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How likely is a lack of DNA match with a distant relative?
How likely is a lack of DNA match with a distant relative?
I have recently gotten interested in ancestry research and have had a DNA analysis performed by a prominent commercial provider.
I've been working on my family tree for a few months now and have gotten into contact with a lot of distant relatives of mine, which has generally been quite delightful. In one particular case, we discovered that we actually have a double-relationship about 5-7 generations back in time, depending on how you count (common links go back to about ~1790).
We found this quite interesting, and this distant relative had a DNA analysis performed on their own genome as well.
Much to our surprise, however, we didn't find any commonalities in our DNA, which seems odd given the double-relation, and the fact that we have what we believe to be original and authentic documents of all the relatives forming the link.
Of course, we began speculating about the possible reasons for this. Maybe a misattributed child somewhere in the family tree? However, this seems unlikely, given the double nature of the link - most likely, we would need two misattributed children to explain the lack of any commonalities.
The other explanation would of course be that the DNA analysis provided by these companies is less reliable than we think, and that just by random mutations and "unlucky" inheritance, any common DNA might have been lost or scrambled beyond recognition.
I would like to calculate the probabilities of this happening in order to judge whether it makes sense to dig further into the original documents to try and clear up this mystery, or whether a mismatch by chance alone is sufficiently likely to explain this oddity. Of course, I don't need super precise numbers, but a back-of-the-envelope estimation would be nice - are we talking a few percent, or one in a billion? Also, I would be curious anyway on how to calculate probabilities like this, given the publicly available data on these tests.
What are the relevant quantities for this calculation (number of SNPs, I suppose), and how would one define and calculate a probability like this?
About myself
I'm a physicist with a strong background in data analysis with some basic understanding of biology and genetics. Don't be afraid to hit me with those numbers and probabilities, but please explain any genetics jargon you're going to use!

Welcome! I think what renders this question difficult to answer is we don't know what test your commercial company employs. There are very, very many ways to compare DNA between individuals. It's complex: you can share a polymorphic gene variant with a great ape of another species that you wouldn't share with a grandparent, and parts of DNA are inherited paternally/maternally e.g. mitochondrial DNA is used to perform maternal ancestry tracing. To get an accurate picture, ideally one looks through the entire genome. If you provide the company/test name, it might help specify an approximation.

I didn't know if providing a concrete company name was against the site policies, but I'm happy to provide it. I was using the DNA Test Kit from myheritage.com.

myheritage.com uses autosomal DNA testing for ethnicity estimate and DNA matching. I assume you went for the latter. I know that different testing companies use different matching algorithms, so some estimates and likenesses for an individual will vary between tests, quite more than one might expect. I think this question is unanswerable in the way that you want; we can't perform an informed calculation for specific regions or genes, but we have no idea which regions myheritage.com uses nor prioritizes, nor with which weight. I hope you can see now that it is probably an intractable question!

I think the most help we could offer would be if you narrowed or refocused your question, perhaps after reading up a little about genealogical DNA testing. The wiki entry is more comprehensive than an answer you could expect here.

Thanks a lot for the Wiki pointer, I will take some time to study that article and see whether this helps me!

This may help you: https://dnapainter.com/tools/sharedcmv4

Also related: https://en.wikipedia.org/wiki/Pedigree_collapse

What is a 'double-relationship'?

Just so you know, "Genealogy & Family History Beta Stack Exchange" exists. -  https://genealogy.stackexchange.com/

With "double-relationship" I mean something like this: my father has a common ancestor with his mother, and my mother has a common ancestor with his father.

There's a very detailed analysis published by the International Society of Genetic Genealogy here with lots of charts and stats, including stats from various commercial providers.

Note that there are also "non-paternity events". That is, the actual father is not the stated father. These happen frequently enough that, excluding a solely maternal lineage, the family tree some generations back is typically not the real tree. You can see the effect here: https://isogg.org/wiki/Non-paternity_event#Table:_Cumulative_effects_of_NPE

First, if you haven't read it already, I highly recommend Carl Zimmer's "She has her mother's laugh." for anyone interested in ancestry/genealogy.
In it, he presents the following figure showing the probability of sharing any autosomal DNA with a given ancestor as a function of the number of generations separating you from that ancestor. (notably, this analysis excludes the very real possibility of intermarriage within a family tree).

So, for example, if you were to look at one single ancestor from 10 generations before you, there's a little less than a 50% chance that you share any of that ancestor's DNA (remember that at 10 generations you have roughly 1,024 ancestors).
So, at 5-7 generations there's still a high probability that you both have at least some genetic material from the same common ancestor(s). But, it's much less likely that you both share the same pieces of that genetic material (probably in the 10-14 range on this graph).
Plus, very few (probably none) of the commercial DNA ancestry sites do full genome sequencing for ancestry comparisons. They look at a limited number of specific regions that can help identify familial relations. So, even if you do share common ancestral DNA, it's less likely that it would be detected without whole genome comparison.
Image Credit: https://gcbias.org/2013/11/11/how-does-your-number-of-genetic-ancestors-grow-back-over-time/
Edit
I just wanted to edit and reference that the above analysis was calculated by Graham Coop and colleagues. I did a little more digging and he's got a blog post (How many genomic blocks do you share with a cousin?) with a more relevant analysis for you're specific question, showing the probability of two "cousins" having zero shared DNA blocks as a function of how many generations back the two shared common ancestors.

Reference: https://gcbias.org/2013/12/02/how-many-genomic-blocks-do-you-share-with-a-cousin/

Nice answer.  Another factor that might be significant is that there might be parallel relationships that I'm not sure have a specific term in English.  That is, siblings who each couple with other siblings.  For example, two brothers who marry two sisters.  The children of these couplings then are cousins on both sides.  This situation is probably was probably rather common in times when families were large, communities were mostly small and transportation was limited.

you have roughly 1,024 ancestors well, you definitely don't have more; you might have less.

It seems to me that this answer is presented in a way that inappropriately suggests that there is something universal about these graphs. If I'm understanding correctly, then the results shown on these graphs depend entirely on which regions of the genome are used.

@BenCrowell - According to the Coop Lab website, these calculations do seem to apply universally (at least with respect to autosomal inheritance), and are not limited to region-specific analyses. I've updated the references to link to the source page for both figures in the answer. Dr. Coop does a pretty good job of walking through these calculations and providing primary references to backup any claims. He has a number of other posts on the topic of genetic genealogy as well.

This doesn't seem to account for the most probable explanation: what we might politely call "misattributed paternity".  (IOW, "Your father's not your father".)  While estimates of the rate vary widely, 10% seems about average from a quick search.  If I'm doing the math correctly, that means that in 6 generations it's about 50-50 that there's at least one such event.

@jamesqf - In this particular context, that wouldn't really be a question of biology, per se, nor would it necessarily be the most probable explanation. Two people with a single shared ancestor 6 generations back would only have about 1 in 5 chances of sharing any common ancestral DNA (yes, that's assuming no misattributed paternity or maternity).

@MikeyC: Perhaps I'm misinterpreting the first graph?  It seems to show the probability of sharing some DNA with an ancestor 6 generations back as close to 1.0.

@jamesqf - That's correct, but I was speaking within the context of the original question, which is about sharing DNA with a contemporaneous relative (i.e. someone with whom at lease one common ancestor is shared). This point is better illustrated in the second figure. Even though there's a high probability of both individuals having at least some DNA from the same common ancestor after 6 generations, it much less likely that they will share any DNA with eachother (~20%).

5-7 generations is a long time
Mother and child or brother and sister each share 50% of their DNA.  If you find a link between two people that is five generations back, that means you take 50% of 50% of 50% ... for five generations.  For both you and the other.  Then there is a brother-sister link.  That means that 2^11 = 1 in 2048 pieces of DNA are held in common between the two of you.
If your ancestor had some unique form (allele) of a gene, the relationship could still be proved!  However, at least a quick glance at myheritage.com doesn't make me think they are doing a full genome sequence from scratch.  If they are focusing on known variations in the genome, (maybe SNPs, single nucleotide polymorphisms) then by definition those variations should not be unique.  There will be a certain percentage of identical forms between the results for any two people and the effect of changing that by 0.05% will be minimal.
Oh, hold on a minute...
After I received an unwarranted number of upvotes, the other response raised a great point: there will be potentially recognizable regions that have not been recombined in 11 generations.  A previous StackExchange question cited that about 53 meiotic crossovers per meiosis were observed in careful measurements of 8 human cells.  A genealogist addressing the question cites figures of 42 for females and 22 for males during gametogenesis. Taking a figure of 3.3E9 basepairs / (32 crossovers x 11 first-degree steps + 23 chromosomal ends), that means the segments of non-recombined DNA should still be about 9 million basepairs long!  With one SNP every 1000 basepairs or so, that gives 9000 SNPs in a row!  That's true, of course, only if you do inherit such a piece - the overall odds should be low, since that's 1/352 of the genome and only 1/2048 is inherited on average.  But ... that's still a 17% chance that a large block of syntenic SNPs might be found - one so large that it should jump out of the statistics if the myheritage data set contains a large number of SNPs.  That probability would be larger if your common ancestor was mostly via the maternal lineage.  It seems surprising to study linkage disequilibrium between two individuals, but with the preexisting SNP data set that isn't really the case.

+1.  Ancestry sites do use SNP arrays (source), so you're correct, and most determinations of relatedness are statistical

Your statement about a brother and sister is wrong. It's possible for a full brother and sister to share no non-mitochondrial DNA (e.g. each received the opposite contribution from each parent). However, sharing no such DNA is extremely unlikely, just as much so as non-twin brother and sister sharing 98% of their DNA. On average, it will be about a 48% share, but any amount between 0% and 98% is possible (can't be 100% and opposite sex). OTOH, two brothers or two sisters must share at least one chromosome from their father (i.e. either the X or Y chromosome from their father).

@Makyen: I don't think I said anything to disagree with what you said (aside from my ignoring mitochondrial DNA, that is - you remind me that if the genetic relationship happens to be entirely maternal, they should see a very clear confirmation by that means!).

@MikeSerfas Your first sentence in this answer says "... brother and sister each share 50% of their DNA." That's what I was saying is inaccurate.

When used to predict a simple numerical expected value for the overall amount of shared DNA, we can use the average figure.  Besides, the binomial distribution gives a >98% probability of inheriting more than 6 and fewer than 17 chromosomes in common even without crossing over - adding say 64 more fragments (they overlap, so I can't really use binomial distribution accurately in that case) would give 38% to 62% shared genes.

It's not all that surprising for no actual segments of the genome to be shared between distant relatives.
The back of the envelope figure I've heard is that there's about one crossover per chromosome arm per generation. So, when you're composing the chromosomes for your child, you pick a point along each arm of each chromosome, and splice your two chromosomes together at that point to make the chromosome to pass along.
This means that there's a fairly limited number of chances to share DNA: if you overlay all the crossover points that happened between you and your relative, they don't define that many distinct segments. Each segment has a chance to be shared or not shared via descent from the common ancestor in question, but can't really be fractionally shared.
23 chromosomes * 5 generations * 2 lines of descent * ~2 crossovers per chromosome * 1 segment created per crossover = ~460 segments

If each segment has a 1 in 2048 chance of being shared, as @Mike Serfas suggests, then it has a 2047/2048 chance of not being shared, and if you AND together not being shared across all the segments you get:
(2047/2048) ^ 460 ~= 0.799

So there's about an 80% chance of seeing what you observed, by my back of the envelope math. If you fudge the numbers up and down a bit, the probability still stays in the realm of "could go either way".

This calculation doesn't seem to have enough connection to the way the tests are actually done to tell us anything useful. These companies pick certain specific parts of the genome to look at, and those are parts that may be identical in people who are unrelated. The calculation suggests that I would have zero DNA in common with a human if our last common ancestor was many generations back, whereas in fact I have quite a bit of DNA in common with all humans, and even with my dog.

+1.  I handwaved this issue out of mind, but as you showed here, it is quite relevant.


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Why can a gene lack of a binding site be expressed in skin cells?

In order for a specific gene to be expressed in the mammal’s cells, all of the gene’s binding sites must be bound by transcriptional activators. The mammal’s skin cells contain activators that bind to sites B, D, and E, while the mammal’s liver cells contain activators that bind to sites A, C, and E. (From Khan academy)

Why can both Gene 2 and Gene 4 be expressed in skin cells? I think Gene 4 can't since it doesn't have site E.

You understand this wrong: All present enhancers of a gene must be bound by a enhancing factor, not all factors of a certain cell types have to be bound. So when skin cells contain activators for B, D and E they can activate gene 2 and 4 of your example, but not gene 3 since the activators for A and C are missing.
So when you have a gene containing any combination of B, D and E, its activation in skin cells is possible according to this model. The same is true for any combination of A, C and E for liver cells. The special case would be a gene having E as the only enhancer as this could be activated in both, liver and skin cells.

This is the right answer, but enhancers tend to act in surprising ways.  The question works tautologically if you define expression as the highest level of expression, the binding sites as only those with an observed positive effect on expression, and ignore all other interactions.  Otherwise you could be in for surprises. :)

@MikeSerfas I know, I worked for quite a while on the regulation of gene expression and enhancers. Sometimes they bind coordinated, sometimes seemingly identical sites are only bound under certain conditions etc. This is a simplified example, for this purpose this should be fine I think.

source: Stack Exchange

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

sort: votes


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Types of structures formed by various types of lipid molecules
Since Phosphatidylcholine (PC) and phosphatidylserine (PS) are roughly cylindrical in shape , they tend to form flat bilayers. Phosphatidylethanolamine (PE) on the other hand is conical in shape which bends the lipid bilayer when present asymmetrically along with PC and PS. What kind of structure will form when PE is present exclusively?

PCs are lipids with large head groups, so are more of a cylindrical shape, as a result, they tend to form flat bilayers.
PE is a lipid with a small head group, so is in a conical shape. However, they are generally present as inverted cones, providing maximum curvature to the membranes.
So, PEs are generally found in highly curved membranes , for eg:- viral budding, microvilli, micelle, internal vesicles formed for transportation, Inner mitochondrial membrane, Gram-negative bacterial membranes.
You can check out this article, where researchers performed lipid content profiling for E.coli. (https://www.sciencedirect.com/science/article/pii/S0014579315006912)

You can also check out this research article for lipid profiling of rat intestinal microvilli.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1186751/pdf/biochemj00720-0057.pdf)

Add figures to this answer if possible to make it complete.

Welcome to Biology.SE. This doesn't seem to be answering the original question, which was what would happen if only PE was present.

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


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How to identify the GPD gene when the sequence varies between organisms?
I'm reading a paper on genetic transformation of a fungi and the plasmid used in the paper uses two forms of the same GPD (glyceraldehyde3-phosphate dehydrogenase) promoter to drive a GFP gene, one from Agaricus bisporus and one from Lentinula edodes (GenBank: GQ457137.1).
However, I noticed that the sequences for the aforementioned GPD promoters do not match the reference sequence in GenBank (NC_007251.2) which itself is derived from another organism.
Why are there different sequences for the same promoter? Furthermore, how would I identify the GPD gene in another organism if I'm unable to compare it to a known sequence?
The organism I wish to transform has had it's complete genome sequenced and my transformation would be much more effective if I could use a native promoter like GPD.

I think in general you are looking for a more general answer about finding homologous sequences or analogous sequences. There is a lot of discussion about how you define a homolog/analog and whether it is a sequence homolog or a functional homolog/analog. This question gives a good answer about potential tools to use. You might also be inte

Nice synthetic biology question; want to support the SynBio SE proposal? https://area51.stackexchange.com/proposals/125068/synthetic-biology?referrer=NDY5ZDU3MWM0Mzc2NmU5OWNjMmZjYjRlYzRmOWJhNzRiYjhmNzIzNjAxYTFkYmE5NmZjMjMxZjY2MTkzMzM2MSlXfcGon_KIsoktWMGcYchcm3KOxHLit6rYuYwj6cmN0

@jakebeal Supported!

@doremi Thank you!

I might be misunderstanding you here, but I take from your links above that you want to match the GPD promoter regions from two (distantly related) fungi Agaricus bisporus and Lentinula edodes, to the GPD promoter of Leishmania major, which belongs to a completely different Kingdom!
Promoter regions tend to be relatively poorly conserved between species compared with protein coding regions, even for closely related species. Given the evolutionary distance between the species you are mentioning, the chance you will find any homology between their promoter regions is probably zero.

Furthermore, how would I identify the GPD gene in another organism if I'm unable to compare it to a known sequence?

What I would do is to take the translated GPD protein sequence, which for Lentinula edodes would be GenBank BAA83550.1. I would then use that to search for protein matches using blastp, specifically subsetting for Leishmania major; and use the result to locate the coding gene in the genome. You can also do this in one single step with tblastn, which looks for matches in a translated nucleotide database (see this tblastn example query).
You can then simply take the 1000 bp or so upstream of the coding region to represent your GPD promoter.

This might be an ignorant question, but how can completely different sequences produce the same GPD dehydrogenase? In the blastp, for example, even the translated proteins only have 40% homology in some cases.

As an added example, the GPD protein sequences for KT067727.1 and KM273235.1 are both from the same species (the one I'm transforming), but they vary wildly. How am I to know which one I can use?

This section is not a good place to answer your first question, but in short: not all residues are equally important for an enzyme's activity. See this Wikipedia article on active sites for some intuition.

The two proteins are probably paralogs. Which promoter to choose depends on your experiment and what you might know about each gene's expression. Compare for example the GPD equivalents in budding yeast: TDH1, TDH2, and TDH3. The latter two are expressed in exponentially growing cells, whereas TDH1 is apparently only found in stationary phase.

Related to this question, I want to replace the gpdA promoter from that plasmid with the GPD promoter from KT067727.1 or KM273235.1 (my target organism). If I have the organism in-hand, how am I supposed to design a primer to clone the promoter if the seq varies even within the same species? If I just had it synthesized, how would I decide which accession to use?

To get a comprehensive answer to this you will want to post a separate question where you explain in detail what it is that you want to do. But you cannot expect to use the same primers to clone two different promoters, even if these code for proteins with the same function - same species or not.

I want to clone the same promoter, but am stumped as to why it differs within the same organism. I'll post a clarifying question shortly.

As promised, link to the follow-up question.


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Do people need nitrogen from air for health?
Can people breath totally nitrogen-free atmosphere for a long time? I know, nitrogen is essential for life, and in big quantities, but maybe people can take it entirely from food, from proteins, etc?

Some short comments - Nitrogen gas is pretty much inert and nutritional nitrogen is mainly obtained from the diet. Inhaling pure oxygen will kill you in the longer run. So what exactly is your question? If N2 gas has dietary value, or whether nitrogen-less air where ~79% of some other non-toxic gas substitutes for N2 can sustain life, or whether 100% O2 can possibly sustain life?

Do people need nitrogen from air for health?

No. This is well established!

Can people breath totally nitrogen-free atmosphere for a long time?

Yes. Also well established!

I know, nitrogen is essential for life, and in big quantities, but
maybe people can take it entirely from food, from proteins, etc?

As expounded on in the comments by AliceD, nitrogen gas (N2) is entirely taken in by humans from their diet, since atmospheric N2 is pretty inert. It is also not necessary for gas exchange to take place in the lungs.
Some extra questions as an addendum:

Can one substitute N2 in atmospheric air with another gas, and sustain human life?

Yes. All side effects would be attributable to the effects of the substituting gas (e.g. it may be heavier or lighter or equally or more reactive than N2).

Can 100% O2 sustain human life?

No, and such a case has never been recorded. Oxygen toxicity following hyperoxia is very dangerous. Ironically, too much oxygen damages lung tissue and epithelial membranes via oxidation and render the lungs unable to exchange gases correctly; and so death by suffocation follows in such extreme cases such as with 100% O2.

A pedantic point: dietary nitrogen is 'fixed' nitrogen, not N(2) which (to quote the Wikipedia article) is 'metabolically useless" to all but a few (very important) microorganisms. N(2) is, however, primarily responsible for 'the bends' (decompression sickness). (Nitrogen 'fixation' is why the Harber process is so important)

Is it known that none of the microbes in the microbiome require nitrogen in the air from inside the intestines for protein synthesis?

Do they have on ISS nitrogen-based air?

I think negative effects of oxygen come frm its partial pressure, not from its percentage. Thus, 100% oxygen at 20% atmospheric pressure should be harmless, no?

Oxygen toxicity depends on partial pressure, sure. That relates to how many O2 molecules there are. Fewer make it less toxic, no doubt. But the act of breathing in low atmospheric pressure is more difficult too, it's another problem entirely. During inhalation, lung volume increases, lung pressure decreases below that of atmospheric pressure. This draws air into the lungs. At lower atmospheric pressure, less total air is drawn in, so breathing is more difficult at lower atmospheric pressures (or at higher altitudes due to the same phenomenon). So you're describing a trade-off.


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Is chloride necessary for animals?
Of the twelve well-known atomic constituents of our body eleven elements have specific properties obviously relevant to their rôle, making them indispensable. Oxygen (electronegativity and valence), carbon and hydrogen (both elements have virtually unique properties), nitrogen (amino group), calcium (calcium(II) is necessary for bones in vertebrates), phosphorus (use of phosphate in nucleotides and ATP), sulfur (–S–S– bridges), sodium (Na+ is a small cation), potassium (K+ is somewhat larger, together with its companion and presumed substitute Rb+), iron (used in hemoglobin because of properties of a transition metal), magnesium (Mg2+ takes part in the ATP cycle, if not anything else).
What about chlorine? A search resulted in

Chloride is involved in the exchange of oxygen and carbon dioxide in the red cells.
In this, chloride passes into the plasma (chloride shift) and bicarbonate into the cells.

(https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/chloride), certain use by muscle cells and also some mention of ligand-gated chloride ion channels in neurons. Chloride in stomach secretion may be dismissed because is used as a generic acid (that is, to complement H+), not for its own special properties. And no mention of biological chlorine compounds other than ionic (such as, having a C–Cl bound) can be quickly found.
Which cells absolutely need specifically Cl− to function? Is the anion mandatory for animals to live?

I am not sure I am clear  what you are asking, but mutations in the chloride channel are known to cause cystic fibrosis (a major breakthrough in the understanding of this disease)

@user338907 relevant, but again: so named “chloride channels” are not necessarily selective. Whereas a sodium channel hardly can pump anything but Na⁺ (the rare Li⁺, perhaps?), anion channels conduct mostly Cl⁻ because of abundance, but generally who-knows-what.

OK. As regards your second-last sentence, there is Gribble, and chloramphenicol comes to mind. (Extending things to the halogens, there is  fluroacetate)

My answer may be a little basic, but I think it is comprehensive:
Many elements are special; for instance, many metal ions such as iron or cobalt are required as cofactors or in catalytic sites due to their chemistry. Oxygen is highly electronegative, that also grants it some of its functions. But... without delving too much into things... chloride is the most basic constituent of saline, without which it would not be saline. Here are 3 very, very important and yet

It works well with alkali and alkaline earth metals, hydrogen, and many compounds... it's a natural pairing!
You cannot separate positive and negative charges in a solution at a macroscopic level. It's not a feasible thing to avoid harboring chlorine atoms as part of biochemistry.
It accounts for a large portion of extracellular fluid tonicity.
etc...

Thus, most inter- and extra-cellular fluid is relatively chloride ion rich, across the entire bush of life. To my knowledge there is no life, tissue or cell on this planet that does not contain chloride ions as part of its makeup by necessity. It is simply heavily constrained in evolution as a basic component. It's just not practical to obtain K+ or Na+ or Ca2+ ions without Cl-, it is so common in nature.
If you want specific examples, you can always mention its indispensable roles in neuron firing (transmission of axon potentials) and general cellular homeostasis, which is dependent on electrochemistry and osmolarity and stuff like that which is heavily influenced and dependent on the presence of a regulated concentration of solvated Cl-.

Ī̲  didn’t discuss abundance of elements on Earth (or elsewhere in the known universe), nor hinted that natural abundance of nutrients has something to do with the question. Please, keep your stuff to the topic.

Neither did I, as I'm sure you will agree. I see 3 posed questions, perhaps I can restate the answers more tersely. Is chloride necessary for animals? Which cells absolutely need specifically Cl- to function? Is it mandatory? The answers are yes, all, and yes. All animals can and do suffer chloride deficiency. I think the answer can also be extended to most microbes. This does not rule out the possibility that one could engineer a synthetic life to use bromine or fluorine, but I presume you know why neither would be a good elemental substitute. They are very different physicochemical anions.

That Wikipedia article states that so named chloride channels may conduct many different ions. An empty-worded statement about necessity of Cl⁻ may not count to qualify an answer.

There are very many membrane channels that are partially or entirely non-selective, including anion and cation channels. I don't really understand how that is relevant, but I wish you luck on getting an answer that you are looking for! Though I would caution you against looking for answers at bio.SE where the lack of chlorine is a strained, imagined hypothetical. Along those lines, we can speculate and opine all day about silicon-based lifeforms. But that's all fantasy and science fiction until we see a proof of concept. Best of luck!


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How does expansion of the skin via mitosis influence the density of its specialised nerve endings
I found a reddit question Do nerves & nerve endings expand with skin or does skin expansion causes loss of nerve density where a user references the study Assessment of Epidermal Nerve Fibers: A New Diagnostic and Predictive Tool for Peripheral Neuropathies which states that intraepidermal nerves fiber density is not dependent on weight

No significant relationship of race, height, or weight on IENF density has been reported

Reasoning that if additional nerves are not generated in response to expansion of the skin, then one should expect a negative relationship between nerve density and weight.
My question is, upon expansion via mitosis, will sensitive skin rich in specialised nerve endings such as the Meissners corpuscles generate more of this same type of nerve endings?
Specifically i’m curious about the inner foreskin and innervation of new tissue created under foreskin restoration if that makes a difference

Foreskin restoration is the process of expanding the skin on the penis
to reconstruct an organ similar to the foreskin, which has been
removed by circumcision or injury. Foreskin restoration is primarily
accomplished by stretching the residual skin of the penis


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How is the renal osmotic gradient maintained even though the blood osmolarity changes?
I am a high school student and I am a little confused in 2 things related to our urinary system:

We know in our kidneys a countercurrent mechanism exists due to which there is a steep gradient of osmolarity is observed as we go deep inside the medulla and due to which water gets reabsorbed from the descending limb of Henle's loop into the ascending limb of vasa recta but due to the countercurrent of vasa recta osmolarity of blood doesn't changes but as collecting duct descends deep into the medulla it also loses water. Where does this water get drained? Does it get absorbed into a blood vessel? I don't think so because if the blood  is also moving down with the collecting duct then it should also lose water as osmolarity increases as we go down.

We know that ADH increases the water reabsorption from the distal parts of nephron via aquaporins but if more aquaporins are there the collecting duct should pass urine of 1200mosml osmolarity, shouldn't it? and in that case will the concentration gradient in the medulla be maintained? if yes then how?  I am not able to imagine how our kidney would behave if blood of increased osmolarity get into it.

The water doesn't get drained.  As blood flows down a vas rectum, in any given section of the arteriole the tonicity is slightly higher outside the arteriole vs inside the arteriole.  This results in a small amount of water flowing out of the arteriole to attempt to equilibrate the osmolarity.  But before this has even finished happening, the blood has flowed down another quarter of a millimeter (or whatever) where the tonicity is even higher outside the arteriole.  In other words, down the entire vas rectum the water is flowing out.  But when the vas rectum comes back up, the situation is reversed, so the same quantity of water ends up diffusing back into the blood vessel.  Thus the osmolarity at any given level of the medulla remains constant.

Correct, the maximum osmolarity of urine is 1,200 mosm/L.  The concentration gradient in the medulla will change very slightly (temporarily), but don't forget that even as the urine in the collecting tubule is being concentrated to that maximum concentration, the whole process of creating the concentration gradient is actively happening in loops of Henle all around the collecting duct.  So even if the initial effect of having a bit more water in the medulla from the collecting tubule would be to slightly lower the extracellular osmolarity, in the grand scheme of things it changes nothing since the rest of the nephron is still actively creating an effective osmolarity gradient.

References

Any physiology textbook... for instance (among others), I have Human Physiology, from Cells to Systems - in the First Canadian Edition it's pp. 553-63.

I want to know that if urine is already getting maximum concentrated {1200mosml/lit} then how the hell ADH works? what's the point of adding more aquaporins into the collecting duct and DCT if urine is already getting maximum concentrated by absorbing water? I think urine will get 1200 mosml/lit concentration only if ADH acts on it , i.e collecting duct is not so permeable for water i.e it doesn't allow water to get maximally reabsorbed on its own, it only does it when ADH acts on it? but if that's the case then osmolarity inside medulla shouldn't be maintained because pumps are actively

continuing- pumping out Na+ ions even when the collecting duct is not allowing water to reabsorb so, the concentration should increase inside the medulla ? 1200mosml/lit is the maximum concentration in medulla only when water is getting reabsorbed from collecting duct , but when its not being done then it should increase?

@ArunBhardwaj ADH is what allows the urine to be concentrated to that extent.  In the absence of ADH, the aquoporins are endocytosed, so that water is no longer able to flow down its osmolarity gradient, and the urine is consequently much more dilute.  In other words, ADH is not a water-removing mechanism so much as a control mechanism - the nephron is designed such that the urine will become concentrated by default - if it can escape the tubule.  The presence of ADH allows it to escape, the absence of ADH prevents its escape (via presence/absence of aquaporins).

but in the absence of ADH , the Na+ pumps in the ascending limb of henle's loop should also decrease or work slowly .otherwise the concentration inside medulla would increase much higher than 1200mosml/lit ,isn't it? because now no water is coming out through collecting duct it is only coming out through descending limb of henle's loop.


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Can any gas other than nitrogen cause decompression sickness (the bends)?
I know that our bodies use most of the oxygen we breathe in during a dive but, wouldn't our tissues, under pressure, absorb more oxygen than we need?  For instance, in normal circumstances, we don't use all the oxygen in each breath and we exhale some (this is what 'rebreathers' are for, right?)
Couldn't any gas we breathe in under pressure cause decompression sickness when we decompress?
Read this, from NASA:

"Astronauts put on their spacesuits several hours before a spacewalk.
The suits are pressurized. This means that the suits are filled with
oxygen.
Once in their suits, astronauts breathe pure oxygen for a few hours.
Breathing only oxygen gets rid of all the nitrogen in an astronaut's
body. If they didn't get rid of the nitrogen, the astronauts might get
gas bubbles in their body when they walked in space. These gas bubbles
can cause astronauts to feel pain in their shoulders, elbows, wrists
and knees. This pain is called getting "the bends" because it affects
the places where the body bends. Scuba divers can also get "the
bends."

Yes, it is possible to get decompression sickness with other gasses, such as the "oxygen bends" or oxygen decompression.  For instance, in this study, they demonstrated that oxygen decompression sickness in mice.  Another study demonstrates a more common non-nitrogen decompression sickness - helium bends.
Undoubtedly you will be wondering at this point why breathing pure oxygen would diminish (or, in certain circumstances, completely remove) the risk of bends as compared with nitrogen.  The reason is simply that oxygen, unlike nitrogen gas, is constantly being metabolized by the body tissues.  Consequently, even if the oxygen levels in your body fluids become elevated, they would have to be way higher than normal levels (like in the first study linked) before you would start to have it accumulating enough to form bubbles.
The body is designed for the shipping and handling of oxygen (think haemoglobin & myoglobin).  Nitrogen, on the other hand, is relatively incidentally present - so long as atmospheric pressure remains relatively constant (which it did until we devised technology allowing us to radically change it), it's present in low levels in all the body tissues without causing any trouble.

Also interesting in this context: https://en.wikipedia.org/wiki/Saturation_diving


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How to replace intron region in a plasmid?
I'm considering working with the plasmid pRFHUE-eGFP and would like to replace the gpdA intron (which is the eGFP promoter region) with a promoter from another organism.
What would be a good strategy for replacing the intron if I already have the other gene in-hand?
Would I cut out the fragment between the SalI and SmaI restriction sites and then insert the new promoter with compatible overhangs there?

Your strategy would work, but if possible you might be better off using XmaI rather than SmaI, as the latter is a blunt-end cutting enzyme.
Furthermore, your strategy would not replace the entire gpdA promoter, if that's what you're after. You might wanna refer to their paper, where it's clear from Fig. 1 that the promoter region is much longer than the region between SalI and SmaI:

I've been appreciating your on-point synthetic biology answers! Want to support the proposal for a dedicated SynBio StackExchange site? https://area51.stackexchange.com/proposals/125068/synthetic-biology

Thanks @jakebeal, but I'm of the humble opinion that Synthetic Biology questions should remain part of SE Biology. :)

Your call, of course; my own reasoning is spelled out in https://area51.meta.stackexchange.com/a/32413/211190

Your answer has pointed out that the plasmid on AddGene and the one referenced in the paper are different. The directionality is reversed,  they vary by 8bp in size and the annotations don't match. I wonder why this might be.

For what it's worth, I'm self-learning synbio. There aren't any focused places on the web for me to get support (diybio forums maybe?). I see pros/cons for a dedicated SE, pro: draw-in synbio focused expertise to central place, con: I appear to be getting my answers from SE Bio already.

Note that what you refer to as directionality here is irrelevant: one map is simply displayed as the reverse complement of the other. Second, annotations might differ because the authors chose a certain vocabulary for the paper, whereas the plasmid map you got from AddGene might be automatically annotated based on the DNA sequence (just guessing). And I wouldn't pay too much attention to the 8 bp difference in size.


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Regarding secondary growth in dicotyledonous angiosperms

I had read that (and as this image shows) the secondary and primary phloem eventually get crushed due to the repeated division of cells forming the secondary xylem, during secondary growth in dicotyledonous stems. While the primary xylem remains intact, the secondary and primary phloem are crushed.
My question: Is the phloem crushed to such an extent that it is not usable by the plant to conduct organic solutes? Then how does it compensate for this? Does the xylem take over the functions of the phloem?


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What is a good book to start with if I'm interested in Gene clustering analysis?
As a beginner, I would like to learn more about gene clustering analysis, namely discovering groups of correlated genes potentially coregulated or associated to some conditions or finding patterns in gene expression data, identification of coexpressed genes from microarray data.
I was looking up for some books, but all of them are a little too much biology-heavy for me, given the fact that I have a Computer Science background. I would like to dive into algorithms such as hierarchical clustering, k-means algorithm, pattern-based clustering and other methods, so a book addressing these would be of real help.
If you have any suggestions, I would be grateful.

Usually, people do not ask for book recommendations on this site. Quora, Researchgate, Reddit, or maybe Biostars are the perfect choices to look for such questions. Still, to give you a clue to continue, If you've previously read some books about "Biostatistics", "Bioinformatics", "R/Python programming" and have a general understanding of what is a protein and what is DNA ("General Biochemistry"), the next step should be reading research papers, indeed. If you lack the mentioned principles, then the best strategy would be reading those first.

Just one more thing. In the case of Bioinformatics, always, always read books that are recent and new. Do not read old books (before 2005 or even 2010) as the area has evolved pretty much in recent years and many old links and websites are not available now


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Are the antibodies developed by differing vaccines still the same?
If one person gets an mRNA vaccine that teaches their body to deal with a specific virus, and another person gets a similar but different mRNA vaccine, and another person gets a more "classic" vaccine with modified/weakened/dead virus cells, will there be any real difference in the antibodies developed by the three different people?
My gut instinct says that the antibodies/proteins developed by all of the people will be mostly identical, but I'm not a biologist.
I'm having difficulty finding articles/research on this. Full disclosure: this somewhat pertains to the SARS-CoV-2 and the varying vaccines, but it is also a more general question. I was hoping to find research on this, but it is proving difficult to google for such a verbose subject.

The mRNA may encode different antigenes, e.g. different parts of SARS-CoV-2's spike protein, or other parts of its membrane or hull. See https://www.nature.com/articles/s41422-020-00392-7. The immune response will/would differ accordingly even in the same individual. Obviously, inactivated viruses will expose several proteins, but not in isolation, and have a different response yet.

In the COVID-19 pandemic, there has been some discussion on the effectiveness when people receive the first dose with one vaccine an the second dose with a different one.

"differing vaccines" - Do they differ? All Covid-19 vaccines seem to code for the same spike, in full length (m-RNA- and vector-vaccines only differ in their being based on either RNA or DNA), and differences if there are pertain to coding specific promoting oder stop codons only? And even protein vaccines do not differ in that respect. Don't they all use the same spike antigen with all its epitopes?

Due to the nature of the immune system, even people who receive the same vaccine will have a different set of antibodies.
Our immune systems generate a vast number of essentially random recognition combinations, unique to every individual. This leads to a polyclonal response to both infections and vaccines, involving multiple antibodies and the fine details of those antibodies differ based on the specific antibodies in the "library" that the person's body has generated.
Now, different antigens do result in different antibodies being selected for, so one might expect there to be additional differences due to getting an mRNA coding for a SARS-CoV-2 spike protein vs. getting a whole inactivated virus. There's a reason that the spike protein is the preferred target, however, in that its position on the outside of the virus leads it to be a focal point for the response to an inactivated virus.
Bottom line: the responses will differ, but will likely always have a varied set of antibodies targeting the spike protein in any case.

Great answer! I have a question. Won't all antibodies be targeted to antigens on the surface of the protein? Is it possible / useful for an antigen to bind to other types of proteins?

Antibodies do show up against non-structural proteins as well (e.g., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812099/).  I believe this is more significant for antigen presentation, whereas the surface proteins are more significant for neutralization of extracellular viruses.

Do the antibody tests just look at common antibodies that should be shared across almost almost individuals who have developed a resistance to the virus? Even when the tests work as desired, could they still miss resistance in a person who has different antibodies for Sars-Cov-2 than the ones being tested for? If so, is this a common issue?

@tparker Antibody tests don't actually check for specific antibodies. Instead, they present pieces of the antigen (in this case, various fragments of SARS-CoV-2 virus) and measure how many antibodies in a person's blood will bind to them.

Would be interesting to know about the role of the MHC which differs from person to person (does MHC type depend on the cell type, by the way? For instance, do B- and T-cells differ in their MHC?)

@PeterBernhard That sounds like a whole new question or two to ask...


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Identify black insect on Granadilla plant in South Africa
Planted a granadilla tree 3 weeks ago and these guys appeared on the new growth.
Never seen them before.

You can use an app like iNaturalist to both make a formal observation for the scientific community, but also to identify organisms with pictures. You'll need to take clear photos, especially of identifying features in order to get accurate suggestions.

See the guidelines at https://biology.stackexchange.com/tags/species-identification/info for species ID questions.

Welcome to Biology.SE! In addition to following @doremi's advice, please click on the species-identification tag for important information about such questions. In particular, please [edit] in size information. Note that this insect has been asked about before on this site, but did not get an answer. Consequently, you should try other resources such as iNaturalist. If you find out, please follow the [answer] guide and post it here. Thanks!


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What is this red little cocoon like creature here?
I found this bug here outdoor on the wall of my backyard. I’m in California.
Red and looks like a cocoon, notice some tiny dots on its back. About 1cm.
Does anyone know what kind of insect is this? Seen it there for a few days now.
Thanks

"Seen it there for a few days now" On the exact same spot or was it moving?

On the exact same spot!

This looks like a lady beetle pupa.  Given the appearance and your description of it's size, my guess would be of Harmonia axyridis.
Here'a link, with a picture of another pupa about half way down the page: https://edis.ifas.ufl.edu/publication/in361. This species has a diversity of colorations, both on the adults and the pupa.
Here's an example of another pupa of what is most likely the same species (from https://bugguide.net/node/view/410817/bgimage):


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Do spring varietes of cereals have a process of vernalization?
I was wondering about this question - Do spring varieties of cereals have some process of vernalization?
It would be nice to have some description of the main processes' differences of spring and winter varieties.
Thanks!

The answer depends to some degree on what you mean by "some process of vernalization". As far as I know, the difference between winter and spring varieties is a matter mostly of how strong the response is, not whether the response exists.
One paper writes in the abstract:

Wheat cultivars are classified as two general types: winter wheat with variable low temperature requirement for a proper flowering time (vernalization) and spring wheat without the requirement, based on their qualitative vernalization requirement. Winter wheat cultivars are classified as three types, weak winter, semi-winter and strong winter, according to their quantitative vernalization requirement to reach a vernalization saturation point or achieve the maximum vernalization effect.

The difference is not whether vernalization exists as a process, so much as whether it is required for timely reproductive transition.
See the figure below (from this paper), showing spring (LEG) and winter (MIR) varieties of wheat after various vernalization periods. Basically, even the spring variety has a weak vernalization response; it's just much less notable than the strong response of the winter variety.

With legend:

Frost tolerance (LT50), apical development (DC = decimal code) and days to heading of ‘Mironovskaya’ (MIR) winter wheat and ‘Leguan’ (LEG) spring wheat plants during 12 weeks of acclimation at 2 °C and two photoperiods, 16 h (long day) or 8 h (short day). Vertical bars indicate LSD0·05 and asterisks indicate that the plants had not reached heading by 100 d.


text:
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:
Identifying Promoters in Non-homologous Sequences within the Same Organism
In this paper, the authors cloned a GPD promoter for use in driving a GFP gene from Lentinula edodes using a set of provided primers. The primers were derived from the following accession GQ457137.1 containing the GPD gene for this organism.
In fact, there are three accessions in GenBank containing gpd promoter sequences for Lentinula edodes, each of varied size and homology to the aforementioned sequence used in the paper.
I am working on defining a transformation protocol for Psilocybe cubensis (of which there are no published transformations) and I would like to design some primers as done in the paper above in order to clone the GPD promoter for this organism from its DNA; however, just as with L. edodes, there are multiple accessions of GPD in psilocybe cubensis: KM273235.1 and KT067727.1
In my case; however, there is no literature referencing either of these accessions and so I don't know which of these accession I could or should use to design my primers.
I have the following questions:

Why does the same promoter within the same organism have such varied sequences?
If the promoter sequence varies even within the same organism, the how can anyone extract the promoter with certainty since the organism may carry a different sequence for the promoter?
Generally, I'm trying to find the GPD promoter for P. cubensis (or any strong promoter) and clone it for use in my plasmid for transformation. I'm stuck as to how to go about finding a suitable candidate.

Thank you.

Why does the same promoter within the same organism have such varied sequences?

While there may be other reasons, the fact that the same species has several genes encoding GPD proteins is an indication that this enzymatic activity is important for different mechanisms, times or conditions. For example, I mentioned in a comment to one of your previous questions that the three GPD-encoding genes in budding yeast (TDH1, TDH2 and TDH3) are expressed during different growth phases. Therefore, although the proteins encoded by these genes might share both sequence homology and function, their promoter regions most likely will not. We even expect their promoters to be different, to allow for such differential expression. Put differently: if the three TDH promoters were all highly similar, we would expect them to also be active at the same times, effectively rendering the three genes redundant.
There is therefore no reason for assuming that promoters driving the expression of two different genes will share any homology, just because the encoded proteins happen to share function.

If the promoter sequence varies even within the same organism, the how can anyone extract the promoter with certainty since the organism may carry a different sequence for the promoter?

The only way of knowing exactly what region upstream of a gene that regulates it's expression (i.e., what functional elements that defines its promoter) is to characterize the promoter region. This is way beyond the scope of your work. What we tend to do in budding yeast when we clone an uncharacterized promoter, is to simply take 1000 bp upstream of a gene's start codon, and assume that this includes all elements necessary for proper regulation of the gene in question (e.g. possible transcription factor binding sites (TFBSs), transcriptional start site (TSS), etc). 1000 bp is a relatively safe length in budding yeast, since the distance between genes rarely exceeds this, and we tend to assume that promoter regions don't overlap neighboring genes' coding regions. But this might be different in your species. Also, if you know the location your gene's TSS, this would be a safer reference point than the start codon.

Generally, I'm trying to find the GPD promoter for P. cubensis (or any strong promoter) and clone it for use in my plasmid for transformation. I'm stuck as to how to go about finding a suitable candidate.

My guess is that the authors that cloned the GPD promoter from Lentinula edodes either already knew that this specific gene is highly expressed and therefore selected its promoter; alternatively they might have cloned all GPD promoter variants, and then simply published the one that they saw worked best.
If you don't have any information about the expression of the GPD-encoding genes from your species, any decision as to which promoter to choose will inevitably be more or less guesswork. It seems to me that the evolutionary distance between Lentinula edodes and Psilocybe cubensis is way too large to make any direct inferences. Nevertheless, with the lack of better options here is what I suggest:

Try to identify which of Psilocybe cubensis's GPD proteins is most similar (in terms of sequence homology) to the protein the authors chose for their Lentinula edodes GPD promoter. This might indicate that these are direct orthologs, and with a bit of luck may also share similar relative expression patterns and/or levels. You could also do a similar matching with the Tdh3 protein from budding yeast, since TDH3 is indeed a very strong promoter (article behind paywall, but easy to find elsewhere). If you still don't know which of the promoters to choose, proceed with both candidates and see which one works best (although that means doubled cost and effort).

Once you have identified your candidate GPD gene, you define an appropriate region upstream of your gene’s coding region as the promoter region. This can be arbitrarily picking 1000 bp, or the entire intergenic region, as @Cholpisit suggests.

Design your primers for cloning this region into your target vector, upstream of GFP.

I really appreciate your effort to help, but I can't help but feel like you aren't quite understanding what I'm asking even though I've taken a best effort to elucidate it as clearly as possible. Furthermore, I'm asking these questions specifically to learn and reconcile my ignorance before actually designing the primers or running the experiment - you're first sentence seems to presume otherwise. This conversation format doesn't really accommodates a proper discussion where some of the miscommunication could probably be resolved in a few quick back/forth in a chat.

Anywho, I will digest the info further and see if I can think of a way to progress the conversation forward. I am sincerely grateful for your efforts.

If you don't feel my response answer your question(s) you can wait with accepting it and see if someone else addresses it better :)

My intent was not to insinuate that you are not trying to understand, I just think that if you don't understand why homology between promoters of paralogous genes is unlikely, you will probably want to understand that before you go about with your endeavor. But explaining why this is the case is a completely different question. In any case, I will edit that comment out from my answer. Also, if you can point out exactly what parts you didn't get answered, you might get better answer from me or from others.

I accepted it to ensure my comments didn't take away from the effort you put into the response! Duly noted re: the other parts.

I have rewritten parts of my answer, hope it's clearer now. If not, we might be able to continue the discussion in the chat, but I'm not sure how that works.

Let us continue this discussion in chat.

Left you some messages in the chat. We're in diff timezones so might be tough to hop on at the same time.

I'm not well-verse in fungal transcriptional system but I did some digging in bacteria before, so not entirely sure this perspective will help.
The promoter region of any gene should be upstream of the transcriptional unit and usually remains in the intergenic region, not being part of the CDS of interest and the adjacent gene. If we're digging a promoter of an essential gene, probably constitutively express with decent strength, ones might be able to chop the whole intergenic region and the part of the adjacent genes (in case they contribute to the transcriptional control). A well-annotated genome would be required for this approach.
Considering the different promoter/gene annotations available in the database. It might be hard to pinpoint if they're the same strain/substrain or not and that may affect the genetic variation to a certain level.

The doubting 3 GPD promoters of Lentinula edodes you mentioned are from unpublished sources from 2 teams. Do we know if they're exactly the same strain? As for those two sequences from the same team, they share sequence similarity to a certain level, GQ457137      is part of GQ457138 according to the alignment.
As for the P. cubensis GPD promoter, you can try chopping the intergenic sequence upstream of the coding sequence as gaspanic mentioned above. The GPD accessions KM273235 and KT067727 might be referring to different strains as well. Depending on the strain you're working on, you may prefer the sequence submitted as that strain. However, you'll have to look for more information since those deposited sequences refer to partial CDS, not the promoter itself like in the case of Lentinula edodes.


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What is the purpose of an siRNA screen in drug discovery?
In the paper "A genome-wide siRNA screen identifies a druggable host pathway essential for the Ebola virus life cycle" by Martin et al. the authors try to disrupt the Ebola life-cycle by screening which human genes participate in it's replications:

In order to identify host factors involved in the EBOV life cycle, we performed a genome-wide siRNA screen comprising 64,755 individual siRNAs against 21,566 human genes to assess their activity in EBOV genome replication and transcription. As a screening platform, we used reverse genetics-based life cycle modelling systems that recapitulate these processes without the need for a BSL4 laboratory.

This helped them find a pathway.
What is siRNA screening and how does it help find a pathway?
The tag [rna-interference] references siRNA:

A post-transcriptional mechanism of gene-regulation/silencing mediated by small RNAs (siRNA)

However, I can't tell if siRNA refers to "small RNAs" or the whole process.

According to the Labome article "siRNAs and shRNAs: Tools for Protein Knockdown by Gene Silencing" siRNA does stand for small interfering RNA.
siRNA is used to silence genes via mRNA degredation:

NA interference (RNAi) is the process by which the expression of a target gene is effectively silenced or knocked down by the selective inactivation of its corresponding mRNA
[...]
The silencing mechanisms can either lead to the degradation of a target mRNA, as induced by small interfering RNAs (siRNAs) or short hairpin RNAs (shRNAs), or the suppression of translation of specific mRNAs, as induced by microRNA (miRNA).

There are also Wikipedia articles discussing these concepts that didn't come up in my search somehow, but a colleague linked me to:

Gene knockdown
Small interfering RNAs


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Type B Nerve fibres cause exactly what kind of autonomic sensation to the preganglionic neurons?
Ganong's Review of Medical Physiology (25th ed) presents the Erlanger and Gasser classification of mammalian Nerve Fibres as such:

Type B Fibres are concerned with Preganglionic autonomic sensations, but there is no mention of this being sympathetic or parasympathetic. Does it mean that it is both?
The table does specify it as sympathetic for the Type C Fibres, though.
(I have tried searching this on google, but I can't seem to find anything specific.)


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Are there any online resources that have a list of post-translational modifications and their molecular weight?
I am studying a protein and I am interested in learning about all the post-translational modifications that it has (as I am analysing it via Western blot). I have found a list of the post-translational modifications that it has, however, I want to know what are the molecular weights of the post-translational modifications (in daltons/kilodaltons). I have found this site but I am not sure what the difference is between 'Monoisotopic Mass Change' and 'Average Mass Change' and what units the values are in.
I was wondering if there are any reliable online resources that have a list of all the post-translational modifications that exist and their associated molecular weights? Any insights are appreciated.

To a man with a hammer, everything looks like a nail. If you want to know what modifications a protein might have you use the most appropriate method. Western blots of SDS gels isn’t it. Your intelligence is the resource you need to consult. Calculate the molecular weight of an acetyl group and then what increase N-acetylation will have on the molecular weight of your protein. Then determine whether SDS gel electrophoresis can resolve that difference. You have accepted an answer to your question, but it is not an answer to your — or anyone else’s biological problem.

You've found one. Since the differences between the "Monoisotopic" and "Average" columns in the Sigma-Aldrich link you found are extremely low, functionally we can say they are approximately equal. The masses are in atomic mass units, or Daltons.
However, these numbers are from actual mass changes seen in modified peptides analyzed by LC/MS/MS, typically from digested proteins. Mass spec is a highly precise platform, as you can see by the number of decimal places in the numbers in the table. When estimating protein size by Western blot, the margin of error is at least 1 kilodalton for smaller (10-50 kDa) proteins and 5-10 kDa or more for larger ones. Since a single phosphorylation event would only change the mass of a target protein by 0.08 kDa, determining that by Western blot is essentially impossible. However, evidence shows that proteins modified by a single phosphorylation event typically also have (sometimes many) other post-translational modifications (PTMs) as well, including other phospho sites, methylation, acetylation, glycosylation, etc., that can visibly affect a modified protein's mobility in an SDS-PAGE gel.
Another factor to think about is that in denaturing SDS-PAGE gels (which most Western blots are generated from), migration rates are not only influenced by total molecular mass, but also by charge, as the proteins are migrating in an electrical field. When these proteins are linearized by SDS, a charged detergent, their overall charge is roughly proportional to their size. However, charged PTMs like phosphorylation will affect that overall charge, and may modify the migration rate according to that charge in addition to their extra mass.
Combine all this together, and you have PTM-modified proteins migrating at somewhat different rates than one might expect based on the physical mass of the modification(s) alone. When you start combining multiple PTMs, especially different kinds of PTMs (phosphorylation and acetylation, for example), it can become very difficult or impossible to predict what the expected apparent molecular masses will be.


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Do "shooting" animals exist?
The well-known cartoon imagery of porcupines shooting their quills at opponents in a fight is just that: a silly cartoon concept that isn't real.  But it makes me wonder, does that mechanism exist elsewhere in nature?
Are there any animals whose bodies produce solid projectiles that are used as launched/thrown weapons?  (Not looking for liquid ranged weapons such as skunk spray, bombardier beetles, etc.)

Clarity please. Are you excluding humans? Does this "production" exclude use of tools? Would you include the poo projectiles produced by primates?

@tyersome Yes, when I say "animals whose bodies produce solid projectiles," I mean produced biologically by the body, not produced externally by the use of tools.

Tarantulas can eject lots of bristle at potential predators. They often kick the bristles off with their legs, and I was told that they can eject them by tensioning their skin, but that's probably false, so I won't write a reply, here's a pic: https://www.youtube.com/watch?v=1cPxqjSG6HU

I don't know if it counts as shooting, horned lizard can "shoot jets of blood from their eyes for distances of up to five feet", according to an xkcd "what if" which points to Wikipedia page about horned lizard.

While not a solid produced by their body, pistol shrimp shoot "cavitation bubbles" to stun and even kill small fish! https://en.m.wikipedia.org/wiki/Alpheidae

Not projectile, but bonkers. Horned Lizards can shoot blood from their eyes when endangered: https://biology.stackexchange.com/questions/19794/how-did-the-horned-lizard-evolve

There's also the mantis shrimp, which has two appendages that can be fired at a target so quickly that they boil the water around them: https://en.wikipedia.org/wiki/Mantis_shrimp - however those are permanent appendages, not projectiles.

Many species of caterpillars eject their poop in pellet form at high speed.  It has been theorized that they do this to avoid drawing the attention of predators, so I suppose you could argue that this is a defensive mechanism; but it's not really a weapon.

https://en.wikipedia.org/wiki/Urticating_hair - "Urticating hairs or urticating bristles are one of the primary defense mechanisms used by numerous plants, almost all New World tarantulas, and various lepidopteran caterpillars. ... Many tarantula species eject bristles from their abdomens, directing them toward potential attackers"

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A good exemple should be the “harpoon” in cone snails (Conidae), which is created from a modified tooth inside their proboscis.

(Cone snail with proboscis, from KQED.org)
The harpoon is launched at prey at close distance, and is used to poison and stun prey, and later to pull them in. According to high-speed camera capture the harpoon is launched in just 200 microseconds, with an acceleration similar to a gun. The “harpoon“ structure is also very similar to a human made harpoon (see picture below)

(from KQED.org, Courtesy Manuel Jimenez Tenorio, Universidad de Cádiz)

(from KQED.org, Courtesy Joseph Schulz, Occidental College)
These harpoons are not re-used, and a cone snail can have up to 20 harpoons at different stages of development (see Cone snail toxicity).
It is also worth noting that the harpoon and its venom is a potent defence weapon also against humans. One cone snail can contain poison to kill about 700 people, and people stung by cone snails can get severely injured or even die (fatality reported to 15-75% according to Kapil et al, see below).
If you would include use of tools, in projectile use/shooting animals, apes and elephants are known to use stones as throwing weapons (see wiki-page linked below).
Sources:
https://www.kqed.org/science/1923898/watch-these-snails-stab-fish-and-swallow-them-whole
wikipedia: projectile use by non-human organisms  (with other examples of projectile use)
Kapil S, Hendriksen S, Cooper JS. Cone Snail Toxicity. [Updated 2020 Sep 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. www.ncbi.nlm.nih.gov

An excellent example (unless you consider this a tool) of a weapon using animal would be the "web casting spiders" which are a diverse group of spiders known as the Deinopidae. These spiders create a special elastic web that they hold between their fore-feet, and then dangling down from a surface, they expand and push the web onto their prey.
There is an excellent video from the BBC of this happening here

Although not a hard projectile the Archerfish shoots water
https://en.wikipedia.org/wiki/Archerfish

Humans can also shoot water from their mouths, but not three metres

@user253751 - If you search for spitting world records you may be surprised

"Not looking for liquid ranged weapons"

Can't find it at the moment, but I remember lizards shooting blood from their eyes, most likely from What if? blog by xkcd.

@valisstillwithMonica Here ya go.  It's a defense mechanism

+1 because it's still the physical effects of the projectile that the fish is going for, not like skunk spray which is basically chemical (odour), not impact or making a bug's wings wet.

It is a common notion that porcupines can shoots spines but in reality, they can't. But there are some animals that can shoot/throw projectiles at the target as a result of either offensive or defensive mechanism. The projectile can be anything ranging from spikes or thorn to big objects like rocks, sticks, nuts or even faeces. You can find the details in the Wikipedia article.
The Wikipedia article mentions tarantulas that have a dense covering of hairs called urticating hairs on the abdomen that they sometimes use as protection against enemies. They can kick these hairs off by flicking them into the air at a target using their back pairs of legs. These fine hairs are barbed and designed to irritate and can be lethal to small animals such as rodents as well as humans.
Sea cucumber can expel its internal organs through its anus which can be sticky and sometimes contain a toxic chemical that can kill predators.

Spitting spiders will shoot their strands of web (extremely quickly) toward prey:
https://www.youtube.com/watch?v=DFozCr_tj8I

There is a plant called Sphagnum that disperses its seeds through an explosion that functions similar to that of a cap gun. It's pretty sick.
here it is in action

OP wants to know shooting "animals" not plants.

@NilayGhosh the question text wonders "does that mechanism exist elsewhere in nature?" so plants would be included there. Possibly the title only mentions "animals" as the questioner hadn't considered plants as a possibility - however this appears to be a seed dispersal tactic rather than a weapon

@MartinSmith I would think so but again in 2nd para, it is written "Are there any animals whose bodies ...". If OP were to consider both animals and plants, then the question would be too broad. Also, the other answers involved animals. So, this is an odd-one out.

No, there are not animals which produce solid projectiles to shoot/launch/throw for defence or hunting. I think these criteria mean "aimed and detached".
There are tethered projectiles like cnidocyst in Cnidaria, but they don't detach (Wikipedia/cnidocyte). Harpoon-like organ in cone snails which is mentioned by @fileunderwater doesn't detach from the body (albeit detaches internally) and it must work in this way in order for the snail to hold and draw its prey (Wikipedia/cone snail). Spitting spider which is mentioned by @JimN doesn't store solid silk to shoot, it sprays the materials (Wikipedia/spider silk). It seems that the nearest thing is the urticating hairs in tarantula which is mentioned by @NilayGhosh; but tarantula doesn't shoot, it detaches hairs to make them airborne (Wikipedia/urticating hair). As the question has those criteria, these don't count.
There is a similar question on the possibility of that ability in worldbuilding.stackexchange (link) which you can review.

You should remove the first line of your post, as other posts have proved it false. "Never say never."

@LevelRiverSt What other answers prove this one false? serekani already specifically mentions some of them and says why they don't meet the criteria in the question (a solid projectile shot by an animal). The question doesn't disallow tethered projectiles, so you could argue that's an unnecessary limitation, but I think it's an interesting point to bring up.

@kwc 1. sea snail harpoon - complies with question, shoots, does not detach in use, but "is not re-used" so it must detach afterwards. 2. Of the spider answers, the spitting spider web is clearly projected & detaches in use (at least some parts) and works because it is toxic and sticky. (Watch the video.) It may not be hard, but it's not a liquid or a gas, most definitely a solid. This post then almost contradicts itself because it mentions urticating hairs, which are clearly produced by the animal's body and are solid (though having watched a video they are perhaps not really a projectile.)

@kwc the sea cucumber internal organs and pufferfish look like examples that fit the criteria, but following your comment I haven't been able to substantiate that they actually detach (all I've seen shows them remaining attached.) Equally, its pretty much impossible to substantiate a claim that there is no animal in existence that produces solid projectiles that shoot and detach, which is why I think it is unwise to say it. Consider how many species there are out there still to be discovered.

I know and admire that stackexchange community is passionate in and enjoy learning, researching and exchanging knowledge, and these are the most important things beside providing an answer. But there should be an answer at the end if possible. When and if OP tweaks the question a little bit, one or some of these animals are the answer.

@LevelRiverSt I understand the point:"Never say never." But it isn't necessary or customary to add "as long as we know" to every statement. If one asks if there are any fish species which lay egg on ice, the answer is no. Of course the question can be edited numerous times to try to fit the question to an answer, but this can make asking a question meaningless from the very beginning most of the time.

@serenaki your post has a box above it saying Want to improve this post? Add citations from reputable sources by editing the post. Posts with unsourced content may be edited or deleted which drew my eye to it. I would upvote it if you removed that first line, because I don't believe it's definitely true (and having watched some spitting spider videos I think it's false.) If you changed it to say you don't know of any such animal, that would not be overstating the case. The rest of the answer is good and interesting.

So if you would be shot by a human-made whale harpoon, you wouldn't consider this a death by a "...solid projectile(s) that are used as [a] launched/thrown weapon..."? In that case you are using a pretty limiting definition of launched projectile weapon. Especially considering that wire-guided missiles were common anti-tank weapons up to the 70s.

Fieldfares guard their nests by attacking predators with their poop. Arguably feces is undigested material, but it does contain some secretions made in the body. Admittedly, fieldfare poop is more of a paste than a solid.
https://www.youtube.com/watch?v=Fdrl__ggV9k

I think it would be well argued that bird poop is a liquid generally - there are seabirds that projectile vomit to protect chicks, which would be also considered a liquid. I think the main criterion to the question is created and solid.


text:
Does a virus that spreads more rapidly have less chance to evolve?
Now that the COVID-19 pandemic has been going on for a while, there are reports of many new variants, which have presumably arisen in the past year through mutation and spread through natural selection.
I'll assume that the outcomes of COVID-19 infection are either death or a successful immuse , others would have developed antibodies. Suppose for the purposes of discussion that those are the two end consequences (or correct my answer in your thinking.)
If eighteen months ago, everyone in the planet had been infected with COVID-19 in one very bad day, then many people would die, and the others would end up with antibodies. That might stop the spread of the disease, which would stop its evolution. (Feel free to address Typhoid Mary-like scenarios in the answer; or of course any misconceptions in this paragraph.)
Is there a perspective from which—or set of circumstances under which—drawing out a pandemic can actually worsen the effect of a disease by giving it more chance to evolve?
(I've put the question in terms of COVID-19, but I think it's really a generally question, no less applicable to COVID-20 and above. :-) Please feel free to answer in general terms. I am not looking for a discussion about what public health measures may or not be appropriate to the current pandemic.)

Just guessing: if it has 10 generations of reproduction in your cells rather than 100, i.e. it gestates longer before transmittal, that's a factor... however it could reproduce 100 times in 2 days or 10 times in 3 days. As the other answers state, the virus also has an independent mutation rate per division, so that's 2 only half related factors, plus theres lots of others.

Any evolutionary process has two components to it:

generation of genetic diversity in a population, and
shifts in the distribution of genetic variants under selective pressure.

For a virus like SARS-CoV-2, every infection results in a vast amount of replication, some of which will be variants generated through imperfect replication. Thus, the more rapidly a virus is spreading, the more opportunity it has to generate genetic diversity. Conversely, if there's not many infections going on, then there won't be much evolution because there won't be much diversity generation.
With regards to selection, the more actions that we take against the virus (e.g., mask wearing, social distancing, vaccination), the more selective pressure that it is under, since these actions differentiate between strains that are more or less effective in evading them. If the pressure goes too high, however, this breaks down. With highly effective countermeasures (e.g., rapid vaccine distribution while not letting our guard down), then there won't be much evolution because most variants won't have an opportunity to infect any new host: each new generation of infections will be driven more by countermeasure failures unrelated to viral efficacy, and thus there will actually be little effective selection.
The highest opportunity for evolutionary change, then, is with poorly coordinated countermeasures. This produces an intermediate rate of spreading, with both much viral replication and many opportunities for selective pressure on infections.  It's really much the same as the problem with stopping a course of antibiotics prematurely, only on a societal rather than individual scale.
Bottom line: countermeasures are still a good idea, even when potential evolution of variants is included. People and governments that don't take the problem seriously, however, are threats to all the rest of us.

So a virus that spreads more rapidly has higher population and therefore higher chance of mutations, and also more variable habitats. also perhaps less gestation mutations.

RNA viruses, like SARS-CoV-2, influenza, HIV, etc all have high mutation rates caused by an error-prone RNA replicating protein (known as an RNA dependent RNA polymerase or RdRP) that they use to reproduce their RNA genetic component. The error rates are high enough in these viruses that you can say that the virus exists not as a single species, but as something known as a quasi-species, which you can visualize as a cloud of individual virions, each with genetic variants from the "original" genome, some of which will be more "fit" than others in terms of evolution. These more fit ones are the variants that you see being talked about in the news.  Note that the error rate of the RdRP is in terms of base changes per 1000 bases per 1 replication cycle, and the number is usually around 3-4.
The fitness of a virus is not necessarily related to any one variant, often a number of seemingly unrelated mutations in several proteins are required to make it fitter in any of the following characteristics:

Evading immune response
transmission
Invasion of the host/infectivity
viral titre (how many viral particles are produced)
replication rate
host-range (what species it can infect)
Tissues it can infect

Often, being better at one of these features means that it does poorly in others. A fine example of this is the H5N1 influenza that raged across the world a few years ago - it was great at killing people and even better at killing birds (it is an avian virus), but it was terrible at actually infecting people, it just couldn't sustain transmission in humans and even those exposed on a regular basis (i.e. working with chickens in endemic virus areas) didn't often get infected, even if they seroconverted.
SARS-CoV-2 has hit a pretty sweet-spot, it can transmit really well, it is highly infectious, has a fairly broad host-range, and has a long lag-time (~2 weeks) before people know they are infected, and some never do show symptoms. On the other hand, in some people it isn't at all great at evading the immune system, it actually seems to potentiate it, causing something known as a cytokine storm, where the immune system goes into hyperdrive and causes serious inflammation. This is what actually kills people - the swelling of their airways in response to the infection limits oxygen transport and slowly suffocates them.
Now, you talked about antibodies: Antibodies are not the be-all and end-all like they are often considered. An antibody response to an infection does not necessarily mean that you can not get an infection from it again, it simply means that the infection is minimized to some extent. The extent of the protection is highly dependent on the individual (i.e. your response will be different to mine), and on the organism with which you are infected. If you had say Smallpox and survived, you (and I too, if infected) would likely have a life-long immunity to smallpox. However, have an infection with a different pox virus, such as Orf virus, and you might only be protected for 6 months.
You, yourself (assuming you are >10 years old) and everyone around you is likely to have antibodies against at least 1 of the influenza viruses, but this won't stop you from getting sick from them again, it might however limit your infection so that you don't feel so bad for as long (and can then spread it more effectively...). So you have antibodies, but they don't eliminate the flu, and as a consequence we have a vaccine against influenza. Now the vaccine also doesn't cause complete protection, but that's beside the point. The reason you need to get an influenza vaccine each year is because the viruses have mutated over that year so that they are no longer the same as the previous year's flu viruses, so your body doesn't fully protect against the new viruses.
In the case of the SARS-CoV-2 vaccines being distributed currently world-wide. If you have been following the data, even in a fairly superficial manner, you will have seen something like "the Pfizer vaccine has a 95% protection rate" this means that it protects against 95% of illness from SARS-CoV-2 (i.e. symptomatic infection and actual infection in 95% of people). However, you might have also heard about people being concerned that there is less protection against the "South African" variant. This is an example of evolution causing an escape mutant. Evolutionary pressure has been applied to the virus, and it has produced a means to get around that pressure, to some extent. This will be an on-going process in terms of SARS-CoV-2; we will need new vaccines regularly to cope with the new variants as they arise.
TLDR: the virus will evolve anyway, the evolution happens in as little as a single cycle of virus replication.

Notes that influenza is actually much more complicated case that is not just based on mutation, due to its segmented genome.

@jakebeal yes, assuming genetic drift not shift. Genetic drift is the major component to needing a new vaccine... source: me who used to work at a WHO collaborating center for influenza research...

Are there models which could indicate the increase in variance due to systemic pressure (vaccines being applied to the population at a certain rate without a 100% coverage over time)? Or, could the hypothesis hold that given the slow rate of vaccination in densely populated areas, the evolutionary pressure in selection increases fitness rate and overall rate of variations in the virus? Any references besides adjusted SIR models with time-varying I and R0 rates, or modifications to  Fisher's fundamental theorem of natural selection?

@Moreaki - no idea. I would guess, not being an evolutionary biologist, that the standard models will apply.


text:
If excess sodium is bad for humans, why don't our bodies just remove it?
This is one of those questions where I realized two everyday facts don't connect for me. Excessive sodium in the diet is supposed to be bad for us. But surely our bodies have mechanisms for getting rid of excess sodium. (I don't know the details, but I know enough about neurons to know that our cells can move sodium when they need to.) Why don't our bodies just keep our sodium levels at a healthy level?

Are you talking about the long or short term effects of excess sodium?

I was thinking about blood pressure and stuff like that, but if the answer would be different for different conditions, that would be interesting too.

Because evolution doesn't care about what's good or bad, just about what lets organisms pass on their genes.  The bad effects of things like high blood pressure usually don't show up until long after most people have done their gene-passing.


text:
Mathematical/statistical models for forecasting population distributions of age, sex, weight, and height
I come from a mathematical background but I have no experience with the topic of mathematical biology.
Are there well established mathematical/statistical models for forecasting the evolution of population distributions of biometric parameter such as age, sex, weight, and height? For instance, I have often heard that the proportion of elderly people in the population is projected to increase. What models are being used to generate forecasts such as these?

It's not possible to accurately predict the course of evolution in humans. I imagine the models you are thinking of are based on socioeconomics rather than biology.

You better let the national statistics offices of every country know then because they all make future projections of age and gender population distributions. Health bodies make projections of weight distribution. So I am wondering what models are being used to generate these type of projections. I am particularly interested in models that take a stochastic viewpoint, although I am also interesting hearing about deterministic models.

Those models aren't base on biological evolution which is what I interpret your question to be asking about.

I get where your coming from. The models I am looking for information on relate to population dynamics which is a field of mathematical biology.

It might be irrelevant to your question but search for "allometry".

The term you are looking for is demography - there are literally thousands of papers published on this topic.
Each of your topics mentioned has its own models and prevailing theories, so without an exact question it is very hard to answer as to which model you might find best.
Having said that there are well established models of things like geometric growth of populations (proposed by Thomas Malthus in 1798). The United Nations does a lot of modeling of populations and the like. You might be interested in their freely available publications and information here.


text:
Would anything limit an "invasive species" T. rex introduction now besides equilibration with available prey or intervention by humans?
In the video Two-and-a-half billion T. rex roamed Earth, study finds contains a short explanation of the results in Science Absolute abundance and preservation rate of Tyrannosaurus rex by the corresponding author of the paper.
I'd like to understand better what is known about T. rex's adaptability and range of environments where it was thought to flourish. It's hard to imagine what things were like back then, so using modern flora/fauna and climate distributions as reference points will help me to understand this better.
Based on that knowledge and reference frame, I'd like to ask about the following Gedankenexperiment:
Question: Would anything limit an "invasive species" T. rex introduction now besides running out of food or intervention by humans?
Would they basically thrive over much of the Earth's surface and eat all the other mammals? Or without a supply of dead and rotting dinosaur cadavers would these giant scavengers with excellent olfaction quickly deplete a small region and die of starvation?
Currently there is not likely enough DNA to reconstruct a full genome nor a scheme to build and incubate a dinosaur egg for it (as far as I know), so we are not at any risk of this happening in the near future.

Fun question, there are too many ecology variables to give a definitive answer, perhaps T-rex was an ambush specialist... folks on a paleontology forum would know. If the oxygen levels were OK and there were many buffalo, hippos, rhinos and elephants, i'm pretty sure T-Rex would be unstoppable!

It seems that if the current earth could support terrestrial predators/scavengers the size of T.rex, there would be one already. Terror birds were around relatively recently (2 million years ago) but instead of getting larger, they went extinct

@timeskull I'd always thought that population dynamics was more complicated than that, and that there could be multiple equilibrium points or alternative stable states especially when there's been a significant change in the status of a keystone predator.

@aliential I've added a bounty.

@timeskull ditto.

@uhoh T-rex maximum speed was 20mph and a buffalo is 35mph, I think it's really one for reddit/paleontology :) velociraptor and triceratops would be more invasive... It's only recently that scientists agreed T-rex went 20 rather than 45 mph. 2 many science variables.

@aliential Who needs buffalos there are billions of easy livestock humans have confined with fences and pens a rex can step/reach over. Also remember there is decent evidence T-rex are pack hunters.

Lots of things could impact a reintroduced invasive species.

Disease/sickness: although no close relatives are present that is not a guarantee,  many diseases jump species. Parasites likewise could cause problems, especially newer parasites the dino may not have a good defense for. Even modern Fungus could pose a problem for eggs.

Predators: While an adult t-rex is predator proof eggs and newborns are not. Rats and other small mammals as well as many birds have been the demise of many ground nesting birds.

Poisons: there are plenty of animals and plants that are poisonous enough kill a t-rex that the rex may not recognize as dangerous. Remember there are a lot of things around a t-rex did not evolve with. This is more dependent on location, a t-rex dropped in Australia might kill itself with its first meal.

Human stuff: I am not talking about humans killing them. I am thinking of the things humans make killing them. things like walking into power lines, eating weird plastic human garbage, car accidents ( a car moving at speed could easily cripple a rex), even something as simple as getting hit by trains


text:
What disease / parasite / fungi has affected the mango in the picture?

The mango is found to have some kind of fungi / worm on it's surface . This has affected a huge number of mangoes in the same tree . It can be described as white and fibrous / weblike structure near the top of the mango .

What about the inside of the mango, did the insect make tunnels? if so, photo of slice please. What region of the world are you in?

If you zoom in on your picture, you will see that the small orange blobs have legs. These are red spider mites (Tetranychus urticae), which is a very common pest species of plants world-wide. They are called spider mites as they may spin webs on the plants they are feeding off. You have quite the infestation in the picture. It will take quite a bit of pest control to get this under control. I suggest spraying with Neem oil.
The mites feed by puncturing the cells of the plant they are feeding off and sucking the cytoplasm out. This puncturing results in damage to the plant, which might cause invasion from a bacterium or fungus. In your case I would guess a fungus, probably a sooty mold. Sooty molds grow on sugary excretions from parasitic animals (like spider mites) or on secretions from the fruit itself.