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identification of most Active gene/protein isoform
I am investigating a gene, and on ensemble, it has multiple variants. How can i know which gene or protein isoform is most active?

Welcome to SE Biology. Please read the Help on asking good questions, and then take care to explain precisely what you mean, providing adequate context. You capitalized the wrong word in your title, and the one you did capitalize is ill chosen, as it suggests a comparison of their fundamental properties, whereas I imagine you are interested in the relative expression of the transcripts encoding the different protein isoforms. Depending on the organism, this may vary with tissue, developmental stage etc.  But the simple answer is you can’t tell from Ensembl: you need to search the literature.

While David has a point that for specific genes you should look at in vivo data, significant amounts of work has been done to identify representative transcripts, often using direct experimental evidence.
One such effort is MANE-Select. When in doubt, or specifically when doing high-throughput or computational work, I would choose the MANE-Select transcript.
The idea behind it is to find a single transcript that is agreed upon by NCBI and ENSEMBL and to go through various steps of automated and manual curation to provide a "ground truth" expression product for a particular gene.
In vivo data includes techniques such as 5' RACE and CAGE to identify transcript coordinates that broadly agree with transcription starts and stops, among other steps.
Note: MANE-Select is only for human genes so far as I know.


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helm notation for ribosyl in a siRNA
I need the helm notation for the compounds in this patent by Dicerna: WO2023220351A1.
The chemical modifications, defined on page 141, are all like 5'rXmXrXmXrXrXrXrXrXrXrXrXrXmXrXmXrXrXrXrXrXrXrXXXX 3', where the X are to be replaced by the base. without prefix is a nucleotide, with an m is an m-2'-OMe modified nucleotide. The helmet notations would be r{X}P and [m]{X}P in these cases.
I don't get the rX. The patent says it's a r- ribosyl modified nucleotide, but I don't know what is this, and don't find any reference.
Which is the helm for the r prefix? Any other tip (a better name for instance) would be very useful too.

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Adh2 promoter in saccharomyces cerevisiae
I'm looking at expressing a protein in saccharomyces cerevisiae using the Adh2 promoter. My understanding is that the gene will be repressed by the presence of glucose, but when glucose runs out it should be activated. If my strain has deletions in ethanol biosynthesis, will Adh2 promoter still work?

Why wouldn't it? As long as you haven't deleted the transcription factor(s) that bind to the Adh2 promoter, it should work just fine.

I'm coming across publications talking about ethanol encouraging dimerization of the transcription factor into it's active state, and I just wanted confirmation if ethanol is necessary.

Ah. In that case, feel free to ignore what I said and do more research. I don't know much about Adh2 specifically (although I'm fairly well informed about transcription factors in general), so you'll have to see if the promoter is absolutely dependent on EtOH, or if that's just one way it's activated.

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Does alternative splicing contribute to the diversity of enzymes?
I understand the role of alternative splicing in generating protein diversity, but for enzymes specifically, is alternative splicing responsible for the diversity of it? My professor told me something similar to the 1941 “one gene one enzyme” theory, and he said that “Enzyme diversity is coded for in the DNA, each enzyme is coded for by a separate gene, and splicing doesn’t  generate the diversity.” I am a little confused because I thought one exception to the one-gene-one-enzyme theory was the mechanisms of alternative splicing… (obviously DNA itself also creates diversity but I don’t get why alternative splicing is not responsible for it)

It would help to get the exact words of your professor. AS definitely affects protein function (many papers out there, here is one random example). It may not dramatically affect qualitative enzymatic behavior but it certainly can change function.

Please define precisely your usage of the word “diversity” as it applies to enzymes, and explain why you think enzyme diversity (as you intend it) differs from protein diversity in general. At the moment this is quite unclear to me.

The "One-Gene-One-Enzyme" theory is rather outdated now and many of these "One-Gene-X" terms to define how genes work can be inaccurate. For example, after many modifications to that term, biochemist and geneticist George Beadle and geneticist Edward Tatum came up with the term "One-Gene-One-Polypeptide", and even then there are caveats. One is that Alternative Splicing means that one gene may code for more than "One" polypeptide. And two, that genes do not always code for polypeptides, that is, they may code for RNA strands that work to regulate gene expression (regulatory RNA), in fact, genes that encode for proteins constitute only around 1.5% of the human genome! (Source for this passage: Campbell's Biology 12th edition)
Back to the main issue, I wouldn't say that alternative splicing creates a "diversity" in genetic products, I think it is better worded that alternative splicing allows a greater range of products to be formed.
I do not have a specific, well-detailed example of how different enzymes are formed from the same gene that comes to mind, but it is definitely possible that if you can form different proteins from the same gene by shuffling the exon sequences, it can be possible that the shifting of the domains or usage of different subunits of an enzymatic protein by splicing exons in different fashions can affect how it functions.
I did, however, find a publication on PubMed whose abstract states that there are isoforms (protein variants) of Base excision repair enzymes (though at the time of the publication, their function does not seem to be explored).
There is also an example given on Wikipedia on protein variants that uses AMPK as an example of an enzyme formed by alternative splicing of subunits, where some combinations of subunits are more ideal in their function according to where they are located, such as the liver having a different preferred/abundant form of AMPK than human skeletal muscle.
I hope this answer gives you a nice clarification, if anyone finds something inaccurate please feel free to criticize!

There are a lot of different mechanisms by which the "one-gene-one-enzyme" theory doesn't work. Alternative splicing is definitely one of them, but there are other biological processes like post-translational changes that can affect enzyme function. Also, it is very important to take into account that there are many enzymes that work as functional complexes with multiple subunits in which every subunit might (or might not) be coded by a gene with a certain pattern of splicing.
In summary, alternative splicing does contribute to the diversity in enzymes.

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Phenotype-to-genotype mapping
My understanding is that GWAS or QTL attemp to extract potential SNP candidates responsible of a particular trait.
However, is there any framework that attempts to do the opposite? This is, link the phenotypic value of traits to the distribution of allelic frequencies.
For example, given a set of traits construct a classifier (i.e. SVM) for a given SNP and try to predict its allele.

https://en.wikipedia.org/wiki/Phenome-wide_association_study

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mendelian inheritance calculating probabilities help
In a recent exam our teacher gave us the following questions:

Assume that D, E, F, G, H, and I are autosomal genes on different
chromosomes. From the mating (parent A) DdeeFfGGHhIi x (parent B)
DdEEFFGgHhii:
a. What is the probability that one of the offspring
will have the genotype DdEeFFGghhIi?
b. What is the probability that
one of the offspring will be heterozygous for each allele?

Is there any way of answering these questions without drawing a super large Punnett square?
Thanks in advance for helping out.

You need to understand that each locus follows a law of independent assortment. This means, each probability of combinations are multiples of the probability of each element. For example, Dd x Dd goes by

DD (1/4) : Dd (2/4) : dd (1/4)

and Ff x FF goes by

Ff (2/4) : FF (2/4)

If the case is DdFf x DdFF, it is

DDFf (2/16) : DDFF (2/16) : DdFf (4/16) : DdFF (4/16) : ddFf (2/16) : ddFF (2/16).

You can verify my countings by making a Punnett square. However, notice on the first case, the probability of DDFf is basically DD * Ff itself, 1/4 * 2/4 = 2/16. So as others.
To solve your problem, use Punnett squares (or just directly doing it with no issue) for each of the locus. Like this:

Dd x Dd -> DD : Dd : dd
ee x EE -> Ee
Ff x FF -> Ff : FF

What is the probability of having DDEeFF?

DD * Ee * FF -> 1/4 * 4/4 * 2/4 = 8/64

Try this on the question asked. Remember, solve smaller Punnett squares, and multiply for your desired genotype
Good luck!

The hint that the loci independently assort comes from being on separate chromosomes. If they were close together on the same chromosome we would strongly suspect dependence. If the on different chromosomes was absent, I would suspect that the exam wants me to assume independence but I might be temped to include Fre'chet bounds anyway.

I see, @AgnesianOperator. In the case of nonindependently assorting genes, we can opt to genetic linkage. If so, there would be usually two types of questions, First, calculating each probability with genetic distance information in centimorgans. Second, determining the genetic distances between loci from an observed distribution table.
Fre'chet's inequalities are something interesting, but I have not been updated that it is used in genetic mapping or genetic analysis. I would search for more if I missed it.

Yes, using centimorgans is fine if you know the conditional probability of recombination given centimorgans. Haldane's map is an example that might be suitable for a student exercise. I think we agree that in an empirical research setting the data distribution must be considered.

The Fre'chet bounds work for any probability distribution, so they certainly apply whenever we are considering recombination probabilities. Their main limitation is that they can be conservative; the price of assuming very little. If you can make more assumptions about the probability function, then sometimes you can put tighter bounds on the joint distribution.


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Is it possible to genetically alter human beings to see parts of the infrared?
Most electron transitions take place in the infrared region,The ability to see this part of the electromagnetic spectrum without reliance on sophisticated technology would have tremendous advantages. Is it possible to manipulate human genes to see this part of the spectrum?

Our heads are warm, so the receptors that react to infrared radiation would be set off constantly by ambient radiation, not just radiation that comes in through the eye.  Note that the animals that do see infrared are cold blooded.
So it would be a massive genetic engineering project to get working infrared vision, to either make human heads be room temperature, or to thermally insulate eyeballs from the surrounding tissue.

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Is the blastopore imaginary?
I've been told in my zoology class that the blastopore is an imaginary pore found in gastrula, from which mouth develops first in protostomes and anus develops first in deuterostomes. But we've also been told about the famous blastopore grafting in newts experiment by Spemann-Mangold. So how can you graft something which is imaginary? Is the blastopore really an imaginary pore?

Ithink they were referring to the fact it is not actually a pore in the normal sense of the word but instead an invagination. It has been imaged many times https://www.researchgate.net/profile/Jr-Kai_Yu/publication/6564822/figure/fig2/AS:281320203800598@1444083371979/Figure-2-Expression-of-Nodal-the-Nodal-antagonist-Lefty-and-organizer-related.png

From Merriam-Webster:

Definition of pore
1 :  a minute opening especially in an animal or plant; especially :  one by which matter passes through a membrane

The blastopore is a real thing, it is not imaginary. It is the point where the mouth or anus eventually develops. I'm guessing the reason your zoology class referred to it as imaginary, however, is probably because it isn't really a pore (and especially it is not a pore into the blastocoel). It sort of looks like a pore, but it's just a little indentation (and may even be considered a blastopore before the indent forms); it doesn't really become an opening until later, and the process of gastrulation doesn't actually involve anything going inside the blastopore, it's just a folding in of the cells on themselves.
In summary, I think your understanding is sound, good job, and I just wouldn't get too hung up on the "imaginary" part.

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Why don't plants use radio waves?
I heard that the Earth's atmosphere is opaque at most wavelengths and only allows visible light and radio waves through, so why have plants evolved to only absorb visible light?

Probably because radio waves have super low energy.

@AlwaysConfused even humans don't use it naturally. I ain't sure, but as Alex says, there is probably no molecule which can release electrons by getting energy in RF range.

@AlwaysConfused some of your questions can be researched by  googling. Also, comments on StackExchange are for discussing posted question, not other stuff like random ideas

Possible duplicate of Why do some bad traits evolve, and good ones don't?

@AlwaysConfused Comments are not for extended discussion. You can use the chat if you want.

Even if the atmosphere is mostly transparent in the radio domain, most of sunlight is visible light.
Also, to make photosynthesis work, you need photons of high energy (say: wavelength shorter than 700nm) in order to excite electrons in the reaction centres. Radio waves cannot do that.
The most widespread photosynthetic organisms make use of visible light and water, which are plentiful on Earth.


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Intron sequences in course of evolution
In course of evolution did some exons become intronic  sequences or will introns in some species acts as exons in other species.

There are alternative exons (and cassette exons). See alternative splicing.


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Does the cell release the empty capsids?
The virus via the spike of the capsid connects to a receptor in a cell, then the DNA enters the cell wall.
My question is what happens to the capsid - does it stay connected to the receptor or is getting loose.
(e.g disconnected from the cell).

Which virus, and where did you read this? Please provide details — preferably with a link — to your source so that we can try to help you.

I mean any virus. Does it connect to a receptor? After the DNA gets in, what happens to the capsid?

But only certain viruses have spikes, and different viruses use different strategies to enter cells, and those surrounded by a membrane will behave differently to those that don’t, and how long is a piece of string. I suggest you read a little about viruses in general (try Wikipedia), and then about coronaviruses, if that is your interest (try the links on Meta). However it is my understanding that decapsidation generally occurs within the cell, and the capsid proteins are left as litter.

I understood that this is true only for a certain type of viruses namely the bacteriophages. In that case can their capsids gained from a culture be used to induce antibodies?

If your real concern is raising antibodies to capsid proteins, that is a different question. If your interest in antibodies is for detection of viruses or as antiviral agents I suggest you might like to look at some of the links on the Meta page devoted to reputable sources of information about coronavirus.


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Why is ACE2 not used as drug against covid?
Can ACE2 be produced and used as drug against covid? I read it is the receptor molecule. If it is in the organism the virus should bind to it and could not attack cells anymore? Is that right?

There's a Cell pre-print by Monteil et al. (DOI: 10.1016/j.cell.2020.04.004) which argues that human recombinant soluble ACE2 protein can competitively bind to SARS-CoV-2 virus and reduce its ability to infect and replicate:

Here, we report that clinical-grade human recombinant soluble ACE2 (hrsACE2), which has already been tested in phase 1 and phase 2 clinical trials (Haschke et al., 2013, Khan et al., 2017), can reduce viral growth in Vero E6 cells by a factor of 1,000-5,000. Moreover, we show that human blood vessel organoids and kidney organoids can be readily infected, which can be significantly inhibited by hrsACE2 at the early stage of infection.

Though it is not perfect, in that other factors and receptors may be implicated in infectivity:

Our data now show that this clinical-grade human ACE2 molecule - but not mouse soluble ACE2 - can significantly inhibit SARS-CoV-2 infections and reduce viral load by a factor of 1,000-5,000. However, as observed in antibody neutralizing experiments of many viruses, the inhibition is not complete, though clearly dose-dependent. This may be due to the fact that there might be other co-receptors/auxiliary proteins or even other mechanisms by which viruses can enter cells, as had been initially proposed for SARS (Jeffers et al., 2004; Qi et al., 2020).

One person is right to comment that these are in vitro studies. In other words, they treat cell cultures on the functional equivalent of a Petri dish: Vero cell lines or simulations of human tissues (organoids), and they see what happens.
The in vitro studies are useful and important but it is a big step from those to 1) treating people in vivo — designing a drug that can actually and safely target the virus where it infects respiratory and renal tissues — and, 2) making and distributing that drug in quantity, cheaply, safely, etc.
But the larger point of these studies is to show that scientists are definitely thinking about the mechanisms by which the virus infects cells, and to see if there are ways to interfere with and limit the virus, by doing so.
Like your thought to use ACE2, some researchers have looked at other viruses, like poliovirus and HIV, to see if there are similar soluble ligands that they can bond to antibodies and deliver safely to humans, as a general therapeutic idea.
They found that HIV-1, which uses binding to the CD4 receptor as a means to infect T cells, could develop mutational resistance to soluble CD4 and use other mechanisms to cause infection. But by adding a second receptor CCR5 to the immunoglobulin, other researchers were able to limit the ability of HIV-1 virus to evolve resistance to both receptors, which provides some possibility of this approach as a vaccine, down the road.
These issues all complicate use of receptors as a way to "fake out" the virus. But it is an avenue being explored, especially for this virus during a time of emergency.

It should be noted that the study referenced is in vitro and no efficacy has been demonstrated in actual infected individuals, though there are earlier trials (I assume these are the citations in the quote) showing clinical efficacy in ARDS - I believe that relates to the enzymatic activity of ACE2, though, not anything to do with binding to viral particles, and I don't know of any proof-of-concept that would suggest the receptors make it into the lungs where the virus is.

Good points, definitely. Read the preprint in depth.

@AlexReynolds thank you. In that regard I have a question. Has someone tried to use human cells with artificially damaged cell interior that will accept the virus by its ACE2 and other receptors (but not reproduced it and finally destroy it)?

I don't know if such a therapy exists. Maybe others would know. Usually these are immunoglobulins, immune system proteins with unique bits attached that a virus would bind to, instead of the receptors on a lung or other cell that it would normally try to infect.

What about any side-effect of "taking away", i.e. scavenging, the natural ligand of ACE2 (which is physiologically expressed on membranes of epithelia and neurons too(?), thus especially  leading to a lack of counterbalancing of high blood pressurem as ACE2-axis is considering beneficially downregulating the AngioensinII-AT2-axis?


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Can skeletal morphology change in adults?
I'm just a curious layman, so be gentle. I read around that things like the cranial1 and pelvic2 morphology change with age, but I also read seemingly contradictory information that bones are 'completely ossified' around age 25 (can't post a third link for reference) and that's often cited as meaning "done changing."
Wikipedia (my trusty friend) also describes 'bone remodeling' as a lifelong process, yet also describes ossification (not a lifelong process) as a key component.
So I'm confused. What actually changes in terms of bone morphology throughout an adult's life? Does bone tissue continue to form in adults? Do bones "bend" and flatten ever so slightly into new forms? Additional reading would be appreciated as well.
Thanks

+1 for writing a good question. Somebody competent will answer.

The statement "  bones are 'completely ossified' around age 25" means that all bones are now osseous i.e. there is no cartilage or membranous present after 25yrs. This doesn't mean that bone resorption and ossification doesn't take place. The term Ossifocation has different meaning in different context.

Bone never stops changing.
Your bones are constantly being broken down and reformed on a microscopic level. Your bones are done growing at a certain point but they continue to be reshaped. Remember bone exists to supply calcium (and to a lesser extent phosphorus), to your muscles, Your body needs to break down the surface of the bones for this calcium.*  So bone is dissolved and redeposited constantly, this regulated mineral levels but also allows the bone to slowly reshape itself.
Bone will slowly reshape itself to resist any stress it experiences, for instance if you build muscle the attachment point for the muscle will become more rugged to strengthen the attachment. A runner's leg bones will get thicker and denser to resist the greater stresses. Joint surfaces can even reshape with repetitive motion.
*bone originally evolved as armor but this has been lost in modern vertebrates. Vertebrate muscle requires calcium to function, Vertebrates have lost the armor but not the need for a calcium store, and have repurposed into a structural support. Vertebrates without structural bone need to have massive calcium levels in their body tissue instead.
for continued reading there is a whole series of books by R. Mcneill Alexander that cover bones in fascinating detail.

"bone exists first and foremost to supply calcium to your muscles" - What makes you so sure of claiming that? Bones certainly did not evolve for this reason. Also see: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3237026/

oops that was my bad, forgot to add phosphate, good catch. But if you read carefully that source supports my claim, calcium phosphate is resistant to the acidic conditions produced my active muscles creating a calcium and phosphate store that can be modulated. bone did evolve for that reason.

The structural use of bone (originally armor) could only occurred after the ability to deposit calcium phosphate had evolved.

@john What does 'joint surfaces can even respade' mean? Respade means to turn over(Wikitionary). Please can you explain,what do you mean by the above statement?

dyslexia plus a typo, "reshape" I'll fix that.

@adjan Bone evolved first just to rid the body of calcium, This was easily turned into external armor/skeleton. Bone then became biochemically important for how vertebrate muscles work. As armor was lost the calcium was still needed so it shifted to internal storage and reinforcing existing structural tissue. Out of the current uses of bone calcium regulation would be the most primitive. Structurally bone could be replaced but its calcium store function cannot.

@John - Bones are indeed the body's main repository for the critical-to-life element, Calcium. But to say that's why they evolved is a teleological argument. There's a difference.

no there are clear adaptations to make bone better calcium stores, I think you are confusing "evolved to" with "only evolved to"


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official authoritative source for bacterial shape classification
I'm a bit disappointed but after several hours of search, I could not find an official authoritative source for bacterial shape classification. I find a lot, I mean a lot of links but no original sources, even on  Microbiology society no source....
I believe a convention, workshop or another authoritative source must at one point have worked on this matter...

Oxford English Dictionary? Or, as Steve Jobs said about pornography, I know it when I see it.

Shape based classification is somewhat obsolete.

I am well aware that phenotypic classification for prokaryote is obsolete, but I would like to find the source that describes the official acknowledged bacterial shapes.


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When there is incomplete dominance of one allele, is one allele still considered recessive?
When you have incomplete dominance between two alleles of a gene (say, on two different tail lengths blending into an intermediate tail length or two rose colours blending together), can you still call an allele recessive or dominant? If so, how would you tell which to call "dominant" and which to call "recessive"? Do you compare protein expression or measure the difference between the phenotypes of the two homozygous variants or something?
This is purely a terminology question -- I'm aware that the distinction might be a bit meaningless in practice. The closest I could find to an answer is this question, though I'm unsure whether they're measuring tail length to determine the difference between codominance and partial dominance or what.

No - if we have a phenotype, in your case the tail, which we can measure and treat as a numeric variable, and if a heterozygote's phenotype is exactly half-way between that of the two homozygotes, the phenotype is considered not to exhibit. Dominance exists only when the heterozygote's phenotypic value lies closer to one homozygote than the other.


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How do viroids and virusoids cause infection to a specific host ? How could they indentify the host without protein?
We know, the capsule provides specific  pathogenecity for the virus right ? Then ,  how do viroids and virusoids cause infection to a specific host ? How could they indentify the host without protein ? Seems like they could infect any possible living being ? Please make it clear

Welcome to Biology.SE! Thank you for taking the [tour], but please also go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, I suggest adding more information about viroids and virusoids (including references and links). It would be especially helpful if you were to discuss what you have learned about their host specificity. This will both help you get better answers and demonstrate that you have done the expect prior research. Also note that your first sentence is not relevant to enveloped viruses! Thanks!

Wikipedia says that virusoids have a protein coating, which presumably is involved in infectivity.


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Do whales really sleep "head down"?
Currently there is a broadcast in German TV (see https://en.wikipedia.org/wiki/The_Swarm_(TV_series)) where there was a scene of multiple whales sleeping in suspended state, vertically heads down.
The whales were not moving any fins.
The scene looked impressive, but I wonder:
The lungs had some air inside, and when being in suspended state the other parts of the body must have a tendency to sink, as otherwise the whale would surface (by the rules of physics).
Assuming that the lungs are in the front part of the body, I'd assume that that part of the body would have a tendency to surface, while the tail has a tendency to sink (submerge).
So the scene in the film was just opposite to my expectations.
Thus my question: Was the scene real, or was it just artistic fiction?

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site 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. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Well, the best resource that I could find (https://marinepath.com/why-do-sperm-whales-sleep-vertically/) was that sperm whales do sleep vertically, but the text did not mention whether "head up" or "head down".


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How do roots of a seedling know the direction to grow?
When a seedling starts to grow covered by soil, I thought directions are clear:

Roots grow following gravity (down to the water), and the cotyledons
(right word?) grow against gravity, so that they'll reach sunlight eventually.

Once the roots "find water" they'll follow it, while the cotyledons
grow towards the light with the usual mechanism that the lit side
grows a bit slower.

However when watching my paprika seeds grow, I found one case where the roots grew "up in the sky" while the cotyledons were still sticking in the soil.
After some time the roots started their way down, however.
It could be that the strange situation was caused by a rather wet environment (a glass covered with plastic foil), however.
Here are some photos I took (not the best due to small size and using a macro lens):

From these observations I might guess that roots need some initial "dryness" to "know" the direction to avoid, and it seems the roots are important to let the cotyledons grow upwards, to that they reach sunlight eventually.
(another interesting question would be: What triggers the seed to start growing? Is it "temperature plus moisture plus sunlight", or is it just "temperature plus moisture"?
I had to wait quite some while when the seeds refused to "come out")
Who can explain the details?

What triggers seed germination depends a bit on the plant species, usually moisture is required for germination. In addition, some seeds only germinate after a period of cold, or other stimulus. The terms of interest are seed germination (what you call growing), and seed dormancy. Breaking seed dormancy is required for germination.

Plants moving toward/away from light, water, temperature, and gravity are referred to as tropism.
Phototropism
Liscum et al. (2014) provide a nice review.

Phototropism, or the differential cell elongation exhibited by a plant organ in response to directional blue light, provides the plant with a means to optimize photosynthetic light capture in the aerial portion and water and nutrient acquisition in the roots. Tremendous advances have been made in our understanding of the molecular, biochemical, and cellular bases of phototropism in recent years. Six photoreceptors and their associated signaling pathways have been linked to phototropic responses under various conditions.

Gravitropism
Chin et al. (2022) and Sato et al. (2015) provide reviews.

The physiological process of root gravitropism comprises gravity perception, signal transmission, growth response, and the re-establishment of normal growth. Gravity perception is best explained by the starch–statolith hypothesis that states that dense starch-filled amyloplasts or statoliths within columella cells sediment in the direction of gravity, resulting in the generation of a signal that causes asymmetric growth. Though little is known about the gravity receptor(s), the role of auxin linking gravity sensing to the response is well established. Auxin influx and efflux carriers facilitate creation of a differential auxin gradient between the upper and lower side of gravistimulated roots. This asymmetric auxin gradient causes differential growth responses in the graviresponding tissue of the elongation zone, leading to root curvature

I agree that those are the two mechanisms I had suspected, but still there is something unknown: Obviously roots are not phototropic (as an  empiric heuristic "water is not where sunlight is"), but the question is: "Are roots gravitropic?" (as I would expect, but the photo arises some doubts). So is there a third mechanism like "hydrotropism", and if so to roots use gravitropism or hydrotropism, or a combination of both?


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Has the speed of animals changed over time?
I am not a biologist but always had the following questions:
Evolution theory says that the fittest of the fittest pass their genes on. Perhaps an oversimplification, but this would mean that slower lions would be less likely to pass on their genes. For example, lions that are slower would eat less, become weaker, be less attractive to their mates ... and therefore, be less likely to pass on their genes compared to lions that could run faster. And evolution theory also would suggest that the speed of a lion cub would be statistically closer to its parents - faster lions are more likely to produce faster lion cubs and vice versa. Obviously, there is probably a terminal speed - that is, lions wont eventually run at the speed of light, and likely plateau at some speed after many evolutions ... and then the rate of increase will likely be negligible from generation to generation.
This brings me to my question:

Do we know if animals like lions are running faster than they were 1 million years ago?
If we define a new ratio variable as R = (average speed of lions)/(average speed of gazelles) ... do we know if this variable R has remained relatively constant over the past 1 million years?

Thanks!
Notes:

These animals have mutated millions of years ago and their current form might have mutated from their old form. Therefore, a given lion from a  certain species 10 million years ago might be a new species of lion, making any comparison somewhat irrelevant (i.e. comparing apples to oranges)

We assume that animals become faster each year - but its possible that they no longer need to be as fast due to environmental changes (e.g. deforestation caused by humans has changed the habitat of their prey and the prey is easier to catch, and requires less energy to chase).

fitness is relative not absolute, thick insulation is a great adaptation in the artic and horrible in the desert. every adaptation has its cost. the more you are adapted for speed the less you are adapted for anything else, like strength or robustness, just look at cheetah. super fast but easily bodied by basically any other predator.

Modern lions are less than 1 million years old. Last common ancestor ~500,000 years ago. Also - fastest =! fittest evolutionarily speaking for lions. They are mostly stealth hunters - jump and pounce, or short charge.


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What is the biological pathway for the biodegradation of DDT (pesticide)?
There are various micro organisms which can degrade DDT. Which micro organism is most frequently used for biodegradation of DDT and what is the metabolic pathway by which DDT is degraded?


text:
How do animals that live in dens keep the dens from flooding?
When it rains heavily or flooding starts what do animals like foxes,wolves, and any other animal that makes a den or lives underground do.? Do their den's/home's flood?

this depends a lot on the animal but generally the shape or location of the den. Simply don't build dens in places prone to flooding, otherwise the shape of the den works.
Foxes for instance which do build dens is places were flooding can occur build V shaped tunnels to their natal dens, so water would have to run uphill to reach the places they actually use. Beavers likewise dig there dens upwards.
here is picture from something completely unrelated that can help.

https://www.jstor.org/stable/41713116


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How do I identify the carbonyl atoms in a PDB file
Can I infer it from the atom name alone? Or do I need to look at the structure of the residue it is in?

Can you add background to your research, why you need to know, and explain what PDB is?

PDB is a file format that was used with the Protein Data Bank to record information on the position and relations of atoms in a molecule.

Looking at the ATOM records for an Ala residue, as an example:

ATOM    132  N   ALA A  33       0.179 -33.349   1.978  1.00 18.93           N
ATOM    133  CA  ALA A  33       0.316 -32.425   0.863  1.00 21.72           C
ATOM    134  C   ALA A  33      -0.617 -32.824  -0.275  1.00 24.91           C
ATOM    135  O   ALA A  33      -0.538 -33.915  -0.831  1.00 23.04           O
ATOM    136  CB  ALA A  33       1.764 -32.365   0.428  1.00 15.90           C

I've bolded the name field. The carbonyl carbon is designated C and the carbonyl oxygen is designated O. See here for a note on nomenclature:

Atoms names follow the recommendations of described in Pure & Appl. Chem., 70, 117-142, 199

And from that IUPAC publication:

In the peptide backbone, the nitrogen is denoted by N, its attached hydrogen by H, and the carbonyl carbon and oxygen by C and 0, respectively (ref. 20).


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meaning of the name "Dictyostelium discoideum"
Dictyostelium discoideum is a well-known species of slime mould.
Does anyone know what the name means?
Here's my best guess.
I found the 1935 article in which it was first described, but there doesn't seem to be an explanation for the species name 'discoideum'.
It might mean 'disk shaped', as in disk+oid plus an agreement morpheme -eum, because in Picture A in plate I, the sorocarp is described as having an 'expanded basal disk'.
The genus name 'dictyostelium' seems to be a reference to the stalk of the sorocarp, and how it resembles a 'dictyostele' or fern stem ('dictyo' meaning 'mesh' + 'stele' meaning upright stone),
which seems plausible but strange, because I don't think the stalk has any internal structure like an actual dictyostele.
So if that's right, the overall name would be a physical description of the fruiting body, something like 'thing with a fern-like stem on a disk-like base'.
Is any of that even close?

Brefeld described Dictyostelium in 1869. The book/article is viewable here

I worked through the article as best I could. (I don't speak German.) Unfortunately, Brefeld doesn't say why he chose the name Dictyostelium, just "it may be called Dictyostelium mucoroides" (p15) The article suggests he thought it might be a primitive mushroom, or something between amoeba and true fungus. "Mucoroides" seems to mean "like the mucor species," which are fungi that produce a tiny stem with a spore. It sounds like he was using analogies with other species to choose the name.

I think your analysis is correct.
Dictyostelium generally means net-like pillar. Dictyo references a net or mesh, and stele originates from the Greek stēlē: to stand or pillar. However, as you point out, "stele" is also the word for the central vascular tissue in vascular plants. The stele can take on several different architectural arrangements, including a net, or dictyostele, in some ferns.
As I don't read German either, it's unclear to me if Brefeld was referencing the structure in ferns, or just describing D. mucoroides on its own terms, perhaps envisioning the gathering of cells to form the stalk as being like a net. See, for example, this image of a Dictyostelium aggregation.

"Discoideum," as you note, means "disk-shaped," and Raper in his description references "expanded disklike bases" and "basal disks."

Dyctio means to throw, to cast [a net], stellum is star shape, discoideum is a grammatical varian of disk / disk shaped.


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What is the point of Meiosis II, considering Meiosis I already produced haploid cells?
Meiosis I is required so that the 2N cells become 1N, and so a 1N sperm and 1N egg can fuse to become 2N again.
But why is meiosis II required? Why does our body need to go from  2 1N cells to 4 1N cells? Can't it just use one of the 2N cells after Meiosis 1?

Source

After meiosis I, those n=23 chromosomes have two chromatides. Meiosis II just separates them into single chromatides.

befor a cell enters its division its heridity material is in a form of a coilled and condensed material called chromatin whose amount is 2N and is diploid 2n However when the cell enters its interphase  its chromatin dobbles but its no of chromosomes remain 46 so  when cell enters meiosis 1 it produces two daughter  haploid cells 2n having 2  same   sister chromatids attach to same centeromere as cells at the end of meiosis 1 are  haploid 1n but amount still remains 2N to half the amount of chromatin meiosis 2 occur so that 4 daughter cells with haploid no of chomosomes 1n as well as halfed amount of chromatin 1N o can be produced

Welcome to Biology.SE! Please add some references to your answer.


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Can ACE2 receptors be syntesized?
I read that there are labs that can produces the spikes of the coronavirus. I wonder can they also synthesize ACE2 receptors or parts of them? If yes, can they be used as drugs?

It seems like Alex Reynolds gave a good answer when you asked a similar question: https://biology.stackexchange.com/a/93416/52196

You might spellcheck your title.

The Wuhan institue of virology Discovery paper transfected the ACE2 gene (from human, bats, mice) to HeLa cells making those transfected with human-ACE2 susceptible to SARS-CoV-2, thus proving the virus relies on this receptor for entry. Transfection means synthesizing the DNA gene in a plasmid form then adding lipofectamine to force entry into the cytoplasm then nucleus, the corresponding protein is synthesized by ribosomes and gets expressed on the cell's surface (due to a signal peptide)

The drugs you are referring to are called receptor mimics or peptide inhibitors.  Yes, molecular mimics for human ACE2 can and have been synthesized.  Binding of these mimics to coronavirus spike proteins leads to sequestration or inactivation of viral particles.

Relevant literature:
Romano M, Ruggiero A, Squeglia F, Berisio R. An engineered stable mini-protein to plug SARS-Cov-2 Spikes. bioRxiv. 2020.
Han Y and Král P. Computational Design of ACE2-Based Peptide Inhibitors of SARS-CoV-2. ACS Nano. 2020;14(4): 5143-5147.
Walls AC, Xiong X, Park YJ, et al. Unexpected Receptor Functional Mimicry Elucidates Activation of Coronavirus Fusion. Cell. 2019;176(5):1026-1039.e15.

Thank you very much for the exhaustive answer. Can these be effective drugs against covid and eliminate it? Are there clinical trials on the run? I see the articles are from very recent.

I'm not sure if any of the proposed drugs are currently in trials -- I'll be sure to update my answer if I find out.


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How can I introduce Na+ in cells?
If in a solution with living cells Na+ ions are included do the cells intake it only because of the concentration?

May I suggest you look up ion transporters and ion regulation and how they work.

Also maybe explain what you're trying to accomplish.

@BryanKrause I want to feed the cells with Na+ so they get a charge. So I think to pour more Na+ in the solution. Will they eat it?

@bob1 I don't want to get into some difficult stuff. Just want to know the result and practical ways to put charge in a cell.

@Mercury In that case you need to include that information in the question - because we don't know what you want to do and why. I read it as a question on physiology of ion uptake, not a practical question.

Neurophysiologists do this with patch clamp, placing a glass pipette against the membrane and using suction to pierce it; you need to gain access to the cell physically.
Doing this will fill the cell with whatever solution you have in your pipette; you'll need to use something similar to what the cell has inside, but you can tweak it a bit, like adding more sodium. If you just want to change the charge of the cell, you can do that with your patch clamp amplifier directly.
There is no other way to do this. Ions move by diffusion through membrane pores called ion channels; any positive charges moving across a membrane carry with them a positive charge that will repel further positive charges from moving across that membrane. If you use the patch clamp technique to tweak things, ions will keep moving according to their charge and permeability; any space that you make more positive will result in positive ions leaving that space and negative ions coming in.
You will kill cells if you disrupt things too much. Most of the energy that biological systems use goes, in one way or another, towards maintaining the specific environment that a given biological cell or organism is adapted to.


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What's a name for this type of setae on a crayfish
What's a name for this type of setae? It's found an the base of the antennal peduncle of a crayfish. They are roughly cone shaped. They look like spines but are flexible. Would they simply be called conical setae?


text:
bilateral symmetry: word for clockwise rotation on right and counterclockwise on left
It seems like there should be some terminology for bilaterally symmetric organisms that could be used in descriptions, where a clockwise rotation on the right is equivalent to counterclockwise rotation on the left. Is there a name for this type of rotation?

I'm a little confused by your description - do you mean mirrored motions - like if you swim the breast-stroke or butterfly (or bird's wings flapping etc?). If so there are so many motions possible, there isn't a single term.

radial symmetry?


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Free diving physiological changes
When training for free diving, there are several physiological and psychological changes that enable this activity, however one of the changes that I do not understand is increased resistance to blood acidification.
Part of the resistance to pain is psychological but from my understanding the body itself is also less sensitive to the carbon dioxide buildup in the blood itself, so I am wondering how this happens. Is this a change in the nervous system, blood or chemoreceptors themselves?

According to Libretexts Medicine link There are two types of chemoreceptors that help regulate breathing. Those with the most impact, the central chemoreceptors, can be desensitized. The relevant quote is:

Central chemoreceptors: These are located on the ventrolateral surface of medulla oblongata and detect changes in the pH of spinal fluid. They can be desensitized over time from chronic hypoxia (oxygen deficiency) and increased carbon dioxide.
Peripheral chemoreceptors: These include the aortic body, which detects changes in blood oxygen and carbon dioxide, but not pH, and the carotid body which detects all three. They do not desensitize, and have less of an impact on the respiratory rate compared to the central chemoreceptors.

From FreediveUK website. There are two types of breath training necessary. One is psychological, to learn to control the breathing reflex due to high CO2 levels and the other is to train the body to operate with lower levels of O2. They also mention the mammalian dive reflex which produces a physiological response:
When the face is submerged and water fills the nostrils, sensory receptors sensitive to wetness within the nasal cavity and other areas of the face supplied by the fifth (V) cranial nerve (the trigeminal nerve) relay the information to the brain.1 The tenth (X) cranial nerve, (the vagus nerve) – part of the autonomic nervous system – then produces bradycardia and other neural pathways elicit peripheral vasoconstriction, restricting blood from limbs and all organs to preserve blood and oxygen for the heart and the brain (and lungs), concentrating flow in a heart–brain circuit and allowing the animal to conserve oxygen.

As an aside: If you go to the freediveuk website they have an article warning about using hyperventilation. You would think this would help, and it was actually taught for many years as a technique. But it turns out that this greatly lowers the concentration of CO2 and you do need a high level of CO2 to signal that it's time to surface. What can happen is that the diver stays down too long, so uses too much O2 and as the diver gets close to the surface the O2 partial pressure decreases and the O2 level in the blood falls so low that the diver blacks out.


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How does the brain activate retinal cones in darkness?
The activation of retinal cones by light is how vision is formed; yet there are other methods, such as mechanical one, for activating light, such as pressure photopsia/phosphenes. This occurs when ones rubs their eyes strong enough.
Yet even without light or mechanical pressure, at complete darkness, there can still be vision generated. I understand the underlying reason for this is the brain's necessity for stimuli; yet how do the cones activate in this scenario?

I don't know the answer to this, but a logical possibility is that it's not the cone "activating" but the brain simply amplifying the signal.


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How does red light change the cellular mechanism in cells?
As winter approaches and the amount of sunlight decreases in the northern hemisphere, I have been reading about red light therapy and its supposed beneficial clinical effects.
Yet there is no much explanation for how red light impacts the metabolism and inflammation related to the mitochondria, which is the supposed benefit of this therapy.
Is there any in depth explanation of the impact in the molecular machinery in the body? Does red light impacts/effects change when red light is exposed to different cells/organs?

We ask questions to demonstrate prior research. An example in this case might be to show evidence that red light therapy is effective for something, such that it's appropriate to ask a follow up question about the mechanism.

The claim is that red light therapy decreases inflammation and increases ATP production; my question is the pathway that allows this + the supplementary question.

Okay, but whose claim? What is the source? Demonstrate the research you've done so far.

Sorry for entering the conversation from the side.
I am a little interested in the topic and found this paper.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4126803/
This paper explains here;
The photons are absorbed by mitochondrial chromophores in skin cells. Consequently electron transport, adenosine triphosphate (ATP) nitric oxide release, blood flow, reactive oxygen species increase and diverse signaling pathways get activated.
As my thought, Mitochondria were independent bacteria until they were incorporated into cells, so I don't think it is strange that their activity is activated in response to light.
I believe that the mitochondria had chromophores that absorb red light well out of the wavelengths of light.


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Why does the luminal test need hydrogen peroxide?
In the chemiluminescent reaction of Luminol in an aqueous solution, the luminol needs to react with molecular oxygen to produce a photon of blue light. In the technique, the hemoglobin of blood decomposes hydrogen peroxide to produce oxygen, which then react with the luminol.
My issue is; wouldn't there already be oxygen present within the blood itself or from the environment that would react with the luminol itself? Am I missing something?

wouldn't there already be oxygen present within the blood itself or
from the environment that would react with the luminol itself?

I'd say that's the exact reason why peroxide is added.

Without peroxide, the oxygen in blood stain may not contrast clearly enough with environmental oxygen, and you got uniform background (if detectable) luminescence everywhere.

With peroxide, the iron in blood stain suddenly produce huge extra amount of oxygen, and everywhere else the background is kept low, which gave away where the stains are.

That's if you are looking for the blood (with the help of oxygen). If you are looking for the oxygen itself, there should be other methods (electrochemical  sensors, etc).


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Is this a bedbug or something else?
Found it on my bedsheet close to my pillow. My boyfriend had a couple of welts a few weeks ago on his chest, but we can’t seem to find any other evidence on the mattress or around it.

Welcome Mel. Please take our [tour] and refer to the [help] for our guidelines as and when. Could you add some more detail such as what area of the world you might be in, if there was food involved nearby etc..

Does this answer your question? Insect identification - Is this a bedbug?


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Why did the requirement for coronary circulation arise?
Why the heart does not absorb the blood directly(for it's oxygen requirement) rather than taking it through coronary circulation?
Is it related to the permeability of myocardium?
Having such a circulation system can help in avoiding diseases which arise due to issues in coronary circulation.

Oxygen and nutrients diffuse out of capillaries into surrounding tissue.
If you don't have sufficient density of capillaries, diffusion distances are too long, and tissue becomes anoxic and dead. See for example:
Henquell, L., Odoroff, C. L., & Honig, C. R. (1977). Intercapillary distance and capillary reserve in hypertrophied rat hearts beating in situ. Circulation Research, 41(3), 400-408.
In other words, the heart muscle is far, far too thick, even in a rodent, for enough oxygen to be delivered without vascularization of the myocardium.


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Why do trees grow closer together and lower near the tops of moutains?
I hiked up a ~5000 ft mountain in upstate New York. As I ascended, the trees became less tall. That makes sense to me, because of the harsher environmental conditions. I also observed that the trees became much closer together, as the altitude increased. I am struggling to explain this. Why do these two effects happen?
First image below: Tiny trees, very close together, ~5000ft
Second image below: Mid height trees, somewhat close together, ~4000 ft
Third image below: Tall trees, spaced far apart, ~2000ft

Is it not that the trees grow wider as they get taller?

Are you saying taller trees are also wider, and therefore have to grow further apart, to avoid interfering with each other? Can you give other examples of environmental conditions (not altitude) which stunt trees and cause them to grow closer together?

look up the term "tree line"

Question is, how do conditions just below the treeline influence the spacing between trees? Logically one might imagine that trees get further apart just below the tree line, due to tough growing conditions, but the opposite is true empirically...

To me, it is unclear towhat extent the 5000ft picture is showing individual trees growing closer together or several small trunks or branches coming from one or a smaller number of trees. In Picea at high altitudes it is common to find them crawling close to the ground and/or with several apical tips (due to harsh environmental conditions).
This does not invalidate the question, and the answer from @bob1 is a good starting point. My feeling is just that you might be misinterpreting the first picture a bit.

Even there are few trees, with many trunks, the trunk density per square meter is high, and increases with altitude. So, a slightly modified version of the original question still stands

I'm not from North America, but I think there are a few factors at play here that might answer your question.

There are several species of tree present in your photos. The 2000' photo shows both hardwoods identified by @Eonema (thanks for all of the ID's) as Acer rubrum (Red Maple), A. saccharum (Sugar Maple), and Picea rubens (Red Spruce). The middle (4000') shows mostly a conifer species, which is Balsam Fir (Abies balsamea) with some hardwood Sorbus americana (American Mountain Ash). The top (5000') is the conifer Picea mariana (Black Spruce). Each of these different species have different habits of growth. Conifers tend to grow a single strong trunk with a cone-shape of relatively small limbs. Hardwoods have a different structure with a trunk that spreads and divides into several strong branches to produce a wider top or middle than bottom (arrow head shaped) or a very wide flat top. These different growth forms mean that you get wider spread of the trunks at lower altitudes, where the hardwoods exist. Conifers tend to be tougher, so often grow to higher altitudes than hardwoods. There are also species of plants that are specialist alpine growers and have forms that are naturally short or procumbent.

Competition. In all environments organisms, including trees compete for resources. In lowland sites, resources tend to be more abundant than they are at higher altitude. This means more free water, more nutrients etc, so plants tend to grow taller.  Taller also means wider in the context of trees. In all spaces, competition for light is a big factor. If you observe carefully, saplings of hardwood species under the canopy tend to be thin and not very wide until they reach the canopy, where they spread out - this is from competition for light. At higher altitudes, the plants grow slower and as height and width are somewhat correlated in trees, they tend to be able to grow more densely.

The climate is also gentler at lower altitude - less very strong sunlight, higher temperatures (in general), rain rather than snow/ice, less wind. This means that plants tend to grow faster and get bigger as they have longer growing seasons and are more protected from the elements than at high altitude.

Wind. In exposed places, particularly near ridge tops, there is less to impede the wind, so you get stronger winds. This leads to something called krummholz or wind shaping. It results in low mat like forms of the trees and often includes "tree flagging" (see last two images on Wikipedia page for krummholz above) where you get a stem with branches pointing away from the prevailing wind direction. It is a very strong factor in plant height in exposed places, resulting in shorter stem lengths, and wider and stronger trunks. This effect is thought to be a major driver in shape and height of plants at altitude (see this article for more information).

2,000 ft photo is Acer rubrum, A. saccharum, and Picea rubens; 4,000 ft is Abies balsamea and Sorbus americana; and 5,000 ft is Picea mariana :)

@Eonema Thanks. I'm not good at North American trees. Didn't spot the Ash in the 4000 ft photo.

So at ~5000 ft Picea mariana is growing only ~12 inches tall with only a few inches between individuals. In lowlands, the same species usually grows much taller and more spaced out. High wind, cold, weaker sun, more snow/ice: these factors likely cause the ~5000 ft individuals to remain short. Shortness correlates with lower width. And low width causes a higher density, due to less competition between individuals for light and water. Is that a reasonable summary?

@have_beard_will_ski I think a procumbent/scrambling form of the plant there - basically leaning over with the trunk more or less parallel to the ground and branches radiating from that, or a lack of an obvious trunk, more lots of branches from one spot. The branches etc might touch the ground and root themselves in spots, which would make it hard to tell, but I don't know how much conifers do this. Basically one plant forming the mat rather than lots of plants, so actually low stem density...

... mostly because of the low chance of a seed finding a good microenvironment (warmth, free water, not too windy etc.) suitable for growth of young tender shoots at altitude. Once the mat has formed. it might be suitable for growth from other individuals though, so you might get localized patches of high stem abundance all within one krummholz mat.


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Nature of firefly Luciferase reaction mechanism?
The bioluminescence of the firefly luceferin (FL) is a two step process, with the first step requiring the enzymatic/catalytic ability of the luciferase to convert the FL into  luciferyl adenylate.
Are there any descriptions for the mechanism in which the Luciferase facilitates the reaction of ATP with the firefly luciferin?

I answered a similar question of yours about aequorin, initially explaining how to go about finding the information and subsequently explaining in some detail aspects of the enzyme mechanism. Perhaps you didn't see my expanded answer, but until you respond to that (accepting it if it answers your question) I have no way of knowing whether that type of answer is what is required.  I described how to go about finding literature on enzyme mechanisms. What are the results of your efforts to do that in this case?


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What is happening with this hummingbird and how can I help him?
Today I noticed a hummingbird next to my feeder (California) which looks very strange. From my observation it seems that something sticks from its head. This thing is rigid (does not look like a spider web) and bothers the bird (from time to time the bird tries to use a leg to get rid of it).
The bird can fly (slower than other hummingbirds) and it seems like it eats from the feeder (but puts its head deeper into the feeder than other hummingbirds).

What is this? And more importantly how can I help the bird?

Welcome to Biology.SE! You might have better luck at [Pets.SE], since this is essentially a veterinary question. If you do decide to try there (please check their help section for suitability), please either request migration or delete this post before reposting there (cross-posting is impolite). Good luck!

@tyersome thanks for the reply and sorry if this question is inappropriate here. I was looking at pets but thought that it might not be the right place as hummingbirds are unlikely to be pets (agree that this is more a veterinary question). If you think it is better to migrate it there, please migrate it.

No problem! I've seen a few wild-bird related posts at [Pets.se] , but I'm not active there so I can't guarantee this will work there. I'm not a moderator, so I can't migrate this. If you want to initiate migration, just flag your answer and select "in need of moderator intervention". Enter something like: Please migrate this to Pets.SE, I think it would fit better there because .... Alternatively, you can delete the post from this site and repost it on Pets.SE. ——— It also might be more effective to reach out to a local wild animal rescue organization for advice/help.


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Can plants absorb organic compounds?
Plants are autotrophs, meaning that they grow by building organic matter out of inorganic compounds (and energy).
Is it then also true that plants are generally not capable of absorbing organic compounds? There are certainly some plants that can do it, e.g. carnivorous plants absorbing amino acids of their (dissolved) prey. But what about, say, the common sunflower on my balcony?

Plants growing in tissue culture absorb sucrose.

Yes plants can absorb organic compounds..For example plants can absorb citric acid

Due to citric acid’s ability to chelate metals and be absorbed by plants, it is hypothe-sized that exposure to it will increase the ability of wheat-grass  to  absorb  macro-  and  micro-nutrients,  as  well  as  heavy metals, from soil.

Citric acid chelates absorption
Also plants have the ability to absorb and release sugars.

Plant roots are able to absorb sugars from the rhizosphere but also release sugars and other metabolites that are critical for growth and environmental signaling. Reabsorption of released sugar molecules could help reduce the loss of photosynthetically fixed carbon through the roots

Monosacharid absorption activity
I'm sure there are other examples, feel free to edit the answer.

There are whole groups of plants that don't photosynthesize, but which derive their nutrients from other plants in various ways.
For instance, the common (hereabouts) Snow Plant https://www.fs.fed.us/wildflowers/plant-of-the-week/sarcodes_sanguinea.shtml gets nutrition from soil fungi (mycorhizzae) which in turn get it from conifers.
There are a great many other parasitic plants, which derive some or all of their nutrients from other plants, or from soil fungi.  See e.g. https://en.wikipedia.org/wiki/Parasitic_plant
Then there's the whole subject of mutualistic relationships between plants and mycorrhizae fungi: https://en.wikipedia.org/wiki/Mycorrhiza


text:
Probably a moth larvae but better to confirm

What I know,
It reacts to light
the red seems to be blood but can't say for sure
1 to 10 mm
it has a casing of something soft fabric possibly
it grabs to walls

That's what I thought, but I still have some doubt because it only has one black spot.

This is probably a larvae of Tinea pellionella, the case-bearing clothes moth.
T. pellionella is a species of tineoid moth in the family Tineidae (i.e. the fungus moths).


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Beetle (?) on Acacia (Senegalia) greggii?
I was working on my botany skills and took a photo of Acacia (Senegalia) greggii.  When I reviewed the photos, I saw a beetle (I think it's a bettle) that I had not noticed in the field.  I'd say its body is about 2 cm long.  This plant was growing in a dry wash in Phoenix Arizona USA, and the flowers on the plant were just maturing.  Observed around 9 am and the temperature was about 75-80 F. What species is this insect?

Looks to me like the Longhorn beetle (Schizax senex), possibly a female, but it is hard to judge the length of the antennae. This beetle has long antennae (hence the longhorn name), with the male having antennae that are nearly twice as long as the female. S. senex is the only species of the genus.
They are hirsute with a pale margin to the wing cases. The species was described in 1873 by LeConte, with the description being rather wonderful (in my opinion):

Niger opacicus, pube breve minus subtili cinerea vestitus, prothorace fortus, elytrus subtilius punctatus, his marginae suturali laterali apicali et scutello fulvo-pubescentibus

My very rough translation - better Latin scholars please fix:

Black opaque, hair short with subtle grey arrangement, prothorax strong, wing cases with subtle dots, and the join margins and edges pointed and scutes fawn-coloured and very hairy.

Note that I found this with a very quick google of "beetles arizona" and scanning through the linked arizonensis beetles page, which was at the top of the links provided by google. I am not from the USA or in the USA, so please anyone with a better identification, feel free to chime in.

Looks like a very good match, thanks!


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Is this a bed bug shell?
What is this bug shell I found under the bed at our rental home on the Oregon coast in the US? The head was about the size of a pencil eraser and the body was larger.
Thank you!
-Laura

I have additional photos, but I'm not sure how to post them...

I found another shell that was a bit more recent and definitely a "potato" or "pill" bug. The little projections at the head were similar. Does this photo fit that type of insect?

Confirmed by an entomologist: it's a sow bug (AKA pill bug or potato bug). They like high humidity areas...

In that case you can self-answer. Just write an answer using the box below. I would include the details from the entomologist that confirmed that this is a sow bug rather than anything else, just to make sure that it makes a quality answer. - Don't just write "It is a sow bug, confirmed by an entomolgist" - add some detail.

Entomologist-identification: Sow bug

Welcome. answers to species ID require a link with background information, a photo of the identified species confirming the image in the question and, preferably, your post needs additional detail that supports the ID, such as overlapping natural habitats etc.


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Do you have sharpened senses when you're hungry?
I'm curious if longer periods of hunger lead to a heightened acuity of your senses, especially hearing, which I suspect noticing in myself.
Googling for it mainly revealed "listen to your gut"-type of blog articles, but I did find one blog post that mentions

I had my earphones in a few evenings ago (which, I should add, are noise cancelling and really do the job!) while fasting, and I felt as though every chord, synth and lyric were infinitely clearer. It’s left me speculating about whether, by not feeding one of your senses (in this case, taste), you can sharpen another sense and strengthen it in that moment. They say that’s why a cinematic experience is best in total darkness, because your senses are stimulated and acutely refined.

So there is at least one other person that makes this claim / had hypothesized it at one point.
From an evolutionary perspective I think it'd make sense to increase sensorial input in order to be able to find food easier, when you're getting lower on energy.
Have any studies been made on this theory / is there any merit to it?

I think you need to look into anorexigenic and orexigenic neuropeptids, like AgRP, NPY vs POMC/CART. And the genetic regulatory networks that keep together the body energy intake and out-take. These neuropeptids regulate the activity in mammals and hunger or satiety does have an effect on their proportions in different regions of our body, therefore making  us more active when hungry and less when satiated. I think that this seems like ongoing research and the role of all the involved elements is not fully understood.


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How can I self-learn some ecology without prior exposure?
I am a college student and have just about no experience with Biology. I was homeschooled and took a bit of biology, however, not only did I do very little of the program—but it was at a homeschool event that was taught by parents in the community and sometimes didn't always include the most factual of information.
As such, I would love to expose my self to biology. I love animals and think it might be interesting—but have no exposure to base this off of.
Is there a good book or something I can spend some time reviewing? Are there any resources that may help me better understand what the study of ecology is about and if I am interested in it?

P.S. I am having some struggle formatting this title in a way that would make it easier for fellow students to find this questions. If you have a better way of stating it, please recommend a change.

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works.

This question is quite difficult because we don't know how much biology you have, so even recommendations of text books might be well above what you want. For instance, if you don't have some understanding of evolution, then phylogenies and taxonomy might be a struggle to grasp intellectually.
Your college might have some textbooks available to give you something to browse; try the basic Biology ones aimed at first-year students; they'll be called something like "Biology" or "General Biology". Otherwise try checking out the texts at Libretexts; they have an ecology bookshelf. If these are both beyond you, you will need to look at high-school texts or try taking foundational courses to give you the basics.
There is high-school level information available on sites such as Khan Academy as well as others. I had a quick skim of some of the Khan Academy pages and they seem OK, and they have a decent reputation for free content on many topics.

Thank you so much for your response! Please treat me as if I have no exposure!

@SpreadingKindness I recommend starting by reading Wikipedia or "A very short introduction" type of book to get familiar with the terminology. Such introductory texts can act as an equivalent for lectures. Only after your brain has indexed the rough brushes of ecology should you read the textbook, as the textbook can be daunting and demotivating for beginners.

I agree that a broad balanced textbook on biology and ecology (which should naturally also include some evolution) would be the best bet.


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Can you help me identify which animal this bone belongs to?

I found this interesting bone on the shore of Lefkada in the Ionian sea. I can’t find a similar bone to determine which animal it belongs to, nor can I determine whether it’s from a terrestrial or a marine animal. On the bottom side there was also a brownish gooey substance, but I don’t know it it was decomposed meat or just something else that stuck to it. I thought it was maybe from a caretta caretta but their skeleton is different. As for substance, it felt and looked like a bone, it definitely wasn’t a plant.

What about this specimen makes you think that it's not C. caretta? It looks a lot like a hyoplastron to me. For comparison, see https://www.researchgate.net/figure/Specimens-of-Caretta-caretta-Left-dorsal-carapace-view-and-right-ventral-plastron_fig3_340649642

Looks like a holdfast, probably from a seaweed, to me.

Could you edit to give some idea of scale? Don't suppose that you've a picture in profile, and from below? Maybe a close-up of the surface structure. Can you describe the texture and flexibility of the fringes - were they bone-rigid or softer?

Based on the shape, the location, and the fact that the OP is confident that the specimen is bone and not plant material, this appears to be the hyoplastron of Caretta caretta, the Loggerhead Sea Turtle. The Ionian Sea is in the range of the Loggerhead, with nesting sites on the southern coast of Italy and Southwestern Greece.
I have outlined the specimen in red, for comparison with the hyoplastron outline from Yudha et al (2020) (numbered 10 in their figure). The shape is a very close match. The hyoplastron of the Hawksbill Sea Turtle (also in Yudha et al. 2020) is also a near-match, but the Hawksbill is not thought to occur in the Ionian Sea.

I'd say based on what we've got, this fits perfectly.


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Will carpenter bee larvae die if trapped or find a way to bore out?
I had a carpenter bee problem last year, beginning with the awful sounds the larvae make! The exterminators couldn’t find the bore holes (they were/are inside a gap between top of the foundation and sub floor of what was once a garage).  I eventually hired a contractor, who removed the vinyl siding, and discovered a straight line drill hole up the plywood!  He replaced plywood and insulation, saw no other evidence (except two dead bees), and sealed up the gap. It’s now spring, and I am hearing them once again.  My fear is that there is a gallery in a floor joist. If there ARE larvae and they ARE there, will they eventually just emerge into that now sealed up gap and die, or bore their way through where it was sealed or, worse yet ~ my floor?  Thank you.


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ID microbe found in moss sample (USA)
I found this microbe after putting a wet moss sample under my microscope. It latched on to a piece of moss and scanned the area around it for prey, and when it didn't find any, it slowly swam away. It's fairly large for a microbe, and it's rectangular with two big green spots. I'm not sure if the spots have any significance (I thought for a second it might be mitosis, but I'm not sure).
Some pictures at 250x and 400x:

Any information would be greatly appreciated!

Are you sure it wasn't just moving in water currents on the slide?

I am not 100% sure on this, but it looks very like a diatom. These are a range of very diverse unicellular algae found world-wide in soil and water environments (salt and fresh). There are a huge number of species (also genera, families etc.).
The reasons I think that this is a diatom are that it has what appears to be a thick transparent wall (photos 2 and 3) and has a "cut in half" shape - where the word diatom comes from (dia divided, tomos I cut). Diatoms are usually between 20 and 200 micrometres long, so 250-400x observation fits fairly well.
I think what you have here is a pennate diatom (see images under "classification"). Some pennate diatoms are motile
There's an image of one that resembles yours here (see second image)


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Can a dead fish be made to twitch via electrostimulation?
Galvani in the 1700s famously showed that a dead frog can be made to twitch by electric stimulation. The hind legs are particularly susceptible. Salt helps in the activation, as shown in these videos:
https://www.youtube.com/watch?v=sJifWqUa2pY
https://www.youtube.com/watch?v=2YZJt_Bw3eo
Can the same be accomplished with a fresh dead fish? Fish are more easily available for demonstrations to children. Have you tried this, and if so which part of the fish is most readily stimulated?

This is quite immediately post-mortem; we aren't talking grocery store frogs, if that's what you're thinking.

With fish, the hearts can be stimulated to beat just by prodding them.
Learnt a long time ago, preparing fresh fish given to me by others.

Works with mammals, including humans, too.


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

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

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

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

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


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Estimates for the volume and mass of most ancestral multicellular organism, and a similar question for alive animals with radial symmetry
please I'm interested in an estimate for the volume and weight, the mass, of (most) ancestral multicellular organisms. Wikipedia has the article Multicellular organism, and my main interest are estimates for ancestral eukaryotic groups (the oldest and simplest of these fossiles) in the International System of Units.
Other question of my interest are the same estimates of volume an mass for alive animals with radial symmetry. I apologize if my question bother some user of the site Biology Stack Exchange, I'm not a biologist. Wikipedia has the article Symmetry in biology, and I clarify that the approximations/estimates are for a typical specimen of the cited in this paragraph: alive animals with radial symmetry.

Question. Please provide estimates for the volume and the mass, of (most) ancestral multicellular organisms, and for the volume and the mass of a typical animal (of our geological epoch) with radial simmetry. Many thanks

I'm motivated to ask these questions after I read the book by Walter Álvarez [1], and inspired in  a graphic, the Figure 2.1, that refers the book [2] by John D. Barrow. I know the Spanish editions of these books.
References:
[1] Walter Álvarez, A Most Improbable Journey: A Big History of Our Planet and Ourselves, W. W. Norton & Company, (2016).
[2] John D. Barrow, The Constants of Nature, Jonathan Cape; 1st edition (2002).

Please if my question isn't suitable for the site add a comment, I can to delete the question in next hours.

Welcome to the Biology Stack Exchange. Please take a [tour] and visit the [help] for more information on what we do here and what makes a good question and answer. Note that we usually ask that the OP make some attempt at answering the question for themselves. We also have a requirement for answers backed with references - which might be a challenge for this question. I would guess multicellular algae, <1 mm across and a few micrograms in mass.

Many thanks for you kind messages. I'm mathematician, I am not able to answer my question, I think that I'm not able to answer the kind of questions that I'm asking in this site Biology Stack Exchange, these are of my invention since I'm curious about from the books that I read @bob1 . I don't know how to search information related to Biology, and I add the encyclopedia Wikipedia as general reference for all users and because my English is bad. If you want, please expand you comment in an answer.

The browser of Google has an answer for "What is the oldest known fossils of multicellular eukaryotes?", but I don't know how to estimate the density and length/volume of a fossil (estimates for the organism corresponding to the fossil, when this organism was alive). I'm agree with the requirements of the site and I add the promise of make more attempt of answering my questions @bob1

I'll convert this to an answer...

So, it looks like it all depends on how you define multicellular - living in mats/biofilms, which are often mixed species, isn't necessarily a multicellular organism, even though it can behave like one, but might be one of the steps along the pathway to being multicellular.
In addition, organisms that live as a group/chain of cells (such as Spirogyra, or many bacterial species which grow in clumps or chains such as Staphylococcus aureus or Streptococcus pyogenes) are not necessarily multicellular organisms.
The earliest I could find that seem to fit the description of Eukaryotic and Multicellular is a report in PLoS Biology entitled: "Three-dimensional preservation of cellular and subcellular structures suggests 1.6 billion-year-old crown-group red algae" (Bengtson et al, 2017). In this paper, they discuss fossils of a couple of thallate multicellular red alga from about 1.6 billion years ago (Palaeo–Mesoproterozoic).
They state that the structures are:

The 58–175 μm wide Rafatazmia tubes are up to ca. 2 mm in length

and

The thalli are megascopic, ranging from approximately half a millimetre up to well over 3 mm across.

So - pretty small. I don't know how this equates to mass, but I would guess a wet weight (i.e. living state with no additional water) of about 0.5 grams.
Full reference: Bengtson S, Sallstedt T, Belivanova V, Whitehouse M (2017) Three-dimensional preservation of cellular and subcellular structures suggests 1.6 billion-year-old crown-group red algae. PLoS Biol 15(3): e2000735. https://doi.org/10.1371/journal.pbio.2000735

Thank you very much I will study your post. It looks like one of the most nice posts I've seen on these sites Stack Exchange. The origin of biofilms seems misterious and fascinanting (I didn't know this article of Wikipedia about biofilms). Many thanks for your work (your remarks  and bibliography) that will be interesting for your colleagues; next time I try improve my research about the questions that I'm asking, but your work is unbeatable. My main interest was the details that you've provided.


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Are there any drawbacks to having immutable DNA during lifetime?
Imagine that there is a way to prevent cell DNA from being changed once zygote has been formed. Would this have any negative effects on the target organism? Does DNA change during the lifetime as part of normal operation, or DNA changes are always due to mutations or malfunction?

Mutations in B lymphocytes are necessary to mount a good immune response. This is called somatic hyper mutation. It is a very controlled process, failure of which can lead to ceetainlymphomas

Are you asking about changes in the DNA primary sequence (ATCG), epigenetic changes like DNA methylation, or both? @Polisetty has already mentioned gene rearrangements and somatic hypermutation in certain immune cells (T and B cells, specifically). DNA methylation (along with histone modification) is absolutely essential for regulating the expression of genes in different cellular contexts - you need a way to keep liver enzymes from being expressed in the skin, for example.

It is interesting... do all cells in the body have the same genome? Leaving apart B-cells, T-cells, mosaicism and other gained mutations.

Semantic of the post
This question could arguably be better on-topic on WorldBuilding.SE. The difficulty with the kind of question that ask What if the world was different, it is unclear how different would it exactly so to understand what consequence to draw from this scenario. The other issue is of course that the answer cannot be drawn from empirical studies but only be inspired from current knowledge and make untestable predictions.
Because definitions of epigenetic vary and some of them might be extraordinary broad, I will assume that by mutation, you are referring to any change in the DNA sequence excluding epigenetic changes.
Related post
Does our DNA change during our lives? is a related post.
What do somatic mutations do?
Adaptive Immunity
For species having some form of adaptive immunity, somatic mutations are used for producing a large diversity of antibody than can be tested on the self before being released in the body searching for antigen to bind to. In absence of somatic mutations, the adaptive immunity is pretty much inexistent. This point is probably the most important and has been raised by @Polisetty in the comments.
Cancer
Somatic mutations cause cancers. More generally speaking, somatic mutations create genetic diversity within the body yielding to opportunity for selfish cells that could proliferate to the expense of the rest of the body. In absence of somatic mutations, there would be no (or at least much fewer) cancer. This will affect selection for increased lifespan.
Somatic mutations on genetic diversity
As a fraction of the mutations that are transmitted to the offspring occur before the separation between the somatic lines and the germline, the absence of any somatic mutation would result in a lower mutation rate. This would result in lower genetic diversity overall. It would also affect selection pressure that depend upon the mutation rate and may have other consequences that are hard to predict.
Also, and more importantly, many species undergo asexual reproduction such as budding in plants. In some species, the entire genetic diversity is caused only by somatic mutations. In absence of such mutation, there would be no evolution possible.
What mutations are inherited
If a parent has a mutation in the lineage giving rise to half the gametes, then this mutation will necessarily be passed to half of the offspring. For this reason, offspring tend to share new mutations even if their parent did not have them. Absence of somatic mutations will remove this effect, which I would predict would have little impact on anything!


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Is it possible to have undamaged healthy cell, that is dead?
I am trying to clarify my understanding of how unicellular organisms are alive, given my existing background (computational modelling, unrelated to biology). During my thoughts on subject I have came to a conclusion that any unicellular organism, given it's undamaged, and has enough resources (so it does not undergo autolysis), must be always alive.
Is my conclusion true? In other words, is it possible to have completely undamaged cell that appears healthy, but yet is dead? And by "dead cell" I mean a cell that does not move, does not consume any resources, does not respond to any external stimulus an alive cell would respond to, does not divide, etc.

Would a frozen cell meet your definition?

Your definition of "dead cell" seems to include dormant cells and spores, which, technically, are not dead organisms. So you might want to reconsider your definition: cell death is something irreversible, while dormancy and sporulate state are not.  Anyway the notion of "healthy dead cell" seems a bit oxymoric...

@toriningen, Flo makes a very good point. Assuming you are committed to your definition of "dead cell", changing "dead" to "quiescent" would be advisable. healthy =/= dead

There is a great bit on the podcast "The Infinite Monkey Cage" wherein Brian Cox recurrently asks "When is a strawberry dead?"
If you think about it, it is a difficult question: when a berry is growing on a plant, it is easy to say it is living because the cells are actively dividing and functioning. But when the berry reaches maturity, the autosomal cells no longer divide. This is called Programmed Cell Death or apoptosis. This is a physiological process. However, one could still argue the strawberry is alive in the sense that the seeds are still viable and can actively produce new strawberry plants. These cells are quiescent. What though, if a strawberry is crushed to smithereens or a disease infects all of the cells? In this case the "death" of the cell has ceased function as in apoptosis, but this is externally mediated. This type of non-programmed cell dysfunction is called necrosis.
So, in direct answer to your question, you must taken into account the mechanism (internal or external) for cessation of function and the permanency. Internal and permanent = apoptosis. Internal and temporary = quiescent. External and permanent = necrosis. External and temporary = ...maybe injury?
To be clear, I've used a multicellular plant as an example (because it is easier to relate to than yeast), but the principles are the same for unicellular organisms.
@Flo made the good suggestion to add references for those interested:
Buttner et al. (2006) Why yeast cells can undergo apoptosis: death in times of peace, love, and war. Journal of Cell Biology
Gordeeva et al. (2004) Apoptpsis in unicellular organisms: mechanisms and evolution. Biochemistry

OP was mentioning unicellular organisms. I'm not sure they are concerned by apoptosis. Do you have a reference for apoptosis among unicellular organisms?

@Flo Yes, it is still defined as apoptosis in unicellular organisms. I've added a reference and a note for clarity.

Dead means either at physically decaying stage or at least no longer able to react whatever the future changes of its environment (contrarily to dormancy).
To be in such state, an apparently healty cell would need to have had his epigenetic "program" stuck in some dead-lock bug (I don't know if this exist). I wouldn't say that this states his then an "healty" state.
Now maybe what you do seek for is dormancy state. But since it's waiting for some environmental signal, you could assimilate this to "lacking of a resource".

What do you mean by "epigenetic 'program'"? Why would such a phenomenon need to be epigenetic rather than genetic?

Because the whole expression mechanism is involved. (comprising how DNA locations are packed or exposed to transcription. + the various expression factors).

I can imagine a scenario, as you've proposed, in which a genetic mutation creates downstream effects that disallowed a cell to react to a environmental stimuli, while still preserving pathways for all other homeostatic functions (so, essentially "healthy"). In this case, the issue would be strictly genetic and digital, and not epigenetic.

Then if it is maintaining homeostasy, what would you call it "dead" ?

I only said it would have all mechanisms for homeostatic function, not necessarily in homeostasis, nor actively maintaining homeostasis. In this case I would call it quiescent. See my answer above in which I propose four, more exact alternatives to "dead."


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Are the human genes' promoters all known?
It seems to be a basic question, but I couldn't find a certain answer.
The human genome is known for more than a decade, and is available through several data providers as the NCBI etc. For the genes' promoters however there seems to be much less information. There are some characteristics known (like the TATA box, which appears in ~25% of human genes), some prediction methods (like CpG sites appearance), some rough estimations for the location (100-1000kbp long, in the adjacent 2kbp upstream from the TSS), but I couldn't find any data set with a closed list of human genes' promoters.
Is this really yet to exist?

Not 100%. People are still working on it using by studying nucleosome positioning and transcription factor binding sites and other factors. For many ncRNAs, even the TSS is not well annotated. Techniques like CAGE are quite recent. But you should clarify what you really mean by promoter: the minimal promoter (TATA-box etc) or all TFBS?

@WYSIWYG Thanks! I'm looking for the whole TFBS (as far as I understand). What I'm doing is comparing and trying to optimize CpG islands (CGIs) identifying algorithms (e.g. as Takai's, and recent CpG clustering algorithm). One major parameter for scoring is how well do results lay withing promoters. Sort of chicken and egg situation.
Do you happen to know if CpG methylation suppresses expression only when appears within the promoter area, or in it's surroundings as well (up/downstream)

Nope. The human genome is still quite unexplored, new genes are still being discovered and the annotation of non-protein-coding regions (that include promoters) is still far from being complete. For example, look at the Statistics comparison of the current and previous Human GENCODE Release, it clearly shows that the annotation of the human genome is still an ongoing process.


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Fluorescent protein tags and colocalisation
We want study if 2 proteins A and B are co-located, for that we use 2 FTP(Fluorescent tag proteins) for each protein?and after the expirement these 2 FTP are co-located. Does that mean necessarily protein A and B are co-located?

Is this a homework or test question?

It's a test question, but the correction says no, but i doesn't make sense for me!

Whel, is possible that the adittion of a FTP made them co-localize. Is that the complete question?

this question is unclear. What exactly you have problem with?

"Are protein A and B co-located?" The answer is that it depends. Since your test question included the word "necessarily", this means that the answer to the test question is no. All you have to do is think of at least one plausible counter-example.
Here's a couple:

The flourescently tagged constructs were screwed up somehow, so A, B, and each of their respective tags were actually expressed as 4 separate proteins.
(As per BPinto's comment) the tagged constructs may co-localize even if A and B would not normally do so. This can happen if, for example, the tags bind to each other, or if the tags somehow cause both constructs to get transported to a particular organelle.


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Real embryo pictures: How different zones(speeman organizer, marginal zones...) are known?
In many textbook, figures of embryo are drawn,but in reality how biologist know which zone is this one of  an embryo in gastrulation stade? Except the dorsal lip here i can't localize other thing.