text:
Why do humans share over 99% of their genomes?
From Wikipedia

The haploid human genome (23 chromosomes) is about 3 billion base pairs long and contains around 30,000 genes.[33] Since every base pair can be coded by 2 bits, this is about 750 megabytes of data. An individual somatic (diploid) cell contains twice this amount, that is, about 6 billion base pairs. Men have fewer than women because the Y chromosome is about 57 million base pairs whereas the X is about 156 million. Since individual genomes vary in sequence by less than 1% from each other, the variations of a given human's genome from a common reference can be losslessly compressed to roughly 4 megabytes.

Why do humans share over 99% of their genomes? Is it a historical accident or a result of selective pressure? If a zygote differed in 5% of the base sequence from the common human genome would it automatically be unviable or could it eventually become a healthy baby?

Dogs vary by as much as 25% and  I think the concencus is interbreeding did happen with other human species, so it could probably be much higher, but not just any genes either.

Humans are a very, very young species, we began diverging on the order of 100,000s of years, compared to e.g. crocodiles which have been around for 200m years, so there has barely been any time for differences to accumulate.

But I'm also not sure this question is well posed. Why wouldn't they share 99% of their genomes?

Let's say there is potential human genome that only shares 70% with the common human genome and that results in you being able to run twice as fast as Usain Bolt. Wouldn't that be evolutionarily advantageous at least in some environments? Wouldn't mutations eventually get us there?

@SKG that's kind of too hypothetical to answer really. If they only shared 70% then they sure wouldn't be human in any sense we know. Evolution happens incrementally, not in massive step changes which would alter 30% of the genome.

I guess if the only option to make embryos is natural reproduction then the question cannot be meaningfully considered. However now that we have several tools for targeted mutations (and also gamma rays for untargeted mutations) I think it does become possible to make an embryo sharing 70% with the common human genome and to put it in a womb. It is probably unethical but I wondered if any expert has written about this.

Relevant: https://biology.stackexchange.com/questions/9172/do-apes-and-humans-share-99-of-dna-or-99-of-genes-what-is-the-difference and also https://biology.stackexchange.com/questions/48084/perplexing-by-the-way-of-estimating-the-shared-or-different-genes-between-humans?rq=1 Make sure when you think and talk about %s of "shared" DNA you know what type of "shared" you mean.

Because the 99% is what makes humans human, of course.  The rest is just minor variation. I would imagine that ANY particular species would have a similar percentage of common genome.  Humans (and other mammals) share a large fraction of DNA with plants, because that's what constructs the basic mechanisms of life, such as cell membranes, ion channels, DNA/RNA replication, &c.

@jamesqf Are there any other species that have 23 chromosome pairs and the same number of base pairs in each chromosome as humans? Otherwise I don't understand how can we compare the genomes of different species (it sounds like comparing strings of different lengths).

@SKG just to give you context, the measured divergence between humans and other great apes is ~1%, and there is complete reproductive divergence between these organisms (https://www.sciencedirect.com/science/article/pii/S0002929707640968). To be clear, these percentages reflect the subset of the genome that is comparable ("alignable") in the first place. Any two humans probably have different numbers of bp in their genomes, due to hypervariable repetitive regions. Moreover, it is relatively easy to blow big holes in the human genome ("aneuploidy"), but it has a tendency to kill the human.

also... "Wouldn't mutations eventually get us there?" i mean... there is a nonzero probability of massive divergence like 30%. After all, evolution does happen on that scale given hundreds of millions of years. But it's like randomly flipping 30% of the bits on your computer and expecting it to keep working. Maybe a very controlled "intelligent design" of bit-flips could get you there, but trial-and-error will take trillions of iterations or more. If you want intelligent design, well, we have to understand the code before we can start hacking! We don't understand genomes that well.

@SKG: As I understand it - and this is not my field, so I'm very far from being an expert - what gets compared are genes.  For instance, there are a family of genes that control the formation of various types of potassiim ion channels.  Each gene is made up of a number of base pairs, and can be located on any chromosome. The particular genes can be isolated and compared: https://en.wikipedia.org/wiki/Potassium_channel

@Armand: You have a couple of undefineds in that experiment.  First, what is the average number of offspring per individual?  Second, what fraction of those mutations result in non-viable offspring?

@Armand tl;dr Your thought experiment is really talking about a different measurement from the OP's cited number. Generally, estimates of substitution rate say ~$1x10^{-8}$ (https://www.nature.com/articles/s41467-017-00323-y), 2 orders of magnitude lower than yours. It doesn't include high mutation rate loci, but those usually aren't alignable anyways so they wouldn't show up in this frequently cited estimate. 1% is probably closer to a "true" measure and ~$1x10^{-6}$ might be closer to a "true" mutation rate, but that is counting a bunch of stuff that people don't tend to count.

@MaximilianPress OK, sorry for the distraction here.

No one seems to be able to decide whether this question is worth answering or not, I will put one down just to bring closure, summarizing some of the discussion in the comments. I think that the question merits answering because the genetics community honestly hasn't done a good job of messaging on this topic.
It's a little involved, so I'll break it into parts. It's a bit long, so for a tl;dr you can skip to the conclusions.
what does "less than 1% different" mean?
First, it's important to know what the widely cited statistic of ~0.1% difference between the average pair of humans means. It means that, of alignable sequence, if you look at ~1000 bp, approximately 1 bp will be different. As a point of comparison, most great apes (including humans) differ from each other by 1-2% by this measure.
However, not all of the human genome is thus "alignable" even between two humans. When I say "alignable", what I mean is that I can take a snippets of two sequences (say, a 100 bp region) and 1) confidently determine that the area is the same on the two genomes, and 2) we can actually associate specific ACGT with each other between the two sequence. Such a 100bp snippet is then "alignable" with regard to the two genomes.
When sequence is not alignable, that usually means that it shows redundancy in the genome, which is to say that it is present in more than one copy, or a similar enough sequence is present that my confidence in a unique placement is low.
In other words, the 0.1% statistic is actually based on the subset of the genome where we can perform confident comparisons. If this minority of the genome were representative, this would not be an issue. But the alignable portion of the genome is highly non-representative, as it contains most of the genes that we care so much about, and none of the big important structural pieces like telomeres and centromeres. This non-alignable region is in part so hard to analyze because it has a much higher mutation rate than the rest of the genome; in other words, we expect the non-alignable regions to be more variable than the alignable regions. Probably much of the genetic variation among humans occurs in these regions.
So the 0.1% estimate is a significant underestimate of divergence. It is nonetheless a useful heuristic for thinking about relative degrees of divergence.
Why don't humans vary genetically more than they do?
This is, I believe, the heart of your question. Whether the true difference is 0.1%, or 1%, or 5%, one could ask why it isn't 30% instead, as you do in your comment. It seems that you are at least somewhat interested in this from an adaptationist point of view, namely that one can imagine that all that extra variation could be helpful in making humans "better", however we happen to define "better" (faster, stronger, smarter, disease-resistant).
This framing is closely related to the classic SE Bio catchall question "Why do some bad traits evolve, and good ones don't?" The common logic being: "I can imagine a way that an organism could be better, why isn't it already better in that way?" I'm not sure that you are specifically interested in that as opposed to a more general curiosity, otherwise it'd be easier to mark your question as a duplicate and move on.
There are several related reasons I can think of why the level of divergence is what it is, I'll try to hit them here:
1. Evolution is slow
Commenter @user438383 got at this a bit in comments, noting that humans are very young in evolutionary terms and asking why not 99%? There's some logic under there that isn't stated that I'll try to unpack.
Other commenter @Armand posted and then deleted (after a too-pointed critique from me) a version of a thought-experiment: let's build a toy model of evolution and plug in some numbers and see what comes out. For example, we could then say that the expected probability of a site remaining the same across $n$ generations is $(1 - \mu)^n$ in a single lineage assuming no back-mutation, where $\mu$ is the mutation rate. We know that the average site in the (alignable) genome has a mutation rate of around $\mu = 1 \times 10^{-8}$. So if we were to calculate that probability for the average site for $n = 100,000$ generations (~3 million years, way older than anatomically ), we get:
$ Pr(no\_change\_at\_position) = (1-10^{-8})^{100000} = 0.9990005$
So, under this deeply simple-minded model with arbitrarily defined numbers, you actually get very little expected change at the position even for rather large time-scales. There are tons of problems with this model, as alluded to by @jamesqf, namely that we ignore population dynamics. But it should at least illustrate the scales that we are working with here.
2. Many/most mutations are shared, due to coalescence
Another fun subtlety is that, of the mutations that do occur in our toy model in (1), many or most of those mutations are expected to be shared between all humans due to coalescence. Briefly, under reasonable assumptions about breeding dynamics, you expect that all humans share a surprisingly recent common ancestor. So there is no variation, because all humans share the mutations.
This issue is exacerbated by so-called population bottlenecks, which are inferred to have happened fairly recently for humans.
3. Most mutations don't matter.
We have known for some time that most of the mutations that do occur have no effect, and allele frequencies suggest no selection occurs on most genetic variation. So there does not seem to be any particular advantage or benefit for humans from having more mutations.
In the absence of selection maintaining a new allele, it is usually lost from the population due to random chance, i.e. "genetic drift".
4. Mutations that matter are mostly bad.
Of the mutations that do have some effect, selection mostly tends to remove them because they are deleterious. These alleles are removed from the population at high frequencies, leading to an incentive to minimize mutation rate to maximize viable offspring.
In fact, the burden of past slightly deleterious mutations retained in the population is a significant force in evolution (the "mutational load"); it is simpler to just not have these mutations in the first place.
Conclusion: you should expect human genomes to differ very little from each other in the alignable regions.
To sum up:

There has not been enough time to introduce all that many mutations into the alignable region of the human population genome.
Of the mutations that occurred, most are shared by all humans.
Of the mutations that occurred, most have no effect, of which many are lost due to genetic drift.
Of the mutations that occurred and had some effect, most were deleterious and were purged by selection.

Did you mean unalignable or "ambiguous location for short-reads"?

mm, I suppose that it's worth clarifying that repeatmasker is the latter, which is definitely an overstatement relative to the more traditional "alignable". I will look around and see if there is a better estimate somewhere.

On second thought, RepeatMasker is likely closer to this than any alternatives. But I can certainly improve the explanation to make it less about short read mapping.

I can't help as I'm just discovering the topic but nanopore website referenced this paper which seems to be exactly doing this, evaluating the true underlying diversity not captured by standard pipelines

@reuns, I'm really thinking of the regions that would not be properly alignable even if we had the perfect full telomere-to-telomere assemblies that the nanopore website refers to. These are significant regions including the telomeres, centromeres, pericentromeres, transposable element sequences, etc. In consideration of your point, I have attempted to reframe the alignability section of my answer to correspond more closely to this, as I was unable to locate a reliable estimate of alignability proportions. It is after all not really important what the exact amount is for this answer.

I think you left out an important point: the differences between humans ARE trivial.  A lot of what goes into making a human also goes into making any primate; much of that is shared with all mammals, mammals share a great deal with other vertbrates, and so on back to LUCA.  For instance, this paper compares the HOX genes (which are fundamental to regulating the body plan) of sharks, various fish, mice, and humans: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC403639/  And then there's what we share with archaea: http://www.sci-news.com/biology/archaeal-chromosomes-07611.html

@jamesqf I think that this is implicit, after all the question could be reframed as "why are the differences between humans so trivial?" That said, I could do a better job making it explicit.


text:
Can the effect of an allele on height be context-dependent?
Some data is available on the effect alleles have on height. For example Common DNA Variants Accurately Rank an Individual of Extreme Height
However after browsing the literature I was not able to easily answer the following.
If we take a genome and allow only one gene to change there is going to be an allele maximizing the genetic potential for height. If we take two different genomes and allow one gene to vary are the optimal alleles going to be the same?
If this can happen then linear polygenic scores cannot fully capture the genotype–phenotype map.

Linearity is an assumption of convenience established by Fisher 1918 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456325/) to make the math easier. There really isn't any biological reason to believe it's true; even the existence of dominance is sufficient to make it obvious that linearity isn't complete. I recommend reading about epistasis (https://www.nature.com/articles/nrg2452). That said, linear predictions yield pretty good predictions under the assumption that most pairs of loci don't interact (also shown by Fisher I believe).

See also e.g. https://pubmed.ncbi.nlm.nih.gov/31761530/. Even if polygenic scores can be used for prediction, they're honestly not doing a very good job! They suck even for highly "heritable" traits, showing the weaknesses of the concept of heritability (but that's a different conversation).

Linearity is an assumption of convenience. In fact, since Fisher himself allowed for the effect of dominance in his 1918 paper, it made the math more complicated, not easier (though it may be easier today in, say, GWASs). The additive model was created based on empirical data to address flaws in the prevailing dominance/epistasis model at the time. There are a number of biological reasons why most alleles are additive; deviations from additivity are very rare.

Polygenic scores are empirically doing an excellent job for prediction; in fact, Alzheimer's disease and height are completely "solved" so to speak (i.e., captured ~all SNP heritability). Heart disease polygenic scores predict better than pre-existing conditions or family history.

Polygenic scores are very good at predicting height.
This figure, from https://arxiv.org/pdf/2101.05870.pdf, predicts height using common SNPs at r = ~0.65.
In a different study, "combined with sex, a polygenic risk score captured 71.1% of the total variance in adult height in the UK Biobank."
As you can see below, polygenic scores are about as good as the height of your parents at predicting your height.

Yet another study found an r^2 of ∼0.82. In fact, this is greater than some heritability estimates of height.

A good starting point is to understand why Fisher used a linear/additive model. It wasn't just due to convenience or to make the math easier, though that may have been a factor. Fisher's model was empirically driven. He observed that some physical human traits, like height, were normally distributed, and then found that his additive model correctly predicted how similar in height relatives would be. In fact, he incorporated dominance into his models in the 1918 paper, allowing for effects of both dominance and additivity at the same time. The additive model was created to address the shortcomings of dominance models, which already existed at the time.
Fisher said in 1930: "The biometrical facts as to the inheritance of stature and other human measurements, though first regarded as incompatible with the Mendelian system, have since been shown to be in complete accordance with it, and to reveal features not easily explicable on any other view. The approximately normal distribution of the measurements themselves may be deduced from the simple supposition that the factors affecting human stature are approximately additive in their effects."
Forgetting Fisher's result that many complex traits are highly polygenic is what ultimately led to the candidate gene era and its frequent failures.
So why is the additive model so predictive? Is it just a quirk of chance?
Not quite. It is inherent to natural selection. Additive effects are more stable across generations, as they do not depend on the particular combinations of alleles an individual has (unlike dominance or epistasis). This stability makes additive effects more consistently "visible" to selection.
Imagine if a gene for having a long neck was dominant in giraffes--it would be impossible to eliminate the recessive allele from the population (aside from genetic drift), as there is no phenotypic difference between heterozygous and homozygous long-neck individuals. Now imagine if there was simultaneously a different, additive pathway to having a long neck. Selection would favor increasing neck length via the additive pathway, as there would be decreased risk of one's offspring having a short neck. In this case, selection inherently favors additivity.
The second reason why additive effects are biologically preferred is due to the fact that mutations happen randomly. By definition, in order for a new dominant interaction to occur, two mutations must happen. If the mutations require each other to be useful, they'd have to occur simultaneously to be selected for. On the other hand, a new additive mutation being selected for only requires that a single new mutation is beneficial.
The third reason why additive effects are predominant is because most allele frequencies are biased towards one extreme or another. Therefore, the remaining genetic variation between individuals is likely to be of small effect and polygenic.
The final counterintuitive reason is because multilocus epistasis itself mostly contributes to additive variance.
As you saw from the paper you cited, very tall people are not tall because of rare dominant mutations, but because they happen to have a very large number of "tall height" alleles.
Yes, if you take a genome and allow only one SNP to change, there is going to be some change which maximizes the genetic potential for height; if you repeat this with two genomes, the allele will probably be the same unless the individual already has that allele or has a different ancestry than the first individual.
I'm not sure how this means that a linear polygenic score would not fully capture the genotype–phenotype relationship. You are completely correct that SNP-based polygenic scores cannot capture the full heritability: they can only capture the SNP-heritability at best. You are correct that it is possible for alleles to be context dependent. If there is a strong GxE component, and you are measuring between environments, a SNP-based polygenic score's accuracy would be attenuated for the trait.
There are other factors besides this that limit SNP heritability and the maximum accuracy of SNP-based polygenic scores, such as:

Rare variants (not yet included in many GWAS or polygenic scores)
Large insertions, deletions, duplications, or rearrangements
Gene-gene interactions (e.g., dominance): though additivity is more common, dominance is still extremely important, especially for certain Mendelian diseases or non-polygenic phenotypes.
Copy number variations

TL;DR:
Your intuition is correct, but for many traits like height, linearity happens to be a good assumption due to biological constraints.
P.S.
Since we all learned about dominance in school, it can be surprising to hear that it is really not that common. For example, Okbay et al. 2022 with N = 2,574,253 found that their "dominance GWAS identifies no genome-wide-significant SNPs. Moreover, with high confidence, we can rule out the existence of any common SNPs whose dominance effects explain more than a negligible fraction of the variance in EA." The "combined variance explained by dominance deviations in common SNPs is negligible."
A different study analyzed 70 complex traits on 254,679 individuals in the UK Biobank. The authors "found strong evidence for additive variance," but negligible dominance variance" and "epistatic variance... not significantly different from zero." "Genetic variance for complex traits is predominantly additive." "Epistatic variance is likely to be extremely small in human complex traits." This replicated a similar earlier result that looked at 79 phenotypes. This was replicated again here with 50 phenotypes. Each time, dominance is negligible.
Hill et al. "evaluate the evidence from empirical studies of genetic variance components and find that additive variance typically accounts for over half, and often close to 100%, of the total genetic variance." This is why Crow states "the breeder's custom of ignoring epistasis usually gives a more accurate prediction than if epistatic variance were included in the formulae."
Keightley shows from a biochemical standpoint that polygenicity alone is sufficient for a lack of dominance effects.
Even after accounting for correlations between alleles (LD), "independent of the type and strength of gene interaction, the epistatic variance contributes little to the total."
Twin studies also support the additive model being predominant, with no effect of dominance for most phenotypes.

source: Stack Exchange

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

sort: votes


text:
Identity of plant bearing a cluster of bulbous, glossy red fruits (Oak Ridges Moraine)

Location: Oak Ridges Moraine, Ontario (Durham Region)
Date: October 4, 2021
Site: Full shade; hillside; sugar bush

This isn't a flower, but the cluster of shiny berries containing the seeds of a flower. My best guess is that it is a Jack-in-the-Pulpit (Arisaema triphyllum), but it's a bit hard to tell from the two leaves, which are both decomposing and at a bad angle to tell for sure. But it's definitely in the Arum family.

Their range includes Eastern US and Ontario.
Named because the flower resembles a preacher in a covered pulpit, the flowers are tiny, and bloom on the spadix (the "Jack") of a mature female. When young, the flowers are male; when sufficiently mature, they become female and can form the berry cluster.
From the site linked above:

Berries (¼ inch across) enclosing one to several seeds, at first green, become bright red as female plants begin to wither in late summer and fall.  Berries remain attached to the dry spadix, resulting in an ovoid mass of showy berries up to 2 inches long which stay on the stem even when stem has dried.  A cluster can consist of up to 150 berries, each with 1 to 3 rounded flat-sided light tan seeds.

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


text:
How big does a landmass have to be in order for biota to not undergo island dwarfism or gigantism?
Somebody asked it here, and the answer was basically "there's no specific size". Still, I'd like to ask if there's an average size to it. Would a Greenland-sized landmass cause elephants to evolve into smaller sizes? (On a side note, were there mammoths in Greenland?)

Please don't add extraneous material to your posts, instead if you have questions about site etiquette please use the [meta] site. However, if you are posting using two separate accounts, you may find this information on merging accounts to be of interest.

I don't know the answer properly, so I welcome other input.
You can probably work this out more or less empirically. Going through the (possibly incomplete??) lists of island gigantics and insular dwarfs you can see a list of which islands they have been found on. Also ignoring the dinosaurs, as we don't properly know the size of islands in those cases
The largest listed is Madagascar and it's about 1/4 (actually 0.275) the size of Greenland at about 587,041 km2 / 226,658 mi2 . It may be that this is about the limit.
Note that this answer relies entirely on the current sizes of the islands, it does NOT take into account previous changes in land area from such things as sea levels raising/lowering. I am almost certain that there will be more to it.

Thanks, but Borneo is larger than Madagascar and its native subspecies of Asian elephant is slightly smaller than the others.

@LordNobody - It wasn't on the list of animals with dwarfism on Wikipedia hence my "(possibly incomplete??)" phrase.

Okay, sorry to miss that.


text:
Why are 6 turns of the Calvin cycle needed to make one molecule of glucose?
I‘ve read that 6 turns of the Calvin cycle are required to make 1 glucose molecule.
But, 3CO2 and 3RuBP are used in one cycle and 6 triose phosphate is produced. Only 5 triose phosphate molecules are required for RuBP regeneration. The remaining 1 triose phosphate has 3 carbon atoms in it. Only 3 more carbon atoms are needed, which can be produced again in the next cycle. So, it would seem that, in total, only 2 cycles are needed to produce 1 glucose molecule. Why do most authors write that six are needed 6?

I still think you should state exactly what you mean by a "turn of the cycle", because that is what your (semantic) argument is about. However, as I don't find the answers so far address that point, I have done so myself. But in future, always, always, always clarify your terms. So much time is wasted by people not being clear what they are arguing about.

You're looking at a version of the Calvin cycle that has been simplified to consider 3 "turns" all together as the steps necessary to produce one 3-carbon product. A hint is that you see three CO2 molecules entering rather than one.
You can look for another diagram that has a one-carbon version, like at https://en.m.wikipedia.org/wiki/Calvin_cycle

(image credit: Mike Jones, CC BY-SA 3.0 https://creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons)
However, arguably this diagram doesn't make clear that 2/3rds of the 3-phosphoglycerate gets recycled back into the Calvin cycle in the abstracted "phase 3".
So yes, you need 2*3 = 6 "turns" of the cycle to make a 6-carbon product. Importantly, though, it's not like there is some singular machine performing this cycle - all the steps are free to proceed on their own independently and simultaneously. The Calvin cycle (and the Krebs cycle in complement) are just the simplification down to the minimum individual reactions.

Please include a diagram in your answer, otherwise only those that already understand will be able to follow. Alternatively, comment and vote to close. The question is similarly incomprehensible.

@David Added; I think the question is pretty clear. Textbooks often say you need "6 runs" through the Calvin cycle to make glucose; this makes a lot of sense because you're taking in one carbon through CO2, so to make a 6-carbon sugar you need to do something 6 times. OP also is looking at a picture showing "3CO2 and 3RuBP is used in one cycle and 6 triose phosphate is produced" - this is equivalent to three runs. That's a handy condensed form because you can consider one "free" triose phosphate to be made per 3 CO2; "free" as in it isn't used up in regenerating the reaction products.

Question and Scope of Answer
The question is about metaphors and semantics relating to the carbon stoichiometry of the reactions producing dihydroxyacetone phosphate from carbon dioxide. I have decided to provide a clarification of the carbon stoichiometry, ignoring hydrogen and oxygen stoichiometry (even though I find the reduction and energetics more interesting). The answer depends on what you consider the  metaphor “turn of the cycle” means in relation to this sequence of reactions, and is of little interest or importance.
‘Answer’
The so-called dark reactions of photosynthesis produce one molecule of glucose (hexose) from six molecules of carbon dioxide in a two step process.

6 CO2 → 1 C6H12O6

In the first step — the so-called Calvin Cycle — three molecules of CO2 are converted to the triose, dihydroxyacetone phosphate (DHAP).

3 CO2 → 1 C3H7O3PO32–

In the second step, similar to the final part of gluconeogenesis, two DHAP molecules are converted to glucose.

2 C3H7O3PO32–  → 1 C6H12O6

The reason the reactions of the Calvin Cycle are considered a metabolic cycle is that one of the intermediates, the pentose ribulose 1,5-bisphosphate (RuBP), is consumed by reaction with CO2 to give two molecules of triose:

1 ribulose 1,5-bisphosphate + 1 CO2 → 2 3-phosphoglycerate

The problem with the epithet cycle in this case is that it differs from the tricarboxylic and urea cycles where a single molecule enters the cycle and is converted to a molecule(s) leaving the cycle in a single series of reactions regenerating the molecule with which the input molecule first reacted. In the Calvin Cycle,  the initial reaction between RuBP and CO2 has to occur three times for the stoichiometric production of one molecule of the triose, DHAP.
Many diagrams that represent the series of reactions as a cycle tend to be stoichiometrically incorrect (or more charitably, ignore carbon stoichiometry to emphasize energetics etc.), rendering the metaphorical expression “turn” of the cycle almost meanless. This is unfortunately the case for the diagrams in two other answers — one molecule of RuBP and one molecule of carbon dioxide clearly cannot generate one molecule of triose DHAP and regenerate the RuBP.
The diagram below from Berg et al. is stoichiometric as it considers the total number of molecules to produce one of DHAP. (The three arrows to the product, Ribulose 5-P, imply three molecules are produced.) I have modified the diagram by de-emphasizing other aspects of the reactions than inputs and outputs.

Conclusion
If you consider (as the anonymous source in the question and many others do) that each time one molecule of RuBP reacts with one molecule of CO2 a “turn of a cycle” is initiated, then six “turns” (or “rounds” à la Berg) are required to produce one molecule of glucose; if you consider each series of reactions that produces one molecule of the triose, DHAP, represents one “turn of a cycle” then two “turns” are required. I personally would avoid the metaphor, state what happens, and concentrate on the more interesting aspects of the process, which are the energetics and reductions using the products of the light reaction.

@user338907 — Thanks. Corrected.

I think you didn't got Calvin cycle properly
For ease of understanding, calvin cycle can be described under three stages; Carboxylation, Reduction, and Regeneration

1.CARBOXYLATION-
It is the fixation of CO2 into stable organic intermediate. it is most crucial step of the calvin cycle where CO2 is utilised for the carboxylation of RuBP. This reation is catalysed by the enzyme RuBP carboxylase which results in the formation of two molecules of 3-PGA.

2.REDUCTION-
These are a series of reactions that lead to formqation of glucose. the steps involve utilisation of 2 molecules of ATP for phosphorylation and 2 of NADPH for reduction per CO2 molecule fixed.The fixation of 6 molecules of CO2 and 6 turns of the cycles are required for the formation of one molecule of glucose.

3.REGENERATION-
Regenration of the CO2 acceptor molecule RuBP is crucial if the cycle is to continue uninterrupted. the regeneration steps require one ATP for phosphorylation to form RuBP...
HERE you see only one molecule of CO2 is being used ... and our product i.e, Glucose is a hexose sugar(6-Carbon)... Therefore, we have to carryout calvin cycle six times...
you can check for cycle on link https://en.wikipedia.org/wiki/Calvin_cycle  ....
HOPE IT HELPS

David, I hope now my answer is complete. Thankyou for your suggestion.

Sorry, but I don't think the diagram addresses the question of carbon stoichiometry, which is what I think the question is about. I have added my own answer now, so I have deleted my previous comments.


text:
Are the terms "provirus" and "prophage" interchangeable?
Regarding the difference between proviruses and prophages, Wikipedia states that "these terms should not be used interchangeably. Unlike prophages, proviruses do not excise themselves from the host genome when the host cell is stressed." However, Khan Academy implies at 3:41 that the two terms are interchangeable. Who is correct?

Over some 15 years in academia and research, I've taken graduate-level virology classes, worked in multiple phage research labs, and attended dozens of seminars on both bacterial and eukaryotic viruses. I can't recall ever seeing or hearing the term "provirus" used until reading this post.
Sometimes different disciplines in biology will use the same or similar terms somewhat differently. There are, in fact, several examples of commonly used terms in biology that have no universally agreed upon definition. However, according to at least one source that I just found on a plant viruses, a "Provirus is a permanent part of host genome," meaning it is not excised before reproduction. This other source uses provirus to describe integrated HIV, which also doesn't need to be excised in order to reproduce. So there may be some consistency of usage here.
Ultimately, meaning in language comes from the intersection of use and understanding in context. Any time you're talking about viruses that infect bacteria and/or archaea, the terms "virus" and "viral" can almost always be replaced with "phage", but don't always have to be, so could be somewhat interchangeable in that context. Whereas, to my knowledge, "phage" is never used in describing eukaryotic viruses.
So, if you said "provirus" in a phage biology lecture, your audience would likely understand it to have the same meaning as prophage, but if you said "prophage" to describe an integrated human retrovirus or retroelement, you'll almost certainly confuse a part of your audience, so not really interchangeable at all in that context.

Since phage are bacterial viruses, every prophage is a provirus, but not all proviruses are prophages. The term "provirus" IS a thing in molecular biology, but as you note is probably much more common in work on retroviruses or eukaryotic genome evolution.

@Armand I agree about prophages being proviruses. One difference being that lysogenic prophages are excised from the host genome before a lytic replication cycle can begin, where retroviruses can generate genomic viral RNA (and infectious virions) while the provirus remains integrated on the host genome. So IF being a PERMENANT part of the host genome was a necessary property of all proviruses, then prophages would not technically be proviruses. But that would seem like a pretty arbitrary distinction to make (imho).


text:
What breaks hydrogen bonds while producing sticky ends using restriction endonucleases?
I am a high school student and I am little confused about the uses of restriction endonucleases. Why do hydrogen bonds(base pairing)
break when restriction endonucleases produce sticky ends? If they only break phosphodiester bond, should hydrogen bonds not break on their own? I searched it on few sites but didn't find any discussion.

Which hydrogen bonds are you referring to? If you're referring to base-pairing in the sticky end section, how many adjacent paired bases do you need to keep the sticky ends "stuck" at physiological temperature or at room temperature?

If you could just provide a certain example/illustration for the bonds which you're referring to, then it may help others to understand what issue you're facing.

I am referring to H bonds in base pairing? you should understand it because there are no other H bonds

The short answer is heat. Compared to the covalent phosphodiester bonds, hydrogen bonds (H-bonds) are very weak, and they're much easier to break and re-form. A long enough piece of double-stranded DNA will stick together at physiological temperature because it contains thousands of highly coordinated hydrogen bonds. But even long pieces of double-stranded DNA can easily be denature into single-stranded DNA by heating them up to ~95°C. The handful of H-bonds on a sticky end will spontaneously disassociate quite easily at the restriction enzyme's optimal temperature (usually ~37°C).
A good way to think about this is to imagine the sticky ends as PCR primers. When I'm planning a PCR reaction, I first need to calculate the melting temperature (Tm) of my primers (the single-stranded oligonucleotides that form duplex DNA on a reverse-complimentary sequence of a strand of template DNA). Tm is the temperature at which half of the duplexed DNA primers will disassociate and become single strands. As the temperature increases above the Tm, an even greater proportion of those primers will disassociate into single-stranded DNA.
If I take EcoR1 as an example, the sticky end sequence is AATT. Just four bases with 2 H-bonds per base, for a total of 8 H-bonds (A-T pairs have two H-bonds, G-C pairs have three). When I plug this sequence into a primer Tm calculator like OligoCalc, I get a Tm of 8°C. Meaning, if you kept this reaction at 8°C, half of your sticky ends would become unstuck. This is why the ligation of sticky ends is often performed at a much cooler temperature than the restriction digestion (either room-temperature, or 4-8°C).

but the temperature/heat will be distributed to all nucleotides i.e kinetic energy of all nucleotides will increase not just those cutted by restriction endonuclease so how can only those get seperated?


text:
What species of snake is this? It was sighted in NE New Mexico, Union County
The snake in this photograph was found injured/dead in Clayton, Union, New Mexico (USA) on 10/06/2021. I want to know if it is a juvenile bullsnake or a Chihuahuan Night Snake...or something altogether different.

Can you mention the length of the snake??

This looks like a western hognose snake (Heterodon nasicus).

 Source: Wikipedia
Notice the OP's yellowish ground color with darker circles and elongated dark elliptic shapes on the head. this mirrors descriptions of H. nasicus, e.g.:

The dorsal ground color is light yellowish-tan to grayish-olive, or even a rich brown. There are a series of dark oval middorsal blotches with smaller ones along the sides. The ventral surface is white to yellowish with masses of dark pigment, sometimes with yellow or orange mixed in. The head is marked with long dark blotches

This is a relatively small snake (<20 inches) that is found from southern Canada to northern Mexico (source).

 Source: MN DNR


text:
For which wing characteristic are Plecoptera (stoneflies) named for?
I'm coming across variable etymological meanings for the order Plecoptera (stoneflies).
Some sources indicate the meaning is "wicker/braided-winged", while others suggest "folded/pleated wing" -- both referencing different characteristics of the wings!

From Wikipedia: "The name "Plecoptera" literally means "braided-wings", from the Ancient Greek plekein (πλέκειν, "to braid") and pteryx (πτέρυξ, "wing"). This refers to the complex venation of their two pairs of wings, which are membranous and fold flat over their backs."

From Dr. John Meyer online Entomology class notes (NCSU): "The name Plecoptera, derived from the Greek "pleco" meaning folded and "ptera" meaning wing, refers to the pleated hind wings which fold under the front wings when the insect is at rest."

I understand that my latter source is much more reliable than Wikipedia, but the prior etymology shows up more frequently from searching.

To confuse things more, Merriam-Webster blends these two etymologies together: "New Latin, from pleco- (from Greek plekein to plait, weave) + -ptera"

I'm trying to create a key of insect orders using their names, but this mismatch in characteristic has stumped me as both seem plausible.

 Source: lesinsectesduquebec.com
Anyone know which of these stands true? (reputable source would be appreciated!)
(I don't really care about the etymology per se; I would like a source indicating the proper origin of the order's name so I know which is accurate)

Unfortunately an incomplete answer, hopefully others can add to this or fill out the details missing.
After a bit of searching, I found the original reference:
Plecoptera was named by Burmeister in 1939. I believe that this was a split of a previous clade, probably the Megaloptera.  The book is available on Google books in the following link: Burmeister 1939 Handbuch der Entomologie: Ordnung Gymnognatha.. The relevant clade can be found on page 863. Unfortunately it is in German and using gothic script, so I can't read it. I will attempt to download the PDF and text recover, then pass through a translator, but as a lot of the terms will be specialist I don't hold out much hope.
Edit: it seems the wing position/folding is discussed on the lower part of page 865 and page 866, but the translation is garbled, so a competent German reader would be needed for proper translation. The following is from the top of page 866:

The consequence of this arrangement is that the rear field of the orthoptere
wing can also be folded lengthways, the o
Sembloden, however, is not capable of such a folding. In br
For the Fåden, however, it will be in a state of rest under the Vorde
field bent, and lies with this and the upper wings horizontally or similar
the body, as in the walking orthopedic; while in i
following guild, with the same dislocation of the wing formation and F
tion, the position at rest is po, as with the jumping
Orthopterics, in which the wings form the body like a dady bebeck
Incidentally, there are also individual cases of orthoptera v
where the back panel cannot be folded, e.g. B. in heterosexuals
mia (p. 488.). With regard to the distribution of the veins in the w
As far as the wings are concerned, it should be noted that both wings fit into it
exactly match, which is again not the 3rd with orthopedic patients
is.

However, most of the references that I could find that talked about the name use the "folded" "plecos" form, if that bears any weight. The ptera bit is certainly "wing" as in Archaeopteryx, which translates to (archaeo) old-wing (pteryx).

Thanks for the effort here. It's not everyday you get a description about an insect that includes dady bebecks and heterosexuals :p. Quite amusing. I'll have to ask a German colleague what they think about all this!

@theforestecologist thanks. I thought it was quite amusing myself. I just downloaded the book and captured the text in base Evince on a Linux system. Then copied and pasted into Google translate. As you can see there is a lot missing or problematic, I suspect malformed characters from the printing and distortion/missing from the scanning. It seems that "dady bebeck" is actually "dach bede(ch?) in the original, so it might mean "where the wings cover you like a roof"

What I most appreciate is that I'd come across Burmeister's name in my own research, but the copy of his 1939 manuscript I found only had ~400 pages instead of the complete version you found. The index itself only went up a few hundred pages! I couldn't figure out why there was no mention of Plecoptera, but clearly your longer version makes all clear. (well, at least clearer! :p). My German colleague actually died last night, so improving the translation just became a bit more difficult on my end. Again, thanks for the upfront research! Let's see if someone can help clean up this translation

@theforestecologist. I'm sorry for your loss.  If it is any help, the volume I linked was edition 2, I think noted as "Bd.2 abt.1", so a revision of the one you (and I) found initially. I think that that first edition was a 1835 one, whereas we needed the 1839. The lack of Plecoptera was what gave away that it was the wrong one.

Ah. Good deal. Thanks, bob1


text:
If brine salt percentage is between 1 and 2 percent, can Clostridium botulinum growth prevail over Lactobacillus acidophilus?
After searching in various websites, I found mostly that Clostridium botulinum doesn't grow easily in a salty environment, and that it needs a pH from 4.6 to up;
as I am lactic fermenting some bell peppers, I searched and found that their pH is between 5.5 to 6.5;
I applied a salt concentration of 1 - 2 % on the solution (brine);
I didn't find a clear answer to whether or not the bacteria can grow in those conditions, only that it isn't likely, and most websites make similar statements, therefore looking for clarification
In an environment of about 20 degrees Celsius, salinity of 1-2%, and pH between 5.5 to 6.5 (bell pepper),
is it possible that Clostridium botulinum could grow and compete with Lactobacillus acidophilus?

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

Also note that a "colony" is the form seen on growth media — I think what you want to know is do they grow? In addition, there are standards for naming of species (including bacteria). 1) The genus (first part of the binomial) is written out in full (the first time it is used) and is always capitalized. 2) The whole name should be italicized. I have fixed these problems, but please do some reading and revise your question accordingly as soon as possible to avoid receiving downvotes — if your question is closed editing your post will also allow you to request it be reopened.


text:
Are the complementary base pairs known as genes?
In my text book ,it is written that a chromosome has 1000s of genes and it is distributed throughout the chromatids except in the centromere. But we know that the chromosomes have DNAs inside them which have complementary base pairs. Then are these base pairs known as genes??

A chromatid is a single hundred of million bases DNA molecules, glued to its complement and a chromosome is two identical copies of that chromatid.  You might want to look at https://www.ncbi.nlm.nih.gov/nuccore/NC_000001.11?from=1000&to=100000 you can see that the region 10875..13410 encodes a gene named DDX11L1 whose sequence is given below. So the genes are those kind of annotated pieces of the chromosome sequence, mainly dedicated to understanding the mRNA whence the proteins that will be produced from it.

what do you think is meant by "complementary base pairs"? Have you researched this term at all?

Don't assume a chromosome to be some X-shaped box that contains DNA inside it and DNA as a container of genes.
DNA, genes, Chromatid, Chromosomes are just different names at different levels of the same thing.
In molecular biology, you'll find multiple definitions of certain terms because as new insights are gained by any researcher, the definition gets modified. So one has to always make their concept clear so that they don't get confused between the same yet uniquely different terms.
So, Let's first look at how different their definitions can be:

DNA is a molecule inside cells that contains the genetic information responsible for the development and function of an organism. DNA molecules allow this information to be passed from one generation to the next. DNA is made up of a double-stranded helix held together by weak hydrogen bonds between purine-pyrimidine nucleotide base pairs: adenine (A) paired with thymine (T), and guanine (G) paired with cytosine (C). Also called deoxyribonucleic acid.

GENE, For many years the HGNC has maintained the definition of a gene as “a DNA segment that contributes to phenotype/function. In the absence of demonstrated function a gene may be characterized by sequence, transcription, or homology”. As there is still no universally agreed alternative we continue to use this definition.

Chromosome is a highly coiled structure of DNA molecule. Often observed in X-shaped only. Along with DNA, some proteins are also make up chromosomes.

But Why does DNA need to be coiled tightly into chromosomes?
DNA double helix is like a telephone wire. If length is to be measured, it will go beyond 60 miles. Some even say it can make a trip to the moon more than 150,000 times. Such a long DNA molecule is not only the part of each organism's cell nucleus but also it's invisible to the naked eye. This happens just because of the high packaging and coiling of this long DNA molecule.
Let's see the diagram to get an idea.
At the bottom  of the diagram there is a sequence of nucleotides (ATGC) in different combinations. This can be considered as a gene if it codes for certain protein which is required for the growth or any other function of the body.
Returning back to your question, Complimentary base pairs are not genes.
Genes are the segments of DNA which is a long sequence of nucleotide base pairs that code for any protein or RNA transcript that contributes to any trait/phenotype/function of an individual.
With the tight packaging of DNA double helix along with help of packaging proteins(Histones and Non-histones), the chromatid and chromosomes are made. The packaging of DNA to chromosomes is highly controlled and is a whole different topic in itself.

Firstly, even in the centromere region, complementary base pairs are found, so, if base pairs were to be known as genes, then genes would also be present in the centromeric region.
Secondly, Genes are functional units of DNA made of one or more codons which store information to make protein which gives an organism a certain characteristics.
Basically, DNA is made of two complementary strands of nitrogenous bases [ Adenine(A), Thymine(T), Guanine(G) and Cytosine(C) ]. Read/ Watch
Now that you know the structure of DNA, realize that information may be stored by the order in which the Nitrogenous bases are placed. Exactly this strategy is used by your cells, to build your body, in other words, you.
I am not writing about the process by which that information is interpreted by your body, since that is beyond the scope of the question, still, you can Read/ Watch about it.


text:
An apple sunk in water, looks fine. What could it mean?
I washed a dozen of apple just now and one of them sunk in water. Also surprisingly I was not able to find an answer via googling, all top results were about why they float.
The smallest one. I don't know the variety name, but AFAIK it is an apple, tastes like an apple. Could a fact that it sunk mean some internal spoilage?

Image Source: Infovisual: Apple
I think that the density of the endocarp is more than the mesocarp, and in that small apple, more amount of endocarp is present than mesocarp, making its average density more than water, thus, making it sink. Vice versa for the bigger apples.

Welcome to Biology.SE! This looks like it might be a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion, which is inappropriate for this site. A good example of how to format references.  Please also provide a reference for the image you used. ——— You may also want to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site.

@tyersome Thank you. I will add supporting references as soon as I find them.


text:
Can deterministic and stochastic models be used to models different parts of the same phenomenon?
A biological phenomenon including two different causally dependent phenomenon occurs in the cell. (Phenomenon2 initiates as a result of phenomenon1). Phenomenon1 and phenomenon2 are linked with feedback loops.
The entire phenomenon is wished to be mathematically modeled. Phenomenon2 is already modeled with a deterministic model including 3 PDEs. Since phenomenon1 and phenomenon2 are linked with feedback loops, they will be connected to mathematically model the phenomenon in its entirety.
Can phenomenon1 be modeled with a stochastic model? If not please explain why.

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

I think that the question requires more clarity, sinc eteh answer depends on which stochastic and deterministic models one talks about. The first thing that comes to mind is that deterministic models are often just the averages of stochastic equations.

I would suggest that the physics StackExchange community (https://physics.stackexchange.com/) might be a better place to get a good answer to this question. It seems that you are interested in the problem of modeling generally rather than a specific biological application, and they have more expertise in that domain.

I’m voting to close this question because it does not appear to be about biology as defined in the [help]. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and [ask] a good question.

@RogerVadim I see, thanks.

@MaximilianPress I think you are right, but sometimes different fields might have different perspectives/tools for the same method or for their analysis. I was curious about the approach of an expert in biological modelling on this question. If there was a biological modelling SE I would put it there. Sorry for inconvenience.

@tyersome I can also delete it, if you prefer. Thanks.

If you also can't see any way to make your question fit here, then yes I think it would be best to delete it. Thanks!


text:
Heterozygous traits with advantages over homozygous traits
I used to believe that there are "good" alleles and "bad" alleles and having two "good" alleles could never be worse than having one "good" and one "bad" allele.
However with sickle sell anemia having one "good" and one "bad" allele confers stronger immunity against malaria (though it can also cause hematuria and other generally undesirable outcomes).
Are there any other examples of this?

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

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

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

This is an example of a rather common phenomenon called overdominance or heterozygote advantage. It can be due to many reasons: the two alleles affecting the same phenotypic trait via different paths, the phenotypic train being due to interaction of many linked alleles, the alleles having multiplicative effect, etc.

The heterozygotes may exhibit increased disease resistence. In case of sickle cell disease, the phenotype is related to the infectivity of plasmodium. In the heterozygotes, the infectious agent is less likely to propogate within red blood cells.
Interestingly, researchers have speculated that other alleles in human may confer disease resistence in the heterozygous condition but are detrimental in the homozygous state.
These include PKU(Phenylketonuria) an inborn error of metabolism, in which the heterozygous fetus may be resistent to miscarriage caused by a fungal toxin(Ochratoxin A), and Tay-Sachs disease, in which the heterozygotes may be resistant to Tuberculosis.
You may refer to given link for more details;
https://www.pbs.org/wgbh/evolution/educators/course/session7/explain_b_pop1.html


text:
What terrestrial trait makes cetaceans so successful in an aquatic lifestyle?
Intuitively, I would expect that an organism that has lived in the ocean for millions of years and can breathe underwater should outcompete any newcomer that is not fully adapted for oceanic life. It makes sense that there may be some semiaquatic animals that can outcompete fish in semiaquatic niches, such as seals, crocodiles, and diving birds. And I could see there being short-term instances of odd species that manage to colonize an isolated area that happens to lack competition.
But dolphins and whales are extremely successful across the globe, have been around for millions of years, and a large part of their niche overlaps with the much older and also hugely successful sharks, yet they manage just fine. A common explanation of this is "intelligence" but sharks are now known to be pretty intelligent, and even if they weren't, why wouldn't they be?
This isn't the first time this has happened, either.  Aquatic reptiles like ichthyosaurs, plesiosaurs, and mosasaurs, and even modern sea turtles, represent hugely prolific and long-lasting groups of air-breathing, fully-aquatic animals (sea turtles come on land to lay eggs, but this seems more like a flaw than an advantage), suggesting that there is something in particular about land-dwelling that gives animals returning to the sea a natural advantage not found in their piscine counterparts.
Is there anything specific about evolving on land - some particular trait that doesn't generally evolve in aquatic animals - that cetaceans retained after returning to the sea, and that makes them particularly successful in the aquatic lifestyle?

Do sharks show evidence of great social intelligence?

@ARogueAnt. It's not as well studied as cetaceans, but numerous studies suggest the answer is yes https://www.wired.com/2016/11/two-way-radios-reveal-mysterious-social-lives-sharks/ https://www.smithsonianmag.com/science-nature/forget-jaws-now-its-brains-48249580/ https://www.sciencedaily.com/releases/2016/10/161004224218.htm

@ARogueAnt. At any rate, it wouldn't answer the question - if you would say "their intelligence or social behavior," the question simply becomes "why are air-breathers more likely to be intelligent or social than water-breathers".

I'd consider https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont both on its own and as a partial answer to those questions ("why are air-breathers more likely to be intelligent or social than water-breathers") as well as in conjunction with the answer by timeskull. Natural selection operates on variability that exists; not every possible trait is expressed in a way that can be selected for in every lineage.

You seem to missing the effect of phylogeny. Cetaceans are mammals — their advantages don't necessarily have a direct connection to them having terrestrial ancestors, but instead are likely to be because they are mammals. Please also note that what makes aquatic reptiles successful may have nothing to do with cetaceans, so I would avoid lumping them together in one question.

Thermoregulation and echolocation both depend on evolutions that occurred on land and seem to be less accessible to fish than to the ancestors of mammals. The heat capacity of water is much greater than air, so maintaining an elevated temperature in body tissues is both more difficult and less necessary. Still, some fish lineages have independently evolved partial thermoregulation. From the article Warm eyes provide superior vision in swordfishes:

In these animals, warming the central nervous system and the eyes is the one common feature of this energetically costly adaptation. In the swordfish (Xiphias gladius), a highly specialized heating system located in an extraocular muscle specifically warms the eyes and brain up to 10 degrees C-15 degrees C above ambient water temperatures.

Depending on diving depth, temporal resolution can be more than ten times greater in these fishes than in fishes with eyes at the same temperature as the surrounding water. The enhanced temporal resolution allowed by heated eyes provides warm-blooded and highly visual oceanic predators, such as swordfishes, tunas, and sharks, with a crucial advantage over their agile, cold-blooded prey.

Echolocation in mammals is possible due to the mammalian ear, which is summarized in a previous answer. From Ultrasonic hearing and echolocation in the earliest toothed whales:

The advent of echolocation is thought to be a key innovation that supported exploitation of a vast pelagic biomass—vertically migrating organisms, especially cephalopods—and explosive diversification of odontocetes

We are starting a Bioacoustics Stack Exchange for people interested in the studies of non-human animal sounds and the impacts of sounds on animals. Please join us! https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

Advantages of air breathing over gills? Keeping in mind water-breathing animals could still evolve lungs.
Not being vulnerable to parasites and diseases of the gills, which are obliged to have blood supply close to the water.
Able to colonise water regardless of salinity, able to survive warm water.

Should I answer if I don’t “have citations from a reputable source”?

Air is 20% oxygen. Water at best is 0.01% oxygen. That is a lot more energy to ventilate gills than lungs (ram ventilation still costs energy in the form of extra drag). Also, you can't burn a fire underwater: body heat gets lost in the gills, and the only way large fish keep warm is counter-current heat exchangers and it still isn't as good as lungs.
But unless you are forced to breath air (life on land) evolution isn't innovative enough to develop lungs on it's own.


text:
For a biological AND Gate to work, do the two inputs need to arrive at the same time?
I understand that AND gates require the two inputs to be present for the output to be produced. However, if one input arrives faster than the other input does the output still get produced?  For example, consider the split T7 RNAP Expression System, where one input produces the T7 N-term and the second input produces the T7 C-term and both join to produce the output. So both need to be present to produce the output. If input 1 occurred first than the second input, will the output be 0 or can the N-term wait until the C-term is produced.
Thanks

It depends on what physical/biologic/informatic realization of a gate you are talking about. I suggest that you explain more clearly what you are talking about - as is, there is too much hidden information (known only to you) in your question.

It sounds like you are thinking about this like a programmer rather than a hardware or wetware engineer.

An AND instruction in a computer program is evaluated at a particular time, and only the values at that instant matter. Thus, the concept of a value "arriving" can makes sense and one would need to worry about times of arrival.
An AND gate (whether biological, electrical, or other) operates continuously, and is always producing a signal based on what its input levels were in the recent past, with the time delay dependent on its implementation.  Thus, signals do not so much "arrive" as simply change between high and low levels at particular times.

Thus, when one input goes high before the other, the gate is not yet activated, but there is not reason for it not to activate when the other goes high as well, as long as the first signal hasn't dropped to be low again in the mean time.
Now, with a biological system such as this one, it can also get messy because the high and low levels may not be cleanly separated and there may be significant leakage when only one is high.  In the case of the particular system that you are interested in, it looks like there's significant leakage for many of the configurations, so in many cases the second signal need not even arrive for the system to be at least partially on.


text:
What determines whether a trait brought out through sexual selection is transmitted only to offspring of the same sex or of both sexes?
First of all, let me apologize for my amateurishness. I have no background in biology. Please bear with me.
My question relates to sexual selection, or specifically its most prominent manifestations:

competition among males which is resolved through male conflict
competition among males which is resolved through female decision

Let us postulate the traits that these two forms of selection might bring about, e.g., strength for the former case and attractiveness for the latter. Of course this may vary. Would I be right to say that whether this trait is passed on through the Y chromosome or whether is it passed on somewhere else (and therefore to both male and female offspring) is a question of probability? If so, what do the odds look like?
The aim of my question is really to understand how selection among men has changed the human species in general. It is well-known that aggression, charm, and paternal care are some traits that have evolved among men. But how would we go about measuring the impact of this selection upon the gene pool of the entire species?
Lastly, is there any literature based on evolutionary research that concerns my question in particular?

check out Monoamine Oxidase 1 (MOA1) gene. Very complex question to answer, there are a huge number of factors including things like hormone expression.

Whoops - MAO gene - apparently called MAOA, not sure where I got the 1 from.


text:
What is the difference between cuboidal and columnar epithelium (other than their shape)?
The difference between squamous and cuboidal/columnar epithelium is clear. Squamous is used for filtration and diffusion while cuboidal/columnar is used for absorption and secretion.
But if both of them are used for absorption and secretion, what is the difference? Why would there be two different tissues that have the same function?

I hope this helps..https://pediaa.com/what-is-the-difference-between-cuboidal-and-columnar-cells/. If you still face any issues, let me know I'll give a detailed answer.

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


text:
Contradiction between random molecular collisions and regulated cellular processes
A cell is a chemical system, consisting of billions of molecules, ions, and atoms. These chemical species are constantly engaged in chemical reactions.
Physics gives the impression that chemical species concentrated in a tiny space, such as a cell, are randomly moving and colliding into one another. Any chemical reaction can occur only if the correct reactants collide with one another and get transformed into a raft of products, under exergonic conditions.
It appears that motions and reactions for biochemicals inside a cell are random and unpredictable. However, cell biology is all about highly regulated and coordinated cellular processes, including transcription, translation, vesicular transport, replication, gene regulation, and so on.
Since each of these cellular processes relies on specific biochemicals to undergo correct chemical reactions, it now appears chemical reactions inside a cell are much more predictable and controlled than what physics might suggest, and so are motions of biochemicals.
How do I reconcile these conflicting ideas about the nature of cells?

Short but relevant: https://biology.stackexchange.com/a/104417/59521

"Random" quantum events don't look so random at the chemistry resolution. I think you are conflating the colloquial concept of random to a very special definition of random used by quantumn physticists. Holistic medicine practioners do a similar thing with the special term "energy".

I’m voting to close this question because it makes an assumptions about randomness that are not necessarily true.

Short answer: Unlike the physical model you're describing above, the reality is that localisation of biomolecules in the cell isn't a passive process, instead molecules are actively concentrated where they're required to be by a variety of different mechanisms.
long answer: I think possible 'missing pieces' of this picture which may help you reconcile these ideas are compartmentalisation and intracellular localisation, which extends beyond just the nucleus and membrane-bound organelles.
It's often the case that the constituents required for biochemical reactions are concentrated locally in compartments which facilitate the "collision" of relevant components to progress the reaction. Some examples would include liquid-liquid phase separated compartments or membrane-less organelles (https://www.sciencedirect.com/science/article/pii/S0960982217311090 and https://www.frontiersin.org/articles/10.3389/fmolb.2019.00021/full are some good overviews).
Scaffold proteins also help in this regard (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117218/)
Another example would be the idea of spatially localised transcription hubs where all of the components required for gene regulation and transcription are located in proximity (https://www.scienceopen.com/document_file/6fe11e52-baf9-4ee7-97be-72f3444d1e04/PubMedCentral/6fe11e52-baf9-4ee7-97be-72f3444d1e04.pdf). A specific example would be nuclear speckles (https://academic.oup.com/nar/article/45/18/10350/4101253).
In terms of intracellular signalling it's often the case that molecules involved in cascades are localised in close proximity at the cell membrane (https://pubmed.ncbi.nlm.nih.gov/16467194/). Receptors which sit at the cell membrane but act as transcription factors when active (e.g. nuclear hormone receptors) are actively imported into the nucleus on activation and other signalling molecules are similarly trafficked in an active, directed process (https://cellandbioscience.biomedcentral.com/articles/10.1186/2045-3701-2-13).
Ultimately, most biochemical processes are compartmentalised or otherwise localised through diverse but active mechanisms to facilitate life, as opposed to molecules floating and randomly bumping into each other as you get in a cell-free solution.


text:
How is a thickening of grey matter possible?
There are plenty of studies that document grey matter thickening in certain brain areas as a result of meditation or exercise. However, it's often said that the extent of neurogenesis outside of the hippocampus is negligible. So can certain activities promote significant neurogenesis in the adult brain or can grey matter thickening be explained through other mechanisms (e.g. cell migration)?
An excerpt from Wikipedia article on grey matter:

Grey matter (or gray matter) is a major component of the central nervous system, consisting of neuronal cell bodies, neuropil (dendrites and unmyelinated axons), glial cells (astrocytes and oligodendrocytes), synapses, and capillaries. Grey matter is distinguished from white matter in that it contains numerous cell bodies and relatively few myelinated axons, while white matter contains relatively few cell bodies and is composed chiefly of long-range myelinated axons.

Sources:
Meditation-related increase in grey matter:

https://pubmed.ncbi.nlm.nih.gov/27983555/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004979/

Grey matter increase in response to exercise:

https://academic.oup.com/biomedgerontology/article/61/11/1166/630432

Except in three specific areas (olfactory bulb, dentate gyrus, SVZ) where neurogenesis continues to occur in adult organisms, it is virtually absent from everywhere else, including the cortex. However, there have been many reports that the grey matter of the cortex, i.e. the zone where cell bodies and their processes reside, can enlarge. Cortical expansion has been linked with changes in dendritic branching, neuronal soma size, synapse size, the number of dendritic spines, and the number of glial cells.
References
- Diamond MC, Krech D, Rosenzweig MR. The effects of an enriched environment on the histology of the rat cerebral cortex. J Comp Neurol. 1964;123(1):111 119.
- Diamond MC, Law F, Rhodes H, et al. Increases in cortical depth and glia numbers in rats subjected to enriched environment. J Comp Neurol. 1966;128(1):117 126.
- Diamond MC, Lindner B, Raymond A. Extensive cortical depth measurements and neuron size increases in the cortex of environmentally enriched rats. J Comp Neurol. 1967;131(3):357 364.
- Holloway RL. Dendritic branching: some preliminary results of training and complexity in rat visual cortex.
Brain Res. 1966;2(4):393 396.
- Volkmar FR, Greenough WT. Rearing complexity affects branching of dendrites in the visual cortex of the rat.
Science. 1972;176(4042):1445 1447.
- Greenough WT, Volkmar FR. Pattern of dendritic branching in occipital cortex of rats reared in complex environments. Exp Neurol. 1973;40(2):491 504.
- Uylings HB, Kuypers K, Diamond MC, Veltman WA. Effects of differential environments on plasticity of dendrites of cortical pyramidal neurons in adult rats. Exp Neurol. 1978;62(3):658 677.
- Mollgaard K, Diamond MC, Bennett EL, Rosenzweig MR, Lindner B. Quantitative synaptic changes with differential experience in rat brain. Int J Neurosci. 1971;2(3):113 127.
- West RW, Greenough WT. Effect of environmental complexity on cortical synapses of rats: preliminary results. Behav Biol. 1972;7(2):279 284.
- Altman J, Das GD. Autoradiographic examination of the effects of enriched environment on the rate of glial multiplication in the adult rat brain. Nature. 1964;204(4964):1161 1163.

So, do you think that neuronal migration from the SVZ is unlikely?

I think you could adapt this answer slightly to make it more directly answer the OP's question about gray matter volume. That is, 1) cortical gray matter is not only cell bodies, a Ramon y Cajal drawing would be a good starting point, and  2) that no migration or new cell birth is necessary for gray matter to thicken.


text:
If the AraC protein was a gene repressor when it binds arabinose, would there be high or low transcription levels when arabinose is present?
If the AraC protein were to function as a gene repressor when it binds arabinose, would there be high or low transcription levels when arabinose is present?

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, your question isn't clear and shows no evidence of prior research. Unclear because you haven't specified what gene(s) you are interested in. Under researched because you haven't said where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please note that both of these are considered to be reasons for down-voting and closure on this site.

A repressor inhibits transcription, thus one expects low transcription when the repressor is present.
Thus, if a protein acts as a repressor when it binds arabinose, then when arabinose is present the protein will inhibit transcription.
In the typical synthetic case of AraC and pBAD, AraC+arabinose does not act like a repressor, but an activator of pBAD.  There are some awfully big caveats there, however:

If "high" and "low" transcription levels are not well-defined, you might find yourself be dealing with a different phenomenon entirely.
If you change the promoter or the genetic or environmental context, you may get different effects, up to and including changing the regulatory relationship.
Transcription is also affected by other things, and so if AraC is also affecting other things in the cell, the apparent affect might be inverted as well.

Bottom line: you need to actually define the system better in order to predict the effects.


text:
What is a downstream target?
For example, in a systems biology analysis, what is a "downstream target" and why are these significant in pathway analyses?
I have looked for answers on Google, DuckDuckGo, Wikipedia, etc. but I have not seen a clear definition that explains what it is.
My guess is:
For downstream targets, these are targets (e.g., a protein) that are affected by upstream targets (e.g., another protein) in some kind of pathway (e.g., some pathway related to cancer). It is called a downstream target because it is used to signify where it is in the pathway (located downwards in the pathway) and that it's being affected by something, as opposed to them affecting something (which would make it upstream target)?

Welcome to the site, please visit the [help] and take a [tour]. In particular take a look at the homework page of the help. Because we get a lot of homework questions on here, we have a high standard for helping before you will get an answer. Most of the help requires that you demonstrate that you have done some research to try and find the answers first. As a start, look up the definition of canonical - ignore the definitions that talk about religion...

Is there a particular instance or area of research you're applying this to? You use the cancer tag and molecular biology tag, is it some related field?

I found this via google ("systems biology upstream downstream"), i believe it is the answer to your question: https://en.wikipedia.org/wiki/Upstream_and_downstream_(transduction). It is not a great page as these things go, but it gets the gist that downstream is "stuff affected by the entity in question".

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

Do not vandalize your posts. By posting on this site, you've irrevocably granted the Stack Exchange network the right to distribute that content under the CC BY-SA 4.0 license for as long as it sees fit to do so. For alternatives to deletion, see: I've thought better of my question; can I delete it?

It's mostly just a flowery extra word in there when you also have the word "target".
If you imagine a signalling pathway as a river/stream, then you have some parts of the pathway that are toward the beginning of the river, and you have some that are towards the end of the river, but up/downstream really all depends on where on the river your reference point is. Targets are pretty much always going to be downstream by definition, though, unless you're talking about a feedback loop where two parts of a pathway are connected bidirectionally.
I don't think it makes much sense to have a "definition" for "downstream target" any more than you have a definition for most pairs of adjective-noun; there's no special extra meaning here besides the stream metaphor.
As far as importantance, well, nothing in biology really does anything by itself: everything acts on something else. For a protein or other molecule in a signalling pathway, you can understand the significance of that entity in the pathway only by what other entities it affects.

@luuuna If someone refers to an upstream target, probably something else is doing the targeting.

@luuuna I'm going to let you just think on this. I'd highly recommend working on being more wholistic in your thinking. Knowing these answers really isn't going to teach you any biology.

@luuuna I mean to think less about this narrow question you have and more about everything else going on. Understand what's actually happening and what's important from that, not what these particular words mean just because someone else indicated that's important.


text:
Is Acetyl-CoA ever transported out of the cell, and in that case how?
Acetyl-CoA is sometimes formed as a result of protein katabolism. Certain cells (in the muscle for instance) can't use Acetyl-CoA to synthesize fatty acid. If there is no immediate need for energy, can the Acetyl-CoA then be exported out of the cell, so that it may be used for fatty acid synthesis in other tissues?
If so, how is this accomplished? I know Acetyl-CoA can be transported out of the mitochondria using the citrate shuttle, but how would it pass the cell membrane and get transported in the blood?


text:
Identification of butterfly from its caterpillar stage
Today I visited Bannerghatta national park's butterfly park situated in Bengaluru, Karnataka, India.
I snapped a picture of a caterpillar in butterfly park.
I inquired to caretakers over there for the identification of the caterpillar. However, They were confused and didn't give me any answer.
I tried searching with the google lens application, however, it shows parasitism and not caterpillar identification.
Please help me identify this cute caterpillar.
Below is the picture I took.

Euploea Core.
Pupates into common crow butterfly. (Aka. common Indian crow, common Australian crow, oleander butterfly (link to caterpillar)).
A common butterfly with (according to Wikipedia) 15 subspecies identified, prevalent in south Asia, and Australia - the adult is distasteful to birds as the caterpillar feeds on latex-bearing plants.
The exact mixture of colours in the caterpillar stage will depend on the diet.
It has a neat trick when attacked, it shams death and oozes a sticky fluid which when ingested by birds make them vomit they find it so distasteful. The butterfly will then "miraculously recover" and fly off, with the bird having learned to avoid that type.
Unable to post images at the moment, so put links instead.


text:
Medical Physiology
I've come across the topic of the influence of inhaled ammonia (caustic ammonia) on breathing rate and some cardiovascular changes. All of this stuff is thought to be mediated through the fifth cranial nerve (CNV). I found some articles about:
(1) https://www.ncbi.nlm.nih.gov/books/NBK11036/
(2) https://journals.physiology.org/doi/abs/10.1152/ajplegacy.1928.87.2.319
but the key point here is the scheme of reflex. Are there any articles or textbooks, that contain an explanation of such phenomena from a neurophysiological point of view? Thanks.

Possibly better suited to medical science stack.

Please [edit] your post to have a descriptive title that includes your actual question, not an extremely broad category.


text:
What are these bugs wiggling white fluffy hats?
Seen yesterday (October 10) in Southern Ontario (near Muskoka), near a lake. Maybe 0.5cm in size or so, during the afternoon.
Hundreds of these little bugs seem to be holding or attached to a curly white piece of fluff each and swinging them back and forth wildly.
What are these? And what are they doing?
Video: https://i.imgur.com/t7kWyKr.mp4
Image (image sucks, please see video):

My research suggests the Woolly Aphid or the Beech Blight Aphid

I am not very particular but I think they are Beech blight aphid(Grylloprociphilus imbricator)
Beech blight aphid is a small insect in the order Hemiptera.The aphids form dense colonies on small branches and underside of leaves.
You can get more info https://en.wikipedia.org/wiki/Beech_blight_aphid


text:
What reference genome was used to bootstrap the human genome?
As I understand it, when we map a genome, the process is much more complicated than say copying text out of a book.  The genetic sequence cannot be copied from a genetic sample in a single pass, so instead the sequence is split into many very small sub sequences called reads.  These reads are then assembled into the complete genome using De Bruijn graphs.  To accelerate this process, a reference genome is used to help figure out which subsequences connect to each other.
In the case of the human genome project, obviously no reference human genome existed.  Was some reference genome used?  If so, what was the reference genome?  If not, how were they able to assemble the human genome?
Based on my reading, constructing the final assembly from a De Bruijn graph is NP-Hard.  So, doing the assembly from scratch seems completely intractable.  The human genome is 3,000,000,000 letters, and an individual read is about 300 letters.  This means there are at least 30,000,000 subsequences, and probably many more than that given how redundant the sequencing process is.  NP-hard problems tend to become completely intractable with problem sizes in the hundreds, and this problem size is in the millions if not billions.  That's why it seems essential that the assembly process used some sort of reference to greatly speed things up, but some googling around hasn't identified the reference used.

This seems like it might be more suited to the [HSM.SE] site. The short answer is that the chromosomes aren't one single "string", but 23 separate strings. In addition, IIRC the problem was further simplified by doing (possibly multiple rounds of) sub-cloning. Have you tried searching for something like "history of human genome sequencing project" — I'm certain that you would find as much detail as you want.

The technology that you are speaking about isthe next generation sequencing, which is not the one that was used in the first human genome project. Also, de novo genome assembly (e.g., with de brujin graphs) and genome mapping are different things - the former is done when the reference sequence is not available. Not sure what the OP means by bootstrapping...

Note that, while we have a "complete" human genome, it is not an ungapped genome. Telomere-to-telomere assembly has only been completed for the human X chromosome and chromosome 8, I believe. The unresolved gaps are caused by regions that are hard to assemble like segmental duplications, ribosomal rRNA gene arrays, and satellite arrays. These gaps can only be closed by careful long-read sequencing.

The process that you describe is true in some cases for the problem of shotgun genome assembly, but it does not describe the strategy taken by the HGP. This resource may prove helpful for understanding how a highly iterative procedure leveraging information from many disparate sources (sub-assembly, BACs, physical mapping) was used by HGP to get around the computational issues: https://www.nature.com/scitable/topicpage/dna-sequencing-technologies-key-to-the-human-828/


text:
How is RNA content distributed in daughter cells during cell division?
During cell division, DNA becomes equally distributed between the daughter cells. But how is RNA content distributed in the daughter cells?

I think you will have to be more specific with your question. Are you referring to some specific organism or cell type? Symmetric or asymmetric cell division? Are you interested in specific examples of uneven RNA distribution, or how RNA is generally distributed? My guess is that most RNA is equally distributed between daughter cells, but there are definitely examples of the opposite. ASH1 mRNA in budding yeast, for example.

RNA is either swimming in the cytosol or be associated with the ER (endoplasmatic reticule) during co-translational protein import into the ER (see secretory pathway).
So in order to answer your question: Daughter cells inherit their RNA simply by chance as cytokinesis just cuts the mother in half and each RNA finds itself on either side, OR they are separated just like the ER.
Each cell 'should' have the same copy number of each RNA, but since daughter cells simply produce RNA all the time, there is no need to be as precise as with chromosomes.
However, there are some specialized motor protein complexes that transport specific RNAs to one (like myo4d transporting RNA along actin filaments). This is called 'asymmetric division'. Please start your research here.


text:
Which of dB or dBA are more useful for predicting damage to hearing?
With no information about noise other than its loudness measured in decibels or in A-weighted decibels, which can be used to more accurately predict how much hearing damage may be caused?
Even though dBA is more accurate for how loud something sounds to humans, that doesn't give me any confidence to say that that also means our ears are under more mechanical/physical trauma.


text:
Virus culture in artificial/synthetic medium
I am looking for a publication/paper in a well a circulated magazine/journal/government study on growing virus culture in synthetic or artificial medium. I have found this link on SARS Cov 2 being cultured in  artificial saliva, but are there any sources handy?
https://www.tandfonline.com/doi/full/10.1080/22221751.2020.1777906?scroll=top&needAccess=true
Thanks a lot!

What exactly are you looking for? What is your "goal"? The linked paper is not "culturing" viruses in artificial saliva, but rather looking at viral survival (aka decay rate) in that medium.

In the linked study they didn't grow it in artificial saliva or artificial culture medium (DMEM) - it was grown in cells (as viruses need to be) and then aerosolized for stability testing in the saliva or medium.  In some manner all media used for growing any cells and viruses are artificial - we make and purify compounds that are then mixed to make the final solution. The exact compositions of these solutions are not found in nature at all, but were derived experimentally by cell culture researchers.

Thanks for responding. Apologies, I should have gone through the whole article. The other day I was having a discussion with a colleague (also a buddy from college) on whether viruses can be cultured outside living cells i.e in a synthetic or artificial medium, under the right stimulation. Is it possible? (We were discussing on some vector vaccine)


text:
Grasshopper vs Tarantula?
This past weekend (October 2021) while hiking west of the VLA in New Mexico (near Datil, NM, ~2200m elevation) my wife and I came across a strange sight. A small (5cm long), likely immature, Aphonopelma peloncillo walking near the trail. That was not particularly unusual this time of year. However, as it moved we noticed that it was being followed by a grasshopper, which was roughly as long as the small tarantula. While the tarantula was still, the grasshopper would walk (not hop) up behind it, the tarantula would notice and skitter forward 10-15 cm, and the process repeated itself over a distance of a meter or so. Several times it appeared that the grasshopper made to attack the rear end of the tarantula. Eventually the tarantula said enough is enough and skittered out of sight rapidly. The scene was mesmerizing enough that neither of us got out our phones to take pictures (sigh).
Based on pictures at insectidentification.org and Wikipedia and going by memory (stupid - no pictures), the grasshopper was likely a Differential grasshopper, Melanoplus differentialis. The size (females up to 5 cm) and territory fit. Sources given indicate they eats plants. Given the season it seems unlikely to me that, were they female, they would still be laying eggs - one of the few reasons I can think of they would try to drive off a tarantula.
Is this a known behavior for a grasshopper? Was it protecting territory (do grasshoppers even have territory)? It is hard to imagine that the grasshopper was attempting to prey on the tarantula. Any information (journal articles welcome - I've searched on Web of Science with no success) available?

Welcome to Biology.SE. Interesting question — is there any chance you could provide more details about the grasshopper? Knowing what species it was could help with you getting a better answer. I do know that some species of grasshopper are omnivorous, but I don't know whether they've ever been reported to attack spiders (let alone a tarantula).

What an interesting observation! Perhaps it was a kind of carnivorous orthopteran? I would suggest using BugGuide's Browse tab to narrow down candidates, and check the Data tab for any likely taxon to make sure it is found in New Mexico.


text:
If stomata is closed at night ,how does exchange of oxygen take place at night?
In this article in the second paragraph, it is written that the stomata remains closed at night to reduce water loss. We know that the plants respire and take in oxygen at night. Then how do plants take in oxygen i.e. respiration takes place at night?
Again in this article, it is written that the oxygen during respiration is taken through stomata. Which is correct ??

What does the bar-graph in the first article show about the gaseous exchange at the "closed" stomata?

I can't see where it's written ''closed at night to prevent water loss''? Article is very clear, that stomata closes due to extreme conditions faced by plants. suggest to read it again.

It's clearly written " In leaves, they typically open during the day to favor CO2 diffusion when light is available for photosynthesis, and close at night to limit transpiration and save water". Please read the second paragraph's second line properly..

I recommend looking at figure 1 here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4940480/. Plants don't run out of O2 overnight, they can store it!

Apart from what's written in the article, stomata typically close at night as there's no sunlight so no photosynthesis. Respiration however continues 24/7 but the rates vary. During the night, the rate of respiration drops since stomata are closed. But it never drops to 0. Respiration still happens as oxygen exchange can still be done through the following three routes:
. Direct diffusion of oxygen through the waxy cuticle in minute amounts
. There are small pores in the stem region called lenticels which allow the exchange of oxygen
. Some small open spaces left in the stomata even after the closure of stomata
Here's a link for reference: https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_Biology_(Kimball)/16%3A_The_Anatomy_and_Physiology_of_Plants/16.02%3A_Plant_Physiology/16.2D%3A_Gas_Exchange_in_Plants#:~:text=the%20plasma%20membrane.-,Leaves,stomata%20(singular%20%3D%20stoma).&text=Normally%20stomata%20open%20when%20the,and%20close%20during%20the%20night.
Hope it helps.


text:
What bug has similar legs to a prawn?
This is a bug that I observe in Melbourne.
This bug is living in wet places and jumping a few centimeters while its length is 8.5mm.
It does not have insect legs. It's legs are more similar to prawn.
Sorry my camera cannot capture a better picture as the bug is too small.

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

It is "Lawn Shrimp", an Australian indigenous creature. It is harmless.

Hello ar, welcome to Biology. This answer is very brief and adds little beyond what another answer has already stated except an additional nickname of the species and a great (but redundant) picture. Please refer to our [help] for guidance on how to answer questions. Enjoy the site.

@ARogueAnt., I wonder why you call this answer redundant when the previous answer does not specify the type of the creature. It only refers to the family of it. I see no "lawn shrimp" in the answer above.

Whilst the picture you've supplied appears to belong to the same family as the other answer, lawn shrimp usually refers to Arcitalitrus sylvaticus which is quite a bit smaller than the size specified in the question (and a different colour, but that may not matter). --Unless I've misread or misunderstood the descriptions.

@ARogueAnt., I have no better photo. I removed it.

This is a "sand hopper" (Talitridae), also known as "land hoppers" or "sand fleas". The Talitridae are a cosmopolitan family of arthropods, known for their hopping behaviour when disturbed.
Which of the genera it is from would be impossible to determine without detailed close-up pictures and a bit of expert knowledge which is well outside my expertise.