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Gender and age-specific mutation rate in plants
Background
General concept
According to Cochran and Harpending (2013), mothers transmits on average a number $x$ of new mutations to their offspring. This number $x$ is independent of the age of the Mother. Fathers, however transmit a number of new mutations to their offsprings that is very much dependent on the age of the father for developmental reasons. In short (and probably poorly stated due to my lack of knowledge in physiology), spermatogenesis is a continuous process that occurs during the lifetime of the individual while the creation of ovules occurs once and are then stocked.
Human example
According to Kong et al.(2012), in humans the mother transmit on average $15$ new mutations and the father transmit on average $25 + 2(g-20)\space\space$ new mutations, where $g$ is the age of the father. For example, a 30-year-old father transmits $25 + 2(30-20) = 45\space\space$ new mutations. (This approximation holds only for men older than 20 years).
Question: How about plants?

Do you think that in plants too, male and female organs (or individuals for (gyno/andro)diocious species and eventually sequential hermophroditic species) transmit a different number of new mutations for similar developmental reasons?
Do you think that in plants the number of new mutations is age-dependent in males but not in females alike in humans?
Do we have any estimate of the sex and age-specific number of new mutations transmitted in plants?

The age dependency for males is because of continuous spermatogenesis (older spermatogonia might acquire more mutations). Oogenesis however, happens quite early in development and oocytes are locked at metaphase. Female age also matters and is evident in case of aneuploidies. I dont know the mutation rates in plant germline but I suppose it is higher in pollens because they are more exposed to sunlight and other environmental factors.

Why would age matter in females in case of aneuploidy? It is not evident to me. I didn't think of external factor such as sunlight, that's interesting. So, does pollen go through continuous spermatogenesis in plants too but not ovules just like in animals so that we could expect the same pattern than in animals even increased by the sunlight. @WYSIWYG Thank you

female age correlates with non-disjunction of chromatids- leading to aneuploidy. See this.. Usually in many plants flowering happens throughout life (both gametes produced). Some plants however flower only once per lifetime. For some it is periodic. So depending on the flowering pattern, the spontaneous mutation rates may vary.

@Remi.b: Have a look at these: http://jxb.oxfordjournals.org/content/57/9/1847.full and http://web.udl.es/usuaris/e4650869/docencia/segoncicle/genclin98/recursos_classe_(pdf)/revisionsPDF/mut%26variat.pdf

From Whittle and Johnston (2006):

Specifically, human epidemiological data and/or nucleotide substitution rates of selectively neutral DNA (which equals the mutation rate, Kimura, 1983; Miyata et al., 1987) have shown that more mutations occur in the male than in the female germ line for numerous animal taxa (e.g. humans, mice, chickens, and sheep) and in older rather than younger human males, patterns that each agree with the cell-division hypothesis (i.e. more DNA replications in males and in particular older males; Penrose, 1955; Risch et al., 1987; Becker et al., 1996; Moloney et al., 1996; Li, 1997; Green et al., 1999; Crow, 2000; Li et al., 2002; Makova and Li, 2002). Other data, however, have indicated that the mutation bias reported relative to gender and male age are not generally well correlated with the number of germ cell divisions and that other factors could explain these trends, such as methylation patterns, differential repair, metabolic rates, and preferential transmission of mutations to pro- geny from older males (Risch et al., 1987; Martin and Palumbi, 1993; Drost and Lee, 1995; Bromham et al., 1996; Hurst and Ellegren, 1998; Martin, 1999; Crow, 2000; Huttley et al., 2000; McVean, 2000; Sommer et al., 2001;Hebert et al., 2002; Hurst and Ellegren, 2002; Kumar and Subramanian, 2002; Li et al., 2002; Bartosch-Harlid et al., 2003).

…so basically we don't really know whether difference in gametogenesis between males and females lead to more sex and age-specific mutation rate!
However, Whittle and Johnston (2006) in reviewing many articles also show that old seeds are more likely to carry chromosomal aberration and that old individuals are more likely because of the instability of their metabolism to transmit more mutations but that would be sex independent and would not result in different gametogenesis as I was expecting in asking this question. Also the kind of mutations that become more frequent with all parents are chromosomal abnormalities or important deletion but not so much substitutions (which was also what I was interested in when asking).
Thanks @DevashishDas for finding this article. This other one was interesting as well.

authors: حنين فوزي عبد الحليم


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Components of the concept of Developmental Noise?
Developmental noise is a concept that correspond to the amount of possible phenotypic variance of a given genotype in a given environment.
Intrinsic noise (aka Cellular noise) is a component of developmental noise and it refers to phenotypic variations caused by the stochasticity of biochemical processes.
My question is:
What are the other component(s) of developmental noise?

There are two good papers on this that I like a lot:
Noise in Gene Expression: Origins, Consequences, and Control
Cellular decision making and biological noise: from microbes to mammals.
I think they can tell you better than I can, but the major other source of noise is extrinsic noise. Extrinsic noise typically is taken to means two things (both of which are related):
1. Physical noise from the environment that affects biological processes (thermodynamic fluctuations, for example)
2. Intercellular heterogeneity caused by, for example, unequal division. This is also related to cells not being "well mixed" - essentially, molecules found inside of cells are not evenly distributed throughout it.
There may be other kinds of noise, but I think extrinsic is really the main one you should think about.

These papers sound interesting.

Another source of developmental noise is due to diffusion. Diffusive processes are stochastic and induce noise in morphogen gradients and results in the concentration as being "jagged". Recent results have directly measured the noise in morphogen gradients of the developing zebrafish.
In fact, when you think about the low copy numbers of transcription factors which are thought to be morphogens,there must be a massive amount of noise in gradients which the developing systems have to account for.

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Integration of several environmental signals
I am looking for examples of different functions that are good fit to how signals are computed in order to respond to the environment. Let's make my question more copmrehensible with an example...
One example
I have been told (I haven't found an article yet) that in plants, in order to know if it is overshadowed by a big tree, the plant computes that ratio of two signals (UV intensity over Infrared intensity or something similar) so that it can decide whether or not it should grow bigger leaves or other attributes.
This plant radiation example would be an example of a species that computes the function $\frac{S_1}{S_2}$ (where $S_1$ and $S_2$ are two types of signals) in order to take decisions about their response to the environment.
Question
Can you please give me examples (examples with a diversity different functions, with different numbers of different signals) of organism using environmental signals to adaptively respond to their environment?
For example, can you give me examples of the adaptive response to the environment is giving by the following functions of 2 signals:
Continuous traits:

$f(S_1, S_2)= S_1 + S_2$

Produce a trait value at $K_1 + K_2\cdot \left(S_1 + S_2\right)$

$f(S_1, S_2)= \frac{S_1}{S_2}$

Produce a trait value at $K_1 + K_2\cdot \frac{S_1}{S_2}$

$f(S_1, S_2)= S_1^2 \cdot S_2$

Produce a trait value at $K_1 + K_2\cdot \left(S_1^2 \cdot S_2\right)$

$f(S_1, S_2)= funA(S_1, S_2)$

Produce a trait value at $K_1 + K_2\cdot S_1$ iff $S_1$ is detected.

$f(S_1, S_2)= funB(S_1, S_2)$

Produce a trait value at $K_1 + K_2\cdot S_1$ iff $S_1 < S_2$.

Boolean traits:

$f(S_1, S_2)= OR(S_1, S_2)$

Iff signal 1 or signal 2 is detected, produce the trait

$f(S_1, S_2)= AND(S_1, S_2)$

Iff signal 1 and signal 2 are detected, produce the trait

$f(S_1, S_2)= FunA(S_1, S_2)$

Iff $S_1$ < $S_2$, produce the trait

, where iff means if and only if and $K_1$ and $K_2$ are constant values.
What I am NOT asking
I am NOT interested in the accurate description of the signal transduction (Description of the kinase cascade and names of the genes and transcriptions factors). I am interested in having examples of mathematical functions that are computed by the cell in order to take decision about which phenotype to produce (plasticity).

To me, it is unclear if you are asking for cases where we have mechanistic reason/understanding for assuming a particular function (i.e. basic understanding of how the information is integrated and weighted), or just cases where a particular function shows a good phenomenological fit to data (or both). In the example you give (leaf growth), without knowing anything about this particular case, both could seem plausible to me. My point is that any statistical model that relates environmental drivers to a response can be seen as an example of an integrating function...[cnd]

[cnd:] ..., but in those cases we don't necessarily know how the integration is executed, or even if it takes place in the focal organism. Some factors could just as well be mediated through interacting species.

@fileunderwater You make a good point indeed. I haven't thought about that. I'll go for the statistical fit to the data. I rewrote my question to make this point clear. Thanks. Let me know if anything is still unclear. I welcome you to edit my question if you think can improve it according to my needs.

In that case I find the Q extremely broad, since basically any statistically fitted model relating a response (physiological, reproductive etc) to one or many environmental factors will do as an answer. Sifting through the litterature you will find supported examples of almost anything, from single regressions, multiple regressions, quadratic relationships, non-linear responses, custom functions and a mixture of all of the above. It is certainly possible to answer the Q with examples, but I dont know what would constitute a good answer, except maybe giving a taxonomy of functions incl examples

I think I understand what you mean and see what the depressant side of my question. I don't think it is easy to find an example where the function is complicated (something like $\frac{S_1+S_2}{S_3^2}$ or even something like $\frac{S_1}{S_2}$). The perfect answer would contain many referenced examples where different functions fit the way the environmental signals predict the environment.

What you are looking for sounds like the mechanism for a fold-change detector. I would recommend looking at these two papers:
The incoherent feedforward loop can provide fold-change detection in gene regulation
As an example of this working in a real system, I recommend looking at the NFkB pathway, as recently detailed by Suzanne Gaudet:
Fold Change of Nuclear NF-κB Determines TNF-Induced Transcription in Single Cells
Here are a few others that I found just by searching for "Fold change detection"
Comparing Apples and Oranges: Fold-Change Detection of Multiple Simultaneous Inputs
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057455
Efficient fold-change detection based on protein-protein interactions
I'm sure by looking at the referenced papers in the above you can find more examples as well.

Thank you! Seems very interesting, I wasn't aware of this kind of signal. I think your answer partially answers my question. Fold-change detector might be considered as one type of function I am interested in. As fileunderwater complained about my question, it is possible that indeed this post is hard to answer because it is poorly defined. I welcome questions and comments to help me improving my question.

I don't think that any other kind of function, which was not classified as a fold change detector would satisfy your requirements. In fact, the example you gave (of plant radiation) is exactly this.

oh really? Ok, I probably misunderstood the concept of fold-change detector then. I thought that a fold-change detector is the kind of detector that does not only sense the absolute value of a signal but sense a change in the signal intensity. So that the concept of fold-change detection would have no relationship with how several signals are computed to determine the phenotype to adopt as in the examples in my post. So, did I missunderstood the concept of fold-change detector?

I see - I am not sure if the question is clear to me, but with your recent addition, it is.
Given what you now have, I would recommend looking at Uri Alon's book - he certainly has examples of the logical operations (OR, AND, etc.) that you discuss. I doubt the more complicated mathematical functions you give exist.

Sorry about that. If you feel you can clarify things in my question, please feel free to edit it or to give suggestions on how to improve it.

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What does uniprot consider "unambiguous" evidence for the subcellular domain of a protein?
Uniprot has annotation for subcellular location of protein domains. This topological domain information of proteins is under the TOPO_DOM flag.
In most cases the subcellular location is assigned by rigorous sequence analysis both for the experimentally verified and predicted subcellular locations. Sometimes more reliable information is available...

... when the experimental technique used allows the unambiguous
  assignment of the transmembrane boundary to a particular position
  (X-ray crystallography, etc.), the ‘Sequence analysis’ qualifier is
  not added in the topological domain annotation. In this case, the
  positions of the topological domains can be propagated ‘By
  similarity’.

What evidence is available that constitutes "unambiguous assignment" so that the by similarity qualifier can be used?

Following your question, we have updated the documentation for topological domains in UniProtKB:
http://www.uniprot.org/help/topo_dom
I hope you will find it more informative now. Please don't hesitate to contact the UniProt helpdesk if you have any additional questions (or, if you prefer to discuss here, a short note to the helpdesk would help us spot your posting more reliably, since we cannot closely monitor all forums as you may understand).


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Do anaerobic organisms that have a terminal electron acceptor other than oxygen have a Citric Acid cycle?
I have been teaching for a while (College level) and realize that I need to make sure I'm accurate as students get more savvy, and more information is published. I teach that anaerobic respiration and fermentation are different. In fermentation the NAD+ are re-generated and Glycolysis can go ~16x faster. But when I talk about anaerobic respiration I say that the process is the "same" as aerobic respiration just a different electron acceptor. But I admit I don't know much more than that, and as I do research, for example into sulfur-reducing bacteria, I am not finding clear information.
I've been assuming that strict anaerobes don't just rely on fermentation and utilize an Electron transport chain, ETC to generate ATP. But do they use a cycle like the Citric Acid cycle? In other words can they fully oxidize glucose/pyruvate/acetyl-CoA?
If they don't fully oxidize glucose and/or pyruvate, what are the consequences of building up pyruvate (biochemically)?
If they don't fully oxidize glucose, how do they produce enough electron carriers (NADH, FADH2) to make enough ATP in their ETC? Or do they just require less ATP per glucose to survive?
Sorry if there are false assumptions in this question, I really want to understand and make sure I'm giving out accurate info.

I have revised your title so that it describes your concern more precisely, and avoids the rather unfortunate phrase "alternative electron acceptor" (not "alternate") which in plain English implies (wrongly) that the organism has alternatives. Unfortunately this whole field is riddled with unfortunate but accepted nomenclature. Please read my answer carefully and let me know whether you require clarification. It is difficult to find details of the metabolism of these organisms in text books, because of their complexity and difficulty of study.

Terminology

“I teach that anaerobic respiration and fermentation are different.”

Although not conforming to the historic or lay use of the terms “respiration” and “fermentation” the poster is correct regarding the current scientific usage of these terms, as evidenced by the following quotations from the Wikipedia article on fermentation:

“The definition of fermentation has evolved over the years. The most
modern definition is catabolism where organic compounds are both the
electron donor and acceptor. A common electron donor is glucose, and
pyruvate is a common electron acceptor. This definition distinguishes
fermentation from aerobic respiration, where oxygen is the acceptor,
and types of anaerobic respiration where inorganic compound is the
acceptor.”

This is developed in more detail in the Wikipedia article on Anaerobic respiration.
However, given the confusing nature of the terminology, if I were teaching this myself I would  first stress the fundamental difference between the two ways of converting metabolic ‘energy’ to ATP: 1. Directly phosphorylating ADP in a metabolic reaction, and 2. Establishing an electrochemical gradient across a membrane that drives the multi-subunit ATP synthase that produces ATP from ADP and inorganic phosphate. Indeed, depending on the background of one’s students, the use of the word “oxidation” to “mean removal of electrons” may need emphasizing.
N.B. The regeneration of NADH+ in fermentation is to allow the process to continue at all, not to accelerate 16x or by any other factor as stated in the question.
Necessity of  the Tricarboxylic Acid Cycle for Anaerobic Respiration

“Do anaerobic organisms that have a terminal electron acceptor other
than oxygen have a Citric Acid cycle?”

No, not necessarily. Some may, but others only have genes for some of the enzymes of the tricarboxylic acid cycle, as a genomic analysis by Huynen et al. demonstrated (relevant details in footnote).

I say that the process is the “same“ as aerobic respiration just a
different electron acceptor.

No, that is incorrect. Certainly a system analagous to the mitochondrial electron transport system must be present to establish an electrochemical gradient. However the assumption that the process is the same in other respects and  “glucose/pyruvate/acetyl-CoA” must be involved and provide the electrons through generation of NADH in the tricarboxylic acid cycle is unfounded. Bacteria that utilize ‘unusual’ terminal electron acceptors generally occupy ‘unusual’ ecological niches, with ‘unusual’ sources of carbon and reducing power.
An example: bacteria of the Desulfovibrio genus
I found it difficult to find detailed metabolic information about bacteria which employ terminal electron acceptor other than oxygen. This may reflect the fact that many occupy extreme ecological niches and are difficult to study in the laboratory. In addition the situation is often confused by alternative methods of oxidation (some are also fermenters) and the possibility of symbiotic relationships with other bacteria). One more tractible example is found in members of the Desulfovibrio genus, which employ sulphate as their terminal electron acceptor, and use hydrogen and various organic acids as the source of reductive energy. With metabolic observations supplemented by genomic and transcriptomic analysis the model below has been proposed for the flow of electrons during sulphate respiration in D. vulgaris.

From a 2011 review by Keller and Wall which should be consulted for further details.
It should be emphasized that the pyruvate generated when lactate is oxidized is converted to acetate as an end-product and not converted into acetyl-CoA for input into a tricarboxylic acid cycle. Genome sequencing indicates that genes for most of the enzymes of the cycle are present, except for citrate synthase and perhaps 2-ketoglutarate dehydrogenase. It should be explained that the presence of an incomplete tricarboxylic acid cycle allows other metabolic interconversions to occur, and, to quote Huynen et al.,

“it has been argued that the CAC evolved originally as two separate
pathways stemming from pyruvate, with an oxidative branch leading to
2-ketoglutarate and a reductive branch leading to succinyl CoA
[Melendez-Hevia, E., Wadell, T.G. and Cascante, M. (1996) J. Mol.
Evol. 43, 293–303]”.

Footnote: Hynen et al. and incomplete tricarboxylic acid cycles
At least one of the bacteria the genome of which Hynen et al. found to lack enzymes of the tricarboxylic acid cycle — Methanocaldococcus jannaschii — uses an alternative electron acceptor. It is only capable of growth on carbon dioxide and hydrogen as an energy source, and lacks genes for the first three enzymes of the oxidative cycle: citrate synthase, iconitase and isocitrate dehydrogenase. A detailed consideration of the energetics of such methanogens can be found in a review by Thauer et al..

There are a number of pathways involved in anaerobic respiration. It's not like the Krebs cycle (TCA) where there's only one pathway in aerobic respiration. To be clear my professional background is carbon fixation. The reason aerobic respiration is important is it can get conflagrated (how do you spell it?) anyway mixed up - with the rTCA (described below) 'cause its the same genes but reverse process. If that happens it’s a disaster :-) because the calculations are kaput.
Anyway, here's a number of examples.
Lactic Acid
Found in: Certainly in mammals, I would suspect its in all vertebrates and some bacteria Lactobacillus is one
Pyruvate is converted to Lactic Acid (C3H5O3) in the absence of oxygen.
Classic fermentation such as making beer, thats yeasts, and some bacteria.
Pyruvate to Ethanol (C2H5OH) + Carbon Dioxide (CO2).
This occurs in brewing and baking processes.
Methanogenesis
Produces methane (CH4) which occurs in methanogen bacteria which include archaea and bacteria in the stomachs of ruminants in the digestion of cellulose from grass. This does occur in the soil in the degradation of living matter and also found in high abundance in peat bogs.
Sulfur reducing bacteria
Produces hydrogen sulfide (H2S) and are found in hydro-thermal vents and thought to be the origin of respiration, not necessarily these bacteria but biochemical process in the first life-forms.

Its important to distinguish this from bacteria that are purely involved in  carbon-fixation e.g. the Arnon-Buchanan cycle - this is the reverse TCA, which is performed mostly by chemolithotrophs, a diverse group of bacteria.   The reason I brought this up is that rTCA - the exact reverse of the Krebs cycle in aerobic respiration, is carbon fixation but not respiration.
Methanogens both fix CO2, i.e. carbon fixation but this is also their pathway of respiration.

As for citations, most of this pretty basic so:
Lactic acid.
Alberts, B., et al. (2014). Molecular Biology of the Cell (6th ed.). Garland Science.
Sulfur reduction and alcohol fermentation
Madigan, M. T., et al (2020). Brock Biology of Microorganisms (16th ed.). Pearson.
For methanogenesis (what I know most about):
Thauer, R. K., and Shima, S. (2008). "Methane as Fuel for Anaerobic Microorganisms." Annual Review of Microbiology, 62(1), 43–64.

Final point, just waving my arms about a bit, I'd suggest the diversity of anaerobic respiration infers one of these was the ancestral pathway of respiration (it's a hot topic).

Hans Adolf Krebs, Nobel laureate.

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Methods of denaturing BL21 E.coli other than using lysis buffer and sonication
The goal is to try different denaturing methods for BL21 E.coli. However, finding detailed paper on this is challenging as most articles do not seem to include the details of their denaturing procedure. I am currently using lysis buffer and sonication but I would like to try something else. Any detailed suggestions with reason would be of help.

By "denaturing methods", do you mean lysis methods? "Denature" typically refers to the unfolding of structured macromolecules (protein, DNA) and not whole cells.

A detergent-containing lysis buffer along with sonication is basically the gold standard for E. coli lysis (which I'm assuming you mean instead of "denaturing", which is something different). Why do you need to try something else? What are you studying, or what are you trying to purify?

Yes you are right I am trying to alter various methods for the disruption, Lysis of E.coli BLC21 currently I am using sonication and a Lysis buffer that contains 20 mM Tris-HCl, 50 mM NaCl plus 10% lysozyme. But we are looking at a better way or alternative ways that may give similar or better results?

There's Ye Olde french press method. https://en.wikipedia.org/wiki/French_pressure_cell_press

https://www.google.com/search?q=methods+for+e+coli+cell+lysis THere are a large number of such detailed protocols described

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Can the UGA codon be used as a drop-in replacement when adapting genes for Paramecium?
Question
It is well established that Paramecium translate UAG and UAA mRNA codons to amino acid, although they are STOP codons in most other eukaryotes. (https://www.nature.com/articles/314188a0)
Suppose I wish to express a particular bacterial gene in Paramecium by translation of its mRNA in a similar fashion to the SARS-CoV-2 (COVID-19) vaccines. The gene is AlkB from Alcanivorax borkumensis, which encodes foralkane hydroxylase (https://www.ncbi.nlm.nih.gov/nuccore/AB110225).
The coding DNA sequence of this gene ends with TAA (UAA in mRNA). As explained above, this won't be translated correctly by Paramecium. Could I simply replace the DNA TAA/mRNA UAA  with DNA TGA / RNA UGA in order to get it translated to the same protein in Paramecium?
Evidence of Research
This is only some of the research I have done for this question. More can be provided, if required.
Search on this site for previous similar questions https://biology.stackexchange.com/search?*q=can+i+switch+codons+with+their+equivalents yielded nothing
Paper  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5409834/
Not useful because it only states that switching mRNAs that mean the same thing may make translation take longer due to rare tRNAs. The only STOP tRNA in Paramecium has the anti codon ACU, as proved above.
Paper
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3549826/
Not useful because it's about bacteria.

Welcome to SE Biology. I have edited your question to improve the likelihood of its receiving attention and a positive response. This consisted of removing much inessential and repetitive material, and the over "loud" appearance through abnormally large text in headings. I also replaced the opening statement that "It is commonly known". Your view of what biological facts are known to this audience is irrelevant to the question, and off by a mile, in a way that antagonizes people who do not know. Likewise, we don't need to be told to click on links to find something out. But I'll answer it.

Hi @David! Thank you so much for your lovely edits & answer, it made the question a lot better! I didn't mean to really offend anyone, thank you for correcting the language used. :)

Preamble
The choice of the organism and gene for expression is not explained, although I gather the bacterium is able to degrade oil components using this enzyme. However one wonders why anyone should wish to express the enzyme in Paramecium, which to my knowledge has not been used to express foreign nucleic acid sequences. The mode of delivery of foreign genes or mRNAs is an important consideration in their expression, but I shall ignore this in my answer. However as Covid vaccines are invoked in the question, a study of papers reviewing the structural features of mRNAs that facilitated their expression (e.g. this one) is advised.
Answer

In principle, replacing a UAA stop codon by a UGA stop codon should still allow termination of translation, especially in an environment in which UAA is the only stop codon. The only possible problem I can see is that of possible readthough, which can occur in certain sequence environments. However if the protein is terminated properly in the bacterium, there seems no reason to expect a disfavoured environment in Paramecium.

As we are considering the expression of a bacterial mRNA in a eukaryotic environment, the differences in bacterial and eukaryotic translational initiation (see any decent biochemistry text or search this site) need to be considered as well as termination. In brief, eukaryotic initiation occurs at a capped 5′-end, with the ribosomes then progressing to what is generally (but not always) the first AUG. An mRNA containing the bacterial coding sequence would have to be synthesized that facilitates this. In addition, polyadenylation of the 3′-end is required to ensure a stable mRNA. A close examination of the features of Paramecium mRNA sequences would be prudent before undertaking such a project.

Thank you - that answer is so great and I understand now  Unfortunately I cannot up-vote yet, but it is a great answer well-written well answer well worthy of one.

I'll definitely do the research you suggested, looks like a great rabbit hole to go down...


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Recycling of nitrogen in hibernating mammals
Hibernating mammals are required to undergo profound changes in metabolism. In addition to the more studied requirement of providing energy, there are problems in relation to nitrogen metabolism because of the continued turnover of muscle protein and the need to dispose of the urea produced in the absence of urination.
In an abstract written over forty years ago Nelson states that to solve this problem urea is reconverted to amino acids:

“The urea that is formed is hydrolyzed and the nitrogen released is
combined with glycerol to form amino acids, which reenter protein
synthetic pathways.”

Is this correct and, if so, where does the process take place and what are the precise biochemical reactions involved?
N.B.
I am particularly interested in the hibernating bear.

some context https://www.nps.gov/katm/blogs/hibernation-in-bears.htm

Summary
The hibernating animal in which the recycling of nitrogen has been best studied is the ground squirrel. Recent studies in this species by Regan et al. (Science (2022) 375, 460–463) have provided strong experimental support to an idea proposed some time ago. This is that the ureases of gut microbiota hydrolyse urea to carbon dioxide and ammonia, the latter being incorporated into amino acids by these symbiotic bacteria. Some of the synthesized amino acids are taken up by the mammalian host and are used for its protein synthesis. It is reasonable to expect that intestinal microbiota may also play a role in other hibernators such as bears, but this remains to be established.
Proposals: Importance and Limitations
R. A. Nelson performed pioneering experiments in hibernating bears. He recognized that muscle protein did turnover, that this entailed disposal of nitrogen as urea, but that the blood concentration of urea was not raised (if it had been it would eventually have reached toxic concentrations) despite the fact that hibernating bears do not urinate. He realized that these two problems could be resolved if the nitrogen in the urea was somehow converted to nitrogen in amino acids, allowing synthesis of muscle protein to replace that which was degraded.

[Simplified diagram showing fate of nitrogen from amino acids resulting from protein breakdown in mammals]
In order to be incorporated into amino acids, nitrogen released from urea (as ammonia) needs a carbon skeleton to be integrated into, and Nelson proposed that this was supplied by glycerol produced from the lipolysis of triglycerides, which after phosphorylation can enter the pathway of glycolysis/gluconeogenesis in liver. Although the major rationale of this is gluconeogenesis to provide glucose for the brain, Nelson performed experiments with  14C-glycerol which showed that some radioactive label entered alanine, presumably by transamination of pyruvate produced by glycolysis of phosphoglycerate.
There are, in my opinion, two major limitations to this proposal. First, it would require a urease to be present in the liver to produce the ammonia for the transamination of pyruvate. There is no evidence of any mammalian urease, either experimentally or from the predictions of genomic sequences. Second, it would not explain how the degraded essential amino acids — amino acids the carbon skeleton of which mammals cannot synthesize — were replaced.
These difficulties were overcome in the proposal of Riedesel and Steffen for a role of gut microbes — rather than the animal itself — in recycling urea, although these authors studied small hibernating rodents, rather than bears. Their abstract specifically mentions:

…the potential for urea recycling by intestinal microbiota…

They had no experimental evidence that this occurred, but they argued for its feasibility in the context of contemporary knowledge at the time:

“Several monogastric mammalian species, including man, have been shown
to harbor microorganisms capable of urease activity (Long et al. Am.
J. Clin. Nutr. 31: 1367–1382, 1978).”

[Conversion of urea to ammonia and carbon dioxide by microbial ureases]
Evidence for role of gut symbiots in ground squirrels
The difficulty in performing experiments on either the microbiota or the animals themselves meant that it was over 40 years after the proposal of Riedesel and Steffen before Regan and associates published a paper with confirming evidence in the prestigious journal Science. They injected ground squirrels with 13C,15N-urea and determined its metabolic fate over the hibernation period by detecting the presence of these (stable, non-radioactive) isotopes using modern spectrographic methods. They also examined the abundance of urease gene sequences in ten individual bacterial taxa of the the metagenome. Their findings are conveniently summarized in the figure below, taken from their paper.

…and what happened to Goldilocks?
It remains to be established whether urea recycling through microbiota also occurs in bears, where hibernation has some different features. A 2021 review by Bertile
et al.  of protein sparing in hibernation includes a consideration of bears in an extensive and comprehensive coverage of this topic. There seems to be some reluctance to the idea of a major role for microbiota in urea cycling in bears, and the authors emphasize other factors that could contribute to protein sparing. It seems to me, as an outsider, that this reluctance will turn out to be unjustified, but, in the absence of experimental evidence, no conclusion is possible at present.

The ability for gut microbes to convert urea is not limited to hibernating animals. Cows  can do it too. Though only with ingested food. https://www.yara.com/industrial-nitrogen/animal-nutrition/animal-grade-urea/#:~:text=Urea%20can%20be%20used%20to,grazing%20feed%20quality%20is%20poor.

I finally managed to get the 1980 volume of Federation Proceedings with the articles by Nelson and by Riedesel and Steffen. I have made a final revision of my answer in the light of this (and also cut some fat). Because Federation Proceedings seems not to be available on line, and the effort of retrieving volumes from university library archives is considerable, I have temporarily posted scans of the two articles for any interested readers to check (linked names above).

@AsekuVena — Urease-producing bacteria are, in fact, found in the human microbiota (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4263730/) as well as in the stomach and urinogenital tract. The sort of questions of interest in relation to hibernating mammals  are whether the bacteria are relatively more abundant or have more active urease activity compared with non-hibernators (or in hibernators outside the hibernation period).


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

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

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

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

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

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

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

@John — Thanks for picking up the typo.


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Is there a paradox in the field of immunology for elderly people?
Say you have an 80 year-old. If you spray an anti-bacterial on their door knobs, keys, floors, walls, bathroom etc you would have fewer bacteria. But by doing that, I would think that you would weaken their immune system, so if they returned to a higher-density bacteria environment, they would be weaker then if you hadn’t put them in the more sterile environment.
Obviously, this paradox does not apply to toddlers, which is the best time to expose someone to bacteria/viruses.

You do not weaken the immune system by removing bacteria. Additionally, with the methods available at home, you will not be able to kill all bacteria. So this is nonsense.

@Chris it's like that for me with allergies. If I'm not exposed to cats for a while, I get re-allergic to cars. If I don't eat ice cream for a year, I end up gassing a lot when I have ice cream for the 1st time. If I don't read while in motion, I'll eventually get motion sickness from reading again.
Isn't our body constantly fighting decomposition, so constantly fighting bacteria from taking over our body? So what do you think happens when our body is put in a sterile environment, and then put back in the previous environment?

@NealConroy nothing, your examples are allergic (aka abnormal ) reactions and lactose breakdown which has nothing to do with the immune system.  one way to treat allergic reactions is controlled exposure thus reducing the immune system response, if we went by that example it should make the immune system stronger. But neither is good model for how the normal immune system works.

@John well why is it when we die, the bacteria take over and eat our flesh? Because we are no longer fighting it. So basically, when we are alive our body is constantly fighting against decay.

To borrow a phrase that was widely heard during the last three years: "Immunology is complicated". You seem to be assuming it functions similarly to a muscle that atrophies with disuse. This is far too simplistic.
For example, I was immunized against smallpox when I was three or so. I've never been exposed to smallpox and I'm in my sixties now, but the odds are that I retain strong immunity to smallpox. To highlight just one of the immune subsystems, there is a class of immune cells called Memory B cells. Their job is to "record" chemical signals from pathogens you have encountered, either from infection or vaccination. These cells then hang out in your blood for decades. If the Memory B cells encounter that pathogen again, they activate and interact with other parts of the immune system and vastly accelerate an immune response to kill off the pathogen.
Notice that I said "odds". There are many probabilistic aspects to the immune system. When you get vaccinated or sick with an infection, you will generate millions of Memory B cells targeted at that infection. As I said, these cells can remain dormant in your blood stream for decades. As you age, some of them will die off, and if you are unlucky, enough of them may die off that they may not be able to respond effectively to their target pathogen. The gradual dying off of Memory B cells, is just one aspect of the overall decline of the immune system with age. In other situations older folks may still have well functioning Memory B cells, but the other systems that do the actual killing may have become weakened and ineffective. This is the motivation for being particularly careful with sanitation around the elderly: they may no longer be able to mount a strong immune response even to pathogens they've seen and fought off many times before.

If I'm not exposed to cats for a while, I get re-allergic to cars. If
I don't eat ice cream for a year, I end up gassing a lot when I have
ice cream for the 1st time.

Your experience may very well be an example of the ability of the immune system to form long-lasting "memories". Note that it isn't the cat hair or the ice cream itself that causes the unpleasant symptoms, it's your immune system's response to them that causes the problems. At some point you were exposed to cat hair and your immune system erroneously decided it was pathogenic, and "memorized" how to recognize it so it could mount a response the next time it encountered it. However, it seems that continued exposure to small doses of an antigen can eventually convince the immune system (at least temporarily) that the substance is OK and doesn't require an immune response. Exactly how this happens is not well understood. This isn't a case of the immune system "forgetting" how to deal with a threat, it's more like it remembering all too well its first impression.
An excellent popular book on the immune system and its complexities is "An Elegant Defense".

Charles, 1st off I thought allergies, and bodies immune system to bacteria and viruses, are separate? My allergies to cats is just red eyes and blowing nose. So, yes, I asked an immunology professor, your environment changes, your allergy-immune system changes. Somehow, bacteria and virus immune system retains a lot longer.

Like I said, "Immunology is complicated". Allergies and responses to pathogens differ, but do involve shared subsystems of the overall immune system. The "memory" for allergens also involves Memory B cells, but usually of a different subtype, than handles pathogens.

Charles, but the part that is much more complicated in immunology is allergies, as opposed to bacteria and viruses. Immune system to bacteria is pretty straightforward, immunity to viruses is rather moot, as viruses change over time. It'd be interesting to see what kinds of things our immunity loses quickest to least. Could very well be motion sickness.

"Immune system to bacteria is pretty straightforward" need citation! Here is a research project for you: tell me how many classes of cells are involved in the human immune response to a bacterial infection. "immunity to viruses is rather moot, as viruses change over time": some do, some don't, as is also the case with bacteria (that's why we're having to deal with anti-biotic resistant strains of bacteria now). "Could very well be motion sickness." OK, you've lost me now. Motion sickness doesn't having anything to do with the immune system (cont)

Charles, I was allergic to acts, at age 12, got my1st kitten, was allergic to it for a day and a half. Then slept with the cat for 6 years, then moved out for college at age 18, at age 19, came back to mom's house and allergies to cat all over, and this time, it took weeks to get over. But lose it within a year. Same thing with motion sickess. 1 time, I read something so interesting while in a bus, that when I got off the bus, I had to throw up. But the next day, I was able to read while on bus/train no problem, so played video games. But within a year, had to start all over... Viruses seem to

Viruses seem to change 50% in about 4 years, so it seems to be much easier to keep track of bacterial immunity. But I don't know a good example of it. As winter colds are caused by viruses. By the way, regarding motion sickness, I constantly threw up in the car at age 4 over long-distance highways, so got immune to that quick. I have a feeling, if I went to jail for a year, and come out, rode a public bus, I'd feel dizzy. But I ride the bus every day. If I don't ride the playground swings for a while, it feels a little dizzy too.

Motion sickness is caused by a conflict between neural input from the vestibular system and your visual system. It is sometimes treated with anti-histamines, but that's simply to suppress your impulse to vomit.

With respect Neal, you're telling your self 'just-so' stories linking your issues, and you are fixating on things like "Viruses seem to change 50% in about 4 years" that simply aren't true. Rather than spin your stories explaining a sample set of 1, I urge you to do some reading on the subject.

Charles, viruses specifically for rotavirus and norovirus, that cause gastroenteritis.

Let us continue this discussion in chat.

I seem to have lost my ability to post in the chat, here's my reply: Charles I didn't change my point. The sickness from sewers was the 2 viruses. And after 4 years, I got sick again at some 50% intensity, hence my logic. I realize now the microbio professor is not the immunology professor. Though the immunology professor should know more about microbio than the microbio professor knows about immunology, so I know now to ask the immunology professor. Which I lost touch of. But they did back my allegation on cats, that my allergies to cats was lost after losing exposure for over a year.

I also seem to have problems tagging people @Charles E. Grant

No paradox, elderly people have fewer reserves of naive cells. This means that you cannot really make your adaptive immune system stronger, as over the life most of its cells have matured to handle the pathogens that have been encountered.

Well my argument was that you could make an elderly person's immune system weaker, from putting them in a sterile environment, and that is the dis-service.

I like the question BTW, upvoted. It definitely makes you think the broader and nuanced implications of a hardline discipline, in this case epidemiology. Epidemiologic recommendations never compromise.
Two points, the first is focused on "diseases of the elderly" in particular norovirus:

For an 80-year-old, the immune system is naturally in decline due to aging, a process called immunosenescence. This decline includes reduced T-cell function, which impairs the body’s ability to respond to infections. I have done T-cell work (bioinformatics not wet-lab) CD8 particularly are key to fighting viruses, a bit like soldiers of the immune system. However, with age, they’re fewer in number, less responsive, and slower to act. This makes the elderly more vulnerable to infections like norovirus, which is "harmless" to most (well you're unwell - but its okay), this isn't a cool infection for the elderly.

So, thats the build-up that the other poster described, which leads onto sterilizing the environment: this reduces norovirus on door handles, floors, and walls might seem logical to minimize infection risk is essential because otherwise there's an epidemic, especially in care homes. This virus is notoriously infectious and can spread rapidly, especially in immunologically vulnerable populations like the elderly. Reducing surface contamination is essential in such cases. So, the logic of disinfecting key areas like door handles and bathrooms holds here to prevent severe illness: got to help out people with aging immune systems, especially in care-homes.

I am aware of the concept of "immune workout" but I would suggest it is more impactful during earlier stages of life. For toddlers, early exposure is critical because their immune systems are still developing, and exposure helps build a diverse immune repertoire. By the time someone reaches 80, their immune system is not developing anymore—it’s declining. The ability to "train" it is limited.

I guess the sort of answer you are looking for is about moderation. My original training is different, its about stopping infections (epidemiology). Here it's important to mitigate high-risk areas where dangerous pathogens thrive. For an 80-year-old, focus on cleaning to prevent exposure to truly harmful bacteria and viruses. This would also extend to hand-washing and hygienic food preparation.
Senescent T Cells in Age-Related Diseases Pei-Jie Yu, Mei Zhou, Yan Liu, Jie Du, 2024. Aging and disease. DOI: 10.14336/AD.2024.0219
Human T cell aging and the impact of persistent viral infections T. Fül T. Fülöp A. Larbi A. Larbi G. Pawelec G. Pawelec.  2013 Front. Immunol. Vol 4 https://doi.org/10.3389/fimmu.2013.00271
Norovirus outbreaks in the USA:
https://www.cdc.gov/norovirus/outbreak-basics/index.html

Rigid epdemiologic recommendations/policy has resulted in big gains in reducing hospital acquired infections, MRSA is a great example. So strict sterile procedures do work. Just saying.

Why the downvote? It is a reasonable answer following a collaboration with an internationally recognised expert in the field of norovirus epidemiology. Thats care homes are heavily sanitised.

Actually I realize this is a dual question. Immunity to viruses and immunity to bacteria. Does the aging body respond to both the same? Most things that deactivate viruses on surfaces also kill bacteria, though most things that kill bacteria does not deactivate viruses (usually deactivates few viruses).

Viruses are more susceptible to disinfectant that bacteria. Bacteria can acquire anti-bacterial resistance, viruses cannot. The FDA banned anti-bacterial agents in household products because of hospital-acquired resistance in hospital acquired bacterial diseases, i.e. the handwashing gel used wasn't working any more.

So you think viruses are pretty weak to 3% hydrogen peroxide? I buy 12% hydrogen peroxide at a salon store in the U.S.

Yes, this will kill most pathogens. I forgot my biochemistry but metabolising H2O2 during infections is pivotal to parasite survival in the host (we're talking very small concentrations, not 2% which is huge). It's extremely toxic. 70% ethanol (alcohol) is a very good disinfectant BTW against viruses and disinfectant per se, in the USA I suspect that is called "rubbing alcohol".


text:
What is the genus of this fungus?

I'm struggling to identify this fungus. Is it Aspergillus sp. or Penicillium sp.?

Welcome to the Biology Stack Exchange. You would need to provide much clearer photos and some photographs down a microscope of the structures seen, particularly the sporangia for ID.


text:
Why is the codon size three, rather than four?
The genetic code consists of triplets, each of which (apart from the stop codons) yields an amino acid when the mRNA is translated.
But why did triplets evolve, rather than a longer or shorter codon size?

Does this answer your question? How did the genetic code evolve?. It and similar questions in our archive have answers that discuss this topic at length.

The reason is pretty simple: It comes from the number of amino acids used to make proteins and thus with the necessary number of possible combinations and robustness of the system.
We have 20 amino acids which are coded by the triplets plus one start and two stop codons. If any of these would only be coded by one base, we already need 23 codons. However, in such a case there would be no redundancy in this system, since any change of a base would lead to an amino acid exchange which can negatively affect a proteins function.
To calculate the number of possible amino acids use the number of bases on the RNA and the length of the codon.
If the codon has a length of 2, you have (sic 2^4=16) $4^2 = 16$ possible combinations. This is obviously not enough for what is needed. (sic 3^4=64) $4^3 = 64$, which is enough to have some redundancies in the code and not every altered base leads to an exchange of an amino acid. It therefore also adds some additional robustness to the code.
If your codon had a length of 4, there would be 4^4=256 combinations, which is way more than needed. This adds a lot of complexity to the translation. [codon length of 4] raises the number of necessary nucleotide by a third, which costs the cells a lot of energy. The extra energy expense on nucleic acid lengths is negligible compared to that of maintaining the extra tRNA synthetases and tRNAs.
The codon triplets are evolutionary well conserved, there is even a mathematical paper available which states that organisms with codons of n>3 will reduce their codon size to a triplet code by evolution.
Reference

Codon Size Reduction as the Origin of the Triplet Genetic Code

"[codon length of 4] raises the number of necessary nucleotide by a third, which costs the cells a lot of energy". The extra energy expense on nucleic acid lengths is neglectable compared to that of maintaining the extra tRNA synthetases and tRNAs. This should be at least some orders of magnitude.

(Just meant as a slight expansion to your answer, which is good overall.)

@KaPy3141 Thanks for the expansion, you're welcome. I added this.

This answer takes it for granted that the codon size is a function of the number of amino acids used for protein synthesis (20), rather than the other way around. That seems reasonable to me, but including a mention of whatever support exists for it would benefit the answer.

@timeskull It evolved this way because of 20 amino acids. I will see to phrase this more clear.

@Chris "It evolved this way because of 20 amino acids". And what makes you think that the genetic code didn't arise until all the synthesis of all 20 amino acids had developed? What if I suggested the evidence suggests it evolved at a time when there were fewer than 16 amino acids, or argued that 20 amino acids aren't needed. I would stick to the question, which I'm surprised you even answered, or having decided it wasn't homework, didn't clean up. I'll do so, but vote to close. However, if people want to discuss other aspects of the genetic code, they should formulate a question.

@David We don't know and we cannot. But seeing the universality of the code suggests that. You can of course argue that all life forms that use less amino acids didn't make it over time. There is no solution to it.


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How to elute the protein that is bound to biotinylated RNA immobilized with streptavidin?
I would like to test the proteins that bind to biotinylated-RNA by mass spectrometry , I was using Dynabeads™ MyOne™ Streptavidin C1 (invitrogen) coupled with biotinylated-RNA,than mix these beads up with cell lysate to achieve protein-RNA interacted solution, so does anybody know the better idea to elute that protein out of the mixed reagent?

What does the manual say about elution?

It doesn't have any info about elution

If your end goal is mass spec, you could do an on-bead digestion of the protein. Alternatively you could elute the protein with SDS buffer and do the digest in a gel. It should also be possible to break the protein-RNA interaction (eg with salt, cosolvents, and/or pH)

any specific protocol or detail with it?


text:
Fixation rate at neutral loci
It is a classical result that the expected time for a neutral mutation to occur and to get fixed is $2 N \mu \frac{1}{2N} = \mu$, where $N$ is the population size and $\mu$ is the neutral mutation rate (wiki).
I am not sure I understand what this actually mean. What is the probability of (at least) one fixation event to occur in $\frac{1}{\mu}$ generations? Is it 0.5? Could we calculate the probability that (at least) one fixation event occurs in $n$ generations? For example after $n=\frac{\mu}{10}$ generations, is the probability of observing (at least) one fixation event equal to $0.1$ or is it more complicated?
UPDATE
Following @DanielWeissman comments:
Let's consider we are starting with an initially monomorphic population (population of clones). In addition to that, let's consider that the population is relatively small $N\mu < 1$

You should probably specify whether you're considering an initially monomorphic population, or a steady-state population (with infinite alleles), or something else.

I didn't realize that would matter. Let's consider an initially monomorphic population. (see update)

First of all, the $\mu$ is not expected time for a mutation to occur and get fixed; it is the rate at which mutations are fixed in the population. The basic result states that if neutral mutations arise at a locus at rate $\mu$ within individuals, mutations at this locus will be fixed in the population at rate $\mu$ as well.
The expected time for a given neutral mutation to fix after arising, given that it is not lost from the population, is approximately $4N_e$, where $N_e$ is the effective population size. Kimura and Ohta (1969) derive this result using a diffusion approximation; Kingman (1982) develops coalescent theory and in the process obtains what in my opinion is a more elegant derivation of the same approximation.
Now what is the probability that some mutation goes to fixation in the population as a function of time? Even though the fixation rate in the population is $\mu$, this does not mean that with probability 0.5 some mutation fixes within $1/\mu$ time units. That probability will depend on the distribution of fixation events in the population. Here's a good way to think about it. If fixation events were evenly spaced and occurred at rate $\mu$, then with probability 1 you would have a mutation within an interval of length $1/\mu$. If fixation events were highly clumped, then you would have a very low probability of having a fixation event within an interval of length $1/\mu$ -- but if you did have one event, you would probably have many. If fixation events are distributed as a Poisson process--which I suspect they would be in a purely neutral model--the probability of having a fixation event within a time interval $1/\mu$ would be given by a (negative) exponential distribution and thus the probability of having at least one fixation event in a time interval of length $1/\mu$ would be $1-\frac{1}{e}$.

This final answer isn't quite correct -- it neglects the drift time mentioned in the second paragraph. If $N\mu \ll 1$ it's a good approximation though. (If $N\mu \gg 1$, the process of fixation is almost deterministic.)

@DanielWeissman Thank you for the informative correction.


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Why are most transcription factors enhancing the expression rather than repressing?
One can classify the effects of Transcription Factors (TF) on gene expression into two types: it either enhance or repress the gene expression.
I have always been told that most of transcription factors functions act to enhance gene expression rather than repress gene expression. Assuming this is true, my question is why are activators more common than repressors?. Is there for example a mechanistic explanation for that (cost less energy to enhance or the enhancement pathway is easier to evolve)?

From wikipedia

While activators can interact directly or indirectly with the core machinery of transcription through enhancer binding, repressors predominantly recruit co-repressor complexes leading to transcriptional repression by chromatin condensation of enhancer regions.

The mechanisms are different and it sounds a likely cause of the overrepresentation of enhancement function of transcription factors in genomes but it is not obvious to me why activators and repressors have to have use different mechanisms and it is not obvious to me either why these different mechanisms would yield to a ratio of repressors to activators other than $\frac{1}{2}$.

Do you have a reference for this claim? Also, keep in mind that simply the absence of an activator can be repressive. In other words, one mechanism of repressing gene expression is to not express the activator.

They do not fall into clear groups. A transcription factor can activate one gene and repress another. Either by binding to its regulatory region or by upregulating another suppressor (which would be a secondary effect).

No I don't unfortunately. But as I have heard that several times I kinda felt that this was common knowledge. "absence of an activator can be repressive". That sounds weird to me. Isn't just a matter of relativity? The point is that still, activators are more common than repressors (assuming this is true) and so why? is it easier to evolve activator than suppressor?

@Chris Oh good point! But still most functions are repressive (assuming this is true) so the question still hold. If it is not common knowledge that activators are more common than repressors I may have better to first ask a question about that to make sure my assumption is correct.

Hypothesizing I would say this is because of different control pathways. You can turn on genes on a pretty sensitive way (fine regulated and only a few at a time with a lot of regulators). You can then use different circuits to regulate the downregulation.

Also worth mentioning is that the same protein can directly activate or repress the same gene depending on post-translational modifications.

I edited my post following your comments on the categorization of TF into groups. I now made sure that I categorized the function/activity/role of a TF and not the TF by itself. It might still have some cases that won't let easily fall into one of my two bins but I think it generally speaking offer a good categorization.

@Remi.b This is tending to be opinion-based. There are some situations where repressive control is favourable and there are others where activation is better. You really need to add details and also provide the reference for Repressors < Activators.

I too have heard the statement "TFs generally enhance expression", but it should be something more like "TFs work to enhance correct expression by repression or expression."

I can answer this question only based on guesses because I am not really sure about your claim that activators are higher in number than repressors. So consider this as an extended comment.

While activators can interact directly or indirectly with the core
  machinery of transcription through enhancer binding, repressors
  predominantly recruit co-repressor complexes leading to
  transcriptional repression by chromatin condensation of enhancer
  regions

Not really true. A repressor can simply sit on the the promoter and prevent RNAP from binding the to the latter.

Abstract
Transcriptional repressors are usually viewed as proteins that bind to
  promoters in a way that impedes subsequent binding of RNA polymerase.
  Although this repression mechanism is found at several promoters,
  there is a growing list of repressors that inhibit transcription
  initiation in other ways. For example, several repressors allow the
  simultaneous binding of RNA polymerase to the promoter, but interfere
  with subsequent events of the initiation process, eventually
  inhibiting transcription initiation. The recent increase in the number
  of repressors for which the repression mechanism has been
  characterized in detail has shown an amazing variety of strategies to
  repress transcription initiation. It is not surprising to find that
  the repression mechanism used is usually exquisitely adapted to the
  characteristics of the promoter and of the repressor involved.

Some justification on why the number activators would be more:
A network perspective:
Lets assume an that gene-A somehow causes the repression of the gene-B. This repression can be either direct (A being a repressor of B) or indirect via some other genes. In the case of indirect regulation you just need one repressor in the network path A → B to result in repression of the latter.
So all repressive paths would minimally require only one repressor, all other steps in the path can be activation; whereas in an activating path you would need 'n' activators for 'n' steps.
Post-transcriptional Regulation:
Now if you include post-transcriptional regulation then you can find more number of repressors: miRNAs (2588 reported in humans: miRbase-21) and many proteins as well (For an e.g. see here). Most cases of events leading to translational activation are actually derepression. It is logical in a way because an mRNA is a temporary product; it should not by default require an additional signal to start producing proteins.

Thanks. I appreciate these speculations based on my non-referenced statement. Your explanations make quite intuitive sense.


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What is Environmental Robustness? Is it different from plasticity?
Hansen (2006) in his review uses the concept of environmental robustness independently of the other concepts of robustness (at pages 139 and 140) without defining it.
How is the term environmental robustness usually defined?
The concept of robustness (aka genetic robustness) can be further decoupled into mutational robustness, developmental robustness and maybe some others. I think envirnmental robustness is one of these sub-categories of (genetic) robustness.
Intuitively, I understand environmental robustness as something that is very close to plasticity in the broad sense. What I call plasticity in the broad sense is any phenotypic response to an environment whether or not the response is adaptive or not. Therefore, plasticity in the broad sense is adaptive plasticity + non-adaptive plasticity. I would intuitively think that a genotype is environmentally robust if the phenotype it produces varies little with environment, that is if this genotype has low plasticity (in the broad sense). Am I using a more or less standard definition of environmental robustness?

I think robustness and plasticity are different concepts, although related to each other.
I would define plasticity as the property of a system to adapt to external changes. As defined in the wikipedia page for phenotypic plasticity:

Phenotypic plasticity is the ability of an organism to change its phenotype in response to changes in the environment.

I think this definition agrees with the one in your question.
Robustness in biological systems, however, is defined as (wikipedia article):

Robustness of a biological system (also called biological or genetic robustness) is the persistence of a certain characteristic or trait in a system under perturbations or conditions of uncertainty.

From this article three references are cited, all of which give some definition of robustness in their introductions/abstracts:
Felix and Wagner (Heredity 2008):

Robustness, the persistence of an organismal trait under perturbations, is a ubiquitous property of complex living systems.

Kitano (Nature Reviews Genetics 2004):

Robustness is a property that allows a system to maintain its functions despite external and internal perturbations.

Stelling et al. (Cell 2004):

Robustness, the ability to maintain performance in the face of perturbations and uncertainty, is a long-recognized key property of living systems.

All these definitions imply that robustness is the ability to remain unperturbed under external or environmental perturbations. In a sense this looks like the opposite to plasticity, which is the ability to change under external perturbations. Personally, I think that robustness is accomplished because biological plasticity allows organisms to compensate (with some limits) the external perturbation in order to maintain their state.

This is sort of how I understand Hansen as well. The problem here is that robust is a rather vague word, similar to the observation by Pimm (1991) that ecologists had been using stability in at least five different ways when discussing population and community stability (he mentions: mathematical stability, resilience, persistence, resistance, variability)

@ddiez Thanks for your answer. The concept of (genetic) robustness is further decoupled into subconcepts that are mutational robustness, developmental robustness and environmental robustness (and maybe some others). My question is about environmental robustness. I don't think Hansen meant genetic robustness when saying environmental robustness, but I think he rather meant some subset of robustness. I might be wrong though. I'll edit my question to clarify my understanding of the subconcepts of robustness.

@fileunderwater completely agree robustness is defined in a vague way. I think we all understand the concept, but how to quantify it? For example, it makes sense to imagine some system to be more robust than another to perturbations, but for me there is no clear way to measure it.

@Remi.b thank you for showing us Hansen's review- looks interesting. I will read it (only skimmed over it a bit) and think a bit more about your comments (and maybe modify my answer accordingly). I think the source of confusion is, as fileunderwater mentioned, that usually the term is just vaguely defined.

I am just summarizing ddiez's answer with a small addition.
Robustness is the ability of the system to maintain its steady state or at the very least qualitative nature of the steady state with minor changes in the parameters of the system.
This is different from stability which actually means the ability of the system to return to its steady state when it is slightly displaced from there. A stable system will reach the steady state irrespective of the initial condition. In multistable systems the state where the system eventually converges, will depend on the initial condition.
So stability is meant in the sense of perturbation in the state and robustness, of perturbation in the system parameters.
So, if you have a model and you do a random sampling of parameters drawn from a uniform distribution of lets say ±2×mean, you will end up with a many sets of parameters with fluctuations from the mean values. Now, if you solve for the steady state at each parameter value you will get a distribution. Less the variance of this distribution, more robust is the system (based on the model).
We had discussed plasticity in this post. Plasticity may be in a way synonymous with adaptive; if a system takes an input and gives an output then how plastic a system is can be defined as how fast or easily does a system reach the new steady state. In this case the input is a parameter of the model and only that is changed.
If I put these concepts in the perspective of an organism's metabolism then:

Robustness would refer to how (in)sensitive the metabolic flux is to the minor changes in rates of different reactions (by changes in the enzyme structures perhaps).
Stability would refer to whether the system gets back (or how fast it gets back) to its original state if you add some extra or remove a metabolite.
Plasticity would refer to how fast would the system adapt or reach the new steady state when there is a change of diet/available nutrients.

Having said that I also feel, as fileunderwater said, that definitions are not universal and different people mean different things. Mathematically speaking environment is  an extrinsic parameter i.e. Input. Environmental robustness should mean the maintenance of the steady state response to changes in the input. This makes sense for example in the case of maintenance of body temperature in homeotherms. Environmental plasticity is also important in certain situations.

thanks for your answer. I copy-paste here the comment I made to ddiez "The concept of (genetic) robustness is further decoupled into subconcepts that are mutational robustness, developmental robustness and environmental robustness (and maybe some others). My question is about environmental robustness. I don't think Hansen meant genetic robustness when saying environmental robustness, but I think he rather meant some subset of robustness. I might be wrong though. I'll edit my question to clarify my understanding of the subconcepts of robustness."

Also, it is a bit counter-intuitive to me to define plasticity as the speed at which phenotypic changes occur, rather than the magnitude of the change or the range of environment toward which phenotypic response occurs.

@Remi.b Not really the speed but response time is one way of quantifying a plastic response. How quickly you adjust is important. The magnitude of the perturbation cannot be controlled by the system and you would want to adjust to the new environment without making a great change in your system composition. So magnitude of change has to be minimized and response time too. I think you can define all subsets of robustness depending on what kinds of parameters you perturb.


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Puffball growing on a tree: What kind of mushroom is this?
What kind of mushroom/fungus is the one shown in the photos?
Description: Looks similar in size (~4-5 cm as I  remember) and shape to a puffball. It is not hard to the touch, unlike typical mushrooms that grow on trees. Several balls were growing individually (not in clusters) from the 2-3 m tall stump of a broken tree, at multiple locations from the bottom to the top. They were breaking through the bark from the inside.
Time and location: Saxony, Germany, in a mixed forest. Early September.

Very interesting! Do you happen to know the species of tree this stump is from? Knowing the "host" can be important for identifying fungi. The leaves in the background look like they could be from European beech, but the bark doesn't look right to me ...

@tyersome Yes, the background is beech. This tree I don't know, and I can't tell from the photo. If I get the chance to go back this week, I'll take a closer look and will try to figure it out. Maybe by then the mushroom fruiting bodies will have developed enough to give us some more hints.

Most trees are beech in this forest, but there's also plenty of oak, birch, conifers, and other things.

they look like mosaic puffball mushrooms (Lycoperdon utriforme), which do grow in Germany, but they don't grow on trees :-/ I don't know what these are

I believe these are Fomitopsis betulina (= Piptoporus betulinus), the Birch Conk (or Birch Polypore or Tinder Polypore), a common mushroom throughout the Northern hemisphere.

Fig. 1. Young Fomitopsis betulina emerging from a downed birch log. image: Eric (CC BY-SA 3.0)
The diagnostic features here are the scattered fruiting on dead wood, the off-white, crackling surface, and the shape. F. betulina is not a puffball, but a polypore like other shelf fungi that grow off the sides of dead trees. Unlike other shelf fungi, they remain fairly soft. These young specimens resemble puffballs, but will expand to expose the pores on their underside. Read about F. betulina and see images of mature mushrooms here and here.
F. betulina grows exclusively on birch, and the snag it is growing on appears to be birch based on the light color and horizontal lenticels. Birches do have similar leaves to beeches, though the surrounding trees could be different species.

Thanks for the guess! Looking at photos of F. betulina, the top and the bottom looks different (the top is brownish and round, the bottom is flat). This one was more or less symmetric. I don't recall seeing any which looked asymmetric, but then it was two years ago ... Yes, this is a lone birch stump and the surrounding trees are beeches.

@Szabolcs The mature mushrooms I linked earlier don't really look like what you found, but see the image I just added - when they're young, they don't have the pore surface on the bottom.

Looks convincing enough!


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What species of poplar tree is this?
I am looking for information on how to identify a poplar (Populus) tree. It is located in Dresden, Germany, next to a small stream. The city tree database lists it as Populus nigra. However, it appears different from other individuals of this species, and I have found inaccuracies in this database before, thus I do not trust it. In particular, the leaves are very large (I estimated ~15 cm) and firm.
There is an old individual (in rather bad shape) with furrowed "woven-looking" bark at the base, but turning smooth not much higher. This one is shown in the last photo below. There are several much younger individuals directly next to it, with smooth grey bark (see photo). Many of the leaves have some brown discolouration on the underside. Some of this can be seen in the photo below, although this leaf is cleaner than the rest.

I can take more photos of specific parts of the tree if this will help identification.

The Pl@ntNet app does not give any results with high confidence. Its best guess is Populus trichocarpa.

I think your conclusion of Populus nigra is correct. See for example this set of observations that only shows P. nigra and P. tremula observed in Dresden, and this set that only shows nine Populus species observed in Germany.
A good field guide, or better yet a "flora" (not sure the German translation, maybe pflanzenwelt?) of your area, or of Germany, should include a technical description of all the species expected to be found in the area.

First of all, thanks for taking the time to respond. This tree is in the city though, and there is no reason to think that it is native here. Many city trees aren't. I'm aware of which poplars are common here, but the very reason this caught my eye is that it looks clearly different from them. So I don't think iNaturalist observations are very relevant.


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Looking for proteins that play a role in cardiovascular diseases (disease ontology)
I'm looking for proteins that (probably) play a role in cardiovascular diseases. I have to compile a list of them. It's recommended to use The Disease Ontology. But if I'm correct this specific protein information is not imported into the database.  Could someone suggest how to use Disease Ontology for this purpose? Or, failing this, is there another tool or resource I can use for this purpose?
Cross posted:

https://bioinformatics.stackexchange.com/questions/22911/looking-for-proteins-play-role-in-cardiovascular-diseases-disease-ontology
https://www.biostars.org/p/9602811/

I see that you have crossposted this question to biostars and bioinformatics SE. In such cases it is considered polite to link your questions to each other, so that we don't spend a lot of time answering a question that's already been answered.

"Cardiovascular disease" is a very big topic, it involves a large number of biological processes. I think you may need to get more specific.
I would suggest relying on Gene Ontology, which has protein annotations for various biological structures, processes, etc.
One approach would be to try to link between Disease Ontology and Gene Ontology using for example MeSH terms, to which both seem to have mappings.
As another approach, you might focus on whatever specific disease you find interesting, look for its etiology (possibly using disease ontology or even just review papers), and use that to look things up on Gene Ontology.


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What is this insect (possibly a cockroach)?
I'm looking to identify this insect, found inside a (basement) bathroom by the sink. Wondering if it's perhaps an oriental cockroach / water bug, but the images don't look quite the same, and the bug didn't run from the light like most cockroaches would. The size is also wrong - this one was only about half an inch long, approximately 13 mm.
Note: this is the second odd bug we've found inside; the first looked like a wood roach (but now I'm second-guessing that identification).
I'm located in the northeastern US, in Massachusetts. Both bugs were found in the late evening, if that matters - between 8 and 9 pm.

The bug pictured is not an Oriental coachroach but a female Uhler's Wood Cockroach (Parcoblatta uhleriana). And according to wikipedia:

Parcoblatta uhleriana, the Uhler's wood cockroach, is a species of Parcoblatta native to the United States and Canada. It is a forest species also found in disturbed and urban environments. The male of the species flies freely, while the female does not fly

Identification
This species can be narrowed down to the family Blattodea (Coachroaches and Termites). Due to the flat, oval-shaped bodies with six legs and long antennae.
From there, the genus is easily determined as the genus Parcoblatta, better known as North American Wood Cockroaches. This helpful article describes wood cockroaches:

Their body color ranges from a light reddish-brown to dark brown. The outer edge of the “shield” immediately behind the head is paler in color; these pale edges continue onto the wings of the adult males. Wood cockroaches have long antennae and legs; the legs have distinct spines along their length

Determining an exact species is a little bit more tricky. As there are four different types of wood cockroaches that live in the Massachusetts area:

Virginia Wood Cockroach (Parcoblatta virginica)
Pennsylvania Wood Cockroach (Parcoblatta pennsylvanica)
Western Wood Cockroach (Parcoblatta americana)
Uhler's Wood Cockroach (Parcoblatta uhleriana)

Fortunately, because the bug pictured happens to be a female there are a few discerning features that aid to narrow down the species. The shiny black color and separated tegmina are two features that instantly classify this bug as being Parcoblatta uhleriana:

Females are readily distinguished from allied species by their short, separated tegmina and shining black color, while males are more difficult to separate from P. fulvescens and P. virginica.  Source: https://en.wikipedia.org/wiki/Parcoblatta_uhleriana

Confirming Media

Here is an Oriental Cockroach (Blatta orientalis), note the similarities and the differences:

Image one referance: https://www.inaturalist.org/photos/78245311, Photo 78245311, (c) Sequoia Janirella Wrens, some rights reserved (CC BY-NC), uploaded by Sequoia Janirella Wrens
Image two reference: https://www.inaturalist.org/photos/305200867, Photo 305200867, (c) Dave Eib, some rights reserved (CC BY-NC), uploaded by Dave Eib
Image three reference: https://www.inaturalist.org/photos/37765231, Photo 37765231, (c) Katja Schulz, some rights reserved (CC BY), uploaded by Katja Schulz

This is guaranteed to be a cockroach. The head shape, antennae structure and pronotum (the little plate on top just behind that partially hides the head), as well as the 2 cerci at the tip of the abdomen and the overall flattened shape are all classic roach anatomical traits. It may be a nymph of a winged species, given the spike-like structures in the metathorax look a lot like underdeveloped wings. That said, it does seem different from an oriental cockroach, especially given the strange shape of the mesothorax, even if the overall appearance and behavior seem rather similar (oriental cockroaches can grow to up to an inch, are similar in color and have wings, but don't fly and are not particularly fast or good at climbing). Them not immediately running away from light isn't exactly a guarantee that they're not roaches, as members of many different cockroach species won't always book it the moment they're exposed to light, potentially an initial freeze reaction to try and remain unnoticed by not moving (which makes it all the worse when they feel they're not safe and suddenly start running away).

(an oriental cockroach - picture from planetnatural.com)
It is guaranteed to not be a waterbug. Those guys aren't cockroaches, but a species of aquatic insects related to stink beetles. they have piercing/sucking mouthparts, lack antennae and have a different limb structure, specialized for swimming and grabbing prey, while this bug has a limbs structure more similar to a cockroach and better for moving fast on land.

(Waterbug and cockroach compared - picture from family handyman)
This side by side comparison of an American cockroach and what seem to be a giant waterbug or a similar species shows it well: The water bug has large raptorial front limbs and lacks antennae. Its head is also more visible overall.


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Timing of events in responses of trees to pruning
Original Post
I recently pruned a shrub of all of its leafy branches.  A week or so later it started sending out new branches.  I am making the assumption that those branches would not have grown where they did if I had not pruned the shrub.  This observation made me wonder how quickly does a plant notice the loss of a limb and begin to grow new limbs?  More generally, how quickly does information about one part of a plant propagate/diffuse/transport to other parts of the plant, and what is(are) the mechanism(s) of that information transfer?  Unless the information transport mechanism and speed can vary wildly from species to species, I can't imagine the speed is very fast, as some boughs that I lopped off of a different tree started to have new growth a month or so after I cut them off (new spring leaves).
EDIT
From the comment provided (Thank you! It was very helpful!), I have learned that I really did not know what I did not know.  My background is physics and classical mechanics with very limited biology (one college class) and chemistry (high school).  After reading the referenced article I feel like I have a very basic understanding of shoot branching.  I still have a question relevant to my original question, so I will briefly summarize what I understand and then ask my question.
A plant has a dominant tip which generates hormones, such as auxin and possibly others, that stop the growth of other buds along the branch.  Those other buds are always present and are potentially created because of gene mutation during the growth of the branch (this is a guess; the article did not say where these secondary buds come from).  Thus, the "signal" for the other buds to grow from the decapitation is the loss of a source of auxin, and the speed at which this "signal" propagates would be the speed at which the concentration of the relevant inhibiting hormones decreases.
So, here is another, perhaps simple, question: how quickly does the vasculature of a plant exchange chemicals?  From this paper it looks like it is either on the order of hours (from bud growth plots) to minutes (from sugar counts).
To be honest, there is a lot about this topic that fascinates and confuses me, but I know that this post is not the place for an extended series of questions, so I will leave it at the one question above.

Hi and welcome. Maybe a bit more detail would help you get an answer. What do you know about plant vasculature and apical dominance? You're asking about auxin transport. This site strongly recommends evidence of prior research attempting to answer your question (e.g. a quote and a link) (so we know what you know.)

We try to avoid unjustified anthropomorphic expressions in biology, which is why I have edited your title to remove the word "notice". The replacement tries to reflect the rephrasing of the question in your edit.


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Questions regarding serial passage of virus through animals arising from the paper The proximal origin of SARS-CoV-2
In this answer on bioinformatics.stackexchange.com to the question inquiring about the validity of the paper Kristian G. Andersen et al, The proximal origin of SARS-CoV-2, the author asserts the following two points, which I do not understand.

Serial passage of a virus through either animals will always attenuate the virulence, say the affinity to the ACE2 receptor, of the virus. My question: Could people artificially select for thus increase the virulence of the virus?
We can always tell whether a virus is artificially serially passed because we know the mutational patterns of other serially passed viruses. My question: How does this distinguish artificial from natural passage?

No. Serial passage through animals attenuate the virulence of a virus In It's ORIGINAL Host. it can cause and will cause an increased virulence in the animals that were used in serial passage, and, if the animals have similar receptors as humans, increase the virulence in humans as well. like the two experiments that passed bird flu across ferrets until they become virulent and airborne across them.
https://www.cidrap.umn.edu/news-perspective/2014/04/experiments-render-h7n1-virus-more-contagious-ferrets
https://www.scientificamerican.com/article/pandemic-bird-flu-studies-public/
https://science.sciencemag.org/content/336/6088/1534.full
https://jvi.asm.org/content/88/12/6623

+1. Any comments on the second question?

It is hard to visualize but according to virologists passage into (mice) cells is very different to passage into (mice) lungs. The later greatly increases virulence (when the virus comes from another species) while the former is more likely to produce an attenuated vaccine strain. My opinion is that a last possibility, passage into cells then  once adapted passage into lungs may produce a more virulent variant. @Hans

@reuns: By "cells" do you mean in vitro, or tissue samples in a petri dish, and by "lungs" do you mean, in vivo, or lungs in a living animal? In the papers cited, the virus is first modified then serially passed in vivo amongst ferrets.  ferrets have the human-like ACE2 receptor.
By the way, do you know the reason for the large difference between passing in vitro and in vivo? I understand they are generally not equivalent. I am asking the reason about the large difference in this particular case

In-vitro : immortalized cell lines. The exact process of SARS-CoV-2 passage into mice lungs is described in there.
The 1st Wuhan institute of virology paper was showing that hela cells stopped to be susceptible when replacing human-ACE2 by mouse-ACE2, so the overall mechanism is quite complex. @Hans

@reuns: Nice reference. This supports the answer negating the assertion of attenuating virulence.


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Did most pandemics originate from Asia/China?
This question may be on the borderline of well-posed-ness. Let me ask it. Then please tell me if or where it can be improved.
Is it statistically true that the majority of the pandemics or epidemics originate from Asia particularly China? If not, is there a geographic concentration of the origin of pandemics? If so, why?

According to Merriam-Webster Dictionary a Pandemic is:

an outbreak of a disease that occurs over a wide geographic area and affects an exceptionally high proportion of the population : a pandemic outbreak of a disease

Epidemics are considered a smaller scale version of a pandemic affecting a smaller region, community or population. Epidemics are obviously more common than Pandemics for that reason.
COVID-19 is believed to have become a pandemic event because it has affected multiple continents and most if not all Nations of the world. These extent of pandemics though rare in the past may become increasingly frequent as our world continues to become more globalized if further precautions are not continuously developed.
According to this list, Around 5 of the world's Pandemics have likely started or been mainly spread from and within China, They are:

Third Plague - 1885
Asian Flu 1957
Hong Kong Flu - 1968
SARS 2002
Coronavirus Disease - 2019

These are 5 out of the 20 pandemics in the list. Would that count as a majority? Depends on how you look at it. For one country to start so many does make it unique and a possible majority but we must also consider the size of the country's population relative to the rest of the world. For such a large country (currently 1.4 Billion people which is about 18% of the world's population) with a large portion of the population being poor it is almost expected that China suffers more epidemics than most countries.
Pandemics and Epidemics start for a wide variety of reasons (some quick-search articles that explain: 1, 2, 3) and many of these pandemics develop because of unique environments or pathogens existing in 'coincidence' with each other.
Generally, lack of hygiene, low economic wealth, lack of healthcare products including vaccines coupled with a high population are common societal trends for the beginning of an epidemic. However the pathogens have their own characteristics that make them effective at causing an outbreak. This includes but definitely is not limited to: rapid mutation rate, easy transmission such as through air (e.g. SARS) or water sources (e.g. ebola virus), and zoonotic capabilities (being able to infect more than one species such as swine flu).
Two sources that must be strongly suggested to check out for anybody interested in these sort of topics are the Center for Disease Control and Prevention and the World Health Organization

Thank you for your informative answer. Since as you say, the number of pandemics is small, I have added epidemics to the question so as to make any conclusion drawn from the statistics more accurate. Would you like to revise your answer accordingly?

Epidemics may be even more evenly distributed across the world. this link (https://en.wikipedia.org/wiki/Category:21st-century_epidemics) is a quick search of all the epidemics (and pandemics in the 21st century), You may notice some other continents or countries having more epidemics than China such as India. If you look into the 20th century (https://en.wikipedia.org/wiki/Category:20th-century_epidemics) The distribution of epidemics changes drastically with the US having several more than most others.

The reasons I mentioned still remain true. But there is of course unique characteristics of each country and each disease that infects them that makes each epidemic its own study.


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Population genetics and the fitness probability distribution. Why is the arithmetic mean all we need?
When recording change in allele frequency in diploid, bi-allelic, infinite and panmixic population we usually use this kind of equation:
$\delta_p = \frac{p * q *( p (w11 - w12) + q * (w12 - w22))}{\bar{w}}$
$\bar{w} = p^2 * w11 + 2*p*q*w12+q^2*w22$
$\delta_p$ = change of $p$ (frequency of one of the allele) from one time step to another
$w11$ is the mean fitness of individuals of genotype 11. $p$ and $q$ are the allele frequencies.
The only indicators for the fitness distribution is the arithmetic mean. Why don't we include other indicator of the probability distribution of fitness? The skew, the sd, the median for examples. Could you argue why we don't need to care about the probability distribution of fitness of individuals with genotypes 11 (for example)? In other words, why is the mean fitness (=w11) a sufficient statistics?
I wouldn't be able to answer if one asks me:

Why don't you take the median instead of the arithmetic mean?"
Why don't you care about the variance, the skew (or any other moment) of your distribution?
What if the traits were not countinuous but discrete (sex is a discrete trait for example)?

Could you point us to where you have seen the statement "we don't care about the prob... the mean fitness is a sufficient statistic"

@GriffinEvo I am stating that we don't care about the probability distribution, distribution skew, etc... as only the mean fitness per genotype and overall mean fitness (pondered by their frequency) appear in the equation.

Thanks kmm. I didn't Mathjax. Can we make the overline over w for mean.w ?

@GriffinEvo To add to my last comment. Does it make sense? Do you know any mathematical formulation that take into account other indications (sd, normal/poisson, skew, etc...) of the probability distribution of fitness when describing a change in allele frequency over time due to natural selection?

I doubt it is going to be the case where evaluating the mean is going to be adequate for describing the population fitness.  Its just a common compromise in experimental and mathematical fitness... this would presuppose that the distribution of fitness is gaussian, extrapolating to a large population.  even then you'd need to have an estimate of standard deviation.

@shigeta so you think our models depend on this very strong assumptions that fitness is normally distributed with a given sd (maybe 1). Isn't it weird that we never tell this assumption when talking about this formula although we talk quite a lot of the assumptions of panmixia in introductory class of evolution?

Wonder if studies often don't have a large enough sampling to justify an SD calculation.  For such studies posting a mean value might be all you can do.  Also the stats training of the authors is not great in many cases.  more recent studies have been larger scale and more rigorous and take years and whole crews of biologists.  If you were to post some paper links i'd try to turn this into a response.

It's simplest to think about a haploid population with size $N$. Say there are two alleles, $A$ and $a$, with $A$ having frequency $p$ in this generation. Each $A$ individual will have some realized fitness (i.e., number of offspring) in this generation; let's call this number $w_A^{(i)}$ for the $i^\text{th}$ individual. The total number of $A$ individuals in the next generation is then $\sum_{i=1}^{Np}w_A^{(i)}=Npw_A$, where $w_A$ is the arithmetic mean of the fitness distribution, $w_A\equiv\sum_{i=1}^{Np}w_A^{(i)}/(Np)$. So regardless of how weird the distribution of the $w_A^{(i)}$ was, all that matters (in the large-$N$ limit) is the arithmetic mean.