formation takes some time to develop and become big enough to see, the nodules are often easily seen about the time the seasonal plants mature as this is also when the nodules get large. However, nodulation starts within 48 h post-inoculation1, so if you took a root tip and looked with sectioning and a microscope you could find nodule initiation at about 48 h.
ref:

Dasharath Prasad Lohar, Natalya Sharopova, Gabriella Endre, Silvia Peñuela, Deborah Samac, Christopher Town, Kevin A.T. Silverstein, Kathryn A. VandenBosch, Transcript Analysis of Early Nodulation Events in Medicago truncatula      , Plant Physiology, Volume 140, Issue 1, January 2006, Pages 221–234, https://doi.org/10.1104/pp.105.070326


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Do some animals have a notion of cooking?
Humans turned the concept of feeding themselves into a whole field in which they rearrange ingredients so as to obtain specific flavours and so on. It's more effort than just feeding ourselves.
Do some animals have a similar behaviour ? I guess at smaller scales of course, but did we already observe animals associate certain ingredients just for the propose of it tasting good or something like that?

This question has been asked before: https://biology.stackexchange.com/questions/42422/do-any-animals-prepare-food


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Is urethra a part of male accessory duct system?
In my textbook it is written that male accessory duct system constitutes the rete testis , vasa efferentia , epididymis and the vas deferens . Can urethra be also included here ?

Did you consider exploring what these other structures are accessory to? This line of thinking might help here.

Thank you for your suggestion. But is it because that urethra has only role in providing a comman passage for urine and sperm , but it doesn't have any role in functional maturation of spermatozoa , so it's not part of accessory duct system ?

I don't really find this terminology occurring very frequently, so it seems mostly something special to your textbook and others like it. Really the primary content I find online about this particular accessory duct is in the form of multiple-choice homework cheat sites. For example, this search for "accessory duct" epididymis vas deferens includes very few results and some are false-positives.
That said, a duct is:

a bodily tube or vessel especially when carrying the secretion of a gland

Accessory, in this context, has meaning along the lines of additional/supplementary/auxiliary, or not the main/primary, as in the accessory duct of the pancreas. So, an "accessory duct", where the adjective "accessory" modifies "duct", is "another duct in addition to the primary/main one".
The main duct, in this case, would seem to be the urethra itself, something common with the female urogenital anatomy, whereas the male accessory duct is the additional ductwork needed to attach the sperm-producing testis to the outside world. So, no, if you're taking the urethra to be the main duct, it doesn't make sense for it to be an accessory to itself.


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Variance in epigenetic drift rate between different species
My question relates to the prospect of (near?) future control of biological aging.
As I understand, it has been recently demonstrated by Prof. David Sinclair's group that epigenetic drift appears to be a major driver of aging, and demonstrated it may be reversed by applying a certain subset of Yamanaka factors. In particular, upon fixing DNA aberrations, epigenetic information tends to be restored with less fidelity than the DNA itself. In the mice in the experiment, the degree of epigenetic changes corresponded well to an aged phenotype in these mice, which was also apparently reversed by applying the above said Yamanaka factors.
See https://www.sciencedirect.com/science/article/abs/pii/S0092867422015707 for more details..
My question is regarding on the existence of "Horvath clocks" that provide a certain measure of epigenetic drift that can be compared across species. That is, do we have some kind a way to measure more of an "absolute" amount of epigenetic drift, allowing to compare this amount in say, mice, dogs and humans? My hope is that this absolute amount would be much greater in shorter lived species, to an extent providing an approximate explanation to the major differences between the lifespans of these species, to further support Sinclair's theory.
Maybe this measure can not be summarized by a single number, even, but rather depend on epigenetic drift in particular DNA regions/presence of certain methylation patterns etc.?

I am not an expert, but having a clear definition / source cited of what you mean by "epigenetic drift" and "Horvath clocks" would be helpful. E.g. in some organisms there is no DNA methylation. What do you do then? Also, my (out of date) recollection was that epigenetic clocks are not uncontroversial as a method of measuring age. Is that really so good of a measure of age? Clarifying and citing sources would again be helpful here.

The fact that some species have no DNA methylation indeed complicates the picture (so lets focus on mammals). I am not an expert either, just a longevity enthusiast.. Regarding a definition and utility of "epigenetic drift" - this is in a sense part of my question. I know that the amount of change relatively to youthful patters ("Horvath clocks") are problematic for estimating age, especially following some intervention, even inside a given species. My question is whether there is any work trying to explain inter-species lifespan differences by such "drift rate".


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How does sperm gets oxygen in the female reproductive tract?
At the time of insemination, sperm along with seminal plasma enters in female reproductive tract and the plasma contains fructose for providing the energy to sperm
If the fructose follows just EMP pathway (and not further Krebs cycle). Then what's the need of mitochondria. and if it does enters in Citric acid cycle and further performs oxidative phosphorylation, from where does the oxygen comes?

Do you think it is anaerobic in the reproductive tract? How do you think the cells of the reproductive tract survive?

Do you think, the cells of female reproductive tract provide oxygen to spermatozoa, well what makes you think that? I wonder if you are considering the glandular secretions to contain dissolved oxygen (do share the references of your idea if possible)

No, I was thinking more along the lines of where do the cells get there O2 from and why would the spermatozoon be any different?

Why it wouldn't be different, when a cell is not any association with any tissue fluid, what can be the transporting medium for oxygen from a foreign body of female.

Kindly upvote the question, for a better reach, Purpose is just to get the query solved asap.

Glycolysis and oxidative respiration are the main sources of ATP production in a sperm which causes oxygen regulating inside the sperm and makes it capable to move itself in the reproductive tract. But, the nutrients required for the survival of sperm are limited INSIDE THE SPERM.
But, as it enters the reproductive tract, the female body gives all the nourishment required for the sperm to survive, resulting in increased lifespan of the sperm (4-5 days).
Source: Oxidative phosphorylation versus glycolysis: what fuel do spermatozoa use?

"which causes oxygen regulating inside the sperm" what does it mean? Kindly clarify the source (precise) of oxygen.

I wrote "OXYGEN" to make you easily understand the process going on. Actually the sperm doesn't require any external oxygen. It is ATP (Adenosine Triphosphate) the energy source that provides the energy required by the sperm to travel to the ova (or the egg). This is the process of ATP formation:  ATP can be formed by 2 processes: oxidative respiration and glycolysis, both of which occur in bovine spermatozoa. Oxidative respiration occurs within the mitochondria, located in the midpiece of the spermatozoon, and results, in the case of glucose, in 36 ATPs being formed per molecule.

Full Article Source: https://onlinelibrary.wiley.com/doi/full/10.2164/jandrol.107.003533#:~:text=ATP%20can%20be%20formed%20by,ATPs%20being%20formed%20per%20molecule.

You should first understand the question, before jumping to answer it. Read the question asked.

Wait, What?? "Sperm doesn't require any external oxygen. ATPs are formed by glycolysis and oxidative respiration". Does your theory says oxidative respiration occurs without oxygen?? and the article, it doesn't holds any relevance related to question.

"Does your theory says oxidative respiration occurs without oxygen??" I didn't say that sperms don't require ANY oxygen. I said that sperms don't require EXTERNAL OXYGEN. that means the don't require external respiration mechanism. The oxygen formed from ATP synthesis is enough for them to move and fuse with the ova.

I gave you the source article to make you understand the process of ATP synthesis in Sperms.

I request you to kindly read the question asked.

Thats what I am trying to answer. The oxygen required comes from ATP synthesis.

Does ATP synthesis yields Oxygen?


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Are bacteria repelled by self-lysis products?
Intuitively, it seems like treating your own lysis products as chemorepellants would make sense, since getting away from a place where your kind are dying would be a Good Idea, but I can't find any papers that explicitly say so. Does anyone here have insight into the behavior of bacteria in the presence of high concentrations of chemicals that are normally inside of cells?

What specific chemicals or substances are you thinking about? What would only be found inside a bacterial cell and not in the general environment?


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Did predators evolve eyes first?
I'm an engineer and biology is my weakest point, so please forgive if this question is dumb.
Lately I've been wondering, "Why do animals that have eyes tend to have exactly 2 of them?" The closest related answer I can find is that 2 eyes provide depth perception. However:

That answer really only answers why animals have more than 1 eye; it doesn't say why animals have 2 (as opposed to 3, or more); and
Depth perception can only explain animals near the top of the food chain - wolves, bears, humans - but not animals closer to the middle of the food chain - penguins, squirrels, or fish.

Predators typically have depth perception. Prey typically do not, even if they still have 2 eyes. I'm painting an entire kingdom in broad strokes, and obviously there are exceptions. Big sharks are pretty close to the top of the food chain, but they don't seem to have depth perception. (If they can turn their eyes 90 degrees forward they might get depth perception, but only over a narrow range. I mention this because I read a statement that animals with eyes on the sides of their heads have more depth perception, but I don't see how that can be true.)
This shortcoming of depth perception can be overcome if predators evolved vision first, and then some of their descendants evolved into predators while others evolved into prey.
So here's my question:
Did (near) apex predators evolve vision first? Or, is there any evidence to suggest that that's what happened?

2 eyes, one on each side of the head allows perception of a 360-view. This is common in prey animals.

Additionally: Prey animals also need some food, take penguins for example. They need to fish, in order to be successful, they need 3D information. Also this is very useful for perception of their environment.

Bilateral symmetry is pretty ancient, and 2 eyes may just be a natural consequence of that. It's likely useful enough that both predators and prey can get advantages from it.

2?  eyes have evolved many many times. When eyes first show up in the fossil record a lot of things have them some have 2 some have 5

"Why do animals that have eyes tend to have exactly 2 of them?" I think this is a wrong assumption. Most species probably have a different number than 2. Did you know that bees, flies, and wasps typically have five, not two, eyes?

Your focus on depth perception seems very terrestrial-centric. It is less important if you do not need to leap and the types of animals with the first vision would have been aquatic.

I'm also no biologist, but equivalent to the question about two eyes probably is the question about (most) animals being symmetric. Also it seems I recently discovered that hornets have three smaller eyes on the top of their heads (see also http://www.hornissenschutz.de/grbilder/ocellen3.htm); why three? ;-)

"I read a statement that animals with eyes on the sides of their heads have more depth perception, but I don't see how that can be true." I think what you read was regarding hammerhead sharks. Their elongated head shape gives them better depth perception than other sharks that have eyes on both sides of their head. (https://science.fau.edu/shark_lab/pdfs/mtk09.pdf#:~:text=Several%20factors%20that%20influence%20the%20evolution%20of%20the,and%20is%20consistent%20with%20the%20%E2%80%98enhanced%20binocularfield%E2%80%99%20hypothesis.)

Short answer
Complex eyes may have evolved first in predator species, specifically in box jellyfish. Trilobites are another group of animals where complex eyes may have evolved first. The trilobites covered a vast range of species in many different flavors, with variable life styles and variable diets.
Background
The biggest question here is what is vision? If you call the sensation of light vision, then vision evolved perhaps 1.5 billion years ago (Williams, 2016) as a mechanism of phototaxis in unicellular, photosynthesizing microorganisms (prokaryotes); phototaxis being the moving towards light (Jekely, 2009). Also negative phototaxis existed early, as a protective mechanism against too much illumination. The present day relatives, tiny single celled algae, even have what you can call eyes, namely orange-colored eyespots (Fig. 1). These pigments, however, do not collect light, but block it to give direction to light. From there on evolution of vision becomes a much more complicated matter and can fill libraries.
Nonetheless, I think that's exactly what you are interested in since you are talking apex predators, i.e., I reckon, multicellular creatures, perhaps even with furry or feathered coats and clawed paws. If that is what you are looking for in terms of vision, we are further down on the path of visual evolution.
Cnidarians such as the box jelly fish are relatively primitive species that feature eyes (Fig. 2) and are thought to have appeared in the Precambrian Period between 635 and 541 million years ago. The trilobytes, marine arthropods, also featured relatively complex eyes (Fig. 3) and first appeared around 521 mln years ago. I think, from a quick search, that these taxa are among the first to have featured complex eyes (Williams, 2016). Both the cnidaria and trilobites (why I keep on typing trilobytes, I must be geeked) are considered predators, but trilobites may also have been detritus feeders, scavengers or even filter feeders. The cnidaria have their hallmark nettle cells with which they can paralyze their prey. Since the Cnidaria precede the trilobites, and are considered predators, I reckon we can hypothesize that complex eyes evolved first in predator species, although some attribute the first eyes to the trilobites.
References
- Jekely, Philos Trans R Soc Lond B Biol Sci (2009); 364(1531): 2795–808
- Williams, Eye (2016); 30(2): 173–8

Fig. 1. Eye spots in Euglena cells. source: ThoughtCo

Fig. 2. Eyes in a box jellyfish. source: box jellyfish

Fig. 3. Trilobite fossil showing its insect like eyes. source: Museum fur Naturkunde, Berlin

These images are great nightmare material.

Importantly, cnidarians have more than 2 eyes. Having 2 eyes is more a consequence of bilateral symmetry as all animals with bilateral symmetry have approximately 2 of everything.

@BryanKrause very wrong, some of the first bilaterally symmetric animals with eyes have 5 eyes, 3 eyes, or 2 eyes.

@BryanKrause Yes, and there many examples of extant bilaterally symmetric animals with > 2 eyes, eg many spiders have 8. Eyes have evolved independently something like 22 times, so there is vast variety that eludes simple generalizations.

great, now I want a 100 trilobyte drive...

Mostly a great answer, but Euglena are no more the "present day relatives" of photosynthetic prokaryotes than we are.

AliceD's answer is great but just to address your points 1 and 2.

Eyes are expensive. From a study on fish loosing their vision in caves.

The cost of vision was calculated to be 15% of resting metabolism for a 1-g fish, decreasing to 5% in an 8.5-g fish as relative eye and brain size declined during growth.

Why would prey animals/middle of the chain animals not want depth perception? Squirrels certainly need it for their acrobatics!

Finally, from this answer, you don't always need two eyes/overlapping vision to get depth perception.

I was told by a coworker who had lens replacement eye surgery that he was told that he would be really hungry for a while since his brain would be unaccustomed to processing all the extra visual detail. And he said the doctor was correct. Apparently it far surpasses the clarity he had with glasses.

Eyes evolved multiple independent times in convergent evolution.
Almost all the vertebrates have eyes. Those few that doesn't lost their eyes through evolution and live in deep ocean of in caves where there is no light.
Going back from vertebrates into other chordates, we note that tunicates have very simple eyes in their larval stage and lose them as adults. So, it is likely that the common ancestor of vertebrates and tunicates already had eyes. Going back into the evolutionary tree, lancelets have very simple eyes and have more than two, so it is here that things start to get interesting.
Going further back into the evolution tree, we look into other deuterostomes, where we find equinodermatas and hemichordatas, which does not have eyes.
So, the common ancestor of all chordates should have primitive eyes. Those became more complex as they evolved until the appearance of the first fish.
Parallel to that, in convergent evolution, Panarthopodas (arthopodes, tardigrades and onychophora) also developed eyes and some mollusca too. So, eyesight evolved at least three times (likely much more) independently in the animal kingdom except if this was a crazy result of horizontal gene transfers (which is possible due to participation of viruses and parasites doing strange things, but still unlikely).
Also, some jellyfishes also have eyes and some nematodes and annelids also sense light, but they have no eyesight yet.
Let's focus on chordates. The primitive eyed chordate probably had a very poor and simple vision, like lancelets do today, and likely fed on plancton and detritus living in the late Eadiacaran or early Cambrian, it could also eat small invertebrates. The line between sensing light and having true eyesight is blurry, but it was crossed somewhere by an early chordate. Also, the animal kingdom was very poorly developed at those times. So, it was in fact a predator, but not in the sense that you were thinking, it was not anything similar to apex predators we have today, since even a herbivore animal is also a predator of plants. Also, the apex predator at the time were probably jellyfish, which never developed eyesight because they lack brains, only having very simple and rudimentary nerve networks.
In fact, a couple of years ago I had read out somewhere (don't remember where though) that one hypothesis about what triggered the Cambrian explosion was the evolution of eyesight in animals starting an arms race. This could make many animals orders coevolving really fast or become extinct, and even plants would also quickly evolve spines, toxins and thick protective coats against better herbivores, leading to a Cambrian world much different than the previous Eadiacaran world.
So, no, the eyes didn't evolved into a predator because it was a predator. The first eyed animals had very poor eyesight without any depth perception. It likely evolved firstly to avoid the sun, or to locate the sun and floating algae, avoid dangers (including predators) and to better locate food (which is not the same thing as hunting, since searching for cabbage is not what people would call as hunting). But once it developed, it started to evolve quickly both for predators and prey.
After the first fishes appeared in mid-Cambrian, those who tended to be prey needed to scan the environment better to detect, evade and hide from predators and they did that by gradually moving their eyes to the sides of the head. Those who were predators, needed to attack the prey precisely in order to ensure it won't escape, evolving better depth perception with binocular vision which is better done by having both eyes in the front of the skull. Invertebrates with eyesight did roughly the same thing. So neither the evolved first, they both co-evolved together. Or if one did evolved first, it was by a very small margin. Also, since the first sighted animals had very poor eyesight, they could not perceive depth, that only came after some reasonable eyesight was evolved.
Also, flying animals, even when being prey, also needed very good depth perception without losing panoramic vision, which they attained by having very specific head shapes. But this only happened much later, roughly into late Silurian or early to middle Devonian for insects, into the late Jurassic for pterodactyls, into the middle Cretaceous for birds and middle or late Eocene for bats.
Animals and plants without eyesight were limited in developing toxins, poisons, carapaces and spines as a defense, but some sighted animals needed to develop those too as protection from predation.
A few references
https://www.jstor.org/stable/1311112
https://royalsocietypublishing.org/doi/10.1098/rspb.2014.1729
https://evolution-outreach.biomedcentral.com/articles/10.1007/s12052-008-0085-0
https://www.nhm.ac.uk/discover/eyes-on-the-prize-evolution-of-vision.html
https://www.nature.com/articles/srep02751
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783037/
https://www.sciencedirect.com/science/article/pii/S2667242122000203

The reference link dump format isn't very useful to someone hoping to better understand aspects of your answer. Better to connect specific statements to specific points made.

@BryanKrause I just joined this community today, I am still not used to the style of this one. I will try to edit that though.

Understood, I appreciate your efforts very much, I think it'll be an excellent answer especially for your first contribution here.

@VictorStafusa-BozoNaCadeia if you click the edit link on either mine or AliceD's answers you'll see how we've linked specific points to references. You can do that yourself when you edit your answer by highlighting a piece of text, then clicking the "link" button in the editor, and then pasting the link. You'll end up with a hyperlink on the text you highlighted.

For example you might link within the body of your post to a popularized account of the role of eyesight theorized to connect the Cambrian explosion to brain development, or link to peer reviewed scientific literature on the subject.  Help your Readers by describing what they might expect to find by following your links.


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Identify this insect in Texas
Please help identify the insect in the attached picture.  It was found in the Dallas/Fort Worth area in Texas, today, April 18 2023.  It is about 0.25 inches long.
Update in response to comment:  It was found in the backyard of my house, in shallow soil that I had recently been digging in and re-grading.  The white background in the picture is a potting soil bag I flicked it onto to get a better look.

The thorax is all wrong for a juvenile cockroach as others have suggested. (A cockroach would have an enlarged prothorax covering the head, as well as plate-like meso-and meto-thoraxes). Also, the antennae are too short.
Instead...
Based on the size, location (soil), and body shape (especially indent at base of pornotum, apparent split between elytra seen at the right of your image, and the short filliform antennae), it is much more likely this is some species of ground beetle (Carabidae).

According to Wikipedia, "All carabids...have a groove on their fore leg tibiae bearing a comb of hairs used for cleaning their antennae." However, your image does not provide enough clarity to effectively check (though perhaps th right leg showing a spur associated with this groove?).

According to Wikipedia:

more than 40,000 species worldwide, around 2,000 of which are found in North America and 2,700 in Europe.[3] As of 2015, it is one of the 10 most species-rich animal families

As such, I do not intend to try to identify this to species.

Here is a key to Oregon species to demonstrate variability in morphology as well as to emphasize structures to emphasize when trying to ID to species level.

Although I do not believe this to be your species, I wanted to include an image of an example specimen for reference:

 Amber-colored Ground Beetle - Platynus brunneomarginatus. Photo  credit: Jim Moore (2018); Bugguide.net

Thanks @theforestecologist, that is great.  Eliminating roach as a possibility helps a lot.

Another possible difficulty with this specimen is the teneral appearance (I find it possible that the animal had only recently emerged from its pupa); the same animal seen a few hours (or more) later might be considerably darker.


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Why is iron transported across membranes in the ferrous form?
Iron in the diet of animals is predominantly in the ferric form, but it must be reduced to the ferric form by a specific ferrireductase before it can be transported across the cell membrane into the cell:

To be absorbed, dietary iron… must be in its ferrous Fe2+ form. A ferric
reductase enzyme on the enterocytes’ brush border, duodenal cytochrome
B (Dcytb), reduces ferric Fe3+ to Fe2+. A protein called divalent
metal transporter 1 (DMT1), which can transport several divalent
metals across the plasma membrane, then transports iron across the
enterocyte’s cell membrane into the cell.

(https://en.wikipedia.org/wiki/Human_iron_metabolism)
Why is this necessary?

This is not my subject, but from scanning the introductions to a couple of reviews on the general topic of iron metabolism, the following factors seem to be important:

Ferric iron is less soluble than ferrous iron [1].

Ferric iron is potentially toxic in the cell because it can be reduced by oxygen, giving reactive oxygen species which are dangerous to the cell [2].

[1] Srai et al. (2002)
[2] Kaplan (2002)

@John — Thanks for picking up the typo.


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Can somebody explain why mouse and cow are the least related based on this sequenece alignment?

Answer key says out of the choices, the mouse and cow and the least related. Is it because they have the most number of differences out of the four choices? (Hedgehog/Horse is 5, dog/horse is 3, mouse/cow is 7, and mouse/dog is 3). I know there are more complex ways to make the tree, as shown in this video: https://www.youtube.com/watch?v=09eD4A_HxVQ, but I just wanted to know if my logic is correct here. This is for AP biology and we did not learn anything about the technique used in the video. Thank you.

Welcome to the site. The image is confusing as there is no reference sequence - normally you would have a sequence to compare them all to. As this is clearly homework - what do you know about genetic difference; how might we measure this? Do you think having a greater number of differences leads to more or less similarity?

I would think having a greater number of differences would lead to less similarity. The video I referenced also didn't have a reference sequence, but I don't think we're supposed to do it that way.

So, you have your answer, and you knew it all along. The reference sequence makes it easier for multiple comparisons, but as the answers in your question are binary, you take one as reference and calculate the numbers of differences between the two, then do the same for the next pair (as you obviously did).

That sounds good. I guess my problem is dog/cow and cow/horse both have eight differences, so I'm guessing the only way to tell would be to do the complex way to actually make up the phylogenetic tree?

The problem there only exists in your mind - those weren't part of the options you were given, so you don't have to worry about that part. No need for a tree.

Yep I'm just trying to understand it the best I can. I don't think what we learn in school tells us the whole picture. I tried the method and what I got is this: https://imgur.com/a/4CA13aI  I'm not sure if it's right, but this would say that cow/mouse and cow/hedgehog are the most distantly related, which is different from dog/cow and dog/horse if you just go by how many different nucleotides. So it's like you get different answers by using different methods.

The question says nothing about phylogenetic trees and nor should you as it would be absurd to try to construct one from these contrived data. I loath and detest MCQs in teaching, but the question is clearly testing one idea — that the longer evolutionary time there is between the organisms from which sequences have been derived, the greater chance there is of mutations occurring. You would do better to ponder the simplification in the scoring system — why is a transition scored the same as a transversion (not to mention the convenient absence of insertions and deletions).

By asking about the "least closely related" the question is implicitly asking about a phylogeny—one cannot answer properly without one. While your general statement about time and mutations is true, the seemingly logical corollary, that the most differences means least related or the fewest means most related, is not. I agree this isn't a great question, but mostly because it's conflating the issues of character similarity and relatedness, and it's relying on the simplicity of the example to lead to the correct answer just by eyeballing the count of differences.

@Darlingtonia sure you can. which of these 4000 species is least related to X, based on data given,  only one share's no common sites in the sequence, no need to build a tree of all 4000 species, heck you might not even be able to build a tree with the data given, but you can answer the question.

@John That's incorrect because character similarity isn't the same as relatedness. Imagine species A with sequence GGGG, species B with GGGT, and species C with TTTT. The tree would be ((A,B),C). Species A and B are sister to each other, so they are equally related to species C, even though B has higher sequence similarity to C than A to C. Furthermore, sometimes there can be one species that is "least related to X" (but certainly not always), but across any phylogenetic tree there is never a single pair of species that is "least related", there's always multiple equally-related pairs.

@Darlingtonia Sure there are single species that are most distally related, do you know what an outgroup is?  Also species are not always split into two species equally, a species could for instant spawn multiple species or fuse from multiple species, phylogenetic trees are way of organizing and understanding relatedness they are not actual phylogenesis. Don't confuse the model for reality.  Of course character similarity isn't the same as relatedness, its only a predictor, note the questions asks about classification not true relatedness.

An outgroup (assuming it was just one species) would be in the same position as Cow in the example. It would be equally related to all members of the ingroup, so there would be no single pair of species that is "least related". Phylogenies can support hybrid speciation, and this highlights the need to use robust models when inferring relationships from characters; indeed, the complexities you cite highlight the need to construct a tree rather than eyeballing the answer.

Well the mouse has 7 differences and the horse has 8, compared to the cow, on that sequence.

Answer C (Mouse and Cow) is the correct answer to the question, because among the four answer choices, mouse and cow share the earliest common ancestor*.
OP developed this tree** by following the method in the YouTube tutorial.
Under this tree, mouse and cow are more distantly related than the other provided answers because the common ancestor of mouse and cow is deeper in the tree than the common ancestors of the other answer pairs.
However, mouse and cow are not the most distantly related pair across the entire tree. The tree OP constructed*** shows that cow is equally related to each of the four other species. This is because the common ancestor between cow and any other species is the same. Cow/horse are just as distantly-related as cow/mouse, cow/dog, or cow/hedgehog, because each of those pairs diverged at the same point in the tree (with the most recent common ancestor of all five species).
Finally, the algorithm used to construct the tree can make a difference, so it's a little unfair to provide a set of sequences and have someone think up the tree. In this case the question author probably just expected the student to count up the nucleotide differences and select the pair with the most (which most of the time will be the most phylogenetically distant).

*Edit: This originally stated that they were "farthest apart in the tree", but I thought this would lead to confusion with OP's drawing where Cow and Mouse are separated by the greatest horizontal distance in the diagram. To be clear, horizontal distance in the drawing is essentially uninformative to relatedness. One could draw a tree with the same topology as OP's where Cow and Mouse are right next to each other, and it would not change the interpretation.
**I didn't confirm if this is a correct application of that method, but we can assume it is.
***This tree is not accurate to reality. Our best understanding of relationships among these species would put cow sister to horse, who are both sister to dog, who are all sister to hedgehog, who are all sister to mouse. So, basically the exact opposite of this tree. (Although I believe OP correctly constructed their version based on the provided sequences.)

Thank you for the answer. I have a question about how you said the cow is equally related to all four based on the cladogram I drew. I uploaded another one with some characters added on it. https://imgur.com/7Ffr5iK So based on what I understand, you said the cow is equally related to all four have the shared character "red" right? But you would say the hedgehog and the mouse are the most closely related to each other because they share the most number of characters. Thank you.

Not exactly. To talk about relatedness, you need to have the tree, because the shape of the tree (called the topology) shows you which common ancestor is shared by certain species. Now in order to make the tree, we do use characters, but 1) hopefully we have a lot 2) they're usually not as well-behaved as yours 3) if we're asking how a character evolved it hopefully wasn't used to build the tree, and 4) there are many methods of constructing a tree from the characters. Methods like the video just use simple similarity, but really, some evolutionary model should be applied to the characters.

But, yes, mouse and hedgehog are most closely related in that tree. We know that because they share a more recent common ancestor than other pairs; not because their "color" character is most similar. If you added another species, like zebra, you wouldn't be able to say if mouse/hedgehog or horse/zebra we more closely related (although some types of phylogenetic trees do use informative branch lengths, so that could maybe tell you).


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Are the lower layers of skin more electrically sensitive as opposed to simply heat sensitive?
Today while surfing I accidentally rubbed the top layer of skin in my fingertips off from friction against the surfboard.
I didn't think much of it until later in the day when I was using my laptop. I brushed against a USB peripheral (the external case of which is made of metal) which was plugged into my laptop with one of my fingertips and felt an immediate searing pain, not like a burning, but very much like electrical shock.
To verify, I quickly touched it with another of my raw fingertips and experienced pain so great that it caused me to cry out in shock. I adjusted pressure with the tip of my finger, and the more surface contact there was with my finger, the less the pain was. That is, as I pulled my finger away slowly leaving only a tiny bit of skin in contact with the metal it got EXTREMELY painful, as if the fewer the affected nerves the worse the pain.
I then touched it with one of my fingers which had somehow escaped being rubbed raw, and I felt nothing. It simply felt like normal room temperature metal (there was no noticeable heat).
This led me to believe that what I was feeling through my raw fingertips was not simply heat, but electroconductivity against which is usually protected by the outermost epidermis.
Can anyone shed some light on this?

In case this gets closed, here is some basic info, and in more detail here. The basic reason you feel more (and different) in your raw fingertip is that the protective layer of squamous epithelial cells has been removed, exposing raw nerve endings which don't get triggered when the epithelium is intact. If this is not closed, I'll give a full explanation when I have more time.

Sensation comes from receptors, and there are many different types, including free nerve endings, which are responsible for sensations of heat and pain 1. These free nerve endings can be directly stimulated by voltage. (So can other receptors, but these receptors are more readily stimulated by electricity 2.) Everything you "feel" is initially detected by your receptors and transmitted to your brain. What this means is that your skin itself does not feel anything - all sensation (through touch on skin) is conducted by these receptors.
[Most] Receptors lie in the 2nd layer of skin called the dermis, which lies under the epidermis 3. The epidermis has a few sublayers itself, including a [relatively and variably] thick sub-layer composed of cellular remnants and primarily the protein keratin 4. (All receptors lie below this sublayer 5). This layer protects the rest of your body from hazards in the environment. So to gain information from the environment through touch, your receptors have to be extra sensitive.
Now, when you blister or lose a layer of skin, part or all of the epidermis is what is usually lost 6. The net effect of this is you lose distance (and a layer of heat and electrical resistance) between your receptors and the environment - it is no longer protected by the epidermis. So your receptors will be more easily activated by stimuli - such as hot surfaces and your USB port. Additionally, fluids from your extracellular space can more easily "leak"7 and form a thin, sweat-like layer of fluid over the raw skin, which can actually enhance electrical conductivity.

As for why the smaller the contact, the greater the pain? Perhaps someone else can supplement, but my speculation is that when you apply pressure, other receptors (pressure, etc.) are also firing signals. This can cause a net dampening of heat/pain signal from the free nerve endings. Although not exactly the same process, you can think of like lessening the pain in one body part by inflicting pain in another (e.g. squeezing hands really tightly and clenching jaw after stubbing toe). When you are only slightly making contact with the port, only your free nerve endings may be firing, causing uninhibited signal. The pain may not be able to be replicated with intact skin simply because the free nerve endings under the epidermis are not firing - whatever miniscule current passing through the port cannot activate the receptors through an epidermal layer.
Again, this last part is just my reasoning. I don't think this has been studied, and there is so much variability in the human body that you would probably need a personal nerve conduction study for a definite answer to this phenomenon you've experienced.

"...you would probably need a personal nerve conduction study..." No. There's not that much variation in the nervous systems of individuals.

Btw, I'm not a neurologist, but I think your explanation is probably correct. I would liken it to, say, the same amount of pressure applied to a 1 cm^2 section of the fingertip vs. the point of a needle. The first would be noticeable, the second painful.

I don't think it's necessary to speculate about any of this, and I'm not sure what all has been done in humans but certainly has been extensively studied in animal models, I don't think speculation is necessary here.


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What species is this insect?
I would be grateful for help identifying the insect depicted in the attached picture. It was found inside a residential building (ground floor) at the periphery of Valladolid, a city in Yucatán, Mexico. Unfortunately, I am unable to provide a precise size, but from my recollection, it was about 1-2 cm long. By my (highly uneducated) guess, it seems that it might be an early stage of a member of the Triatominae subfamily, but I would appreciate a more precise/informed identification.

it looks like a weevil

This is a weevil, a beetle in the superfamily Curculionoidea. Most weevils are easily identified by the usually-present elongated snout (or rostrum [Davis (2017)] )
There a number of common home-invading weeviles (e.g., see UMN Extension), including a number of nuisance grain weevils (see my previous Bio.SE post). However, your specimen does not look like any of these....
Your specimen reminds me quit a bit of one of the better known species, the boll weevile (Anthonomus grandis), which is native to Mexico but is typically found in/around cotton fields. (I don't suppose you live near or work with cotton?). Though, your specimen is also larger than the typical 0.3-1.0 cm size of the boll weevil.

Field guide to similar weevils available here1.

 Boll weevil. Source: Jones & Williams (2001)
Wikipedia states:

Because so many species exist in such diversity, the higher classification of weevils is in a state of flux.

As such (and since your specimen is not one of the common house pest species I'm used to seeing), I'm going to leave my post open ended unless you end up updating with additional details. I think the boll weevil is ultimately unlikely your specimen (though not impossible), but it should serve as a good example to demonstrate this group and a potential jumping-off point for further investigation.

Also, see Jones et al. (2019) for Emergent and Possible Invasive Pest Species of Weevils in Mexico

 1. Jones R. and M. R. Williams. 2001. A field guide to boll weevil identification. Technical Bulletin 228. Mississippi Agricultural & forestry Experiment Station.


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When shall we call a secondary Oocyte an Ovum?
My common sense tells me that once ovulation has occurred and the secondary Oocyte is out of the Ovary ,it should be called an Ovum, but my son's high school biology text book mentions a secondary Oocyte as an ovum, actually in a bracket after secondary Oocyte.
It further mentions that once the second polar body is released, the secondary Oocyte becomes haploid Ovum (Ootid).
But in some other study materials it is mentioned that the secondary Oocyte undergoes second meiotic division and that the second polar body is formed only after a sperm has entered it and it is then only that a secondary Oocyte becomes an Ovum.
So I am confused.
Can we call the secondary Oocyte, released by a Graafian follicle, an Ovum or not, especially when it has already been "Ovulated", or shall we wait till the release of second polar body, which happens only after a sperm has entered the secondary Oocyte and a haploid Ovum (Ootid) is formed to call it an Ovum?


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Why doesn't the cell just use one messenger?
I recently learned the second messenger model, where adrenaline activates adenyl cyclase, which converts ATP into cAMP. Then cAMP acts as a second messenger which activates portein kinase enzymes. The protein kinase enzyme converts glycogen into glucose.
This is a very complicated pathway for me. Why doesn't the cell just use adrenaline to activate the protein kinase enzyme? Or even more simply, why doesn't adrenaline itself be an enzyme? Doesn't this make things much more easier?
Or in other words, why does natural selection choose to use the more complicated second messenger as opposed to one messenger only?

If you think that second messenger systems are complicated, then do not look into signal transduction cascades. More complexity allows a finer regulation as well as signal amplification.

The question seems to assume an underlying idea: that adrenaline has nothing to do other than cause the conversion of glycogen into glucose.  It has many other functions; if you consider that, perhaps you'll understand why this multi-stage system evolved.

Does this answer your question? Apparent paradox in Glucagon action. It is obviously not the exact same question, but careful reading of my answer will help you understand how the integration of different biochemical responses between tissues is key to hormones and second messenger systems.

A simple explanation for why there are intermediate messengers between stimuli (in this case adrenaline) and the final effector (the kinase).

Multiple messengers in a signalling pathway create different points at which signals can converge or diverge: Many stimuli may have the same end result, so a common secondary messenger is a point in the pathway for these signals to converge, as opposed to having multiple dedicated proteins to produce the same result for each stimulus. cAMP is a good example of such a secondary messenger where the signals from many stimuli can converge. Similarly, secondary messengers can also be points where signals diverge to have very different results, depending on other factors/proteins that may be active in the cell at the time. This way, a cell has common points to combine information from multiple stimuli (which may be be in agreement or conflicting) into an output. If there was a strict 1-1 relationship between stimuli and effectors with no cross-over points, it would be difficult for such cross-talk to happen.

Signal amplification: Many times, cells receive only a few molecules of a stimulus, which may not be enough to trigger a response on its own. However, if there are intermediate steps in the signalling pathway where the signal can be amplified, then very feeble external signals can also be detected. This image illustrates this point:

Image source

There is already an explanation of amplification here which gives the detail needed for a naive student to understand.

The figure is also unintelligible on its own. What is D? I know what a GPCR is, but someone new to the subject would not. Please avoid using abbreviations without defining them.


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Unidentified Fish-like Microorganism from pond water
I was looking at my friends pond water and saw several Daphnia. As I was searching, I noticed a Pliomate Rotifer and some other unidentified Microorganism. It looked almost like a micro fish, with a strange patterned disk around its body

That was under 40x magnification there's another image but with the disk hidden from view.

That photo at 400x or 800x. I did notice some fast moving area near the head almost like cilia, however they were inside and didn't appear to be cilia wiggling. If anybody has seen this type of microorganism before, please do let me know! I'm not sure if it is uni or multicellular given it's size but I'd guess it's multicellular given the tail appendage and complex internals.


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Is it viable to make liquid potassium ferilizer through dissolving very small amounts of potassium chloride in water
I wasn't able to find fertiliser online that was simply potassium chloride and I didnt want to source my potassium chloride solution from potassium sulphate or other general NPK fertilisers for my experiment on the effect of varying K+ concentrations on a plant. maybe 50,100,250,1000 ppm solutions. Or is there another element or component of fertilisers, perhaps compounds that lead to nurtient intake that I am overlooking in my methodology

If you have potassium sulfate (or carbonate) you can precipitate using Calcium salts (nitrate etc). Not all, just most.

the issue here is the chloride not the potassium.  Potassium chloride is very soluble in water. but you could be killing your crops/garden when you spray it on.
Most plants do not tolerate much Chloride ion.  With a limit of 500mg/kg of chloride in soil you will not be able to use much of this stuff.
that's wny potassium phosphates are much more desirable.  the phosphate will be consumed by the plants.


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Why does the thymus gland shrink with age?
What exactly is reason/process/mechanism for which our thymus gland starts to shrink with age? The thymus gland is the site of production of T lymphocytes which are the best defence against infection and even cancer cells, but as we mature, the tissue shrinks and gets replaced by nothing but fat.
Whereas our bone marrow (although it gets reduced cellularity) stays mostly intact and keeps producing red blood cells. I scoured the web for answers but didnt got satisfactory answer, with mostly dealing with effects rather than cause. One Quora answer draws speculation that perhaps with old age, thymus cells accumulate mutations so its better for body to reduce it, but it doesnt seems satisfactory.

@Kshtij Kumar. Intuitively, it must be supposed that 'thymic involution', a process mediated by circulating sex hormones (post-pubertally), occurs because its principal function as the site for maturation of T-lymphocytes has been largely satisfied once processes of their positive and negative selection have been accomplished. Since these T-cells are both long-lived and exposed to the circulation of blood and lymph, these 2 aspects of T-cell maturation are substantially complete in the thymus itself: its role is fulfilled. Incidentally, the original thymocytes are produced in the bone marrow.

If you read the 'Wikipedia' article on the 'thymus' carefully, the mechanisms are mentioned by which these long-lived T-cells are programmed in the thymus to recognise the difference between foreign antigens presented to their surface receptors by the MHC of body cells, and autoantigens deriving within the body itself -- i.e. 'positive selection' ('negative selection' of T-cells reacting to autoantigens results in apoptosis of the thymocyte within the thymic medulla). The inference is that once the bulk of this function is achieved in the thymus, refinement of the process occurs peripherally.


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Short RNA oligos modeling using FARFAR2
Does anyone have experience with modeling short RNA molecules using FARFAR2 server?
Given very short strands, ~20 bases long, I'm getting binding in all bases though only half should bind
Thanks!


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Is it possible to focus only one axis of astigmatism?
When we look at something close, we focus our eyes as a circle. But what if someone has astigmatism and focuses on something close, is it possible for the eyes to "focus" only the axis that needs focusing, thereby getting clear vision without astigmatism? (Provided, of course, that the object is at such a distance that it's possible for the eye muscles to "focus" on it so that that that axis would be focused but the other not.)

What do you mean by "possible"? If it were something humans are generally capable of I don't think there'd be glasses for astigmatism.

@BryanKrause Glasses are for general use. Even if a person can play around looking at something for some time until they succeed, that doesn't mean they can walk around doing it at will throughout the day. I'm asking if it's theoretically possible by spending some time looking at something. Not if people can do away with glasses for astigmatism.


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Why is glucose so common in disaccharides, as opposed to a different monosaccharide?
The three most common disaccharides (sucrose, maltose, and lactose) all contain at least one glucose monomer (sucrose=glucose+fructose, maltose=glucose+glucose, lactose=glucose+galactose), and the vast majority of other disaccharides also contain at least one glucose.
The only outliers to this that I have found are xylobiose (xylose+xylose), rutinulose (rhamnose+fructose), melibulose (galactose+fructose), lactulose (galactose+fructose), and mannobiose (mannose+mannose), and these all seem to be relatively niche/uncommon. Glucose is also one of the only monosaccharides I can find that binds with itself to form a disaccharide, and I have not found any examples of a fructose+fructose or galactose+galactose disaccharide.
What property of glucose makes it so that glucose found in (and is so integral to) so many disaccharides instead of a different monosaccharide, such as fructose or galactose, and why is it able to commonly form a bond with itself, unlike fructose or galactose?
(link to wikipedia article containing list of disaccharides with the monosaccharides they are composed of: https://en.wikipedia.org/wiki/Disaccharide)

What property of glucose makes it so that glucose found in (and is so integral to) so many disaccharides instead of a different monosaccharide, such as fructose or galactose, and why is it able to commonly form a bond with itself, unlike fructose or galactose?

Some readers seem absorbed with the notion that glucose can "form a bond with itself, unlike" other monosaccharides. This hasn't been addressed because it's an incorrect premise. To my knowledge this happens in many hemiacetals/hemiketals in water.
Glucose is a fundamental hexose; the metabolism of glycolysis is truly central to cellular life. This explains why it's so pervasive, in disaccharides or other carbohydrates. To use the wording of the question, the property of glucose that it explains its pervasive representation in disaccharides is its metabolic availability.
So why is glucose metabolism conserved across all three Domains of life? I explore two reasons.

Glucose metabolism could be central because of evolutionary history. Another type of aqueous biochemistry could prevail under terrestrial chemistries. So galactose-based terrestrial biochemistry is equally possible, in which case it would be overrepresented in biomolecules instead of glucose.

The aqueous abiotic (organic) chemistry of carbon (under terrestrial conditions) support glycolysis as a central metabolic pathway. So a galactose-based terrestrial biochemistry is thermodynamically disfavored.

(Same arguments go for pentose phosphate and TCA cycles, and the few other pathways that are so close to energetic equilibrium as to be amphibolic and metabolically central.)
Evolutionary biology provides evidence for explanation (1). This is because all domains of life share conserved enzymatic machinery for glycolysis; "The phylogenetic distribution of the enzymes of the glycolytic pathway confirms that it is indeed an ancient metabolic pathway, and was present (at least in part) when eukaryotes and
prokaryotes diverged about 1800 million years ago."From this reference, p. 224
There are also strong arguments for explanation (2). Below is one article detailing how glycolysis could very plausibly preceed cellular life. Glucose would then be pervasive, in part, because it's a pervasively metabolically-accessible (and chemically stable) sugar, under terrestrial conditions.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4023395/

"Evolutionary biology provides evidence for explanation (1)." Can you provide a link to support this (completely reasonable) statement? Thanks.

Your answer makes no connection between the composition of disaccharides and glycolysis, indeed disaccharides are not even mentioned.

@Ryan.  Perhaps this is a question of stereochemistry.  Ask a chemist.

@anongoodnurse I added an evolutionary biology reference

@jeremiah my reference includes considerations of stereochemistry

@David my answer doesn't reference disacchararides and glycolysis because they do not exist in glycolysis! the preponderance of glucose in sugars, celloses and chitin, etc, is being explained by me in terms of its sheer abundance as a central metabolite

Aren't you putting the cart before the horse? The question isn't "why is glycolysis universal?"

@anongoodnurse my answer is, glucose is preponderant because it's central metabolically, and i gave two possible explanations for this centrality. you asked for a reference as to my claim that it's central for evolutionary reasons, explanation 1.

@Ryan But the question is about disaccharides! The word “glycolysis” doesn’t even appear in the title. I

The paper is about glycolysis, not the ubiquity of glucose. It's like asking for support for democracy in Ancient Greece, and citing the American Constitution.

not following the above analogy, but your persistence motivated a more explicit answer, @David

@Ryan - What came first, glucose or glycolysis? Glycolysis depends of the production of glucose. The principles of democracy (e.g. in Athens) predate the US Constitution, which was heavily influenced by Ancient Greece. Your answer is teleological.

If you want to answer a question on the reason that glucose is the "king" of hexoses, ask it and answer it yourself. However think carefully. Many such evolutionary "why" questions provoke answers that assume that whatever Nature chooses must be the "best". It ain't necessarily so, and stacking up one feeble argument after another doesn't make it so.

glycolysis can be biotic or abiotic. my position would always be to asume abiotic conditions to be ontologically prior. I don't see how my position is teleologica, as well, I haven't asserted a King hexose" type explanation, but I do see how answer 2 is related to that position

Part of the explanation for this preponderance in disacharides is perhaps the dominance of glucose generally, and the clear necessity for it to be stored in organisms. The intuitive explanation for that preponderance, including in polysaccharides generally, likely involves some stereochemical property which distinguishes it from galactose, and broadly speaking, fructose.  The following is an excerpt from the 'Wikipedia' article on Glucose itself; which seems a good starting point.

Glucose is the most abundant monosaccharide. Glucose is also the most
widely used aldohexose in most living organisms. One possible
explanation for this is that glucose has a lower tendency than other
aldohexoses to react nonspecifically with the amine groups of
proteins. This reaction—glycation—impairs or destroys the function of
many proteins (e.g. in glycated hemoglobin). Glucose's low rate of
glycation can be attributed to its having a more stable cyclic form
compared to other aldohexoses, which means it spends less time than
they do in its reactive open-chain form.
The reason for glucose having the most stable cyclic form of all the
aldohexoses is that its hydroxy groups (with the exception of the
hydroxy group on the anomeric carbon of d-glucose) are in the
equatorial position. Presumably, glucose is the most abundant natural
monosaccharide because it is less glycated with proteins than other
monosaccharides. Another hypothesis is that glucose, being the only
d-aldohexose that has all five hydroxy substituents in the equatorial
position in the form of β-d-glucose, is more readily accessible to
chemical reactions, for example esterification or acetal formation.
For this reason, d-glucose is also a highly preferred building block
in natural polysaccharides (glycans). Polysaccharides that are
composed solely of glucose are termed glucans.


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What type of beetle is this? It was on the wall in my backyard
This insect was on the wall in my backyard. I live in Southern California. Does anyone know what is is?

Welcome to the site. We would need at least 1 picture, preferably high quality and close-up of the insect/beetle in question to identify.

The wide, flat body makes me think that's a roach, not a beetle. Beetles normally have an exoskeleton over their wings, not exposed wings. Based on the pic you provided and these two websites, I think it's a German cockroach, Blatella germanica
https://ipm.ucanr.edu/PMG/B/I-OT-BGER-CO.004.html
https://www.corkyspest.com/cockroach-id.html


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Identify a spider which is consuming a fly
can you please identify this spider which was found on indoor banana plant eating(?) a fly?
Located in central europe - Czech Republic, Moravia region. Photo taken in April 23rd. Banana plant is located indoor, behind the window facing southwest side. 228m above the sealine. Googled "webless spiders" but couldn't find anything similar to this one.

Please [edit] your question and add some details like: when did you see this? What time of year? Can you be a bit more precise than "central Europe"? How about habitat? Was this in a house? On a mountain?

Please edit your question to begin title and sentences with a capital letter. This is the form in both English and Czech.

This is something in the Thomisoidea family (Crab and Running Crab spider superfamily).
You can review the community-observed species of crab and running crab spiders in Czechia here: https://www.inaturalist.org/observations?place_id=8264&subview=map&taxon_id=367176&view=species
The two stripes down the carapace are unlike Philodromus, where the stripes in Philodromus are at the edges of the carapace while in this photo, there is clear space between the stripes and the edges of the carapace. In North America, I would has assumed this was Mecaphesa (in the Thomisidae family), but Mecaphesa does not seem to exist in Europe.
But Europe (and Czech, in particular) has the Triangle Crab Spider (Ebrechtella tricuspidata) (this genus does not exist in North America). This Triangle Crab Spider has the same key indicators as in this given photo: short - almost dwarf-like - hind legs. Brown-striped front legs. Green abdomen. Two stripes down the carapace with remaining spacing on the outsides.
This photo was observed in Czechia:

The observation and identification can be found here:
https://inaturalist.org/observations/61869636

thanks for an answer. so according to photos here: https://en.wikipedia.org/wiki/Ebrechtella_tricuspidata the example on the photo should be male, right?

correct. Here is a gallery of males: https://www.inaturalist.org/taxa/360081-Ebrechtella-tricuspidata/browse_photos?quality_grade=any&photo_license=any&term_id=9&term_value_id=11&layout=grid&place_id=97391
and here is a gallery of females:
https://inaturalist.org/taxa/360081-Ebrechtella-tricuspidata/browse_photos?quality_grade=any&photo_license=any&term_id=9&term_value_id=10&layout=grid&place_id=97391


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Does active transport go only against concentration gradient?
Does active transport go only against concentration gradient? Is there any scenario that active transport moves molecules from high to low?

I'd parse this into two sub-questions for yourself. 1) What would the benefit be of using active transport to move something down a concentration gradient? 2) If you artificially or pathologically or experimentally changed concentrations such that something that would ordinarily be moved up a concentration gradient is now moved down, would that interfere with an active transport system already in place?

These questions are the exactly why I'd ask this question. Some of the textbooks and my teacher said the active transport is not always against concentration gradient. I don't think that's right too. An example introduced by my teacher was the active transport was done by small intestine cells from low to high after eating dinner.

If you include the quotes from the textbooks in your question it would significantly help.

If the molecule to be transported has a ionic charge, then the change in free energy is not only due to the concentration gradient, but also on the membrane potential (Vm) and molecule charge (z).
If the electrical free energy necessary to move the molecule surpass the free energy released by the chemical gradient, then an active transport is necessary.

Does active transport go only against concentration gradient? Is there
any scenario that active transport moves molecules from high to low?

What's active transport?
Have you considered the ion transport mechanism of gastric pump?

There are two types of Active transporters. 1) Primary Active Transport is generally energy driven by ATP Hydrolysis. 2) The other category of active transporters do not rely on ATP directly.
One:
The primary term refers to transport mechanisms that are directly coupled to the consumption of metabolic energy ATP.
Thus "pumps" encompasses all transporters capable of thermodynamically uphill transport (so-called active transport). Let's consider a couple popular active transporters (ion pumps) of the cell membrane that are directly fueled by ATP.
Within ion pumps itself there are those active transporters that pumps ion against a concentration gradient e.g. H+,K+-ATPase (gastric proton pump) where high concentration of H+ is actively transported across the appical membrane of parietal cells towards the low concentration of H+ of gastric lumen. Gastric pump maintains a 1H+:1K+ ion stoichiometry, yielding overall electroneutral ion pumping mechanism and cycel. This is a type of active transport mechanism that is specific to a particular physiological task such as digestion.
Then a more popular ion pump of the same family, Na+,K+-ATPase which actively transports ions (3Na+:2K+) across an electrochemical gradient (a combined concentration gradient and an electrical gradients) in basolateral membrane by pumping Na+ from cell interior (cytosol) to cell exterior in exchange for K+ from cell exterior to interior where cytol has high [Na+] concentration and extracellular is high in [K+]. The electrochemical gradient is necessary for the pump's ion pumping activity and infact gradient is maintained by the underlying concentration and asymmetric selective substrate ions (Na+, K+) stoichiometry (3:2). Na+K+-ATPase's active transport is at work in all cells of the body (not just human).
Primary active transporters, such as Ion pumps do infact pumps ion across high to low concentration (concentration gradient). Have you considered H+K+-ATPase?
Two:
The second type of active transporters depend on the electrochemical gradients of other ions as an energy source. They are usually called ion exchangers. These active transporters are able to carry more than one ion up its electrochemical gradient and at the same time taking another ion (most often Na+) down its gradient. e.g. the Na+/Ca2+ exchanger that shares Ca2+ with the PMCA Ca2+ pump.The exchanger keeps intracellular Ca2+ concentrations low. The Na+/H+ exchanger regulate intracellular pH, in this case by acting directly on the concentration of H+.
Such that It is not quite just to simply to characterize that 'all' active transport mechanisms are 'only' based on concentration gradients alone. Further, just because a molecule (substrate) to be actively transported by a transporter, is an ion, it does not engage in a concentration gradient. There are transporters such as P-Type 4 ATPases which are evolved to actively transport phospholipids as substrates that are not cations/ions.
I am not going to contaminate the answer by introducing passive transporters such as ion channels which are crucial to the co-existence and function of the ion regulation of the cells. e.g. ion channels produce electrical signals by diffusing down substrate ions across electrochemical gradients (again a combination of ion concentration and signaling. That means ionic currents depend on the electrochemical gradient across the cell membrane (of some type). In the case of nerve cells, such an electrochemical non-equilibrium is crucial. Diffusion will continue until this gradient has been eliminated. Imagine, with ongoing electrical signaling and ion diffusion, if there's no reserves to constantly replace these ions, these necessary ion concentrations would reach a zero, so is the nerve signaling.