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How exactly do mutations cause genetic variation in bilaterians?
I am trying to understand how mutations cause genetic variance, and I'm stuck on one issue that I'm going to try my best to explain.
(I am specifically talking about mutations that cause a phenotypical change). The question is focused on organisms with a distinct germ-line.
My issue is with trying to understand where mutations need to occur to cause variation. For example, does the mutation need to occur in the DNA of either the specific sperm or the specific egg that gave rise to you?
The body of an organism obviously has a vast, vast number of cells. If a mutation occurred in just one of these cells, then surely it wouldn't have any phenotypical effect. Even as an infant or an embryo, if a mutation occurs in just one of your many cells, that is unlikely to cause any phenotypical changes (phenotypical variance) as your body develops. So, is the only way for a mutation to have a phenotypical effect is for it to occur in the gametes that produced you? That way, all of your DNA would inherit the mutation, since all of your DNA would be replicated from the DNA of the sperm and egg.

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

In addition, I encourage you to think about cancer — are you sure you want to claim that "if a mutation occurs in just one of your many cells, that is unlikely to cause any phenotypical changes (phenotypical variance) as your body develops"?

I actually think this a reasonable question because, although the answer may appear obvious (and the poster argues for it on the basis of logic) my own impression is that it seems to be rarely emphasised in texts. So I can understand the poster wondering why.

The phrase you should look for to understand this is "germline mutation".  Also look up "germ cells", which are handled with kid gloves, so to speak, to avoid mutation as much as possible.

@David — I still feel like the question is under-researched (and that the logic in what is now the final paragraph is dubious). However, in light of Bryan's answer and your feeling that it is of value, I have withdrawn my close vote and made edits. If you have a chance I'd appreciate your checking to make sure I've actually improved the question ...

For example, does the mutation need to occur in the DNA of either the specific sperm or the specific egg that gave rise to you?

To give rise to heritable genetic variation in the sense that it's a mutation that exists in all of your cells and is transmitted (with some probability) to your offspring, yes, it must come from the gametes, with the caveat that it need not occur specifically in the gamete, but in any of the cells giving rise to that gamete in either parent. I suppose it could also occur in the fertilized egg cell, and mutations shortly thereafter may produce a chimera where a substantial fraction, but not all cells carry that mutation, but as mutations are most common during cell division I think it's okay to simplify a bit and presume the source is the gametes for most heritable mutations.
Estimates of how many of these mutations exist per human fertilized egg (relative to their parent genomes) vary, but you can assume that each human has something on the order of dozens in coding regions that their parents lack, plus others in other areas of the genome. A whole human organism has far, far more mutations, and these cause issues with aging and cancer in their cells, but these are not typically heritable.
The number of mutations per replication depends on genome size and also the stringency of that organism's replication machinery. In general, complex eukaryotes have stronger systems for correcting replication errors, so you can expect bacteria to have higher rates of mutation. Some related reading:
Correlation between genome size and mutation rate?
How much variation in mutation rate in there in the human genome?
Bacterial division and mutation rate
Mutation rate in viruses
Veltman, J. A., & Brunner, H. G. (2012). De novo mutations in human genetic disease. Nature Reviews Genetics, 13(8), 565-575.

Each generation (per individual), approximately 74 de novo single-nucleotide variants (SNVs), three novel indels (small insertions or deletions) and 0.02 larger copy number variants (CNVs) arise in our genome

Ségurel, L., Wyman, M. J., & Przeworski, M. (2014). Determinants of mutation rate variation in the human germline. Annu Rev Genomics Hum Genet, 15(1), 47-70.


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Data on number of viral replication cycles and their duration doesn't seem to agree with observed duration of infection
I'm trying to model SARS-CoV-2 disease progression in individuals (and have very little background in biology).
At first glance, data from the literature on the duration and number of replication cycles that the virus undergoes over the course of a characteristic infection and the observed real world data on duration of an infection seem contradictory.
In The total number and mass of SARS-CoV-2 virions it was estimated that the virus undergoes 3-7 replication cycles over the course of a typical infection, and in SARS-CoV-2 by the numbers the duration of a replication cycle was taken to be 10hrs.
From this I would expect an infection to last 30-70 hrs (plus the time for the last virions to die out) which roughly is at most 4 days.
However, the median time from onset to clinical recovery for mild cases is around 2 weeks. In more severe cases it can take the patient up to 6 weeks to recover.
What causes this discrepancy?
Is it that symptoms are (partly) caused by our immune system's response to the infection, not directly by the virus itself?
In severe cases lasting up to 6 weeks, would one still expect only 3-7 replication cycles?

The estimates you refer to seem to be of the "Fermi problem" variety - that is, these are "order of magnitude"-style estimates.
There's also the issue that they are talking about "typical" cases, whereas it seems you are talking about more extreme cases. I'm not sure where your estimate of "median time from onset to clinical recovery for mild cases is around 2 weeks" comes from but I suspect you may be referring to something based on hospitalized cases or something similar; the vast majority of COVID-19 cases do not involve hospitalization. There's also no reason to expect that time course of symptoms, which primarily involve activation of the immune system, need relate closely to the time course of viral presence.
In summary, though, when you are doing Fermi estimation, at the very most precise you might expect your estimate to be off by an order of magnitude. That means that, for this type of approach, 4 days and 40 days are the same number. In the first paper you link, note the precision of some of the numbers they are using to estimate:

~10–100 infectious units per cell

3×105–3×108 infectious units produced

You can't expect to get more precise when you're starting with estimates that vary over 1-3 orders of magnitude.

very helpful, thank you for your answer!

This is a great answer, and I think this point is key: There's also no reason to expect that time course of symptoms, which primarily involve activation of the immune system, need relate closely to the time course of viral presence. The period of immune activation does not necessarily stop when the offending pathogen is cleared.

@acvill This is so interesting - so you can be really sick despite your viral load being virtually nonexistent? What exactly is going on in the body? One guess would be that it has to recover from the lung tissue scarring caused by the virus

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snRNAseq vs scRNAseq in cancer
my question is about phagocytosis as response to cancer. It is known that cytotoxic T cell may kill a cancer cell and sends cytokines to phagocytes like macrophage or dendritic cell to engulf and digest the killed cancer cell. From this, my questions:

can one assume that mRNAs of the cancer cells can be captured and sequenced along with those of the phagocyte by scRNAseq? In this case, the phagocyte should show a hybrid expression profile
if 1 holds (that I have observed in practice), can snRNAseq show a similar result? I ask this because in snRNAseq we deal with nuclei not the entire cell. However, I have observed hybrid expression profiles in phagocytes analyzed by snRNASeq.

It might help if you added links or an explanation of the techniques involved, and what you have found out - particularly about transport of foreign nucleic acids to the nucleus...

This is a very interesting question and I will give you an outline of the scenario I think is most likely.
I'm using the same hypothesis to explain another common observation in single nuclei RNA-Seq: In all snRNA-Seq data I have analyzed so far I have found reads for mitochondrial genes although they are not transcribed in the nucleus. How did they get there?
When doing single nuclei RNA-Seq the cells necessarily need to be broken to isolate the nuclei. The nuclear envelope is quite stable but most other cellular membranes will be permeabilized. As a consequence, mRNA from all over the cell is liberated and can stick to the nucleus. When the nuclei are isolated, the mRNAs sticking to them will be isolated too and then will be sequenced as part of that nucleus.
In the end it does not matter if the contaminating mRNA is from mitochondria or from cells taken up via phagocytosis.
I have seen mRNA from hemoglobin sticking to cell membranes in single cell RNA-Seq after > 5 washing steps, so I think it is not unlikely to assume mRNA can stick to the nuclear envelope as well.
You could try and see if the non-phagocyte genes have a higher percentage of splicing than the phagocyte genes. Since most mRNA in the nucleus will not be spliced this would be a hint that these genes come from outside the nucleus. How well this works will depend on the technology you are using. 10X only sequences the very 3' end of the mRNAs and you are not guaranteed to have a splice site in there.

Thank you for your interesting answer. I use 10x which outputs UMI counts for each gene so I don't have transcript/splicing information. When you say most nuclear mRNAs don't undergo splicing, do you mean splicing happen in the cytoplasm? Otherwise why is it that? It is worth mentioning that in the phagocytes showing such hybrid expression profiles, genes coding MHC II we're highly expressed, meaning they were most probably APCs as well

Splicing happens in the nucleus but the spliced mRNA is quickly exported to the cytoplasm. This is why is is recommended by 10X to include introns when mapping single nuclei data (page 9 top of right column).  Unfortunately, I'm not an expert in immunology and cannot comment on the expression of marker genes in your cells of interest.

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Solar Celiac Plexus location in body
Where is the Solar (Celiac) Plexus located in relation to the ribcage? I am reading this on the internet, and trying to learn more.
"The solar plexus — also called the celiac plexus — is a complex system of radiating nerves and ganglia. It's found in the pit of the stomach in front of the aorta."
Can someone point it out in the picture below? The purple and blue areas in the picture is the ribcage.

Since this diagram contains only bones and muscle (diaphragm), you should not expect to find other things on it, like nerves and ganglia.

hi @BryanKrause I am asking about solarplexus location spacial relationship to the rib cage,

Honestly, the Wikipedia article tells you what you need to know here.  It gives a decent illustration (courtesy of Gray's) that shows how these nerves radiate "like rays of the sun" from a spot a little below the diaphragm.  The tougher part is understanding how splanchnic nerves of the sympathetic nervous system work with the vagus nerve of the parasympathetic, etc.  Use a free textbook and start from the basics of the autonomic nervous system (Chapter 15); you'd never believe such a Rube Goldberg mechanism actually evolved!

Pretty much the center of your figure. The yellowish downward pointing arrowhead is where it is, possible represented by the arrowhead. Immediately below the ribs/sturnum


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Protecting linear ssDNA inside a yeast cell
This is kind of a multi-part question :)
Basically, I want a linear single-stranded polydeoxynucleotide to exist inside an S. cerevisiae cell cytoplasm for a long time without being digested. As far as I understand, the main danger to a linear DNA are 5' and 3' exonucleases (am I right?). So, the first question is:
What particular exonucleases digest ssDNA in yeast? What other enzymes do? Maybe something involved in defence against viruses? Which of them, if any, can be safely knocked out (i.e. are not absolutely crucial to the survival and reproduction of the cells)?
The rest of the question is about protecting the 3' end of the molecule against exonucleases (assuming they aren't knocked out). For the application I have in mind, "unnatural" modifications of DNA (like phosphorothioate bonds or 2' modifications of sugars) are unacceptable. Only 3' modifications of the last nucleoside are possible. In particular, I am considering something like:

Where X = -O-, -S-, -NH- or phosphodiester, and R can anything that's either something small (-H, -alkyl, -acyl, ...) or something big but connected by a long spacer (say, a protein on a PEG tether).
Can an effective 3' end protection be achieved this way?
The problem is, according to this, 3' modifications are generally bad at inhibiting exonuclease activity, but I can either use them or knock out nuclease genes (the latter is less preferred).

Would a locked nucleic acid work?

No. I should have probably defined "unnatural" as modified sugars or phosphodiester bonds. A bridged ribose doesn't work as R, too, because it's bulky.

Can you [edit] in some background about why you want to do this? Is it important the the ssDNA not be digested or that there be a high steady state level of the ssDNA? If the latter, there are alternative strategies that would allow you to achieve your desired ends without extensively modifying the yeast genome or expensively modifying the ssDNA. ——— The problem I see is that yeast also has enzymes with ssDNA endonuclease activity (and 5' exonucleases), so 3' end protection (or complete KO of 3' exonucleases) probably wouldn't be sufficient, again depending on your goals ...


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Lumpy green balls on tomato leaf
We live in central Maryland, USA, and pulled this off a tomato plant in our garden this morning (mid-summer). Any idea what these are? Not sure if they’re beneficial or parasitic, but I’d say the latter if I had to guess.

The shape of those looks more like caterpillar droppings (frass) than galls to me, though I've never seen them so green or shiny. Here's an image of tomato hornworm droppings, it looks quite similar to your picture:

If the balls are firmly attached to the leaf then they are galls, if they can be dislodged, then poop is more likely.

On closer look poop, is more likely.

Galls, the plants reaction to certain insects. Generally no action is warranted because of minimal harm to the host plant.


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What does it mean to collapse heterozygous alleles?
I am a bioinformatics rookie. I read a paper, it said:

existing algorithms either collapse heterozygous alleles into one
consensus copy or fail to cleanly separate the haplotypes to produce
high-quality phased assemblies.

So what does it mean to collapse heterozygous alleles?

I suspect this means that either the multiple alleles are represented with an ambiguity code:
Haplotype1:      ATCG
Haplotype2:      ACCG

Consensus:       AYCG

Or, that from a pile up of mapped reads, the "consensus" is simply called as the allele with the majority of reads.
Read1:     ATCG
Read2:     ATCG
Read3:     ATCG
Read4:     ATCG
Read5:     ATCG
Read6:     ACCG
Read7:     ACCG
Read8:     ACCG
Read9:     ACCG

Consensus: ATCG

Without more context, the meaning is unclear.

It would be better to not answer bioinformatics questions with no biological component on this site. It is also best to not answer questions that show no evidence of the expected prior research — this encourages sloppiness on the part of posters and results in an accumulation of poorly formed questions that will be of no use to future users. Note that if you feel compelled to put phrases like "I suspect" into your answer this is a strong indication that the question isn't clear enough — in such cases asking for and awaiting clarification is likely to lead to higher quality posts.

@Darlingtonia - good answer.  Regarding the other comment, it's bad enough to be discouraging to newcomers, but must it now also be discouraged for someone to give a helpful and informative answer?  Based on the logic that helping one curious novice might lead others to come, or that bioinformatics has nothing to do with biology?  It would be much more useful to have a folder or tag system to segregate high- versus low-level questions, as some other forums use.

@tyersome This looks like a typical case where a novice can waste a lot of time trying to find an answer where a more experienced professional can quickly provide a relevant explanation. That said, the original poster could have provided more clues about their previous research efforts. Regarding the absence of biological component in the question, we may add that the question might have been better placed in https://bioinformatics.stackexchange.com/


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Aligning two PDB structures with different numbers of atoms
What options do I have to align two PDB-files of ribosomes but with different number of atoms? I need to do the alignment using selection "name CA or name P", because the ribosome has both protein and RNA.
From my previous work I learned that PyMol can do alignment where it doesn't matter if the number of atoms is different, but there is problem because PyMol can only do the alignment using CA atoms, and thus it ignores my "name P" from rRNA.
I also tried to align the structures in VMD using RMSD Calculator but there needs to be same number of atoms in both selections. I also tried MDAnalysis code but there is also the problem that the selection doesn't have the same number of atoms.
Are there any suggestions on how to perform such an alignment? The best option seems to be PyMol (as it works with a different number of atoms in the two selections), but how do I incorporate the RNA into the alignment?

You may have more luck on SE Bioinformatics. (Oh, and amount of sugar, number of lumps.)

I use ChimeraX for structural superposition and it may work for your needs. See this command specifically. It also has a GUI.

When encountering that problem for single pdb files I often default to using the MultiSeq tool in VMD. This pairs sequence information and structural information to create very good alignments. MultiSeq can also align RNA.
If you require to do this over a trajectory, I would start by doing an alignment with MultiSeq and from this alignment identify residue-residue correspondences. Ignore gaps in the sequence alignment and align the backbone atoms of all other residues. This ensures that the number of atoms is identical in both selection and that you can use the "meausure fit" command in VMD.
In VMD you need to make sure that the selected atoms are in the correct order. Assume that you have two sequences that align like this:
AAAA---AAAA
AAAAEEEAAAA
then you can do
set idA [mol new MoleculeA.pdb]
set selA [atomselect $idA "backbone and resid 1 to 8"]
set idB [mol new MoleculeB.pdb]
set selB [atomselect \$idB"backbone and (resid 1 to 4 or resid 8 to 12)"]
\$selB move [measure fit \$selA \$selB]
Trajectories are then done similarly by moving through with animate goto \$frame in between.
When using the MDAnalysis python library you can make use of a selection dictionary for alignment. The select option of MDAnalysis.analysis.align.AlignTraj can take in a dictionary like this:
{'mobile':"resid 1-8", 'reference':"resid 1-4 or resid 8-12"}


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Need help identifying vascular structures in brain matter
I am working on PET images of the brain. The neuro-oncologist I'm working with identified 2 large high-intensity regions as vascular structures. I've been meaning to ask what structures these are exactly, but he's on vacation so I'm turning to you guys for help.
I've colored the 2 vascular structures in blue and red: The pictures show the axial (upper left), coronal (lower left) and sagittal (lower right) views of the brain.

I've tried googling this, but this turns out to be less straight-forward than I thought and I'd like confirmation from someone that knows what they're talking about.

As these are very large, they seem to me likely to be sinuses; the central one in red right along the midline is the superior sagittal sinus.
I think your blue traces may mark differently named sinuses, though they are all connected.
As a disclaimer, I'm more familiar with venous sinuses in the rodent brain, as they are important to avoid during rodent brain surgeries. Presumably the human ones are good to avoid when you poke things in there, too, but I haven't done as much of that, and anything I've done with human brain anatomy has already had these sorts of artifacts removed. If you need a specific anatomical reference from a cranial anatomy expert, I wouldn't rely on this answer too closely, but hopefully it leads you to where you need.

Thanks! this was actually what I was looking for, I have my sinuses in question to be the superior sagittal sinus and the straight sinus.

@nibs The straight sinus is on the midline; your bottom right image may be straight sinus but the other two are not. Transverse perhaps. Probably far easier to tell if you can threshold your images and look in 3D.


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Is menopause a design or a degradation?
Does menopause appear to be a designed or an accidental phenomenon?
We might say it is "designed" if there is a biological process that triggers it.  Like menarche, where something genetic says, "Time to ramp up these hormones!"  Or perhaps the ovaries say, "Egg count has dropped below a critical level, time to stop the cycle."
We might say it is "accidental" if it is a byproduct of degeneration like all aging processes, and not the consequence of any particular biological mechanism.

Great question. I’ll try and write up a proper answer later, but it’s widely considered that the menopause is adaption to avoid inter generational conflict in humans.

@user438383 — "Widely considered". I look forward to the evidence. Meanwhile, I would observe that most animals don't survive beyond reproductive age, and that this has been a recent development in H.sapiens.

A third idea is that menopause exists to keep women from competing with their own offspring. It forces them to rechanneled resources in helping their descendants which is an advantage in species with such helpless but high energy demand offspring with such slow maturation rates. A woman at menopause age is unlikely to raise new offspring to maturity in the wild, so there is a evolutionary advantage to rechanneling effort into existing offspring.

Just-so stories are a folklore that we love to tell, but it's important not to get too carried away with belief in them.  To conclude the design or purpose of something, or whether it is accidental, implies a very deep understanding of all the possible paths of evolution, a God's-eye view if you will, that typically evades us.  Even so, predictable statistical effects do guide the course of evolution, so we'll attempt to explain anyway.
That said, I'll name two very sensible ways to explain how menopause came to be - almost surely not the only two.  One is that it is rooted in the social nature of humans, by comparison with cetaceans (especially orcas) which have a similar segment of their population.  If eusocial insects can have most females non-reproductive, it seems easy enough to believe that a lesser non-reproductive population is possible.  Johnstone and Cant, 2010 ask why older rather than younger women assume this role.  They conclude that philopatry of males, rather than females, accounts for the uniqueness of these two groups.  When females disperse and males remain, an older female is more related to young individuals than a younger female, because her sons remain in the area.  If the females are philopatric, the effect is reversed.  (Note that in all human populations, including hunter-gatherers, there is a substantial contribution from postmenopausal women)
The other way I'll mention is simply that arrested oocytes have a shelf life.  Huber and Fieder, 2018 argue for this by comparing the age of reproductive senescence with lifespan.  Their curve levels off a little past the point of human menopause, suggesting it is just hard to keep ovaries going very much longer.
Here's where it's important not to get too caught up in the myth.  A sense of "purpose" would make us argue for one explanation or the other -- but the reality of random evolution means that both can be true.  Oocytes could evolve to surpass current limits of reproductive senescence, and existing patterns of philopatry and social behavior could change.  But for now, this combination of young gametes and social assistance from the elderly seems to work.


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Are babies cute, or is cute babies?
I have no doubt that the cuteness of babies is an evolutionary advantage. So the 'why' is clear, a bit of research also explains the mechanics, such as babies having certain features that trigger hormonal reactions. Therefore the 'how' is also fairly clear.
However, this leaves the question for which I did not really find an answer:
Did babies evolve to increasingly trigger cuteness in the brains of adults, or did adult brains evolve to increasingly get attractive to what babies look like?!
In most cases the direction of influence in an evolutionary process is quite clear (e.g. if the sun is bright in an area, humans adapt to it by getting a darker skin, the sun itself did not evolve to become brighter in area's where people with darker skin live).
However, as the appearance etc. of babies and how these are percieved is actually both about humans (who typically are first babies and then become parents) I am now doubting if babies are evolving to be cute, or if cuteness is evolving to match babies!
I am very curious if we know if the evolutionary influence is a one way street, bidirectional, or perhaps we (recognized scientists) actually have concluded that we have no idea. In case it was not clear I am mostly interested in humans though I guess the question may apply to other races as well.

I did think about other things that are typically found to be cute by humans (e.g. baby animals), but these roughly have the same features that we currently find cute in human babies (e.g. being small) so I don't think this rules out an influence in either direction.
My personal intuition is that babies will definitely evolve towards the general current standard of cuteness, but I would not be surprised if the standard of cuteness also evolves towards the general current appearance of babies.

Let's please try to be civil as we offer criticisms of questions posted here. Not every question needs to be about everyone's preferred area of biology, I expect that almost everyone who uses this site regularly has some class of questions that they aren't as interested in.

For OP, I think your question will get a better response if you try to frame it in some existing discussion rather than working from the ground up. Have you found biologists who study "cuteness"? What are the issues they discuss?

I don't think there is a natural selection against babies that are not cute or less cute.

On an intimately related topic, neoteny in humans and its evolution are worth investigating.

Sounds a bit like a chicken-egg question and as such is almost certainly unanswerable.

@DKNguyen - I used to deliver babies. The ugliest baby I ever saw, a truly ugly baby, went on to acquire two siblings. So I believe you're correct.

@anongoodnurse That made me lol. On second thought, that might be just within the  past few thousand years (maybe not even the past few hundred). Maybe a million years ago parents did subconsciously neglect less cute babies when times were hard and they were equally healthy. Especially if they became tied with traits associated with fitness and health (things like facial symmetry, etc). I'd guess it goes back even farther. After all, humans, kittens, puppies, and birds diverged long ago and we find them cute.

I did not expect the statement that babies are cute to be so controversial that it needed support in itself, but have added this link as a reference to show that it is not only my perspective. https://psychology.stackexchange.com/questions/16098/why-baby-animals-seem-cute-to-us
Now of course there are more assumptions (the post rougly explains cute as 'expressing the need for care' and surely it is not proving that this also results in babies actually getting that care, but perhaps we can focus on the mechanics of evolution rather than how I worded the question.

Its a lot easier to change how adult brains think than baby anatomy.
Babies are tightly constrained by development, certain things need to grow faster or earlier than other things. This is why most vertebrate young share many of those features. meanwhile evolving a behavior is one of the easiest things to evolve, a huge portion (~80%) of our genome is devoted to the brain and thus behavior.  A classic example of this interplay is that it is nearly impossible to keep babies from puking, so the brains of parents react differently to the puke of babies. It is also worth noting non-cute babies are usually suffering from, what would be in nature, fatal defects. It is also worth noting people find their own babies cuter than other babies, which means cuteness is also partially subjective.
https://onlinelibrary.wiley.com/doi/abs/10.1002/1097-0355(198121)2:1%3C56::AID-IMHJ2280020109%3E3.0.CO;2-G
If you want a more detailed breakdown you are gong to need to ask a series a questions because cuteness covers a lot of behaviors.

Very nice insight, to be fair I was not sure if I would get any insight at all.
Based on the earlier comments I should perhaps keep my mouth shut at a biology seminar, but at the next birthday party where we run out of topics I will definitely pose that it seems likely that cuteness is for a notable part defined by babies, rather than them only evolving towards it!


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Colorado insect identification
Found this bug in my backyard, but was unable to identify it. Thanks for any hint!
Edit : I live in the south east suburbs of Denver, Centennial.
So this is quite an urban area. I found this bug on my deck, and it escaped going under my deck. The board in the pictures are from my deck (composite, not real wood). My backyard is quite small, mostly grass and not a lot of flowers. The bug's body is around 3/4".

a better location and a descripion of the area you found it will help in identifying the insect,please edit more information into your question.

Thank you, done.

How big is this bug approximately?

Around 3/4" - Edited my description as well. Thank you.


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What are the differences and relationships between online plant taxonomy databases (POWO, WFO, WCSP, WCVP), and is one considered the most reliable?
Each of these databases has their own summary of their aims and process - but they rarely seem to mention each other in comparison. It's hard to figure out what differences or relationships exist between them. It seems like some of them use data from others, but not exclusively.
Should one of these be considered the primary or central source for botanical taxonomy? Are each of these databases reinventing the wheel independently, or are they just presenting the same data with different interfaces? Is any of them considered the most reliable or complete?

World Checklist for Selected Plant Families (WCSP)
World Checklist for Vascular Plants (WCVP)
Plants of the World Online (POWO)
World Flora Online (WFO)

Please check this open access article : https://nph.onlinelibrary.wiley.com/doi/full/10.1111/nph.18961# It proposes a comparison of WFO, WCSP, LCVP and WorldPlants and explain why and how they differ. WCVP, POWO and WCSP are the same basically.


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Can organisms grow on acetic acid?
Can organisms grow on acetic acid and water (with <1%, all inorganic, impurities), i.e. using acetic acid as a carbon / energy source?
If so which concentration of water would it start at? (assuming it doesn't happen without water)

Welcome Hans. We're expected to show our own research into a topic when asking. Please [edit] to tell us what you searched, found and where you got stuck. Also, please take our [tour] and refer to the [help] for guidance. Acetic acid (ethanol oxide) is already pretty stable as it's the metabolic product of several processes, would you perhaps be referring to an extreme environment, perhaps a fictional one? Then [worldbuilding.se] might help there.


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Given that "genetic drift" can happen, why is searching for an adaptive explanation for traits considered an important scientific question?
I saw today on Wikenigma (a wiki for open questions in science) that there are many competing explanations for why zebra stripes are evolutionarily adaptive, and there is no consensus on which one(s) are correct.
The discussion there suggests that scientists are eager to explain the specific adaptive advantage conferred by zebra stripes—for example, to find evidence showing that zebra stripes help the animals regulate their body temperature.
However, we know that there is a phenomenon called genetic drift by which certain genes come to dominate a population "just because": These genes are neutral with respect to evolutionary fitness, but happen to secure a majority early on in the lineage, and this majority grows over time:

Genetic drift is one of the basic mechanisms of evolution.
In each generation, some individuals may, just by chance, leave behind a few more descendants (and genes, of course!) than other individuals. The genes and other genetic elements of the next generation will be those of the “lucky” individuals, not necessarily the healthier or “better” individuals. That, in a nutshell, is genetic drift. It happens to ALL populations — there’s no avoiding the vagaries of chance.
…
Genetic drift affects the genetic makeup of the population, but unlike natural selection, through an entirely random process. So although genetic drift is a mechanism of evolution, it doesn’t work to produce adaptations.

Let's fix the meaning of adaptations here:

An adaptation is a feature that arose and was favored by natural selection for its current function. Adaptations help an organism survive and/or reproduce in its current environment.

(source)
My question is, given that "genetic drift" can happen, why is searching for an adaptive explanation for traits considered an important scientific question?
Non-questions

Zebra stripes are a motivating example for this post, but not the central theme. If you believe that zebra stripes do confer a specific adaptive advantage, then please substitute "zebra stripes" with a trait whose adaptive advantage you cannot identify.

I'm not sure that I see the justification for point 3, as that's the only place that you've specified that the father has some fitness advantage. Zebra stripes have a known adaptive advantage - did you look them up, what did you find? If something is preferentially selected for, then it is by definition a selective advantage, it doesn't make any difference if it's due to the feature being attractive or a good survival trait - see peacock tails as example of female selectivity of non-advantageous trait. Can you clarify?

Point 3 is mentioned in the preceding paragraph. Your first question is addressed by my first "non-question." Your second question feels like a semantic issue: you say "selective" advantage but I chose the word "adaptive" on purpose, because the search for an explanation for zebra stripes seems deliberately targeted toward adaptive explanations and nobody seems content to take "the stripes are attractive" as an answer—and again, the zebra stripes are just an example, and you can substitute peacock tails if you think zebra stripes have an adaptive advantage.

“Can natural selection reward traits…?” Please consider carefully the meaning of the words “selection”, “reward” and “traits”, and you will see that your title is scientifically and linguistically meaningless. Traits may be selected, and one might say that evolution involves the selection of certain traits. That is the only relation between the two. “Reward” is not a feature of evolution in any sense.

“ Now suppose that a strong, adaptively fit male of this species happens to be born with a heritable sexual preference for trait A.” 1. That favors reproduction, which means selection. You can’t make it neutral just by placing a label on it. 2. How do you think traits evolve? A male just happens to be born with an interest in pattern “s”? Why would that happen in one jump? Is preferring a metal vs. a wooden frame a trait that is heritable? Your words… don’t seem to particularly comprehensible, and they certainly don’t mean what you seem to believe they do.

for neutral traits look up something called "genetic drift".

I’m voting to close this question because it is unclear (this includes your explanation for why you think the linked page doesn't answer whatever you are trying to ask) and under researched. In particular, this appears to be based on an inadequate understanding of the basics of evolutionary theory — I encourage you to spend time reading and thinking about the material in this useful introduction to evolutionary theory from UC Berkeley.

I'm frustrated that many of the responses here seem to boil down to pointing out that I have used words in a different sense than evolutionary biologists do. I gave a clear example of what I mean by an "adaptively neutral" trait; while I understand that my example is technically "adaptively positive" in the sense that it favors reproduction, it is obviously qualitatively different from traits such as opposable thumbs that confer a specific biological advantage, and this distinction is at the heart of my question.

@anongoodnurse, I agree that "traits that favor selection" includes "traits that favor reproduction"—that's my point! But if you read the debate about zebra stripes, biologists aren't content with a circular explanation like "zebra stripes favor reproduction"—they are looking for a specific advantage such as "the stripes help them regulate their body temperature." My question is, why do biologists require such a specific explanation, if examples like mine are possible?

A male just happens to be born with an interest in pattern “s”? Why would that happen in one jump? The possibility of this happening follows directly from the following two premises: 1. Sexual preferences are influenced by genetics. 2. There are random variations in genes. Which of these premises is wrong?

At any rate, the concept of "genetic drift" mentioned by @John seems to best capture what I am asking about here. Let me reword my question to use this term in hopes of reducing confusion.

you are still going to have the issue with this being a very opinion based question. but as a side note something like visual patterning is unlikely to be neutral since vison is how predators and mates notice and identify you.

Sure, and I 3iterate: Zebra stripes are a motivating example for this post, but not the central theme. If you believe that zebra stripes do confer a specific adaptive advantage, then please substitute "zebra stripes" with a trait whose adaptive advantage you cannot identify.

@Max That's not really fair and seems to be a goalpost move. You posit that people search for adaptive explanations for things that need not be adaptive. Your evidence is so far one example; if that example isn't valid, why should we take your premise as true?

I don't know if the premise is true—one possible answer to my question is, "The debate about zebra stripes is unusual. In general, biologists assume that most traits arise from evolutionary drift." Is this your answer? I am asking because I don't know, not because I am trying to checkmate biologists. If I had a comprehensive knowledge of biology, then I would have chosen a better example, but then I wouldn't have needed to ask in the first place.

Ok, I will take on face value that you’re not trying to checkmate biologists. In that case, instead of arguing in comments, why not learn from them? You’re not going to get knowledge from arguing illogical arguments. Genetics doesn’t work the way you want it to work. A mutation is a point in a gene. It’s not likely to result in a completely new behavior. There are exceptions, but they are few and far between, and exceedingly difficult to prove. Lactase persistence is one, and it spread rapidly because of survival advantage. In fact, there are several SNP mutations that have similar results. …

…and we know this because of a lot of time, money, and research in different lactase persistent populations. What would prompt research into your scenario? I suspect nothing would, because it’s not a workable hypothesis.

With all due respect, I resent being accused of "arguing" when I have made every effort to understand the comments here, ask follow-up questions, and use your feedback to improve my post. From these two comments, it seems to me that your view is that "most traits, such as zebra stripes, have a specific adaptive advantage and aren't merely due to genetic drift." Is this an accurate summary? If so, please provide it as an answer rather than a comment.

This article may be an interesting read for you. You can also check out the Wikipedia pages on adaptionism and constructive neutral evolution.

The very shortest answer, and in my opinion most ideologically neutral, is that neutral evolution ("genetic drift") is the null hypothesis of evolution.
The burden of proof is always on the person claiming adaptation. If you can't provide sufficient evidence for adaptation, the default is to assume neutrality.

This is a very surprising answer, if true, given that "open questions" surrounding the adaptive benefit of traits seem to be such a hot topic of research. My impression from skimming the Nature article you linked (but I will take a closer look) is that it is arguing that genetic drift should be treated as the null hypothesis, the subtext being that in practice it often isn't.

@Max "selectionist"/"adaptationist" arguments emphasizing the role of active selection in shaping observed diversity are often dominant, yes. It's more fun/publishable/suitable for textbooks to do work on surprising things than on boring things, even if boring things are more numerous. Hyperdarwinist views are emphasized by evo psych, "new atheism", etc.... To a degree you could call it an overreaction against creationism. For an old but well known criticism, see here.

Is "hyperdarwinist" a synonym or antonym of "selectionist" here?

@Max neither - selectionist/neutralist differences are reasonably opposing views about how traits evolve. "hyperdarwinist" are those who unscientifically try and shoe-horn every observation about the natural world into some kind of story about selection.

@Max - you say you just want to learn, but your arguments don’t support your statement.

In order to gain a deeper understanding of the topic, I ask a lot of "why" questions. I am asking in good faith.


text:
What is this unusual butterfly?
Sighted in West London, July 23rd., 2022. The weather was cool and overcast. I could only get a picture of the underwing, but the upper wing was orange towards the head, and white towards the tail, with a black eyespot in the orange section
.
I have tried a Google image search, but I am not finding any results among common UK or European species. The Orange Tip is not a world away, but the underwing is quite different. Could this be a rare visitor? Size, perhaps 4 cm from head to tail.

It's a moth, specifically a Jersey Tiger Moth - can be seen in parts of the UK, more usually the south west, though it seems to be spreading more within the UK. Info here https://butterfly-conservation.org/moths/jersey-tiger

This is clearly correct, but answers are most useful (and to get a better response) if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion and less useful to other users. Posts are expected to be self-sufficient — i.e. not require leaving this site. ——— You may wish to take the [tour] and consult the [help] pages for additional advice on [Answer] effectively on this site.


text:
Does the recent concern over several papers about Aβ*56 call into question the association of Alzheimers Disease with any amyloyd beta oligomer forms?
The news item by Charles Piller just published in Science BLOTS ON A FIELD? A neuroscience image sleuth finds signs of fabrication in scores of Alzheimer’s articles, threatening a reigning theory of the disease highlights the recent news and activity around a series of papers discussion Aβ*56, a specific, proposed type of toxic oligomer of amyloid beta or Aβ.
There are questions of image altering and of the veracity of Aβ*56 isolation and measurements, and expressions of concern have been recently added to online versions of a numnber of papers referring to it going back to the 2006 Nature paper A specific amyloid-β protein assembly in the brain impairs memory.
Several drugs developed for treatment of Alzheimers Disease have targeted Aβ.
I'm having difficulty understanding how far the implications of the recent concern reaches. Is it simply the correlation with the particular form Aβ*56 associating with Alzheimers, or is it the connection between any oligomer of Aβ? Does the recent concern over several papers about it call into question the association of Alzheimers Disease with any Amyloyd beta oligomer forms?

Does the recent concern over several papers about Aβ*56 call into question the association of Alzheimers Disease with any amyloyd beta oligomer forms?

From my understanding, no.  alzforum.org has many great comments on it, e.g. from David Brody:

In my own group, we tried replicating the Aβ *56 western blots for about a year, without success. We then moved on to other things.
Our later work on soluble Aβ aggregates/oligomers from human brain tissue indicated that they are considerably larger than Aβ *56 (Esparza et al., 2013; Esparza et al., 2016).
I think these larger soluble Aβ aggregates/oligomers may still be important potential therapeutic targets, but not Aβ *56.
The strongest evidence comes from the labs of Dennis Selkoe and Dominic Walsh.
References:

Esparza TJ, Zhao H, Cirrito JR, Cairns NJ, Bateman RJ, Holtzman DM, Brody DL. Amyloid-β oligomerization in Alzheimer dementia versus high-pathology controls. Ann Neurol. 2013 Jan;73(1):104-19. PubMed.
Esparza TJ, Wildburger NC, Jiang H, Gangolli M, Cairns NJ, Bateman RJ, Brody DL. Soluble Amyloid-beta Aggregates from Human Alzheimer's Disease Brains. Sci Rep. 2016 Dec 5;6:38187. PubMed.

or from Thomas Bayer:

In my view, Aβ-amyloid oligomers are valuable and realistic drug targets. However, not all Aβ oligomers described in in vivo or in vitro model systems do exist in human brain. Besides full-length Aβ, N-truncated Aβ peptides, pyroglutamate Aβ 3-42 and Aβ 4-42 represent a dominant fraction in the brains of patients with Alzheimer’s disease. Both N-truncated peptides show a high aggregation propensity to form stable aggregates as observed by NMR spectroscopy, for example (Bouter et al., 2013).
References:

Antonios G, Borgers H, Richard BC, Brauß A, Meißner J, Weggen S, Pena V, Pillot T, Davies SL, Bakrania P, Matthews D, Brownlees J, Bouter Y, Bayer TA. Alzheimer therapy with an antibody against N-terminal Abeta 4-X and pyroglutamate Abeta 3-X. Sci Rep. 2015 Dec 2;5:17338. PubMed.

Antonios G, Saiepour N, Bouter Y, Richard BC, Paetau A, Verkkoniemi-Ahola A, Lannfelt L, Ingelsson M, Kovacs GG, Pillot T, Wirths O, Bayer TA. N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody. Acta Neuropathol Commun. 2013 Sep 6;1(1):56. PubMed.

Bakrania P, Hall G, Bouter Y, Bouter C, Beindorff N, Cowan R, Davies S, Price J, Mpamhanga C, Love E, Matthews D, Carr MD, Bayer TA. Discovery of a novel pseudo β-hairpin structure of N-truncated amyloid-β for use as a vaccine against Alzheimer's disease. Mol Psychiatry. 2022 Feb;27(2):840-848. Epub 2021 Nov 15 PubMed.

Bayer TA. N-Truncated Aβ Starting at Position Four-Biochemical Features, Preclinical Models, and Potential as Drug Target in Alzheimer's Disease. Front Aging Neurosci. 2021;13:710579. Epub 2021 Aug 20 PubMed.

Bayer TA. Pyroglutamate Aβ cascade as drug target in Alzheimer's disease. Mol Psychiatry. 2022 Apr;27(4):1880-1885. Epub 2021 Dec 8 PubMed.

Bouter Y, Dietrich K, Wittnam JL, Rezaei-Ghaleh N, Pillot T, Papot-Couturier S, Lefebvre T, Sprenger F, Wirths O, Zweckstetter M, Bayer TA. N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits. Acta Neuropathol. 2013 Aug;126(2):189-205. PubMed.

Bouter Y, Liekefeld H, Pichlo S, Westhoff AC, Fenn L, Bakrania P, Bayer TA. Donanemab detects a minor fraction of amyloid-β plaques in post-mortem brain tissue of patients with Alzheimer's disease and Down syndrome. Acta Neuropathol. 2022 May;143(5):601-603. Epub 2022 Apr 16 PubMed.

Thanks for the link - some very interesting comments on the blog post. One takeaway message from some of the comments is that the Science article contains some misguided views, so they are definitely worth reading to get a more well rounded picture of what happened;


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Are these pineapple seeds starting to germinate?
What is this? Is it the structure from where pineapple seeds grow? The photo is a slice of fruit.

Welcome to Biology.SE. Never seen anything like that inside a pineapple, but it vaguely resembles an inflorescence (grouping of flowers). However it isn't clearly like what is expected for a bromeliad. I'm skeptical that you can get an answer here with this picture. Did you keep this structure and is there any chance you get clearer pictures — ideally using an SLR camera with a macro lens, but borrowing different models of cell-phones might also help (assuming that is what you used). Alternatively, do you have access to an institution with botanists on staff and a dissection microscope?

@tyersome sorry I didn’t keep it. But I understand the limitations of what I’m asking based on this photo only.

Is it the structure from where pineapple seeds grow?
Yes, these are pineapple ovules, which if properly fertilized would develop into seeds.* The structure they're attached to is the placenta, which is found inside a chamber called the locule. In pineapples, three locules together form an ovary. Pineapples are interesting in that the whole fruit is made up of dozens of ovaries all grouped together, each one with a flower facing the outside of the fruit.
See this blog post for a good explanation of what's going on.
Are these pineapple seeds starting to germinate?
No, these have not been fertilized. To germinate the ovule would need to be fertilized, mature into a seed, and then be planted in the right environment for the embryo to continue development.

*Commercial pineapples don't generally produce seeds because pineapples require genetically distinct pollen for fertilization. Commercial pineapples are propagated from cuttings because it's faster and more reliable than trying to obtain seeds.

Awesome answer, thanks! This pineapple did have seeds.


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What are the most intelligent plants?
For intelligence lets adapt the definition from here:

Perception of the surrounding environment
Adaptation to environmental conditions
Communication (in the case of plants, through chemical secretions)
Social interaction (by sending and receiving chemical information) and cooperation for mutual health and safety.

Basically, I'm looking for the spices of plants that demonstrated very high sensitivity and responsivity to their surroundings.
Those intelligent plants are not necessarily the plants that can physically move in seconds like mimosa pudica, rather also those who show any kind of respond even to humans - if we accept some  of the research that have been done in the past years.
Edit: It has been demonstrated conclusively can communicate: i.e., have the ability to send and receive signals. Just, for example, by "Below-ground communication" using chemical cues. Moreover, it has been also demonstrated that plants are aware of their surroundings: the roots can bend to avoid some obstacles. Yet another example of a kind of communication/awareness is the phenomena of Crown_shyness.
There are researchers that are not shy of using the term intelligence here (Some researchers even go further to suggest a kind of memory in plants).
This question adapted the terminology (that is used by some), and provided the reader with the definition and explanation that is too long for the title. I believe the reader should not be deterred here, as ultimately this question is not about semantics. The question basically asks if there is any kind of test or scoring points to distinguish those "intelligence behavior" between plants, as I believe that there are plants that are more "intelligent" than others - but I could not find information about this online.

Welcome to the site. Please take a [tour] and visit the [help]. There you will find lots of good information about what sort of questions to ask, and how you can make a good question/answer. In particular, questions with "most" are likely to be answered as opinion and don't fit the stackexchange format well. We also ask that questions have some evidence of an attempt to answer them by the asker. If you rephrased your title to something like "what is the evidence for communication and intelligence in plants" then you might get a better response.

@bob1, I've taken notice and added some more information. For now, as I explained in the body of the edit, I prefer to keep the title as is. If someone believes he has a better title, he can be free to edit the title.

Users might better give the OP (me) enough time to edit the question after requested before downvoting. or at least explain  why the question was downvoted.

No point in worrying about downvotes, see this main-meta post regarding downvotes and comments. Now you've edited you're much more likely to get upvotes.

there is no evidence plants can perceive their surroundings, plants ae not aware of anything. A plant no more perceives its surroundings then a a TV perceives its remote. individual cells can send an receive signals, adapt and engage in social behaviors, so you have not defined anything the simplest unit of life can do. you are combining several unrelated and basically incomparable metrics and asking us to evaluate their balance, which makes this essentially opinion.

Note that your links are to "popular science" sites or Wikipedia. There is nothing "wrong" with this, but it does suggest that you've done at best a very cursory examination of the available literature. In particular, such sources tend to over-simplify, make extensive use of analogies, and extrapolate well beyond what has actually been shown. This can lead to a (sometimes very) distorted idea of what is known. In your case, you use a lot of terms (e.g.s "intelligence" and "awareness" in a very colloquial fashion — its great that you try to define the former, but I think you will get a  ...

@John what about things like phototropism, geotropism and chemotropism? I think that no perception is a bit strong. Conscious behaviour? no, definitely not, but perception isn't limited to conscious behaviour.

... better response if you determine what terminology is used by people doing this research and use that —  if they do use "intelligence" then tell us exactly how they define it. ——— Also note that even in humans it is quite possible to react without any conscious awareness, which makes your use of "aware" when you appear to mean something more like "responsive" needlessly confusing.

@bob1 again all things single celled organism can do, perceive means being consciously aware of something, which you can't do without a brain.

My vote would be for the aspen. The entire thing. One stand. Communicative, yes. Perceptive, yes. But intelligent? For a plant, maybe.

@John - your comment is dead wrong. Not only can plants respond to temperature, day length, gravity, position of the sun, moisture, etc., there is scientific evidence that they can do more. Your comment is faulty to the degree of harm to science. Any gardener knows plants much better than you do. Biologists should know more, not less, than a hobbiest in the field.

@anongoodnurse, again all things single cells can do, there is no evidence plants are consciously aware of any of this. there is a difference between sensation and perception, plants can sense all those things they perceive nothing. please read my statements with care before you  declare them in error.

@John - I didn’t say anything about consciousness. I said your comment was dead wrong, and it was.

@John- it should not surprise me in the least when people assume that a disagreement is based on lack of careful reading, but… it still does.

@anongoodnurse am curious what statement of mine you think is dead wrong that does not have to do with consciousness? As I said perceive means "consciously aware of"

I’m voting to close this question because: 1) it is asking for something that seems impossible to answer objectively ("most intelligent" is controversial even within humans where we at least roughly agree that "intelligence" is a meaningful concept); and 2) it remains unclear what is meant by "intelligence" in this context and the edits so far have not helped. Please see the [tour], [ask], and other [help] for details.

@tyersome, That's okay if this forum thinks and votes the question is off to close it. But I want to offer my take as to why - by your two points - the question should stay open. (1) It is possible to answer objectively by offering appropriate tests (see my answer); it  simply not possible to answer uniquely. that's was I used plants in the plural. (2) If it is unclear - though it was defined (before the edits) - please explain what is not clear.

The plant genus Cuscuta (dodder, amarbel) might be the most 'intelligent' plant(s). It is based on an agreed definition of intelligence, observations on the plant and what the plant can achieve compared to other plants and without a neural network; although this is not a scientific fact and there isn't a scientific consensus on plant intelligence. They are parasitic plants that can attach themselves on a variety of different plants to hijack them for nutrition and can spread plant diseases as well. They appear to use different senses like smell, taste, touch to be able to interact with their environment and to find other plants/food.
Here is a study from PubMed Central titled The foundations of plant intelligence and I'm including some relevant excerpts that provide a summary, the definition of intelligence and some observations on the dodder plant:

Intelligence is defined for wild plants and its role in fitness identified. Intelligent behaviour exhibited by single cells and systems similarity between the interactome and connectome indicates neural systems are not necessary for intelligent capabilities. Plants sense and respond to many environmental signals that are assessed to competitively optimize acquisition of patchily distributed resources.
I consider that intelligence in most animals and plants is concerned with improved survival in the wild and thus in turn fitness.
Perhaps, the most useful summary is that of Legg & Hunter. They collected some 70 different definitions of intelligence and summarized them as follows:
Intelligence:
(1) is a property that an individual has as it interacts with its environment or environments;
(2) is related to the agent's ability to succeed or profit with respect to some goal or objective; and
(3) depends on how able the agent is to adapt to different objectives or environments.
Observations on the parasitic behaviour of Cuscuta (dodder), indicates it performs analogous behaviour to Lymnea but without the need for control by a simple nervous system. Dodder is a typical parasitic plant in that it searches and locates host plants which in due course it exploits. Some 4500 angiosperm species exhibit varying degrees of parasitism.
The dodder seedling lacks a root. Consequently, it must find water quickly on germination. In this condition, it is clearly in a motivational state of search. The shoot circumnavigates and locates nearby hosts from the volatile organic compounds the host emits, as shown by time lapse.
Kelly offered numerous suitable hosts to dodder by tying them together and found a rejection rate of 50% within a few hours, indicated by the parasite branch growing away. The assessment period is thus completed in this short time and since contact is only surface in character, assessment is probably made of the volatile chemical signature of the host. Dodder is using taste like Lymnea and changing search strategy when the source is not satisfactory.
There is little doubt that a primary problem some biologists have with the concept of plant intelligence is the assumption that intelligence is limited to organisms with some sort of neural network. The observations above show that dodder is capable of equivalent behaviour in the absence of a neural network. Alternative methods of assessment exist in plants. Intelligent behaviour is not dependent on neural activity.
Trewavas A. The foundations of plant intelligence. Interface Focus. 2017 Jun 6;7(3):20160098. doi: 10.1098/rsfs.2016.0098. Epub 2017 Apr 21. PMID: 28479977; PMCID: PMC5413888. - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5413888/

Further sources:

Detection of Different Hosts From a Distance Alters the Behaviour and Bioelectrical Activity of Cuscuta racemosa - https://www.frontiersin.org/articles/10.3389/fpls.2021.594195/full
Understanding interdisciplinary perspectives of plant intelligence: Is it a matter of science, language, or subjectivity? - https://ethnobiomed.biomedcentral.com/articles/10.1186/s13002-022-00539-3
Book: Plant Behaviour and Intelligence By Anthony Trewavas

dodder grows in the direction of certain chemical compounds and away from others and can habituate to signals, which all plants and indeed all cells do, so what makes dodder more "intelligent" the paper offer nothing that all know organisms cannot do. It essentially argue all life is intelligent.

Thanks for your answer and suggestion about tags edit which I've adapted. This is a long article and I intend to read later this week. As I said some researchers prefer to use the term intelligence - I agree - but some might disagree and that's completely fine. The problem starts when people turn away from the given definition of the term (and rather focus on the title) - then the discussion is not fruitful for the actual issue at hand.

@discipulus I think it's wrong to think you can redefine a term without pushback; however you change the definition, terms used in an existing way will always carry baggage. The definition given is so far from the use of "intelligence" in context of animals. By that definition, almost all of biology becomes "intelligence", and therefore the term becomes useless.

@BryanKrause, (1/n) what you and others seem to be missing is that I'm not trying define a term for the sake of the definition. I care not about the term. if it helps, one might replace the word intelligence with the term "fjhdsfjhkds" and reread my question. That's for one. For two, and this follows if one says that this can be applied to all biology -- I won't object and will be tolerative - not necessary because I agree or not, but because it is not the point of the discussion.

@BryanKrause, (2/n) Now, if we want to enter the discussion. First, bear in mind, that however strongly one resists the term intelligence - this precise term was used and is used by more than one researcher. So, we have to accept that at least part of the scientific community believes this term is appropriate.  I have not seen appreciation for this fact here.

@BryanKrause, (3/n) Now, the term intellegence was not born out of void. it makes perfect sense (to me at least) to use this term, if one view things in context. the context clearly was the apparent display of function in plants that wes previously hidden to humans. This is a kind of higher function - like communication. in this sense the plant is indeed intelligent.

@BryanKrause, (4/n) I also think it is wrong to think of perception/sensation only in terms of brain and nervous system. those term (intelegece also) predates the human understanding of the mechanism in the animal kingdom (i.e., nervous system) - hence I see no reason to restrict the terms to nervous system. For 5 year old the plant is aware and perceives no less than humans are. YOu can teach the child the plant has nervous system and the child won't object.

@BryanKrause (5/5) Finally, I don't think it is easy to define intelligence in a way that would match humans and animals and not plants (nor even cells or "all biology" if you will).  without restricting the term and thus - effectively - render it very limited and essentially meaningless.


text:
Why does the concentration gradient of one ion represent the entire cell in the equilibrium potential of an ion?
The Nernst equation for the equilibrium potential of an ion(in this case potassium),
$$E_{eq,K^+} = \frac{RT}{zF} \ln \frac{[K^+]_{o}}{[K^+]_{i}}$$
includes the ratio of the concentration of that specific ion outside of the membrane to the concentration inside. If this is for calculating the diffusional force, why does it ignore other ions? Wouldn't the concentration of other ions inside and outside of the cell also affect this ratio?
For example, some ion might be more abundant inside the membrane than the outside, but some other particle might be more abundant outside, thus creating no diffusional force. However, in the equation this will be taken as if this does indeed generate a force, since it only takes into account the ion more abundant inside.

Welcome to Biology StackExchange. Cross-posting is generally not desired on StackExchange.

Just add up everything of interest. For example, you can include sodium as

which gives you

chlorides, and everything else could be further added in a similar fashion, although likely to diminishing effects. These equations and numbers are from page 107-108 of From Neuron to Brain.


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What nutrients are necessary for Bacillus subtilis germination?
What are the necessary conditions to germinate Bacillus subtilis spores? Under laboratory conditions, spores of B. subtilis are often heat-activated for 30 min at 70°C to increase their germination responses to nutrients. Most papers use either L-valine or L-alanine amino acids to germinate.
However, I would like to know if those are necessary nutrients for germination.
Are there other nutrients that can germinate B. subtilis?

Your own efforts to answer this question? Again.

To get you started in answering your question, here's a good paper: Analysis of the germination of spores of Bacillus subtilis with temperature sensitive spo mutations in the spoVA operon. I would recommend reading section 3.3 - Germination of spoVA mutant spores.


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Do animals exist that grow body parts back into themselves?
goats sometimes grow their horns in a way that it "grows back" into its skull (e.g., https://en.goodtimes.my/2017/11/27/argali-sheeps-majestic-spiral-horns-can-protect-kill/).
However, this is a rare defect and not the "intended" way for the goat to grow, since it seriously hurts the animal.
I wonder, are there any organisms in which body parts merge with another part (as opposed to growing out of another part, as is standard) in this way, where it is not a mistake and instead a feature of the organism?
Thanks!

Would [babirusa[(https://en.wikipedia.org/wiki/Babirusa) count?

Does a narwhal count?

Human infants have 270~300 pcs of bones, that merge into 206 pcs in adults.


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The pollination of lupins
Do lupins produce nectar? According to this study it seems like there are conflicting conclusions regarding this. And in this study the supposed inability for Lupinus argenteus to produce nectar is utilized to study whether the addition of nectar changes pollinator behaviour.
If the answer to this question is no, then why do these bumblebees insert their tongue inside the base of the flower, because it certainly looks like that is what they are doing. Do they do so regardless of whether a flower contains nectar or not, just to verify whether there is any present in the flower? But if pollinators only visit lupins for pollen to eat then why do they stick their tongue inside the banner where it seems to me that there should be either trace amounts or no pollen at all.

Welcome to SE Biology. Please finish reading the Tour before posting. That way you will find out how this site works. I have edited out reference to two questions, as we only take one at a time. I am no botanist, but did you really mean “banner”?

Yes, banner as in the uppermost part of a papilionacepus flower (zygomorphic flower shared by almost all plants of the pea family). My phrasing is not specific enough: the banner in this lupin flower is folded slightly towards the bottom creating a "crevice". It is this crevice that the bees in the video seemingly stick their tongue in.

Ok. Banner it is. I should stick to animals.

Is there some reason to think that all lupines must be the same? If so, then please [edit] that into your post. If not, then is Lupinus argenteus the species of interest and is that species what is being shown in the linked video? Also, what species is the bumblebee? ——— While providing links and sources is good you should also summarize what is in the papers and video; all posts must be self contained (i.e. must not require users to follow links). In addition, it would be great if you extracted and posted relevant frames or short segments as gifs from the video.

The lupine from the video appears to be L. polyphyllus, and this paper suggests L. polyphyllus doesn't produce nectar.


text:
What is a random piece of DNA called?
If I picked up a DNA molecule and randomly snipped out a piece with scissors what is the scientific name for the resulting piece?
I'll confess right up front that I am not an academic or professional. I am retired and write science fiction for a hobby but I like everything in my stories that can be true and correct to be so.
In my current novella I have AI searching through the entire human DNA molecule (coding and non-coding) for a piece of DNA not related to grains but to a grain viroid. I am aware that viroids only infect plants but for my story I need a piece of this viroid to have spliced itself into the DNA of grains. That will then be found in the DNA we share with grains. Like the DNA we share with chickens, fruit flies, and bananas.
In my novella the reason for this is that it is a part of the trigger sequence for human metamorphosis which then takes place over ten thousand years. Just as things like body weight, food scarcity, etc. are triggers for metamorphosis in other animals, eating large amounts of grains is the trigger for human metamorphosis in my current story. Eating large amounts of grains means the development of agriculture and thus civilization. In my fictional universe where earth-like humans are not unique but common (due to convergent evolution) the birth of a new civilization means the beginning of their end unless they can escape the confines of their planet of origin before they destroy themselves via some version of the great filter.
Metamorphosis in other animals is an evolutionary strategy that is believed to have developed for similar reasons.
The metamorphosis that is triggered in humans leads to the development of AI and robotics and the next stage of life for the species. It enables them to spread to other worlds (which our organic bodies can't do in time) just like dragonflies leaving their pond.
"Why is humanity so compelled to create artificial life in its own image? Perhaps the caterpillar feels the same as it builds its chrysalis and for the same reasons." -- quote from my story, Metamorphosis And The Messenger.
So that's the big idea. As I was writing a paragraph about this search I wanted the correct word for a random piece of DNA. Google's AI only responded with names for specific pieces of DNA like genes, bases, exons etc. So since Google's AI is not smart enough to handle my question here I am. Maybe it's just called a "piece" but if there is a proper, scientific name I would prefer to use it.

Not in reference to this specific question necessarily, but it occurs to me you might like our [worldbuilding.se] stack. It exists for the express purpose of helping writers, artists, game-designers etc. design their fictional world. (Take their tour, read-up in their help centre before posting.)

Hi NetCentric, and thanks for posting your question. A few things: (1) you say "the entire human DNA molecule" -- the diploid human genome is comprised of 23 chromosome pairs, so 46 individual molecules (92 if you consider dsDNA to be composed of two interacting ssDNA strands). (2) I agree with Jiminy that your question is likely a better fit for the worldbuilding stack.

Thank you for suggesting the Worldbuilding stack. I was not aware of this resource but will check it out now.

If you were to literally chemically remove a piece, as with restriction enzymes or physical disruption, that would be a "fragment".
If you just mean a focal region of a genome, then "locus" or even just "region" would do.
I'm aware it's a SF premise and not meant to be super robust scientifically, but how do you see a pattern of descent in which a viroid that infected a grain (a plant) gets into a human (an animal that diverged 1 billion years ago, long before there was such a thing as multicellular plants)?
It's formally possible via horizontal gene transfer when people eat grasses I suppose, but then it's not part of the commonly inherited regions that we share with the other organisms you mention, as those branched off long before.
I suggest looking into work on ultraconserved genomic elements as relevant to the mechanism by which the "AI" might work. These methods are relatively commonplace though, not sure that they merit the buzzword though.

Thank you for for answering my question. I really appreciate it. Also thanks for pointing out the pattern of descent and  horizontal gene transfer issues. As I pointed out I like things to be scientifically correct as far as possible so I will see if I can come up with another way to make the connection with agriculture. That part of the story is not yet written. If I can't find another mechanism well that's when the fiction part comes in. Thank you again.

To be clear, the "piece" OP is looking for should probably just be called a "gene". It would be reasonable to say that the AI is checking fragments of DNA for a gene introduced by a viroid, if taking all the premises as reasonable.

It's not clear to me why the AI would need fragments, though; given modernish technology they might as well operate on the whole genome. It seems they're looking for something suspiciously conserved from wheat to humans despite having no known function in either.

@BryanKrause I like "locus" in context as being a bit noncommittal about what exactly the piece of DNA is. If it's a viral genome/viroid relict, then "gene" isn't quite accurate. Yes, I agree that the work on ultraconserved elements could be relevant here; i will update to include.

@MaximilianPress I think of "locus" as a position in a genome rather than something functional. Even if the product is unknown (or if it's unknown that there's even a product vs a regulatory role) wouldn't gene be better?

@BryanKrause We commonly refer to "the YFG1 locus", where YFG1 is a gene. TAIR has genes under "locus" heading: https://www.arabidopsis.org/servlets/TairObject?accession=locus:2043520. I think of "gene" as meaning something rather specific as a defined transcriptional unit. I don't think this is what OP means, since "viroid" or "piece of viroid" is not necessarily transcriptional, and if it is, it is probably not a single unit. If we wanted to look for something in the archaic Johannsen sense of a generic, heritable-material-agnostic "unit of heredity", maybe then "gene" would be appropriate.

@MaximilianPress I think I'm leaning newer, rather than older, the definition that eg Wikipedia captures as "a broad, modern working definition of a gene is any discrete locus of heritable, genomic sequence which affect an organism's traits by being expressed as a functional product or by regulation of gene expression"; specifically that final 'or'. But I suppose it's still unclear whether OP's chunk should be a single gene, or multiple, or what... I still think of "locus" as being a bit more like a street address with reference to a chromosome.

Of course there's a lot of overlap there, too, because if a building is on fire at 11 Wall St., whether you refer to the building or refer to it by address you still mean the same fire.

@BryanKrause Yes I think that we broadly agree, I find the wiki def'n to be a bit too vague but that's really a matter of taste. When we talk about the kind of algorithms that people use for this purpose I think that a "street address" is certainly appropriate, to follow your analogy.

@MaximilianPress Yes, I suppose as long as you phrase it as "you are looking for the place in the genome where this viroid-origin DNA exists" then a "locus" is fine; I still don't think that the thing you find there can be a "locus", but as you say, these can be somewhat interchangeable practically.

@MaximilianPress Thanks for the tip re: ultraconserved genomic elements. It looks like a promising alternative for the story given the pattern of descent issue you pointed out.


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Mapping 23andMe data to academic paper
I'm trying to figure out how to map 23andMe genetic data to a paper but having trouble. I'm able to find the gene here (https://www.ncbi.nlm.nih.gov/gene/1813) but the paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6128289/) mentions an "A1 Allele" while the 23andMe data says it is "AG".
How can I reconcile this data? Or in other words, how can I see which alleles are present in 23andMe data?

I'd be cautious about overinterpreting your genetic results without consulting an expert in genetic counselling. I'm not sure whether your question should be closed as personal medical advice but I don't think I'd feel good about giving an answer here, I think there can be some risk in giving people some Dunning-Kruger style expertise.

@BryanKrause this is purely for research purposes and would absolutely not constitute medical advice to anybody.

@Bryan whilst this certainly seems like the thing an interested amateur would ask, it's also a totally plausible thing a researcher might do as well.

@user438383 A researcher involved in genetics? I kind of highly doubt it...

@bryan  there’s plenty of non-geneticists who dabble in genetics research to support their (often misguided) e.g. sociological research, and who probably have no idea about what a reference allele is or how to parse a vcf file. But maybe I’m being too generous… (I’m a geneticist btw)

Honestly, I'm just interested if my father (who died from alcoholism) and I have the same genetics related to addiction. I'd like to better understand the causes behind his death and if there's some way that I could help people in the future

Honestly, I would appreciate an answer to this question, otherwise, I'm just going to have to post on other forums/rephrase my question until I get an answer

@Rob That is exactly the sort of thing I was warning about interpreting without expert guidance.

As answered in your other question, you should use the rs ID for the allele. This is a systematic method (rather than the informal "A1" terminology) of being very precise about the variant. This ID will be shared / mappable across a dizzying variety of genetic resources, including 23andme.
For this specific variant, the rs ID is rs1800497.

This is very helpful! Thank you!

@Rob — Please take the time to take the [tour] and then consult the [help] starting with [ask]. You have asked what appears to be essentially the same question twice and are now asking a followup question in the comments. Both of these actions are frowned upon on this site — doing this makes it harder (if not impossible) for other users to find material, which is a primary aim of the site. Please see above links for details. ——— In addition, your posts suggest you have a limited understanding of the basics of molecular genetics. If this is true, you would be best to address that ...

@Rob: I can't evaluate the AG issue since I'm not sure what it's referring to at 23andme. I'll note that AG would be the reverse complement of CT. In other words, there are C and T alleles, which if you turn them around are A and G alleles. Just a guess, not sure.

@tyersome I do think that this and the other question are distinct (and potentially useful to answer independent questions)- obviously or I wouldn't have answered both. This question is more about "how do I figure out what to do with 23andme data" and the other one is more along the lines of "how do I look up stuff about a variant". I agree they're closely related, and the answers happen to converge. But knowing about that convergence is pretty specific domain knowledge about human variant databases (IMO).

Just in case anyone finds this useful:
The data from 23andMe contains information about SNPs (single nucleotide polymorphisms), which are basically single base pairs in your DNA, eg. AT, AG, TT, etc.
However, in many academic papers, the authors usually write about entire genes, which are many SNPs that come together to form a trait. Alleles are simply different configurations of these SNPs for the gene that encodes for something.
Eg.

A gene could be the color of your eyes
Some Alleles for the eye color gene could be ones that encode blue, green, or brown eyes
The SNPs inside each Allele would be different, for example, green eyes could be AA, TT, GG whereas blue eyes could be AG, GG, TT

Therefore, since 23andMe contains information about individual SNPs, there's still work required to understand the SNPs for each Allele. I'm currently trying to figure out where I can find this information.


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Could life protect itself from ultraviolet radiation?
I have heard it argued that life as we know it (DNA-, RNA- and protein-based) could not have evolved without the ozone layer to protect it from UV radiations.
It seems to me that mechanisms to deal with this would have evolved. Is there any scientific evidence on this point?

Life on earth predates the ozone layer by over a billion years.

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site. 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. I suggest starting with a search like "UV protection plant" — you will find a lot of information showing that this has happened (obviating you post). Please see the [tour] and [help] starting with [ask] for details.

Donno, maybe intelligent design shouldn't play with UV to start with. Or leap seconds.

If you're interested in hypothetical questions, perhaps relating to a fictional world you are thinking about creating, then [worldbuilding.se] is a splendid resource for that.

Preamble
The original question asked about fair assumptions, but addressed conviction rather than scientific evidence. This site primarily exists to address biological questions that can be answered or at least approached objectively. It certainly does not exit to rehearse people for arguments against those who have already made up their minds on a topic because of religious convictions. So I changed the question to restrict it to UV-resistance of living organisms.
Answer
It is already known that organisms currently exist that are resistant to ultraviolet radiation. The bacterium, Deinococcus radiodurans, an extremophile which is also resistant to other radiation, is a prime example.
In addition, organisms, including higher organisms, have mechanisms for repairing DNA damaged by ultraviolet light, as summarized in this brief Nature Scitable article.
Hence, even without knowing that the ozone layer postdated the origin of life by a billion years (as @canadianer pointed out), there is ample evidence that life would have managed to deal with ultraviolet light.


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How low potassium can potatoes have due to low potassium in soil?
According to Wikipedia 100 grams of potatoes has 2005 milligrams of potassium.
But if there is low potassium in the soil where it grows, it may not be able to acquire so much potassium.
How little of potassium can a healthy-looking potato have?

Do you have any reference that suggests potato potassium concentration is appreciably affected at all by soil potassium? My naive expectation would be that low potassium in the soil would primarily stunt growth, as this is what generally happens with plants more generally.

@BryanKrause no, i do not have references. i think some molecules are acquired if they are present, not if they are not. i think, potatoes have relatively much of potassium, so they may gather it in amounts much more than it is required for their growth.


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Where to search for which sequence of SNPs belong to specific Alleles
I'm trying to find more information about a specific Allele, namely the "A1 allele of the DRD2 gene". How can I find more information about this allele, and which SNPs are part of this Allele?

I doubt this is enough information. Most SNPs have systematic identifiers starting with rs. This should be available via the 23andme interface, either as raw data download or browser (I don't have it these days so I can't check web, but it's definitely in the raw data). Once you have that number it should be extremely easy to find studies for which that variant is relevant, along with any phenotypic associations of the variant.

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

The systematic ID of this allele is rs1800497.
You can use this information to learn a lot about it. Here is one such resource, here is NCBI on it, there is a lot more via google.
Those links should have everything you ever wanted to know about this variant.


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Why isn't the resting membrane potential at equilibrium?
There has been a question asked regarding the purpose of ion pumps, and the main answer was that the resting membrane potential isn't in an equilibrium state, so the potassium keeps flowing out. Other sources claim this, too.
But why is this the case? For example(in this case considering only sodium and potassium), wouldn't potassium be forced out the cell when sodium starts to enter, and in the same way that potassium builds up an electric force to match its diffusional force to reach equilibrium, the electric force of potassium get stronger to the point that it can counter sodium's inflow? This would create a new equilibrium, albeit different from potassium's Nernst potential, but still an equilibrium.

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

Short Answer

This would create a new equilibrium, albeit different from potassium's Nernst potential, but still an equilibrium.

The Nernst equation is how you determine the voltage at which an equal number of potassium ions move in each direction across the membrane; that seems to be what you are calling "equilibrium" for potassium. If you have two ions and you'd like them both to have zero net flow, their Nernst potentials must be identical. The Nernst potential depends on relative concentration; the only way to change Nernst potential is to change relative concentration.
The Goldman equation will help you find a different "equilibrium": the voltage at which net total flow of all ions equals zero. This gives you the membrane potential with multiple ions present; however, at this equilibrium, as you've read, individual ions are not at equilibrium; for a typical neuron, you can expect that at the resting potential given by the Goldman equation you will have about equal potassium leaving the cell as sodium entering.
Longer Answer
In a typical neuron, there is more potassium and less sodium inside the cell relative to outside.
This makes a negative Nernst potential (=reversal potential) for potassium: to stop net flow of potassium down its concentration gradient and out of the cell, you need negative charge inside.
Similarly, there is a positive Nernst potential for sodium: to stop net flow of sodium down its concentration gradient and into the cell, you need positive charge inside.
The resting membrane potential is a weighted sum of these potentials that are driven by concentration gradients. The relative contribution of different ions to the membrane potential depends on their permeability; the more permeable the membrane is to an ion (through specialized channels), the more important that ion is for setting the overall membrane potential.
For a typical neuron, the resting membrane potential is near the potassium reversal potential, but not quite as negative, due to sodium (and other ions, but for now we can just think in terms of these two).
Let's say, for example, potassium reversal is -90 mV, sodium reversal is +50 mV, and the membrane potential is around -70 mV. The reason it's around -70 mV would be because that's precisely the voltage where as many potassium ions are flowing out of the cell as sodium ions are flowing in.
If pumps keep the concentrations of sodium and potassium constant inside and out, this will stay the same indefinitely: concentrations stay the same means reversal potentials stay the same which means the membrane potential stays the same, as long as ion permeabilities stay the same.
However, with no pump, the sodium concentration inside is rising, and the potassium concentration is falling. That means the reversal potentials won't stay the same. As the potassium concentration in and out becomes more similar, the Nernst potential for potassium drifts towards zero: you don't need any voltage to stop net potassium from flowing if the concentration is equal inside and out. As the sodium concentration in and out becomes more similar, the Nernst potential for sodium drifts towards zero. These potentials are not intrinsic to the ions, they are entirely a function of relative concentrations inside and out. If you lose the relative concentration gradients, you lose the voltage, and, importantly, you lose the ability to influence membrane voltage by changing the permeability of particular ions.

What I'm curious about is why potassium just leaves the cell without forming an electric gradient (by leaving behind anions) when sodium starts flowing in. Wouldn't potassium eventually be attracted back, match the sodium inflow, disable more sodium from coming in, and reach an actual equilibrium as the resting membrane potential?
This is the same way the electric force matches the diffusional force to reach the potassium Nernst equilibrium (which is when we're only considering potassium), but this time also matching the added diffusional force by the sodium inflow.

@SentientRays At the resting potential, the sodium entering equals potassium leaving; that's what the Goldman equation tells you: what voltage will the cell be at when the charge moving is equal. If 100 potassium ions leave and 100 sodium ions come in, there's no electrical change: +100 - +100 = 0. If enough ions move so that concentrations change (like if a pump isn't keeping them constant), you need to redo your calculations.

Oh. So then would the reason sodium increases the membrane potential a bit be that there's initially some space for the sodium to go to, therefore making multiple sodium entering equal one potassium ion leaving for a while until it fills up and one sodium equals one potassium? But then, after that other ions will not affect the membrane potential. If calcium enters after potassium and sodium establish themselves, since the cell is in a state where one charge entering one charge leaving, one calcium would kick two ions out and not affect the membrane potential at all.

@SentientRays Not really following and I don't think anything you are writing is grounded in reality. Use the Nernst and Goldman equations, they tell you everything about what will happen in the cell: Goldman equation tells you what the membrane potential will be, Nernst equation tells you the equilibrium for each ion. Ions will always move according to their Nernst potential relative to the membrane potential.

Alright. I was just wondering if you could explain the mechanics behind exactly why ions change the membrane potential before reaching the inflow-outflow balance.

@SentientRays If the membrane potential is more positive than the Goldman equation gives, you can know the change in membrane potential will be towards the Goldman equation potential. That means slightly more positive charge leaving than entering, making the cell more negative and closer to the equilibrium potential.


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How to predict enzyme activity computationally
if I have an enzyme and its corresponding substrate, are there computational methods that I can use to predict its enzymatic activities? I understand that we can determine its activity using various enzyme assays, but I'm not sure whether these activities can be reliably predicted with computer.

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

Specifically, what do you mean by "its enzymatic activities"? Which of the things you understand can be measured experimentally are you asking about?

There are numerous studies using molecular dynamics to analyze enzymatic activity.


text:
Why doesn't HIV give you cancer if retroviral gene therapy gives you cancer?

More than twenty patients have been treated in France and Britain,
with a  high rate of immune system reconstitution observed. Similar
trials were  restricted or halted in the US when leukemia was reported
in patients treated in the French X-SCID gene therapy trial.[2]  To
date, four children in the French trial and one in the British trial
have developed leukemia as a result of insertional mutagenesis by the
retroviral vector.
https://en.wikipedia.org/wiki/Vectors_in_gene_therapy#Retroviruses

HIV doesn’t seem to cause cancer directly, but over time it causes the
immune system to become weaker, putting people living with HIV (PLWH)
at  an increased risk of many types of cancer.
https://www.cancer.org/healthy/cancer-causes/infectious-agents/hiv-infection-aids/hiv-aids-and-cancer.html

Short answer: Most HIV-infected cells will die before transforming into cancer.
Retroviral gene therapy may increase risk of cancer since the integration into the cell's genome can be faulty (strand breaks, insertion into genes, cell stress and innate immune response, etc. ). Infected cells survive but might transform into cancer later in very rare cases.
HIV also causes integration into the host cell genome, probably causing errors, too. But most infected cells will die (apoptosis, overproducing viruses) before transforming into cancer. But as you said, the lack of an immune system increases risk of developing cancer in non-infected tissues.


text:
Vertebra identification
What type of vertebra is this? It was found on a beach in Corea, Maine.

Definitely mammalian and quite large; my very much a guess is seal. Any chance you could post a photo looking straight down from above with the vertebra in the orientation you have in your second photo

Thanks, I added suggested picture.