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Can cell adhesion molecules have intrinsic enzymatic activity?
I am learning about cell adhesion molecules (CAMs), and I know that they mediate cell-cell and cell-extracellular matrix adhesion via homophilic and heterophilic interactions. I have read that CAMs can be divided into four families based on their protein sequence and structure, including the immunoglobulin superfamily, integrins, cadherins and selectins.
I know that immunoglobulin superfamily CAMs are defined as having immunoglobulin domains in their extracellular domain.
However, I was wondering if a protein has immunoglobulin domains in the extracellular domain but a protein kinase domain in the intracellular domain (e.g. TYRO3), can it still be classified as a cell adhesion molecule belong to the immunoglobulin superfamily?
I know that the intracellular domains of CAMs can interact with cytoplasmic proteins, thus regulating intracellular signalling cascades. However, I have never read about CAMs themselves having any intrinsic enzymatic activity.
Any insights are appreciated.

Not related to Ig superfamily CAMs but beta-catenin is a good example of a structural protein that also acts as a signal transducer. Many proteins have dual functions (moonlighting).

Ebnet K (2017) Junctional Adhesion Molecules (JAMs): Cell Adhesion Receptors With Pleiotropic Functions in Cell Physiology and Development." maybe just adds info to the comment above which does not answer your question?  I think any cleaving or phosphorylation can be considered an "enzymatic activity". Maybe you should elaborate on "intrinsic" enzymatic activity". Premise is that CAMS like "antibodies" (immunoglobulins)   "transduce" as a middle part, adhering and detaching, without any cleaving or phosphorylation? Can you give some example for: "CAMs can interact with cytoplasmic proteins"?

No, they can't.
You're right, you "...have never read about "CAMs themselves having any intrinsic enzymatic activity"  - because this category does not exist. There is no explicit definition, any search to no avail. However, categorization as shown by Wikipedia, Immunoglobulin_superfamily does not suggest that categories as defined are not mutually exclusive.  Hence, featuring the immunoglobulin domain cannot turn a tyrosine kinase receptor into a "cellular adhesion molecule".
Interestingly, your question seems to come up both with what those mutually exclusive categories might have in common - the immunoglobulin domain - and what - still - sets them apart: the enzymatic activity.
Some "backbone" to your question might be the question if any receptor that does not have enzymatic activity may be considered or even termed CAM, which is illustrated by the B cell receptor's popularily known presentation of antigen to T4 cells: two cells clung together by receptor, still, that is a receptor, it is no CAM. This it what makes me suggest that categorization is more formal than material.
And, what may not easily be understood in your question:
As you ask about "intrinsic" enzymatic activity you do not seem to inquire about the signaling cascade that ensues the binding of cell adhesion molecules (CAMs) to internal proteins  which, themselves, may be enzymatic. In fact,   cell adhesion molecules do not seem, per se, to be involved in cell signaling at all. That makes differentiating even more intricate: if some CAM as a ligand induces enzymatic activity it might be termed "enzymatic"; however, your question is not about the exclusion of receptor-like ligands from the set of CAMs, but, to the contrary, about the inclusion of proteins that - like tyrosine kinase TYR3 - are considered "receptors" into the set of CAMs (trying to be precise: you do not ask about TYR being included into CAMs but about TYR-like, i.e. receptor-like, proteins, being included in CAM). Those categories "receptors" and "CAMs" are mutually exclusive. A receptor - if defined receptor - even with no enzymatic acitivity is not a CAM.
"CAM" implies non-enzymatic activity, and the enzymatic tyrosine kinases you refer to are,  in concept,  opposed. This isn't trivial as you state that tyrosine kinases have the immunoglobulin-like epitope on the extracellular end. To answer your question: that doesn't change the kinase receptors being excluded from the class of CAM membrane proteins.  Untrivially, what CAMS and Tyr3 (e.g.)  share is their being located on or within the cell membrane. Both's function may be considered  cell to cell communication.
Some reference:
Rüdiger Horstkorte et al., Basic Neurochemistry (Eighth Edition), 2012https://www.sciencedirect.com/science/article/pii/B9780123749475000092
"Ig-like domains are frequently found protein domains. For example, in the human genome, there are more than 750 identified proteins with at least one Ig-like domain. Prominent examples are, in addition to the above-mentioned immunoglobulin-related molecules, receptor tyrosine kinases, co-receptors such as CD4 or CD8 and many cell adhesion molecules."
In literature, it seem's there can't be found any material arguments for delimitation.
CAMs may, in my opinion, be opposed to enzymatic proteins of the cell membrane, especially TYRO3 and other tyrosine kinase receptors, by their working principle: CAMs do not cleave as enzymes do, but adhere as specific ligands, and disolve, or do not adhere but choose. They have perfect fit or don't. They succumb to conformational change, but unlike enzymatic membrane proteines do not inflict it, by cleaving or fusing (phosphorylation). Their conformational change may even be mechanic (pulling two cell membranes tight to each other when fusing cells).
For instance
Integrins (which form a category of CAMs, cp [Wikipedia, Cell adhesion molecules]:2
"Integrins are transmembrane receptors that facilitate cell-cell and cell-extracellular matrix (ECM) adhesion. Upon ligand binding, integrins activate signal transduction pathways..." - This may lead to think of CAMs, e.g. integrin as some form of receptor, as they can bind to ligands themselves, and vice versa categorize enzymatic receptors as CAMs, as in a wider sence, CAMs, e.g. Integrin can support enzymatic receptors, TYR-receptor, moreover:
From Wikipedia, Integrin: "Integrins play an important role in cell signaling by modulating the cell signaling pathways of transmembrane protein kinases such as receptor tyrosine kinases (RTK). While the interaction between integrin and receptor tyrosine kinases originally was thought of as uni-directional and supportive, recent studies indicate that integrins have additional, multi-faceted roles in cell signaling. Integrins can regulate the receptor tyrosine kinase signaling by recruiting specific adaptors to the plasma membrane."


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How many people need to have the same mutation of a gene in order for that gene to be seen as a feasible candidate for a disease?
I am learning about genome-wide association studies (GWAS) and I know that they are used to see whether certain SNPs are associated with a disease of interest. From everything that I have watched and read about GWAS, it seems to me that GWAS can only be used to analyse SNPs in relation to a disease.
However, I was wondering whether GWAS can be used to analyse gene deletions in relation to a specific disease. For example, if you are interested in seeing whether a deletion of a certain gene X is associated with a disease like intellectual disability.
Would it be feasible to recruit thousands of people with intellectual disability and thousands of controls and then sequence their genomes and see whether the deletion of a specific gene is significantly associated with intellectual disability?
I cannot see how else scientists can determine if deletion of a specific gene has a meaningful association with a disease. I know that many mutations in intellectual disability patients are de novo and rare, so it is hard to find a large sample size of intellectual disability patients with a specific mutation. Many journal papers focusing on the deletion of a gene in relation to intellectual disability just reference the cases of individuals carrying the deletion reported in the literature/databases, and use that as evidence to justify the gene as a candidate gene worth investigating.
However, if you have a very small cohort (e.g. < 10) of patients with intellectual disability carrying deletion of a specific gene (and have no other detected mutations), is this strong enough evidence to say that this gene is a plausible candidate for the intellectual disability?
In biological research, how many people with a disease need to be carrying a specific gene mutation in order for that gene to be considered a candidate gene for the disease (is there a minimum value)?

Genomic analysis of copy number variants is routine for GWAS purposes. Here is one early example. In that case I believe they used array CGH rather than sequencing but the principle is the same, and it is more cost effective with sequencing now.
I suggest that you look into the literature of power analysis for GWAS studies. Here is one publication, here are some course materials on the topic.
This is really a statistical question rather than a biological question, at its root.

Short answer: about a million people.
Check out Cochran's formula:

In reality, here's a paper that discusses it more (still using pretty simple assumptions):
"Our results indicate that predictive models for many complex traits, including a variety of human disease susceptibilities (e.g., with additive heritability h 2∼0.5), can be extracted from data sets comprised of n⋆∼100s individuals, where s is the number of distinct causal variants influencing the trait. For example, given a trait controlled by ∼10 k loci, roughly a million individuals would be sufficient for application of the method."
This subject is a lot more rich than I can do justice to here. There have been a handful of papers published on this.

source: Stack Exchange

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What exactly are the gates in Hodgkin Huxley model?

Hodgkin & Huxley found that a model with 4 gates in series produces a good fit to the S-shaped curve of the potassium current during the action potential.

Upon reading about the structure of potassium channels on the wikipedia article, I still wonder whether it is correct to  imagine these four gates in series as an entrance with four doors in series that all have to be open in order to pass? The article always talks about the potassium channel as being a single tetrameric protein. What are the four variables in the HH-equation that are independent and have to be open (or active if they are not actually gates) in the actual potassium gate? And since there are many potassium gates in a membrane, shouldn't the equation account for the actual number of gates, i.e. the parallel ones?

The HH model was from long before the structure of the actual gates was known; now the structures are well known. I'd suggest the wikipedia pages on the HH model or the individual channels (voltage gated sodium and potassium channels) which will talk a lot about the gating.

Looks like you've added a bounty without doing any more of your own reading :(

I did this by accident. I appreciate your comment and I think it did this question justice. I have another open question which I wanted to be answered, but clicked the wrong one. Is there a way to correct this?

No, it's not possible to move a bounty (not even a moderator can do anything about that). I think this is still a good question, I just think it would be improved with a bit of focus on what you know and where the gap in understanding is, hence the comment.

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


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What happens to quality of breast milk when twins of two different sexes are born?
It says here in Scientific American

Mother's milk may be the first food, but it is not created equal. In
humans and other mammals, researchers have found that milk composition
changes depending on the infant's gender and on whether conditions are
good or bad. Understanding those differences can give scientists
insights into human evolution.
Researchers at Michigan State University and other institutions found
that among 72 mothers in rural Kenya, women with sons generally gave
richer milk (2.8 percent fat compared with 0.6 percent for daughters).

Now I'm curious as to what happens when fraternal twins of different genders are born?

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details about what is expected on this site and then [edit] accordingly. I've made some minor edits, but I encourage you to think about whether the last paragraph adds anything to your question — my recommendation would be to delete since it not based on scientific evidence. It would also help if you could indicate where you've looked for answers to this specific question.

@trondhansen is Scientific American not a reliable source? Also it's Kenyan women, I don't know which ethnicity is being reffered in Wikipedia. Does Ethnicity influence nutritional content? Economic status can also influence it.

@MrGreenGold i removed my comment because the article in the scientific american does not have a reliable source and Marissa is a freelance science journalist not a scientist.it is unlikely that the mother produces milk with only 0.6% fat if the baby is a girl and the same mother produces milk with 2.8% fat if the baby is a boy,it is an increase of 5x the fat content(normal fat content in mothersmilk is 4.2%).


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Birds with overlapping summer and winter ranges
My question is about bird species with overlapping summer and winter ranges, like fieldfares. What happens in the overlap area? Do the birds that breed there also stay there, or do they migrate to the south while their place in winter is occupied by their relatives who breed in the north?

It's possible that ranges don't actually overlap for individuals but that ranges between individuals overlap. If I live very far north and you live very far south, my southern range for me might just be your northern range.


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Why does water damage the lungs but amniotic fluid doesn't?
I've read that near-drowning causes lung damage due to water inhalation. How come this is not the case with amniotic fluid? Taking this further, would lukewarm purified oxygenated water cause damage (if hypothetically there was no CO2 buildup in the blood)? Is it the pressure differential and/or movement caused by there being a mix of both liquid and gas inside the lungs at the same time that causes the damage to the lung and alveoli (the motion tearing or crushing alveoli perhaps)? Is it an issue of consistency or temperature? Meaning, if all the air in the respiratory system was instantly changed to oxygenated purified water, would it still cause damage if the water was not the right thickness or temperature? Given the right fluid concoction, is it theoretically possible for full molecular exchange to occur indefinitely in a liquid inside the lungs (both oxygen and CO2)? Can I hypothetically become Aquariumman or a Hairy Porter munching on quality Gillyweed?
I'm very sorry for the long list of queries, but I've searched extensively for the answers to these questions, and yet still haven't found a more detailed answer than what amounts to 'it is normal and healthy for fetuses to circulate amniotic fluid through their lungs, getting water in your lungs is neither of those things, please go see a doctor'. And so that's what I'm hoping to do here. I'd greatly appreciate a more detailed answer from someone who specializes in the respiratory system (being a fan of fishy Superheroes or dodgy Wizards is appreciated but not required). A heartfelt thank you to all who answer my questions, and may everyone who is reading this have many a wonderful weeks ahead! :)

The level of saltiness is critical. Look up Isotonic, compare with hypotonic

You already know that amniotic fluid isn't water. So how is it different? It's an interesting fluid. Tell us what you've learned about how it's different from water. There is no Neonatologist or Pulmonologist here, and if there was, they would not answer so basic a question without evidence (not just guesses or your claim) of trying to find a solution to your question This site requires some research to be shown (hover over the down vote button; it's also a close vote reason.)

Part 1: For proof that my claims of having researched aren't bogus, I shall answer off the top of my head (I've only just noticed the comments). I know that fetal lung fluid is very similar to, and formed from, amniotic fluid (though they're not completely the same), since it has more chlorine (released by the lungs I believe) which is why I indicated purified water in my question. Amniotic fluid itself also has many things in it (enzymes and proteins and such) that facilitates cell growth, which is why I asked whether a special concoction could facilitate molecular exchange. Part 2 cont.

Part 2: I know that some sort of mechanism regulates and maintains the pressure in the fluid in the lungs by releasing the excess, hence my question of whether pressure was an issue. I also know that the sacs that the alveoli are in are very delicate, hence my question of whether the movement could cause damage. As indicated by Wrangler, I know that the amniotic fluid is salty to facilitate chemical reactions, but not so salty as to disrupt cell function. The saltiness also plays a big part in getting the fetal lung fluid out of the lungs just before delivery I believe. Part 3 cont.

Part 3: I have a Fin Econ background and have 0 formalised education in Bio or Chem after grade 10, since I chose physics for my grade 11-12 IBDP. This means all I know about biology after that comes from self research into curious topics in my free time from studying in Uni. This unfortunately severely restricts my ability to understand Bio papers/articles in as much detail as I'd like in a reasonably timely manner. I'm also curious about absolutely everything, not just biology, hence I find myself with a little knowledge about lots of things, rather than in-depth for some, except finance. :)

As you stated, fetal lung fluid is not the same as amniotic fluid, and the direction of fluid flow is from the fetal lung into amniotic fluid/fetal GI tract, not amniotic fluid into fetal lungs. Fetal lung fluid is secreted bu the fetus' developing lungs to keep them expanded. Does this change your question(s) at all?  IOW, amniotic fluid doesn't normally reach fetal alveoli. As to O2 exchange with the right solution, yes, it can occur, but there needs to be a mechanism to circulate the fluid such that O2 is continuously introduced and CO2 removed.

Part 1: Thank you immensely Anongoodnurse for your answer and for such quick replies! However, I was completely certain that fetuses did indeed inhale and exhale amniotic fluid, and that it was only changed (not secreted) into fetal lung fluid by the lungs releasing certain chemicals (such as chlorine) into the amniotic fluid that was being inhaled from around the baby. And I was also absolutely certain that the alveoli/air-sacs were indeed exposed to the fluid as well. Part 2 cont.

Part 2: In fact, I found myself to be so darned certain of these two views that I decided to go back and research them again to see if my memory was failing me and I'd somehow started getting early-onset dementia at 23! (:D) Here're the results of my (admittedly quick and of shallow depth) reconducted research: The Children's Minnesota web page at ChildrensMN.org states that "The unborn baby “breathes” the fluid into the lungs, where it pushes open the air sacs and stimulates them to grow". Part 3 cont.

Part 3: Furthermore, WhatToExpect.com states that "Muscle contractions bring amniotic fluid in and out of the lungs" and that "It may even support the development of alveoli, tiny air sacs on the lungs". This view is supported by many different types of reputable sources as well. For instance, Medical News Today states in a news article that "Developing babies are surrounded by amniotic fluid, and their lungs are filled with this fluid... babies begin taking “practice” breaths. But these breaths... only refill the lungs with more amniotic fluid". Part 4 cont.

Part 4: And also, BabyCenter.com is a parents' help website that states "26 weeks: Baby begins inhaling and exhaling amniotic fluid". These views are even supported by Bio education websites. For example, OpenTextBC.ca is a Canadian education website for British Columbia, and it states that "Fetal breathing movements involve muscle contractions that cause the inhalation of amniotic fluid and exhalation of the same fluid". And another Edu-site called LumenLearning.com has a course that states that "the fetus “practices” breathing by inhaling amniotic fluid in utero".

N.B. Not everything you read on the internet is true.

@ShaptarshiJoarder you should [edit] your question to add all necessary details instead of stating them in comments. Make your question readable, understandable, and self contained so that any user who has a similar question does not need to scroll through comments.

@PolypipeWrangler - Now that few people are looking at this question, it doesn't matter if non-fatal drowning occurs in salt or fresh water, so isotonicity isn't really the issue. People tolerate small amounts of inhaled fluids well enough, but larger amounts can wash away surfactant, and causes shunting.

Thanks for new info @anongoodnurse; in response I read the wikipedia article on pulmonary shunt.

TL;DR: Fetal lungs are filled with lung fluid produced by lung epithelial cells, not amniotic fluid. Amniotic fluid aspiration in utero can be catastrophic. So your question is based on an inaccuracy.

Why does water damage the lungs but amniotic fluid doesn't?

My question back to you is, how do you know that amniotic fluid isn't harmful to fetal lungs?
There is a common misconception that fetal lungs are filled with amniotic fluid. In fact, it's so common that even many physicians mistakenly believe this.
From a book chapter titled Amniotic Fluid: Physiology and Assessment published in 2008, this misconception is discussed briefly:

Because amniotic fluid is more hypotonic than fetal plasma, it is postulated that exposure of amniotic fluid to the fetal alveolar capillary bed results in net movement of water from the amniotic cavity into the fetus. Although radioisotopes have been discovered in fetal lungs after intra-amniotic instillation, this quantity has been small and inconsistent,2 leading investigators to question the actual contribution of fetal respiration to amniotic fluid removal. In fact, surface-active phospholipids originating from the fetal alveoli are found in the amniotic cavity, leading to suggestions that the fetal lungs may actually be a net contributor to amniotic fluid volume.

This, in 2008, despite the fact that fetal lung fluid was shown to be produced by fetal lungs in 1948. (That paper, unfortunately, is unavailable.) By 2018, that misconception was corrected in medical textbooks, e.g. Avery's Diseases of the Newborn, Tenth Edition (2018) in which can be found the following:

Fetal lung fluid is a product of the epithelial lining of the developing lung (Wilson et al., 2007; Helve et al., 2009), averaging 4–6 mL/kg per hour. The resistance imparted by laryngeal abduction results in fluid accumulation to a total volume of 20–30 mL/kg during gestation, which generates an end-expiratory pressure of approximately 2–4 cmH2O. The composition of fetal lung fluid is distinct from that of both amniotic fluid and plasma, as illustrated in Table 42.2.

More succinctly:

During fetal life the lung develops as a liquid-filled organ. This liquid is produced by the fetal lung and leaves via the trachea from where it is either swallowed or enters the amniotic sac. Fetal lung liquid plays a crucial role in the growth and development of the lungs by maintaining them in a distended state.

Fetal lungs produce fluid that keeps the lungs expanded and developing normally. Though there is evidence of diaphragmatic activity as early as 12 weeks gestation, amniotic fluid does not enter the lung with these diaphragmatic movements because the fetal larynx closes during "inhalation" preventing the entrance of amniotic fluid. When it relaxes, a small amount of lung fluid escapes the trachea, some of which is swallowed, and the rest contributes to amniotic fluid.

Fetal breathing movements contribute to the efflux of lung fluid into the AF, but about half of the effluent is swallowed rather than entering the AF.

Amniotic fluid aspiration in utero can cause death because amniotic fluid is loaded with keratinized epithelial cells from the baby's skin and other things that can injure the lungs.
Before the baby's first breath, all the fetal lung fluid is quickly absorbed by the lungs into the interstitial space, allowing for air to enter the lungs.
Edited to add: You wanted a specialist to answer this question.  Well, here is a letter to the editor of Pediatric Pulmonology, a journal about the lungs you referred to in your question, from a Neonatologist,  entitled Fetal lung fluid: Not the same as amniotic fluid. In it, the Neonatologist corrects a mistake by another Neonatologist in one of the articles in this specialty journal! So it shouldn't be a surprise that so many others get it wrong, too.
An exerpt:

However, I wanted to bring attention to a statement in the introduction where the author states that the “preterm infants’ lungs are filled with amniotic fluid”. This is not accurate and appears to be a common misconception, particularly among medical students and junior residents despite recognition of fetal lung fluid as being a separate entity from the amniotic fluid as originally described in 1948 by Jost and Policard.

Thank you so much for this amazingly in-depth and easy-to-understand answer! Finally one of my endless number of curiosities have been quenched. Hope you and your family have a most fantastic week ahead! :)

@ShaptarshiJoarder - Feel free to hit me with another. I learned a fair bit here, too. :)

As soon as I have another biology curiosity that my research can't seem to answer, I'll be sure to do so! It seems fishy wizards shall remain in fiction for now.


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Problem involving genetic interactions in yeast
I'm having difficulty with the following problem:

In yeasts, genes MEC1 and SGS1 favor survival in response to HU
(hydroxyurea). In the figure below, Δ indicates homozygosis for the
mutant allele that causes loss of function. mec1-100 yeasts are
heterozygous (one MEC1 allel is wild and the other is mutant).
a) What genetic interaction do genes SGS1 and MEC1 maintain?
b) How do you explain the results at the molecular level?
c) How do you explain the difference in phenotype between the homozygous and heterozygous yeasts for the allel that causes loss of
function for the MEC1 gene?
d) Why would you combine the sgs1Δ mutant with mec1-100, instead of combining it with mec1Δ?

My attempt to solve this was as follows:
Observing the sgs1 Δ mutant in homozygosis for MEC1, we see that the phenotype that is produced is within a scale close to the WT phenotype. Further, in heterozygosis for mec1-100 without mutation we also see a phenotypical scale similar to the WT. When we see the heterozygotes for mec1-100/sgs1Δ the scale drops abruptly and the phenotype passes to be very far from the WT phenotype. This last one can be explained as an incomplete dominance in which the genotype of mec1 must present both WT allels to achieve its effect, because just one of the WT alleles cannot fulfill its function, so what we see in comparison with the sgs1Δ/MEC1 homozygote dominant is different from mec1-100/sgs1Δ. When we mutate the gen mec1Δ we see that the viability of the cells is reduced, even though the gen sgs1 is still present.
What has been observed and described previously could be explained as a recessive epistasis where regardless of what happens with gen SGS1, if MEC is mutated (double recessive) it masks the effect of Sgs1. That is clearly seen because when mec1 is present, the viability is close to the WT scale while when mec is mutated or in heterozygosis (which would work as a mutant by the incomplete dominance) it does not matter what happens with sgs1 (if it is mutated or not mutated) the phenotype of the molecular pathway is not produced (a phenotype of low viability is produced instead).
At the molecular level, it could be explained as follows:
A substrate exists that uses the enzyme produced by MEC1 to activate the viable molecular pathway. In absence of MEC1 the pathway is not activated, SGS1 uses MEC1 to carry out its function that also promotes viability, therefore if MEC1 does not exist SGS1 does not have an enzyme to interact with.

But turns out that the correct answer for this problem is that the genetic interaction is a redundancy between SGS1 and MEC1.
My question here is:
Can this problem, as expressed in the first paragraph, be taken as a recessive epistasis? Why can't it be considered a recessive epistasis? In cases where we have a logarithmic scale, if the correct answer is a genetic redundancy, can we take it as a viability generated by both genes anyway? Is the viability generated by each gene comparable at all?

This is a well-formulated question, but the prompts suggest that it is an exam question or other similar coursework. If that is true, you should add the "homework" tag. (You have clearly shown your attempt at an answer, which means that this question is appropriate for the SE Biology community.)

@MaximilianPress thanks! Will add it now. Yes, this is from a set of prep exercises for an exam that is driving me a little bit crazy.

Based on the graph of experimental results, WT diploid yeast are able to grow in the presence of HU (hydroxyurea).  Deleting both copies of the MEC1 gene results in cells that stop growing in the presence of HU; therefore the wild-type product of the MEC1 gene is involved in resistance to HU (as described at the start of the homework question).  Deleting both copies of the SGS1 gene has a slight effect on growth in the presence of HU.  From this we infer that the wild-type product of the SGS1 gene has some role in resistance to HU, but these mutant cells can still grow, and therefore contain some other activity (or activities) that provide resistance.
The MEC1 gene is dose-sensitive; when you remove one functional copy with the mec1-100 loss of function allele, the cells resistance (or growth) is intermediate between wild-type cells and the mec1 homozygous null (knockout, or deletion).
mec1-100 heterozygotes, that also lack both wild-type copies of the SGS1 gene have much worse viability/growth/resistance to HU (when compared to either the sgs1 homozygous loss-of-function allele alone OR the mec1 heterozygous loss-of-function allele).  In other words, it appears "more" mutant, or closer in phenotype to the mec1 homozygous mutant.  Therefore the wild-type function of the SGS1 gene overlaps with the wild-type function of the dose-sensitive MEC1 gene.  Two genes with overlapping genetic functions are by definition redundant.
I would've described sgs1 as a recessive enhancer of a mec1 hypomorph.  Historically this can be a powerful way to identify genes that may be involved in the same cellular process.  When I see the term 'recessive epistasis' I think of trying to order genes in a genetic pathway.  As in, which gene is 'upstream' and which gene is 'downstream' in the genetic pathway.  It doesn't make sense (to me) to try to "order" two genes with redundant function.  Sometimes redundant genes encode proteins with homologous sequence (e.g., different classes of tubulins), but sometimes redundant genes indicate that there are parallel pathways at work (and one compensates for the lack of the other).  I suspect that you are using a different definition of 'recessive epistasis'.


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Antigen transfer from baby to mother
When considering immunity in babies, the main mechanism that supports their undeveloped immune system is the transfer of antibodies from mother to baby via breastfeeding.
Case #1: both baby and mother got sick with a virus; the mother then produces large amounts of antibodies that are passed to her baby via breastfeeding.
But what if the mother (for some reason) does not get sick while the baby does?
Case #2: just the baby got sick.
What are the possible scenarios for supporting the baby's immune system in that case? It looks like the number of relevant antibodies is low in the mother.
Another mechanism could be envisioned, namely, the baby transfers antigens to the mother when breastfeeding, which stimulates the mother to produce antibodies and pass them back to the baby. Is this mechanism real? Is it efficient in any sense as compared to Case #1?
(scientific references would be appreciated)

Are you suggesting that in case#2 that the mother has not been exposed to the babies' pathogen? (i.e. is the baby isolated from the mother, more-or-less precluding breastfeeding) Or are you suggesting that the baby has been injected with some sort of antigen for which there is no infectious disease present?

@ARogueAnt. - I believe the OP is asking, what if baby was exposed to the pathogen but mother was not? (Say, baby went to visit grandmother, gets virus from visiting cousin. Baby's infection would precede mother's, if mother did catch baby's virus.) It's a reasonable hypothesis, no "isolation" or "injection" necessary.

To the OP: You say, "When considering immunity in babies, the main mechanism that supports their undeveloped immune system..." Can you support that the child's immune system is "undeveloped", since your question hinges on this? Please provide support in an edit to your question.

@anongoodnurse is it important whether the baby's immune system is developed or not for this question? I'm only asking about the possibility for the mother to do the dirty job of making antibodies while not being sick herself.

If that's what you're asking, then edit your question too include that precise request.


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Calculation of drug efficacy- mathematical biology approach
I am participating in a mathematical biology project.
I would like to discuss the following problem:
Let A be a drug such that $x_{o}$ chemical units of it kills 12% of $y$ cells per 1 day, I would like to calculate the efficacy killing rate of the drug.
My attempt:
Duration of process: 1 day
Killing rate $r$ of cells by drug A:
$$
\begin{aligned}
&100y e^{-r t}=12y \\
&100 e^{-r}=12
\end{aligned}
$$
so
$$
r=2.12 / d a y
$$
Efficacy rate of drug A- meaning in which rate cells are killed
per 1 unit of drug A per 1 day:
$$
\begin{aligned}
p x_{o} &=2.12 / \text { day } \\
p &=\frac{2.12}{x_{o}}\left[\frac{1}{U \cdot d a y}\right]
\end{aligned}
$$
Here $U$ means the chemical units of the drug.
Is it correct biologicaly/physically to decompose the a rate of process into the product of efficacy rate  and the initial amount of drug?
Is there anything wrong in thi process? another way of calculation?


text:
Do color-blind people have more rod cells in their retinae than the normally sighted?
All types of color-blindness are said to be caused by the defect or lack of cone cells in the eyes[1]. Since cone cells sense color[2] and rod cells can only sense light intensity[3], the lack of cone cells would mean that the eye cannot detect color. However, rod cell function better in low light than cone cells. Color-blind people have fewer cone cells than other people. My question is, is it possible that they also have more rod cells than other people?
I am color-blind, and I have observed instances where I was able to see better in low light than other people. For example, most often when I read at night or in low light, people have wondered how I'm able to see in the low light condition. I also do not turn on the light most of the time when I walk around the house at night, whereas other people in the house often cannot see well enough to walk without turning on the light. I also recently noticed that my favorite theme (for VS Code), is actually meant for people who work in low light conditions or at night. But they have also noted that it is suitable for people with color blindness.
All these occurrences made me wonder whether color-blind people have more rod cells than average people, and hence can see better in low light too.
[1] ‘Color Blindness’ entry in Wikipedia
[2] ‘Cone Cell’ entry in Wikipedia
[3] ‘Rod Cell’ entry in Wikipedia

The other people in the house should be around your age for a fair comparison. Because in my experience people 60+ tend to be night blind.

Not an answer, but from a cursory search it appears that only a few samples are known where the counting has been done, individual variation seems to be as much as a ratio of 11:18 or possibly more, and no colour-vision capacity was stated in any case. Lots of confounding factors and little useful data there. Perhaps someone else might dig deeper.

@DKNguyen that's a fair point. I'm only 13, so it will be hard to compare the results, since the "other people" I mentioned are basically just my parents.

@ARogueAnt. I was hoping that there might be some experiments done regarding vision, instead of just counting the cells manually. But again, like DKNguyen mentioned, there are a lot of factors affecting vision, so it might be hard to conduct a controlled experiment.

A friend at lawn bowls remarked that he is red/green colour blind but that he can see movement much more clearly than others. We believe he is correct in this assumption.

Short answer
There are not many studies that have counted rods and cones in the human retina, let alone compared healthy retinas with those of color blind people. Yet direct evidence, as well as circumstantial evidence, point toward a degeneration of cones, rather than substitution of cones with rods.
Background
There are a few points of importance. For one thing, as Fig. 1 shows, rods outnumber cones by a factor of 20 in the human retina (Purves, 2001). Secondly, their distribution is very different, cones being clustered in the center of the retina (the fovea) and rods more eccentrically (Fig. 1) (Wells-Gray et al., 2016). Lastly, and most importantly, the scarce studies out there that actually counted photoreceptors in human retina of colorblind people found that deviant photoreceptor counts were the exception rather than the rule. In those rare cases where a loss of cones was found, it manifested itself as areas in the retina lacking photoreceptors altogether, and not by a substitution of cones by rods (Caroll et al., 2004).
The patchy photoreceptor loss found by Caroll et al. (2004) shows that degeneration can be a hallmark of color blindness, but no evidence is yet found to support de novo appearance of rods.
More circumstantial evidence comes from the facts above that rods appear eccentrically, whereas cones are clustered foveally. So any appearance of rods where the cones are lost is not a parsimonious assumption. Secondly, because rods are so much more abundant, patchy increases in rod numbers replacing cones would, likely, not add noticeable differences in night vision. Lastly, rods wire with rods (to amplify light), and cones with cones (for color vision), so substitution of patches of cones with isolated functional circuits of rods would be quite unlikely to occur in my opinion secondarily to degeneration of cones, as the retinal circuitry is quite complex.

Fig. 1. Retinal distribution of rods and cones. Cones (left) are clustered in a densely packed fovea. Rods are more abundant overall and their distribution is reversed from the cones. source Purves et al. (2001)
References
-Caroll et al., PNAS (2004); 101(22): 8461–6
- Purves et al. (eds.). Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001). Anatomical Distribution of Rods and Cones
- Wells-Gray et al. Eye (2016); 30: 1135–43

that makes sense. Thanks a lot for answering! I've just posted another question (somewhat related), check it out if you're interested https://biology.stackexchange.com/q/107212/68669
Thanks again!

Many people are claiming both experimental and anecdotal evidence that colorblind people see better in low-light, in this question here: https://biology.stackexchange.com/questions/44140/what-is-the-evolutionary-advantage-of-red-green-color-blindness/44147#44147
@AliceD, do you think that although the number of rod cells might be the same, the sensitivity might be more for colorblind people? This might explain why most people report better low-light vision.

@Zo-Bro-23 - To be frank, I have no idea. It's an interesting observation though and I'll look into this further.

@AliceD thanks, that works. Please do let me know if you find out anything else about it...

This paper seems relevant ...


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What is the difference between BSA fraction V and the initial fraction?
I am preparing a supplemented culture medium and I need to use BSA. There is fraction V of BSA that we normally use for immunocytochemistry and there is another type named the initial fraction that is specific for cell culture but we don't have enough amount in the lab currently.
I want to know whether or not I may use the fraction V for cell culture as well.

Welcome to Biology.SE. Who is the manufacturer/provider and have you tried looking this up yourself? I searched using "BSA fraction V" and this was my top result.  Please note that the expectation on this site is that you will demonstrate that you have done some prior research before posting. Please take the [tour] and consult the [help] starting with [ask] for details.

For an extremely specific question like this, I think you will increase the probability of getting a helpful response if you include the actual details of the reagents.  In other words, for me to order those same two types of BSA I would need to know at least the manufacturer's name(s), and the catalog number(s).  From that one could possibly bootstrap their way to an answer. Also, after clicking on the link from @tyersome, I did a quick search and found this Wikipedia entry: https://en.wikipedia.org/wiki/Cohn_process that describes the steps.

Thank you for your comments.
Yes. I checked the manufacturer's protocol, the datasheet, and research gate beforehand but I could not find anything specific. I also asked my supervisor's idea but I was not convinced to use it so I kept on looking for more information. Thank you for the links you shared. I will check them.
By the way, I used the fraction V BSAfor supplementing my culture medium and so far the cells are fine.
The ref number for BSA's:
Bovine serum albumin fraction V REF10735086001, ROCHE
Albumin, Bovine initial fractionation by heat shock, A7906, Sigma
Thank you.


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Are color-blind carriers partially colorblind?
Since color-blindness passes along an recessive gene in the X-chromosome, women are rarely affected, while men are affected more frequently. Women with one copy of the color-blindness gene are said to be "carriers". Women also have something called a "genetic mosaic", due to X-inactivation in the early stages of development. However, which X-chromosome is inactivated depends entirely on chance. My question is, what happens if some of the cone cells in the eye contain a copy of the X-chromosome with the color-blind gene? Will the woman be partially colorblind? I read somewhere that the woman's brain learns to ignore signals from the cone cells that are affected. Is that true?
Sources

X-inactivation and color-blindness
As mentioned in this article,

As we [women with the recessive allele] have several millions photoreceptors (cones) which are responsible for our color vision, the defective signals are in a way oversteered by the correctly working ones.

Edit: In the original post, I also included a follow up question about why color-blindness is still present in the gene pool, but that is answered in this question, so I removed it.

Best practice is to ask one question per post. In addition, I think your second question will find an answer here. If yes, (it does address evolution, camouflage etc.), you might be able to focus your post better by eliminating part II. Adding your sources to part I is important; a Q close vote has been posted, because it seems like you haven't added background research, which we ask every person to do on this site (note that I am quite convinced you did prior research, but please add the relevant links to better frame your question).

Thanks a lot! Like I mentioned in my post, I remember reading about this elsewhere, but I can't seem to find the link now. A mistake on my part. I will try my best to provide relevant links in the future.

Looking at the literature, I find the following passage in a review of the genetics of colorblindness:

Females have two X-chromosomes, and can either be homozygous or heterozygous for the X-chromosome opsin allele. If homozygous, they are dichromatic; however, females who carry both an allele for an L opsin and one for an M opsin have the equivalent of normal human color vision, having both L and M cones because the process of X-inactivation segregates the expression of the L and M opsin genes to separate populations of cones. The significance of this is that in trichromatic female squirrel monkeys, the difference between L and M cones is solely determined by the stochastic choice of which X-chromosome is retained as the active one. Variation in L:M cone ratio in female squirrel monkeys is similar to what is seen in human males with normal color vision. In squirrel monkeys the variation has been attributed to the stochastic process of X-inactivation, influenced by the number of cells present at the time of activation and other random factors in the inactivation process (Jacobs & Williams, 2006).

Boiling this down: X-inactivation happens at a local enough scale that eyes of heterozygous females have active versions of both normal and mutant opsin genes. So they will still see color "similar to what is seen in human males with normal color vision".
Note of course that people with an XX complement can have better possible color perception than XYs, as they have the potential for tetrachromacy:

females who are heterozygous, for example, having OPN1LW genes that encode two spectrally distinct L pigments, would have four different cone types -- two different L, plus M and S -- and thus the potential for having tetrachromatic color vision (Bosten, Robinson, Jordan & Mollon, 2005, Jordan & Mollon, 1993, Jordan & Mollon, 1997). Prior to the discovery of variation in peak sensitivity of pigments underlying normal color vision, it had been appreciated that female carriers of a red-green color vision deficiency have the potential for tetrachromatic color vision (Nagy, MacLeod, Heeyndermann & Eisner, 1981).

Here is a study specifically on color perception in heterozygous women that may answer further questions.
So there are some differences between color perception of heterozygous XX vs XY, they're just not colorblind per se.

ZO-Bro, your second paragraph considers why colorblindness stays constant in the gene pool.  Whether it is an advantage or not in some situations, if it is not really being selected for or against, it will probably hang around indefinitely in roughly the same frequency. Nearsightedness would probably disappear FROM THE POPULATION if we lived on the savanna with only spears and stones.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.


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How long does it take for a new muscle fiber to be connected to motor neuron?
When new muscle fibers are formed through hypertrophy, how long does it take for motor neurons to connect  to the new muscle cells in order to be able to control them?
After taking a break from working out, I noticed that my strength has actually increased and I wondered that maybe although the new muscle cells were already built back when I was working out, they weren't yet connected to the nervous system and so I couldn't "access" this strength.

The question is quite interesting. what is the time required to newly establish a neural connection to newly formed muscles? Unfortunately the answer is NO.
No new muscles are formed by hypertrophy.
This is because you are referring to hypertrophy, not hyperplasia, which are essentially different. Hypertrophy is increase in the muscular fibers due to increase in mitochondria, myofibrils and other cell organelles. The size and volume of cell increases but the number of muscular cells remains same, hence there is no change in the nerve connections. The nerve connections essentially remain same. When you do strength training, the proteins i.e. actin and myosin undergo wear and tear. This damaged is repaired by synthesis of these proteins which is results in muscular hypertrophy.
Hyperplasia is increase in number of cells. Which brings us to next question, do muscle cells divide? The answer is YES, but it is largely restricted. These cells are termed as satellite cells.
So new neural connections are established probably only if new muscle fibers are formed.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

Thanks! So do I understand correctly that generally the total number of muscular cells remains constant, but the size of the cells increases due to strength training? And when does muscular hyperplasia occur and how long does it take for neural connections to be established when it occurs?

@timtam, yes! it is the strength and weight training that causes the muscular hypertrophy.  Muscular hyperplasia occurs during the muscle damage or when satellite cells are stimulated under the influence of growth factors. Although I am unsure of time required for formation of new neural connections for a new muscle fiber, but I think that a new neural connection is established as the muscle fiber is formed.

@TOXIN_SCIENCE thanks. what exactly causes this muscular damage in hyperplasia? Aren't sore muscles from workouts not also damaged muscles? Do you have any literature suggestions to read more about how neurons connect to muscles?


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How do we determine what we call "flexion" and what we call "extension"?
Question:
How did we determine which motion to call "flexion" and which to call "extension" with regard to the wrist and the neck?
Background:
Just to set the stage, I'm not asking for help on homework here. I'm a veterinarian and I teach human anatomy. Terms for joint movements make sense to me on a surface level, but the more I think about them, the more confused I get.
I have read some good comments and sources on biology stackExchange, such as this discussion.
But the more I think about it, the less it all makes sense.
My initial question was "why do we use dorsiflexion and plantar flexion" instead of simply saying "flexion" and "extension?" My confusion is not about plantar/dorsal-- coming from the veterinary side, that part is easy for me. Rather, my confusion is about why we don't simply refer to dorsiflexion as "flexion" and plantar flexion as "extension."
Someone mentioned in the link above that anatomists wanted to emphasize the connection between ankle and wrist in their terms. That made some sense... except that we end up using different terms in the ankle vs the wrist. And in any case when I think about this, I start to wonder-- how do we define flexion or extension of the wrist in the first place? I mean to some degree it's intuitive, thanks to everyday language use. I don't know exactly how that intuition arises-- perhaps by analogy to the elbow and knee, I generally think of "flexion" as being the more active movement for picking something up or moving something, while extension is usually for putting things back down, and flexion tends to make the bigger muscles bulk up. But if we want to be objective about it, how would we do that?
Either movement of the wrist reduces the angle between the hand and the arm. Either movement requires some muscles to relax and their counterparts to contract. Either movement can accomplish important physical functions.
I can understand how we arrive at objective terms for the knee and elbow. If we start in the anatomical position, we cannot significantly reduce the angle between the distal and proximal parts except by moving in one direction-- which we can call flexion. Extension is the opposite, and in the unfortunate event that some external force moves us beyond the normal range, we get hyperextension. So far so good.
But this doesn't apply to the wrist, or for that matter the head, so we're back to the drawing board. Starting from the anatomical position, any movement of the head or hand reduces the angle from 180 degrees to something less than that. (The foot is in fact the only one of these three where it makes much sense to simply use extension and flexion; since we start at 90 degrees from the shin, dorsiflexion reduces the angle, and so could to my mind be called flexion, while plantar flexion increase the angle up to 180 degrees, and so in my mind could simply be called extension. And yet for the foot, we don't use these terms!)
Others have mentioned it has to do with the coronal plane-- reducing the angle between the body part and the coronal plane is flexion. But this doesn't really hold up either; both flexing and extending the head increase the angle between the head and the coronal plane. Same with the wrist. This just doesn't seem universally applicable period.
When it comes to why we use plantar flexion and dorsiflexion of the foot instead of flexion and extension, I can appreciate that the foot is uniquely positioned at a 90-degree angle from the long axis of the body, so that the joint is not, in anatomical position, oriented along the coronal plane, while most other limb joints and the head are. So I am open to this being an explanation for why the standard terms don't apply, but to understand that, I need to understand how and why the other terms do apply more generally.
I am willing to accept it if the best possible answer is "we arrived at these terms through a history of common usage and there is no explanation other than the subjective opinions of early anatomists." But I'd love to know if there is something better.
To summarize my main question is:  how did we determine which motion to call "flexion" and which to call "extension" with regard to the wrist and the neck?

Hi and welcome! On this site, people asking (and answering) questions are expected to provide some evidence of their research into an answer. (Yes, some impulsive people answer questions without such evidence, but it's still expected.) From a biologist/scientist, it's even more reasonable to expect some background research. Did you look for historical references? Or the etymology of flexion/extension? I'm sorry if this sounds silly (especially in the light of my having done it, too) but can you include your research? Thanks!

My guess is simply our anteriorly-oriented world view since both flex anteriorly in anatomical position. Although directionality (anterior vs posterior) aren't necessary to define either flexion/extension (see the post you linked for more detail), I could see the confusion surrounding the otherwise arbitrary choice of using these terms in the fashion chosen vs the opposite convention. I think a solid answer here has to pull out one of the classic Greek texts (or whomever 1st utilized these terms in this fashion) to shed adequate light on this.

You might find more helpful resources by searching for atlanto-occipital and radio-carpal joints more precisely

@theforestecologist - I'm curious why you say Greek. My poking around puts flexion (from flectere, to bend) first used to describe, well, joint flexion, in v. early 1600's. Most scholars in the West used Latin back then, no? I can't seem to get further back to Greek.

@anongoodnurse I just guessed some older language without putting much thought into it (hence my parenthetical). You did the right thing by looking at the etymology (I didn't take the time yesterday to look since I made these comments quickly between tasks). Thanks for following up about it!


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Why does Falconer's formula for broad sense heritability subtract correlation values instead of r^2 values?
Falconer's formula for broad sense heritability is 2*(r_monozygotic - r_dizygotic).
Mayhew and Meyer (2017) states:
"Subtracting the DZ phenotypic correlation from the MZ phenotypic correlation provides an estimate of the variance contributed by genetics when 50% of DNA is shared."
If we are seeking an estimate of the additional variance explained by an additional 50% of shared genes, shouldn't we be subtracting r^2 values rather than r values because r^2 is the proportion of variance explained?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5635617/

Each of these two estimates (DZ correlation and MZ correlation) express a numerical relationship (Pearson correlation) between individuals. Each of these could independently be squared to provide r^2 values, if that were one's goal. And the final quantity (heritability, h^2) that Falconer's formula provides is analogous to a r^2. But that does not mean that all of the intermediate steps can  be easily treated in terms of r^2.
I'll defer to wikipedia and other resources for more details, but in simple terms, variance (in r space) is easy to decompose into contributing factors (e.g. MZ correlation vs. DZ correlation), but r^2 is hard to decompose into contributing factors. See for example the general definition of r^2 given by wikipedia:

When you are computing R^2, you don't sum (or subtract) variances explained by different factors. You compute residuals (differences like MZ vs DZ), square them, and sum them, and then say all the variance that isn't in that residual quantity must come from the model (e.g. is variance explained by the model).
I think one issue here is that people use terms like "variance explained" in slightly informal ways. It applies to both r^2 and the final heritability estimate, but not every intermediate step of the computation of those estimates can be neatly phrased in those terms.
For more background here, I can recommend the wiki page for heritability.

I'm suggesting subtracting r^2 values from each other. Not subtracting an r from an r^2. i.e. 2*(r^2_mz - r^2_dz)

@Ashish ok I misread your question. But the point about the decomposability of r vs. r^2 stands. I'll edit

It is quite common to fit sequential linear regression models where you add a predictor with each model and report the difference in r^2 with each added IV. That difference represents the additional variance explained by the addition of the IV. Similarly, here you're adding 50% of the genome as a predictor. The difference in r^2 has a statistical meaning. Difference in correlations does not correspond to any clear statistical property as far as I can tell. My question is looking for a mathematical explanation of the substantive meaning of a difference in correlations.

@Ashish yes this is a common approach when performing regression analysis, one commonly evaluates models using this approach (though AIC or BIC are probably preferred for penalizing parameters). The r^2 difference is heuristically interesting for evaluating model fit in that case. It is however a different approach from what heritability estimation is trying to do, which is to try to estimate specific quantities of interest within a directly interpretable mathematical framework.


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Can we compare the effectiveness of an inhibitor by checking how much they change Km and Vmax during a reaction?
While comparing two inhibitors, can we check how they alter the Km and Vmax of the reaction and then decide which inhibitor is more potent.
I tried explaining in this way:
While I think the answer should be "no", I am not entirely sure.
I got these statements from Wikibooks :

Competitive inhibitors can only bind to E and not to ES. They increase Km by interfering with the binding of the substrate, but they do not affect Vmax because the inhibitor does not change the catalysis in ES because it cannot bind to ES.
Uncompetitive inhibitors can only bind to the ES complex. Therefore, these inhibitors decrease Km because of increased binding efficiency and decrease Vmax because they interfere with substrate binding and hamper catalysis in the ES complex
Mixed inhibitors can bind to either E or ES complex, but have a preference for one or the other. This can either increase or decrease Km, respectively. Both cause a decrease in Vmax.
Non-competitive inhibitors have identical affinities for E and ES. They do not change Km, but decreases Vmax.

From this it is shown that the inhibitors do affect Vmax and Km. But I can't figure out a way to compare them. Any help?

Why do you think the answer "should be 'no'"? You can certainly compare two inhibitors of the same "class", that is: either compare two competitive or two uncompetitive inhibitors. If competitive inhibitor A increases $K_{\rm M}$ by $10%$ and competitive inhibitor B by $50%$, then – obviously – inhibitor B is more potent than A.

The kinetics of enzyme inhibitors is a basic aspect of biochemistry that is treated in almost every textbook on the subject and can be found in numerous resources for students — PowerPoint slides, lecture notes and the like. Just search for "Enzyme Inhibitors Lecture Notes" or the like. Then decide what it is you want to compare. One competitive inhibitor with another? One non-competitive inhibitor with another?  Or something else? Clearly you cannot compare different types of inhibitor. You need to clarify your problem before you can answer it.


text:
Difference in time tick spends on host based on feeding location
Does the time a tick remains on a host, and the 'health' of a tick vary depending on the location where it feeds on the host? Do they change locations on the host to find a better environment?
I recently realized that what I thought was a skin blemish on our dog was in fact a tick (it was there for weeks-- our dog gets occasional skin growths on her head and perhaps I have been distracted). This tick was on her snout-- and dog ticks most commonly attach to the head, neck and ears.  Ticks frequently get ticks on their head and ears because they stick their head (snouts!) into everything. Apparently, different species will stay and feed for different durations (7-10 days for many, but male American Dog Ticks can remain on the host for an indefinite period of time alternately feeding and mating.  This made me think-- how does finding a very exposed part of a host (snout) affect the health of a tick and the duration of their time on the host? At some point might they decide they need to find a better habitat and move?

Can't be answered the way it's asked; what species of tick? It has nothing to do with bone, and a lot to do with skin thickness. Dog ticks "fall" onto victims, so scalp will be common for people, scalp/back/neck for deer, etc. (Your source refers humans.) Deer ticks are mostly on the ground, and crawl up, so leg/groin are good places. Your dog probably had this tick, gotten from sniffing the ground. They're small, and dog nose epidermis is thin (despite appearances), so they'll dig right in. Thin epidermis means capillaries are near the surface, so within reach for small ticks.

@anongoodnurse Thanks for info & guidance on revising my question. Perhaps it still needs help, and I'm assuming it is a dog tick (I don't actually know).

Dog ticks are big, even the nymphs. It would be very surprising if you didn't notice a dog tick on your dog's nose, because they're big, and when engorged, they are so distended it's disgusting (I don't like ticks.) And no, they don't move around after they've started feeding, maybe because a fully engorged tick can't walk. They drop to the ground and lay eggs. I've read some of what you refer to.

BTW, read carefully. Your article (which I just read) stated male ticks alternately feed and mate; females become engorged. Male ticks do not become engorged. Which further complicated your question.


text:
Non- brown, blue,green eye colour genotypes and genes
In genetics, eye colours (brown, green and blue) are determined by bey2 and gey genes. But what about hazel, grey and amber and more? I read a webpage about hazel eye colour and saw that there is a 3rd gene called 'hey' with 'codes' H and h
Other than B(brown), G(green) and b(blue) but now what does H and h mean when there is one hazel?

Welcome to Biology StackExchange! According to the guidelines of this site, your question might seem a little bit under-researched. You should also provide references to your statements. For example: "eye colours are determined by bey2 and gey genes" is not an accurate statement because (as you can read on Wikipedia) "The genetics and inheritance of eye color in humans is complicated" and "So far, as many as 15 genes have been associated with eye color inheritance".

Therefore, I suggest you read some more (online) resources on this topic, and then try to edit your question into a more detailed and focused one, along with the references you have read :-) There are also some useful answers on this StackExchange, such as Why are human eye colours limited? and How is eye color in humans inherited?.


text:
difference between proximal and distal mechanisms of aging in biogerontology?
In his book Biology of Aging, Roger McDonald describes the difference between causes and mechanisms of aging; and states that the cause of aging is essentially thermodynamic (entropy) and that mechanisms can be divided in distal and proximal.

The scientific and lay literature describing biological aging can be confusing due to the misuse of the words cause and mechanism. Often these two terms are used interchangeably, although they have different meanings in the context of aging

The cause of aging refers to the thermodynamic forces that act continually on the organism throughout its life span. There exists only one cause of aging: increasing entropy.

Alterations in the biomolecules that lead to loss of function are the mechanisms of aging. There exist an infinite number of mechanisms that can be observed [...]
We also distinguish between two types of aging mechanisms: distal and proximal

then defines distal mechanism of aging as

A mechanisms of aging that underlies and is remote from the more obvious direct cause for a time-dependent functional loss. For example, obesity is the distal cause of abnormally high blood glucose concentration. Abnormally high blood glucose concentration results in the time-dependent functional loss of connective tissue due to advanced glycation end products

and proximal mechanism of aging as

A time-dependent alteration to a tissue, cell, or molecular process that lead to a loss in function

personally this seems something that he believes and in that sense not very precise academically or scientifically, because I can't find any reference regarding the subject
my question regards the following, is this information something that he believes in or does it has a foundation in biogerontology? and if the latter, can somebody kindly reference the subject with an article?

Thanks for replacing with text; it seems like if your question is about "proximal/distal" mechanisms, that you've included a bunch of unrelated text about "cause vs mechanism" and then stopped quoting where the section about "distal and proximal" is to begin.

my fundamental question is in fact about proximal/distal mechanisms but the cause/mechanism distinction also worries me, because it is the first time i'm reading it and i have no reference that proves that this is true or unanimous among biogerontologists.. however my priority is the distal/proximal mechanism

It's not uncommon to see an author provide some working definitions to keep readers from getting confused, because biologists don't typically sit everyone down to formally agree on universal definitions for every term in a given field of study. While the first point about cause vs. mechanism is a bit reductive and pedantic (imho), the fact that he even points it out suggests that it's not universally accepted in the literature. The proximal/distal distinction is probably just a useful framework for thinking about mechanisms that he will likely refer back to throughout the text.

thank you all for your contribution in this question; yes, it is likely that i'll choose that path, regarding this subject as a useful framework than a dogmatic definition.. i had the opportunity to read Ernst Mayr’s ‘‘Cause and Effect in Biology’’ where he presents the duality proximate/ultimate which is the most similar i can find in biology, beyond that i can only find related topics with sociology precisely about proximal/distal causes.. and that is another thing they say proximal/distal causes not mechanisms. thank you all again; @MikeyC feel free to write and answer if you'd like


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Does biofilm formation hinder photosythesis?
In photosynthetic bacteria such as Cyanobacteria, Synechocystis sp. PCC 6803, the bacteria need access to both light, CO2, and water to perform photosynthesis.
However, in thick biofilm structures (e.g. a sphere or any 3D shape), I feel that physiologically the cells inside the biofilm 3D structure won't have direct access to sunlight, due to the outer cells forming layers blocking sunlight. Moreover, the inner cells are less likely to have the same access to carbon dioxide and water as the outer cells of the 3D construct.
So, Does the biofilm formation affect the viability and efficiency of the photosynthetic bacteria? or Do the bacteria have a mechanism to transfer the photons of light, gas, and moisture inside the biofilm?

Interesting question, In addition I wonder if the Cyanobacteria in a biofilm perform any activity normally seen in eukaryotic organisms. Namely nutrient transfer

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Most of the constituents of Phototrophic biofilms are transparent by which light can easily pass. Phototrophic biofilm are very essential for the growth of photosynthetic microbs (colonies).Due to the presence of glycolipids the 3D structure act as lens which evenly distribute the light in the Phototrophic biofilm.

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Even if lights pass, does the wavelength delivered get affected. Furthermore, How about the nutrient and gases transfer?


text:
Do schooling fish make sounds that predators could detect?
Do schooling fish make sounds, voluntarily or involuntarily? A general internet search for "schooling fish sounds" doesn't provide many answers, but I found a paper from 1960 describing sounds from some fish in Bermuda. The description of the sound wasn't clear to me.
I'm wondering if there has been recent evidence that predators might clue into the presence of schooling fish as prey by the sounds that they make? And might ocean noise interfere with these interactions?

Yes, fish make sounds that predators can use:

Like us, fish produce sound both unintentionally and intentionally. Unintentional sounds from fish come all the time, resulting from hydrodynamic patterns during swimming and feeding. These sounds can provide information to other fishes. In fact, the fishing industry has recognized predatory fishes’ ability to take advantage of unintentional sounds to find prey and have designed fishing lures that emit low frequency sounds that mimic those produced by injured prey fish.

The opposite is also true:

Many fish take advantage of the noises other species make. We know that some sharks use sound to help them locate prey, while some smaller fish can detect the sounds larger predators make in their hunting. Furthermore, it is believed that a few fish species, including herrings and American shads, can detect the ultrasonic echolocation sound produced by hunting dolphins from a distance of up to 200m.

Interesting tidbit:

The oyster toadfish doesn’t need good looks to attract a mate – just a nice voice. To generate the foghorn sound, the toadfish contracts its sonic muscle against its swim bladder thousands of times a minute. At nearly three times the average wing beat of a hummingbird, toadfish have the fastest known muscle of any vertebrate.

Marine Seismic Part VII: Fish Are Big Talkers

This is a really thoughtful answer! Have you considered joining at the Bioacoustics SE beta?
https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=NmU1NDBjYzAxYjYyYTFkNjAxNjVhYTI4MjliM2MzYjliMjVmNzUwYWZlYmE3ZTNmMTU5ZmE2MWRlYzI0YmY1MYeOtoZRE6WnbORfi0NHJsJJl-XVap8qWmQEw-3uUKCT0

@etgriffiths - Thank you for the compliment, but I know very, very little about bioacoustics!

Piranha's bark as a warning to each other for frenzies.
Most fish have a lateral line, which detects water pressure, so it acts like an ear.
Predators use it to orient themselves towards prey, and to follow the vortices generated by fleeing prey.
Prey use sound to detect water displacement from incoming predators and for schooling, territorial defence and mating.
The lateral line system and the inner ear of fish are often grouped together as the octavolateralis system (OLS). The former hears bass and the latter hears high frequencies.

Seasonally, many adult fishes produce sound to synchronise gamete release in spawning aggregations or in courtship interactions for mate selection, with many of these calls forming sustained choruses lasting from weeks to months (Amorim et al., 2015).
Teleosts have the capacity for complex acoustic interactions (Mensinger, 2014).
When a threat or possibility of a threat exists, fishes produces sounds as spontaneous outbursts. They also use sound to control shoal grouping.
Fishes may also generate sounds in stressful situations including when they are attacked by predators or handled by fishermen.
About 20% of fish are thought to produce sound.
About 2/3rds of fish sense electricity, teleost species.
https://onlinelibrary.wiley.com/doi/10.1111/jfb.13867
https://en.wikipedia.org/wiki/Lateral_line
https://blog.nature.org/science/2018/04/18/what-does-the-fish-say/
Keywords: Bioacoustics, hydrophone

Schooling fish do produce sounds voluntarily and there is a cool library of recordings from various species available via Discovery of Sound in the Sea: https://dosits.org/galleries/audio-gallery/fishes/ Each species page includes information regarding the role of the sounds produced and their properties alongside recordings that you can listen to!
Regarding schooling fish specifically, an example includes herring that produces series of click-like sounds (here [enter link description here][1] is a paper describing these pulses).
Underwater noise can impact the way fish (and other animals) use sound in various ways: it can limit the acoustic space of individuals trying to communicate via sound, which means that finding mates can be harder (particularly for individual animals rather than schooling fish) and predators might not be able to hear vocalising animals until they are relatively close to them.
Predators can also listen to the ambient sound to find fish and sperm whales, killer whales and other marine mammals have even learned to associate the sounds from fishing gear and salmon farming acoustic deterrents with an easy source of food.
I hope this helps and I am happy to share more references to academic papers if this topic is of interest to you. :)
Reference:
Wilson Ben, Batty Robert S. and Dill Lawrence M. 2004. Pacific and Atlantic herring produce burst pulse sounds. Proc. R. Soc. Lond. B. 271S95–S97.
[1]: https://doi.org/10.1098/rsbl.2003.0107

There is also a website at https://fishsounds.net that has a searchable collection of recordings and information about the behaviours with which they were associated. (Disclaimer: I was involved in the making of the website. But it is good and helpful.)

It is a good idea to list the name of websites, and provide a proper citation for papers as links can change and die. Other then that, great answer!

Understood, thank you @etgriffiths! :) I added the reference to the paper I mentioned. @Sarah Vela are you aware of the Bioacoustics Stack Exchange proposal? (I hope it is okay to mention this here) https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=ZjMwMTczNDIwZTFiNmUxNzhjMTBiZDkwYzA2YmRkODNmNDg1ODk0NzBkMzM5NmQ3YWYzZmRlZDViODMzYTE1ZSAFiHme-ipoTC99ChnDokzyCUcQmD_38gXTKUbXa1780

You might find this paper by Torres (2017) interesting.
It reviews the different type and scales of sensory cues used by cetaceans to sense their environment and find their preys, including acoustics:
The author lists a few studies that found evidence of passive listening from dolphins, locating their preys using the fish calls, beyond the echolocation detection range.
Similar mechanisms have been hypothesized in baleen whales, who could use the sound produced by schooling anchovies, herrings and krill as cues to locate food patches, but it remains theoretical.
From there, it is highly likely that increased noise pollution could have masking effect with repercussion on the ability of predators to rely on sound for foraging.


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If I want to study protein translocation with RFP as a reporter should I fuse it to the C or N terminus?
I want to identify the whereabouts of the signal sequence (signal peptide) on a coding gene and I want to infer this by using RFP or GFP fusion and visualising the location of the fluorescence. Can somebody please explain how I might go about this (in layman terms) and how fusion to the C terminus vs the N terminus would alter the results.

What research have you done on your own to try and answer this?

I have been reading a textbook on protein localisation/translocation and looking through the literature but I think I have hit a mental block. I must be missing something.

Well, do you want to track the signal peptide or the main protein? Depending on your answer, that's where you put your [R|G]FP.

I want to track the normal localisation of a protein of interest. I just want to use the fluorescent tag (fused to the protein) so that it is expressed in the organelle its signal sequence specifies under normal conditions - i.e. I want to know its subcellular location.

In relation to above, is your signal peptide cleaved after the protein arrives at its destination or not? If it isn't, you'll have to think of another way to do your experiment.

It is more of a thought experiment than a real one. I am just simply trying to understand how fluorescent tags can be used to discover the localisation of a protein that is known to contain a signal sequence.

For the purposes of this answer, we'll assume that we're working with Aquaporin's Localized Protein, or ALP for short. It has an internal cell membrane localization sequence at its N terminus which gets cleaved by a signal peptidase upon correct localization.
What will happen if we put GFP onto the N-terminal end of ALP, separated by 6 peptide flexible linker sequence? Assuming the signal sequence (SS) still works (and this is not always the case!), after translation the GFP-SS-ALP fusion protein will be shuttled to the interior of the cell membrane, where it is inserted into the membrane and the SS cleaved. This now leaves free GFP, which is soon degraded. Looking at fixed cells under a microscope, you'll see diffuse cytoplasmic staining, meaning you can't really localize it to a specific region. Fail. This process is called "grad school".

Source: biotium.com
However, you keep going. You express C-terminal GFP-tagged ALP, again with a short linker, and end up with SS-ALP-GFP. The same process occurs: translation, transport to the inner cell membrane, anchoring, and cleavage of the SS. So what's different? The GFP is still attached to ALP, and viewing under the microscope will show mainly membrane staining.

Source: biotium.com

I got a good laugh at that grad school bit

Thank you for your response, this makes a lot more sense now. I appreciate it!


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Why doesn't repeated Mantaux testing for Mycobacterium tuberculosis cause an immune response?
I have never had TB but have had multiple TB tests for work. All negative. If you are introducing TB antigen with each test, why isn't a memory of that formed by the adaptive immune system?

It's an interesting question; I've had PPDs yearly for decades. May I ask what you found when you tried to answer this question with a search? Please edit your findings into you question and refine your question accordingly. Thanks!


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Why does the Scatchard plot have a negative gradient?
I am very confused as to why the scatchard plot has a negative gradient. If the x axis shows increasing B, specific binding to a receptor, and on the y axis the specific binding (B)/concentration of ligand ([A]), then why is the gradient negatively sloped. Textbooks will assume that the concentration of ligand remains constant, so it seems intuitive that as you go along the x axis and increase the specific binding to the receptor, the gradient would be positively sloped, as values on the y-axis would also be taking greater values for the specific binding (as it is just B/[A]).
The only way that I can make this work would be that as B increases, then [A] will also have to increase so that overall B/[A] will decrease (and thus provide the negative gradient as seen on the plot) However this is also unintuitive as:
i)We assume that [A] is constant anyway and this is what most textbooks do
ii)Even if [A] can change, we would expect it to get smaller, as [A] represents the concentration of ligand, so as the number of bound receptors (B) rises, then we would think there would be fewer free ligands as they are binding to the receptor.
Any help understanding where I have gone wrong in this reasoning would be greatly appreciated, as I have clearly fundamentally misunderstood either the biology that this is seeking to model, or the mathematical model used to generate the graph.

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I have now edited my question to include additional details.

I think you probably misunderstand which quantities exactly are represented on the Scatchard plot. Let's start from the beginning. Binding between a receptor, $\mathrm R$, and a ligand, $\mathrm L$, can be described as an equilibrium reaction
$$\ce{R + L <=> RL},$$
with the corresponding equilibrium constant
$$K_{\mathrm{eq}} = \frac{[\ce{RL}]}{\ce{[R][L]}}.$$
For the simplicity, we have assumed that only one ligand binds to the receptor. Usually, we use the inverse equilibrium constant, called disociation constant
$$K_{\mathrm d} = \frac{1}{K_{\mathrm{eq}}} = \frac{\ce{[R][L]}}{\ce{[RL]}}.$$
Both the ligand and the receptor can be either free or bound, but their total concentration remains constant. So we write
$$\ce{[L]_{total} = \underbrace{[L]_{free}}_{[L]} + \underbrace{[L]_{bound}}_{[RL]}},$$
$$\ce{[R]_{total} = \underbrace{[R]_{free}}_{[R]} + \underbrace{[R]_{bound}}_{[RL]}}.$$
Let's first look at the fraction of occupied receptors, namely $\ce{[R]_{bound}/[R]_{total}}$
$$\ce{\frac{[R]_{bound}}{[R]_{total}} = \frac{[RL]}{[R]_{free} + [RL]}} = \frac{\frac{\ce{[L][R]}}{K_{\mathrm d}}}{\ce{[R]_{free}} +\frac{\ce{[L][R]}}{K_{\mathrm d}}} =  \frac{\ce{[L]_{free}}}{K_{\mathrm d} + \ce{[L]_{free}}}.$$
This curve is probably familiar to you, and it is usually called saturation curve. It relates the concentration of free ligand with the fraction of occupied receptors.

We are now interested in the ratio between bound and free ligand,
$\ce{[L]_{bound}/[L]_{free}}$. Let's derive this quantity
$$\ce{ [L]_{bound}} = \ce{[RL]} = \frac{\ce{[R][L]}}{K_{\mathrm d}} =
\frac{\ce{[R]_{free}[L]_{free}}}{K_{\mathrm d}},
$$
$$
\ce{ \frac{[L]_{bound}}{[L]_{free}} }  = \frac{\ce{[R]_{free}}}{K_{\mathrm d}}=  \frac{\ce{[R]_{total}}-\ce{[R]_{bound}}}{K_{\mathrm d}} = \frac{\ce{[R]_{total}}}{K_{\mathrm d}} - \frac{\ce{[L]_{bound}}}{K_{\mathrm d}}.
$$
We have obtained the Scatchard equation, relating the concentration of bound ligand with the ratio of bound and free ligand
$$ \boxed{\ce{\color{red}{\frac{[L]_{bound}}{[L]_{free}} }} = \frac{\ce{[R]_{total}}}{K_{\mathrm d}} - \frac{\color{blue}{\ce{[L]_{bound}}}}{K_{\mathrm d}}}.$$

Thank you that makes much more sense


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How to measure tone of the cerebral cortex?
There is a lot of information about the "tone of the cerebral cortex". Some scientific papers describe that the tone could decrease or increase. However it's not clear how do they measure the tone of the cerebral cortex. Any ideas?
In case if they use EEG for that purpose, could you please specify what exact frequency ranges(alpha,beta,etc.) should have to alter to indicate that the tone is to be decreased or increased?
Thank you!

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Tonic is used to describe constant muscular contraction; this word has also come to refer to neural activity that leads to constant muscle contraction, and further to mean constant neural activity more generally, in contrast to "evoked" activity produced by some stimulus.
When they say "tone of cerebral cortex" they mean "tonic activity of cerebral cortex", or in other words, they refer to background firing activity at rest/not specifically evoked by some experimental stimulus.
Action potentials are most associated with gamma and high gamma bands, but you can also speak of tone in other bands. It's quite possible they simply mean EEG amplitude. It's not possible to say for sure, you would want to refer specifically to the methods sections of papers mentioning "tone"; they need not all measure the same thing.


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Does mass spectrometry data have units?
I am reading some journal papers about the proteome of certain brain structures. In these papers, they used mass spectrometry to identify the proteins that were present in the brain structure as well as their abundance. In one paper, they performed high-performance liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. In another paper, they performed nanoLC-high resolution mass spectrometry and used a tandem mass tags (TMT)-based labelling approach.
I am interested in finding out whether certain proteins are expressed in these brain structures. I have downloaded the supplementary tables from the papers that gives information about average level (as they had several samples of the brain structure) of each protein found in that brain structure. However, I am new to analysing mass spectrometry data and I unsure about what are the units of mass spectrometry data. I could not find anything regarding the units of the data in the papers or their supplementary tables.
In general, I was wondering for mass spectrometry data, what are the units used to describe the abundance of a protein in a sample? For example, in RNA-Seq data when quantifying the number of gene transcripts you have normalised read counts such as RPKM/TPM. These values can be averaged across samples such that you get the average RPKM/TPM value for a gene.

Can't you just weigh the sample first?

You really need to refer to either a concrete example in a paper that we can interpret, or state precisely what it is you want to do — compare proteins in one experiment, from different experiments, determine absolute concentrations or what? The “data” is obviously a spectrometries trace in which you can measure the height of a peak, or the area under it. This obviously has no units as such.

@David I am trying to interpret the data from this paper (https://www.sciencedirect.com/science/article/pii/S2211124721012572). In Supplementary Table 1 of this paper (where they show the average levels of each protein in the synaptosomes), I am trying to figure out what the unit of protein abundance is.

@ceno980 — I see you have accepted an answer, but I'll have a look at it tomorrow and add any additional comments I may have.

@David Thank you

As far as I can see from the paper they mention "the availability of lipid standards for quantification" so I imagine that quantification (in standard units of concentration) is  based on comparison of the area under the curves of standards and unknowns.

I think MS data, like other spectroscopy and chromatography data, is usually quantified by comparing peak areas (in arbitrary units) to those of a quantitative standard. So the Y axis is just the intensity of the signal, often which doesn't display its direct experiment readout units  (like current or voltage). In other words, you need the results of control or calibration experiments extraneous to the raw MS data.

I don't think the units are 'arbitrary' per se, but rather are the units that result from integrating the signal with respect to time. If the units of the variables are not arbitrary, which for physical units they are not, then the definite integral's units are not arbitrary either. For someone interested in the concentration of an analyt, it is true that the (usually linear) calibration converts this area measure into units of concentration (or similar) such as Molar. That aside, I think your answer cuts pretty cleanly to the point (+1).


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What did Masatoshi Nei 1972 mean by "However, evolution does not occur so as to assure this property at least at the nucleotide level."?
In Nei 1972 he describes what is now called Nei's standard genetic distance. This math.SE post provides an exerpt to the definition of Nei's standard genetic distance. In this paper he states

In the present measure of genetic distance, the triangle inequality, which is often assumed in numerical taxonomy (see, e.g., Levandowsky and Winter 1971), does not hold. However, evolution does not occur so as to assure this property at least at the nucleotide level.

The triangle inequality can be nice to have, but it is fine that functions do not always have it. But I find his justification for not having it to be perplexing.
What did Nei mean that "evolution does not occur so as to assure this property at least at the nucleotide level"? And in what sense did use this criterion to decide that the other properties of his function were assured by evolution at a nucleotide level?

I don't have access to the paper so it's hard to place the quote in context. A little more surrounding text might help. But at a guess he might mean that the distance between individuals or populations does not satisfy it, because it may not be clear which mutational path is taken. For more on different metrics and the triangle inequality, see introduction here: https://dyerlab.github.io/applied_population_genetics/genetic-distances.html

@MaximilianPress The mutational path lengths may well have been what Nei 1972 was referring to. A metric computed on the nucleotide content alone would not necessarily be comonotonic with such pathlengths.

@MaximilianPress I wish I could send you the link directly. I can access it through my academic institution. Perhaps you can do the same.

No longer in academia unfortunately! And my alternative sources don't seem to be working right now.

I think this is just a way of saying that evolution is not sufficiently deterministic to expect it to follow simple mathematical relationships, and isn't meant to be any more profound than that. I'd think that saying "the purpose of evolution isn't to make neat mathematical results" or "biology doesn't obediently follow the assumptions necessary" would have the same meaning. Or "the triangle inequality doesn't hold here, and that's okay because you shouldn't expect it to". But I don't have access to the original document, either.

@BryanKrause Thank you for your perspective. The concerns about (1) degree of determinism, (2) purpose of evolution, and (3) necessary assumptions are not synonymous. Yet I can see any of them matching Nei's phrasing to an extent. I am sorry to hear that you are also unable to access the original document.

@DifferentialPleiometry Yes, I don't mean to say they are synonymous, just that I think they are all consistent with the intended meaning. I take it as a bit of a droll statement, in the spirit of https://en.wikipedia.org/wiki/All_models_are_wrong, and if so I am very sympathetic with the message it communicates.

@BryanKrause Thank you for reminding me that I want to read Science and Statistics by George Box.

@BryanKrause Having fresh eyes on the paper around the "All models are wrong" quote, I appreciate Box's point of view. I actually didn't know that the paper has a large focus on Fisher's career. I largely agree with Box that when it comes to Statistics, we should be wary of "mathematistry" rather than Math per se.