text:
Resource recommendation: a good book explaining and evaluating the evidence for evolution?
I take a great interest in the intersection between science and religion and evolution is therefore something I often read about. Many of the critics of evolution like to poke "scientific" holes in evolution, perhaps the most common one being that there is simply "not enough" evidence. As someone trained in physics but not biology, I would like a book that is accessible and which summarises the evidence we have accumulated for the evolution of life on Earth. Ideally, I would like a book that remains strictly scientific, without any particular atheistic or religious agenda, and which evaluates each line of evidence rather than simply describing it.
Does anyone have a book recommendation?

I don't think you can do much better than the original: Darwin's "Origin of Species", or failing that, any high school or college biology text.  The "problem" from your point of view is that evolution has for a long time been accepted fact. Modern books would describe evolution rather than argue about it, since at this point trying to convince those who don't accept it is rather like trying to teach a pig to sing: it just wastes your time and annoys the pig :-)

My own favourite, first published in 1958 but with a Canto edition in 1996, is The Theory of Evolution by John Maynard Smith. You can get a 'flavour' of the great man's work here. IMO his book is still one of the very best.

@jamesqf You can obviously do a lot better. Darwin's work was seminal but even ignoring the dated language (his is clearer than most from the period but, nevertheless, language evolves), Darwin's understanding of evolution was simply extremely limited. It's hard to overstate just how much we've learned since then, and, in particular, a modern introduction to evolution is incomplete without discussing evidence from genetics.

Have you tried Berkeley's understanding evolution it is a great supplement for anyone just getting started on the subject. https://evolution.berkeley.edu/evolibrary/home.php

@Konrad Rudolph: But modern texts will (AFAIK, anyway) be written from the point of view that evolution is accepted fact, rather than citing evidence in order to persuade the reader that the theory is correct.

For the love of your own sanity don't read "On the Origin of Species" for a modern reading it is incredibly dry and covers many thing you already know, like that heredity exists, and uses examples you will have no experience with like pigeon breeding, which was very common at the time and nearly non-existent now. Three bloody chapters on pigeon breeding!

I like "The Darwinian Revolution" by Michael Ruse.
It's far more of a history book than a science book. It won't get into the nitty gritty of evidence from molecular biology and modern genetic analyses. What it does do is to chart out how exactly Darwin (and Wallace) came to understand the key features of biological evolution and how the scientific community reacted, both in converting skeptics overnight and hardening a few opponents.
Reading the book, you'll learn how Darwin was a geologist at heart and by training more so than a biologist, and how evolution fits as much into the history of geology as it does in biology. You'll learn how religious thinking was an element to all sorts of competing theories about natural history, with different thinkers taking different approaches and getting stuck in different holes.
You'll also see how Origin was both revolutionary and incremental: really all of the basic concepts were already out there at the time Darwin published, they just hadn't quite been synthesized into a whole.
I think it's a good book to set the table. When considering all the competing theories and evidence, Darwinian evolution comes naturally out of the bodies of evidence collected by others. It explains numerous puzzles that no one else could quite figure out. It emphasizes the places where adherence to faith put up barriers for some scholars in understanding what was otherwise right in front of them. I think it puts more modern opposition to evolution, like "intelligent design", into its own historical context, and after reading it's hard to argue against Dobzhansky: "nothing in biology makes sense except in the light of evolution". It's not that there are particular pieces of evidence for or against evolution, it's that all of biology is the evidence for evolution, and modern biology takes it so much for granted as truth that we hardly notice.
There are reasonable religious arguments to make about the origins of life and the universe itself, but the descent of species from common ancestors and all the phenotypic and molecular connections that link us to all other organisms of life on Earth are unimpeachable.

Ruse wrote a review/afterword of his own book decades after publication, available in PNAS:
Ruse, Michael. "The Darwinian revolution: Rethinking its meaning and significance." Proceedings of the National Academy of Sciences 106.Supplement 1 (2009): 10040-10047.
and another a few years earlier:
Ruse, M. (2005). The Darwinian Revolution, as seen in 1979 and as seen Twenty-Five Years Later in 2004. Journal of the History of Biology, 38(1), 3-17.
if you want to start with something shorter than the original book:
Ruse, M. (1979). The Darwinian Revolution: Science Red in Tooth and Claw.
My copy is of the 1999 second edition, and it looks like there is a newer 2019 version as well.

I can name a few
Your inner fish by Neil Shubin is probably the most inviting for a layman. Just be aware the first chapter is about Shubin personal story and the discovery of Tiktaalik. It is greater starter not because it covers every of lines of evidence but because is covers six or seven specific human centered bits of evidence in great detail. it makes a good starting book if that sounds like your level.
If you want to go into detail, the blind watchmaker by Dawkins is still some of the best in depth explanations of the evidence out there. It also goes into great detail about the part that gives people the most trouble how evolution gives rise to complexity. It also deals with the problems with the lay arguments against evolution. this is the best if you really want to sink your teeth into it and for getting an evaluation of evidence.
If you are just interested in animal evolution Endless Forms Most Beautiful: The New Science of Evo Devo and the Making of the Animal Kingdom by Carrol is you best bet. it is focused on how mutation can change animals by altering regulatory or developmental genes, which is the bulk of evolution in animals. It also delves in many of the modern experiments on such genes which lets you see modern examples of evidence. This is another good one for sinking your teeth into.
As someone trained in physics you may even find a undergraduate population genetics book worth looking into since it will be a more mathematical framework. Although I can't name one off the top of my head.
Evolution: The Triumph of an Idea by Zimmer, is a good middle ground, if you just want a primer on evolution, this is an excellent one. It talks about the modern evolutionary synthesis, the history of evolution and the ideas it is founded on. It is also one of the most accessible books on the subject I have ever seen. If other books are giving you trouble read this first.
DON'T read On the origin of species, is is a dry, dull, long winded book for modern readers, there are three chapters on pigeon breeding for sanity's sake. Darwin was writing an exhaustive book for a different time and many of the chapter are devoted to demonstrating things most modern people already know without question, like that heredity exists.
this question may also be helpful for you. What are the major differences between good study habits for biology vs mathematics?
Also the stated clearly site has some excellent videos on evolution, some of the best out there. I recommend them to my students. It is amazing how much easier a simple animation can make a concept.

I think libraries have been filled on the topic of evolution - it is an immensely broad field of study and can be looked at from a geological time scale (millions of years) to a much smaller scale observable in a scientist's career, since evolution driven by geographical separation can happen over a few generations. Nonetheless I can add my 2 cents worth.
I love the book 'Dinosaurs - A concise natural history' from Fastovsky & Weishampel. Chapter three of this book on dinosaurs features 5 sections that feature many elements that you are after. The sections in this chapter are the following:

Phylogeny
Evolution
Phylogenetic systematics
Cladograms
Logic of science and hypothesis testing

As you can see the chapter builds up to the point where the theory of evolution is explained. It's still a theory, yet the evidence is so overwhelming it's principles are taken as a fact, yet the exact mechanisms behind it and the construction of the 'tree of life' is anything but a fact, but rather based on science, logics and hypothesis testing. The chapter has been really rewarding for me to read and I bet it can help you a lot too. Along the way you'll learn a lot of cool things about dinosaurs too (birds are technically dinosaurs, but flying dinosaurs were not the direct predecessors of birds and so on).
Reference
- Fastovsky & Weishampel. Dinosaurs - a concise natural history. Cambridge University Press. 2010

Recommendation:
A Short History of Humanity by Johannes Krause and Thomas Trappe
Not pure evolution however Johannes Krause is the Director of the Max
Planck Institute of Evolutionary Anthropology and this is a recent book (2021) in a very rapidly changing field of Archaeogenetics.  Covers the extinct species of Neanderthal and modern DNA showing traces of Neanderthal interbreeding with modern humans.

I've read a few on the topic, and what I would recommend would depend on your focus.
For a generally fun, smart, and accessible book on evolution, my favorite is Trilobite: Eyewitness to Evolution, by Richard Fortey.  It's an odd approach to talking about general evolution, but trilobites were around for so long, and they left such perfect fossils, that they teach us a lot about the whole process.  Did you know that when geologists don't know how old a layer of rock is, they often look for which species of trilobite are stuck in it?  Or that they had eyes made of crystal, and were so numerous that the oceans were black with them.
This book broke down evolution for me when I was looking for exactly the clarity that you describe in your question, and allowed me to converse with people in a much more intelligent way.
You might also consider as secondary reading Desmond Morris' The Naked Ape, and others by him. It's more about evolutionary psychology, and is interesting is showing, as he put it, that "Man is not a fallen angel, but a risen ape."  It's really interesting to see how many of our morals, thoughts, actions, cultures, and even gestures come built in from our ape ancestors.  But, psychology is also always a more slippery field, so you may not like some of the assumptions.

If you are looking for something that gives a good overview of all evolutionary processes, I recommend Evolution Unraveled from Randall Harris. The book goes into the best explanation on how evolution could work as observed by science.
For example, as @CaptainSkyfish mentioned with the Trilobites, the book expands on some great questions like how did something with such a complex eye evolve so early?
A great book if you are into coming to heads with what science actually describes around evolution.

Being a physicist myself I would recommend the Gillespie's little book as a crash course on the basic genetic concepts. For the mathy stuff it is worthwhile googling "population genetics" - there are a few excellent sets of lecture notes walking around - such as several version of the Mathematical population genetics by Ewens. Theses might seem not exactly what the question asks about, but to a physicist this would give a rather good idea why genetic models being a lot more serious than most creationists with no math background can imagine.


text:
GC content of a protein-coding region
I have computer science background and I am trying to understand the equation below.
The average value of the G + C content of a protein-coding region is
given by :
(G+C)=  $\sum_{\alpha} (I_\alpha *f _\alpha$ )/3
$I_\alpha$ = Maximum number of nucleotides C and G that appear in one of the
synonomous codons for given amino acid
$f_\alpha$ = Frequency of amino acid α.
Where does the 3 in the denominator come from ?

Each codon codes for one amino acid and every codon contains 3 nucleotides.

source: Stack Exchange

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

sort: votes


text:
Why does the structure for cellular retinol binding protein show interactions with cadmium ions?
A structure of cellular retinol binding protein (1CRB) contains two cadmium ions as ligands. Is Cd2+ a ligand of CRBP and, if so, is that interaction necessary for protein function or is the protein a transporter to remove cadmium? My other thought is that the interaction only appears as a result of the methods the scientists used to determine the structure of the protein.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, your question about whether this is a cadmium transporter can be answered by looking at the entry for the structure you indicated! I also suspect that your last guess can be confirmed by looking at the linked paper. ——— Please also take the tour and then go through the help pages starting with How to Ask questions effectively on this site and edit your question accordingly. Thanks!

As far as I am aware, there is no known requirement for Cd in mammalian systems, but it is extremely toxic (Waalkes & Goering).
It would seem that cadmium is required to get crystals of RBP, and its presence is an artifact of the crystallization process (ref):

Pig holoRBP crystals were obtained at 277 K by the sitting-drop vapor- diffusion method, at a final protein concentration of approximately 8 mg ml ~ and in the presence of 8%(v/v) 2-methyl-2,4- pentanediol, 3mM cadmium acetate, 0.1 M Tris-acetate, pH = 6.8

The only mammalian Cd-binding protein I am aware of is metallothione (ref), which was originally isolated as a Cd-binding protein (ref), and allows safe transport of a highly toxic metal.
Carbonic anhydrase from the marine diatom Thalassiosira weissflogi can use Cd  as active-site metal (typically when Zn is low) and this may explain "the nutrient-like behaviour of cadmium in the ocean" [ref and ref]

Also from the paper you quote: "Cadmium ions represent an absolute requirement for the growth of orthorhombic crystals of... RBP"

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


text:
Is it possible to determine what tissue a DNA sample came from based solely on its sequence?
All cells have the same genome and differ only by the expression pattern. Is it possible to determine the tissue origin of a cell based on its DNA sequence using short tandem repeat (STR) analysis or copy number variation (CNV) analysis?

You say yourself that all cells have the same sequence, so how could you tell them apart based solely on sequence?

I don't know; that's why I am asking. Wikipedia page for STR analysis says that STR analysis can be used to track cancer cell progression, and I found a paper that claims CNV can occur in different tissues. I was wondering whether it would be possible to determine the origin of the cell using these or other similar molecular marker techniques.
http://www.pnas.org/content/109/44/18018.full.pdf

Let me rephrase my question as a statement: if all cells have the same sequence, you cannot differentiate them based on sequence. Cancer cells do not have the same sequence and thus could show STR expansion or CNV. I suppose you could also see mosaicism if such a mutation occurred early in development but I don't know the extent to which this occurs nor how strongly it would correlate with adult tissue types (other than in a broad classification such ecto-, meso-, endoderm). Too which paper are you referring?

Oh I see the paper in your edited comment. Yes they seem to be referring to mosaicism and the variations they discovered appear to be between tissues that developed from the same progenitor. Interesting stuff. If you were trying to determine the tissue from which a cell originates, you may consider profiling gene expression, such as by RNA-Seq

It's like looking at a binary code (101010101011110001110101) and asking "what would this do?" Actually binary is still far better than deciphering a genetic code...

The answer is in the question but I suppose you wanted to ensure you were not missing some info.
Answer
The DNA sequence is the same in all cells of a multicellular organism. Only the expression pattern varies among tissues. It is therefore impossible to tell from the DNA sequence alone what tissue a cell come from.
It would be feasible by looking at the transcriptome or the proteome or eventually by looking at epigenetic modifications.
Potential exception
Of course, as you talk about CNV, if you consider that the number of chromosome is part of the info present in a DNA sequence, then haploid cells (spermatozoids and ovules) are an exception and you could tell them apart. Similarly anucleated cells would be an exception as they contain no nuclear DNA.
Further potential exceptions are explained by @tsttst in his comment.

This answer may be wrong as transcription can affect mutagenesis as shown recently by Sankar et al., Nature 2016, https://www.nature.com/articles/nature18316; while their great study was on bacteria, it could be thinkable that also in animals there is a coupling between transcription and mutagenesis (--> thus tissue-specific transcription profiles may lead to tissue-specific somatic mutation patterns --> which would allow identification of tissue by DNA); P.S.:  A further exception would be https://en.wikipedia.org/wiki/V(D)J_recombination

There was a paper in Science, August of this year (apologies to the author for not remembering their name). They worked up a protocol for single cell bisulfite sequencing and through the use of known marker genes managed to identify multiple neuronal sub-types based on non-CpG methylation across gene bodies.
Non-CpG methylation across gene bodies is seen often to be inversely correlated to gene expression, through this you can infer an expression profile of known marker genes giving you have a solid poke at a cell type with only a DNA sequence.
(Edit: Assuming this holds true in tissues outside of the cortex)

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Why don't restriction endonucleases digest transformed plasmids?
In the textbook that I'm using, it explains that bacteria does not digest its own chromosomal DNA because the sites that would be cut by its own endonuclease are methylated. Is there a similar mechanism involved for protecting its own plasmids? If so, how are plasmids cut while serving as vectors?

You're asking about engineered plasmids, as opposed to natural ones?

Sure, but I guess it can apply to both; for example, if an engineered plasmid is inserted into E. Coli, what prevents E. Coli's own endonuclease from digesting the new plasmid?

Welcome to SE Biology. Your question seems to imply that you think that restriction enzymes are involved in recombination, which is not so. Perhaps I misunderstand, but I do not see what relevance recombination could have. You will need to clarify if your question is not to be closed as unclear.

I'm sorry; I have no idea why I said recombination there at the end. I think I was thinking of ligation during DNA cloning and got confused because of "recombinant DNA."

Laboratory strains used for the purposes of cloning have been genetically engineered to address this issue, typically by deleting genes of the various restriction-modification systems. There are four broad classes of restriction modification systems, which I will discuss individually. Unless individually referenced, most information below is based on the following supplier technical notes:
Promega: What are the effects of the bacterial DNA restriction-modification systems on cloning?
New England Biolabs: Restriction of Foreign DNA by E. coli K-12

Type I
In Escherichia coli, this system consists of the hsdR, hsdM and hsdS genes and is capable of both restricting (digesting) unmethylated DNA and methylating hemimethylated DNA. Knockout of hsdR and/or hsdM prevents restriction and methylation, respectively. This allows engineering of strains for specific purposes. For example, a common E. coli strain used for cloning, DH5α, has the genotype hsdR17 (rK–, mK+) which abrogates restriction activity but maintains methylation activity. This means that exogenous DNA will not be restricted, but will be methylated and therefore able to be subsequently transformed to r+ strains without worry of degradation, if the need may arise.

Type II
This is the class of restriction enzyme commonly used in the lab to cut DNA because they generally recognize short, palindromic sequences and cut within or near the recognition site. The E. coli background strains K and B, from which most lab strains are derived, do not contain Type II enzymes. The Type II enzyme EcoRI, for example, was isolated from the E. coli RY13 strain (Yoshimori, 1971; PhD thesis).

Type III
Similarly to Type II, the K and B strains do not possess this restriction-modification system, which was first characterized in E. coli 15T-.

Type IV
This system differs from the others in that it cleaves methylated and hemimethylated DNA, though it does not recognize methylation by Type I or Type II modification systems, nor Dam or Dcm methylation. In E. coli, this system consists of the mcrA, mcrBC and mrr genes and is most problematic when attempting transformation of DNA from organisms with ubiquitous cytosine or adenine methylation (eg plants and mammals). For example, the lab strain T7 Express, which is derived from the common strain BL21, has the genotype Δ(mcrC-mrr)114::IS10 which deletes mcrBC, hsdRMS and mrr.

Note on Dam and Dcm Methylases
These bacterial enzymes methylate adenine and cytosine residues, respectively, but are not directly involved in the restriction-modification systems discussed above. However, some Type II enzymes used for cloning are sensitive to this methylation and so lab strains are available with these enzymes deleted.

Thank you for coming back and making the detailed edit; I appreciate the explanation!

@JohnSmith You're welcome. If this answered your question, you can click the checkmark next to the answer to mark it as accepted (as well as upvote).

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Explanation of ECG in MI using an electrostatic model
I found a paper presenting an electrostatic model to explain the ECG recorded in various leads. This model essentially calls for considering the depolarization wavefront to be the major contributing factor to the potential difference measured at the leads, especially the limb leads, by means of an aggregation of momentary dipoles with dipole moments organised according to the direction of propagation. It is also used in this book here, under the ECG section under Measurements of cardiac function.
The paper does not explain the observed ECG deformities in case of MI in detail. ST elevation, is a common finding in most MI cases. How do we explain this in light of the aforementioned model?
My thoughts
In the normal case, ST segment is isoelectric, as there is no depolarisation/repolarisation wavefront propagating. How is this isoelectric nature compromised in MI? Assuming most infarcts include muscle death or damage due to focal insufficiency of coronary circulation, even if a region of heart was dead, during the ST segment, the graph should show an isoelectric line (no deflection) as the living tissue will either be depolarised or polarised, (but not switching states) and the dead tissue will have either a completely obliterated membrane polarity or an altered polarity throughout the cardiac cycle. In any case, no part of the heart will be switching its polarity then. Why is then, some resultant dipole (which indicates a propagating wavefront of altering polarities)obsereved during the ST segment?

alternative model
   To explain the elevation, this book (pg 522) provides a two cell model, and explains that the anoxic damage somehow
  causes the basal depolarised state of the cell to have a lower
  membrane potential difference, which causes all the segments of the
  ECG except the ST segment to be lowered, making the ST segment appear
  raised. I don't understand three things regarding this explanation.
  How will anoxic damage cause such a specific alteration in the polarity and the subsequent action potential? How can this two cell
  model be extrapolated to the whole heart with a focal infarct? How
  does this explanation be reconciled with the model presented at the
  head of the question?

Let me know if the question appears too broad and needs to be split, or if my assumptions are wrong in any way.
MI-Myocardial Infarction
PS:-  I seem to have lost the touch with the formatting on this site, and hence don't know which tags to use. Will take some time to get back :)

formatting and tag edits are fine! :) +1

The concentration of K+ inside the cell is 30 time more than outside. Hypoxia causes loss of this intracellular Kalium and consequent/premature repolarization when measuring the potential of action.
As the all the ECG theory is Vector based, any abnormality in the electric pathways and myocytes will result in changes of ECG.
This picture depicts the ST changes due to different extension of injury. In addition, the explanation on this site will probably resolve the issue of understanding.

ADD
The article explains the ECG phenomena as a result of electric propagation of dipoles. If the dipoles propagate towards the lead we get upward wave etc.
As the electrostatic model takes the whole heart as one dipole (as a sum of multiple dipoles) the minor infarcts can be missed on ECG. It is an actual fact, this is why other tests are important (for example, the troponin test).
The confusion point in your understanding is a "dead" tissue. In a case of infarct there is an hypoxic damage which leads to elevated permeability of the cell membrane with resulting K leak (as I explained above there are 30 times more Kalium inside the cell than outside). This means that "dead" area will have abnormal depolarization/repolarization pattern just because there are multiple "non grouped" dipoles in that area (look at the picts). There are diastolic and systolic theories of ST elevation, but none of them has won the battle yet.
With time the scarring tissue replaces the infarcted myocardium and in that case the ST-segment will not be affected and will look nearly normal. This is the case you meant as "dead" tissue - scar tissue does not leak any electrolytes and consequently the ST segment is not affected in a chronic stage.

Thanks for the answer. But I want to understand the genesis of the resting and the repolarised-state dipole which causes the said changes in the graph, considering the electrostatic model presented.

@SatwikPasani I'll read the article and add the explanation if it could be reliable.


text:
Electron transport in granal stacks
See paper for distribution of PS-I and PS-II within grana
As explained in the above paper, the PS-I complex is primarily located within non-appressed thylakoid region and stroma lamella, while PS-II in the appressed regions. Now since non-cyclic electron transfer (non-cyclic photophosphorylation) requires both the photosystems, wouldn't their distribution within grana far from one another hamper their ability to carry out non-cyclic electron transport. Although there are mobile untis to account for the electron transport between marginal PS-I and the PS-II immediately below, but the electron transport to the PS-II units deep in the granal core would still be unaccounted for.

You may find useful this article.

I commented instead of answer because I hadn't understood your question precisely! Maybe the problem is mine, but can you refine this phrase?: "Although there are mobile carriers, but what about the PS-II units far in the centre of large stacks of thylakoids?"

"Although there are mobile untis to account for the electron transport between marginal PS-I and the PS-II immediately below, but the electron transport to the PS-II units deep in the granal core would still be unaccounted for." Edited in answer too.

First a clarification: the mobile units are no so "mobile". Due to (1) the high protein:lipid ratio of the thylakoid membrane and (2) the packing of protein complexes, the rapid diffusion of components along the membrane is hindered.
It has been proposed the existence of small local PQ diffusion microdomains, based upon the percolation theory:

From the percolation theory, above a critical density, immobile or slowly moving transmembrane proteins are, indeed, expected to form flexible 2D networks of closed compartments preventing long range movement of small molecules. (Kirchhoff, H et al. (2000) Biochim. Biophys. Acta 1459, 148–168)

For this reason the PQ are confined, on a short time scale, within these domains, preventing their "dispersion".
In addition of the low diffusion of mobile carriers, the geometry of the granal stacks mantains the contact area between the PSII of the appressed grana and the PSI in the margin annulus domains relatively large, enabling effective linear electron transport in microdomains.
Figure 2b of the paper cited below shows the geometrical organization of the stacked grana and its description says:

The circular border between the appressed domain and the margin annulus (ring) allows a large contact area between the PSII and the PSI domains and efficient linear electron transport from PSII via plastoquinone (PQ), plastocyanin and cytochrome b6f to PSI at a short distance of ~30–60 nm in local domain.

Further informations can be found in Albertsson, P-Å. (2001) Trends Plant Sci. 6, 349–354.


text:
Regulation of Cra protein level in E coli
Catabolite Activator/Repressor, Cra protein (formerly known as Fructure Repressor FruR) plays a significant role in central carbon metabolism of E coli. Its activity is inhibited by fructose-1,6-bisphosphate (FBP); Cra up-regulate gluconeogeneis pathways and down-regulate glycolysis and carbon-uptake pathways. I found enough literature on how Cra plays a regulatory role in metabolism.
However, I am unable to find out explanation of one experimental observation: with increase in glucose uptake rate the transcript level of cra decreases. What is the mechanism for this. Further, are Cra proteins degraded as the glucose uptake rate increase, if so what is the regulatory mechanism?


text:
Why is ammonia converted to urea rather than secreted in the urine?
Since ammonia is highly soluble in water, my senses keep telling me something like, "Just a little bit of water is enough to flush it, given that a lot of it would dissolve per liter of solvent". But who knew, it's exactly the opposite.
I keep seeing articles saying that since ammonia is very soluble in water and it takes lots of water to eliminate this waste in vertebrates. Uric acid, on the other hand, is very easy to eliminate, since it is not easily dissolved in water.
Why does the water solubility of ammonia would make it much harder to eliminate in birds, reptiles or the human body, compared to urea/uric acid?
Humans also eliminate ammonia, but, apparentely, its high solubility in water, and toxicity, would make it so that is actually more favourable to just convert it to urea inside the liver. On the other hand, its quite easy for bony fish to eliminate ammonia as a nitrogenous waste, since there's plenty of water around to help them flush it.
Once again, i don't get it, if ammonia is highly soluble in water, why does it take an ocean for some vertebrates to eliminate?
Some links: https://en.wikipedia.org/wiki/Metabolic_waste
https://courses.lumenlearning.com/boundless-biology/chapter/nitrogenous-wastes/

Welcome to SE Biology. I would advise you to prepare and edit future questions beforehand to produce a more compact and structured question. This will help you examine your logic and assumptions, and will produce something that is more readable and hence likely elicit an answer. In this case you provide no basis for the assumption in your title that ammonia is more difficult (please avoid non-scientific terms like “tougher”) to eliminate than urea. Where did you read that? Why don’t fish have problems? If you didn’t read it anywhere isn’t it just possible that the problem lies elsewhere?

I am trying to help you. Some people charge for this sort of educational advice. I am giving it to you for free. Your link says nothing about ammonia being difficult to eliminate — the erroneous assumption of your question. It does contain the statement "Nitrogenous wastes in the body tend to form toxic ammonia, which must be excreted." If you had read that, then the only question I can imagine you could have is one about why transferring ammonia to the bladder would not be enough to prevent its toxic effects on the body. But that is not what you asked.

I have edited my answer. It would appear that one has to consider the actual mechanism of secretion of ammonia as well as whether there would be any problem with an otherwise toxic concentration of ammonia in the bladder. The problem would seem to be talking about "flushing" and "filtering" without thinking about the mechanism, and not considering the role of ammonia in acid/base balance. It would be good if you removed the red herrings of uric acid and volume of water from your question and title as it might encourage a physiologist to interest himself in your question.

What exactly are you suggesting? Because the question i have in my mind is exactly the one that is written.

I am suggesting that you accept 1. that the toxicity of ammonia means that land animals have to convert it to a non-toxic compound for excretion, 2. That animals that can afford to carry and loose water convert it to urea which is soluble in water, whereas birds which cannot convert it to the insoluble compound uric acid, which is excreted with their faeces. The valid questions then become 1. Would secreting ammonia to the urine in the bladder solve the problem of toxicity? If so 2 Why does this not happen? A title might be "Why is ammonia converted to urea rather than secreted in the urine?"

Further to my reply. I feel that I have answered 2 in relation to the competition with the blood buffering role of ammonia produced in the tubule, although a clearer title of the sort I suggest might elicit a more detailed answer. I assume you do want to understand the system, rather than pretend it doesn't make sense and argue about what people may or may not have written (but not explained).

I'm starting to doubt my ability to comunicate in this language because both 1 and 2 were never really in question for me. I knew that more evolved vertebrates, as they started to populate more dry habitats, had to come up with a solution for the toxicity of ammonia, and that would be the urea and uric acid cycles. What i don't know is if the solubility of ammonia worked as an evolutionary pressure to this shift - in response to dry habitat colonization - or was it simply a matter of toxicity.

@DiegoMenezesPamplona Toxicity. What the sources you are reading (and David's answer) are trying to convey is that a lot of water is needed for ammonia excretion despite the high solubility, not because of it.

In other words, does the fact that ammonia is highly soluble make it more costly for the internal organs to flush it, or was it simply a matter of higher toxicity, when concentrated in the plasma, pushing evolution for a less toxic waste for the same concentration budget?

@BryanKrause But it’s more than that apparently. As far as I can see it’s “would be needed if there were a way of removing blood ammonia by secretion” although I suspect most general authors are not aware of the problem that tubule’s own ammonia generation system poses. The poster has changed his title but not his question which is still obsessed with the irrelevant concern with solubility. Surely there are some molecular physiologists on the list. I remember being involved in teaching acid-base balance to medical students — I was on firm ground with bicarbonate buffering, but not the kidney.

@BryanKrause So you're saying that high solubility doesn't have anything to do with the fact the ammonia needs a lot of water to dilute and flush?  So, for the same degree of water availability, ammonia would be more concentrated in the plasma than urea, for example?

@DiegoMenezesPamplona Yes I am saying the high solubility has nothing to do with needing a lot of water to flush it. No, this does not mean ammonia would be more concentrated in the plasma. It means if you didn't have enough water to dilute the ammonia enough to remain below toxic levels, you would die of ammonia poisoning.

@David Not sure I'm exactly following your point about secretion, but I think if a textbook is mentioning it they probably intend a contrast with uric acid as a nitrogenous wastes strategy rather than saying anything particular about ammonia.

OK. I don't have a queston anymore. I think it's best if @David posts a new one. If you prefer you can write it on the comments and i can edit mine.

What I propose to do is to do a little reading and then edit both question and answer. I live in a part of the world where the sun rarely shines, so that when it does one has to go out and take advantage of it, because it won't last. This week the sun is shining, so it may be next week before I do this. However the point is not to do things in a hurry but do them properly. That way we may increase our understanding of the topic.

The comment of the poster to my request for clarification cites “The formation of ammonia itself requires… large quantities of water to dilute it out of a biological system” I conclude that he assumes that the problem with animals eliminating ammonia as such is one of solubility in water. This is not the case. The solubility of ammonia is such that saturated solutions exceed a concentration of 10 mol/L.
The problem is that ammonia is extremely toxic at low concentrations, so that decreasing its concentration to non-toxic levels would require a large volume of water. The writer of the cited text is, in my reading of it, presenting this as a hypothetical solution, and then rejecting it because the demands of supplying this volume of water would be prohibitive to the organism.
This is not my field, so the best information I have about the toxicity of ammonia comes from an anonymous web page on the University College London web site. It states:

Ammonia is highly toxic. Normally blood ammonium concentration is < 50 µmol /L, and an increase to only 100 µmol /L can lead to disturbance of consciousness. A blood ammonium concentration of 200 µmol /L is associated with coma and convulsions.

The page goes on to state (in red):

200 µmol /L is far too low a concentration of ammonium to affect plasma pH or the normal transport of sodium and potassium ions across nerve cell membranes.

I know almost no physiology, but my inference of the significance of this is that it would be difficult for the kidney to respond to this concentration of ammonia by filtering it out. Hence it needs to be converted to a non-toxic (or much less toxic) compound — urea, in the case of vertebrates.
Further reading suggests that the problem is that there is indeed a renal system involving the proximal tubule for secreting ammonia into the urine by a mechanism coupled to the cation transport and responsive to pH. In fact this system exists to control blood pH by generating ammonia to neutralize blood acid. This would explain the second part of the quotation above — the organism’s mechanism to control blood acid is inconsistent with a secretion mechanism for blood ammonia.
It would be good if a molecular physiologist could comment on or edit this section.

But why do you think it has nothing to do with soulubilty? I have a Portuguese school textbook that, as this website,  states crystal clear that as solubility in water increases, so does the need for water in the process of elimination. It would be great if i could find a peer reviwed article abou this and not just a school textbook. I think your explanation is good enough, but why are you so sure?

You can see this idea literally everywhere, but it's never thoroughly explained. Check this out http://www.bio.miami.edu/dana/dox/nitrogenouswaste.html. Here the relation between solubility and elimination is stated separately from the toxicity, which makes me think that something is missing.

My answer hardly gives the impression that I am “so sure” when I apologise for using an anonymous web page as a source of information and ask for help (answers can be edited) on physiological aspects of the question. As I have a chemical background I knew that ammonia was soluble in water, which is why I felt that solubility was not the problem. As for the Miami U page, that does not impress me. Lists of advantages (like debating arguments) generally contain weak or dubious members to make up the numbers. I imagine a single factor prompted the evolution of ammonia modification. I may be wrong.

You said, quote, "I conclude that he assumes that the problem with animals eliminating ammonia as such is one of solubility in water. This is not the case.". I felt here you were sure about this. The miami page was just to illustrate that this is a common idea which shows up now and then when reading about nitrogenous wastes.

Please don’t take offence. Your written English doesn’t suggest that you are a non-native speaker, but I just wonder whether you are confusing “dilution” with “dissolution” / “dissolving”. Ammonia is so soluble in water that you can dissolve 0.88 g per ml.  None of the texts mention solubility. The Miami U page talks about “more water to dilute”. You can only dilute a solution where the solute is already dissolved. This will decrease its concentration. Why would you do that?

The miami page mentions solubility on the uric acid section. I'm not native and definitely not fluent, so feel free to correct anything.

@DiegoMenezesPamplona It does, but it doesn't mention solubility in the others because it's not a limiting factor for those.

For reference, I am linking this answer of yours: https://biology.stackexchange.com/questions/82379/why-is-urea-not-converted-to-ammonia-in-the-body/82400#82400


text:
Why and how do Stomatal Guard cells turn flaccid at night time and cloudy days, and turgid during the days?
If I'm correct, the guard cells turn turgid during the day and flaccid at nights. What is the reason behind the same and how is it done? (im a noob highschool student, so basic explanations are welcome)

What is the result of each type of guard cell status (turgid or flaccid) on the stomatal opening? What are the functions of the stomatal opening?

(Umm, I forgot to add the 'how' part to my question...) Coming to that; i guess
flaccid = close; - doesn't allow transpiration
turgid = open; - does allow transpiration

There is a good free recent review by Brodribb et al., 2020 which explains much of this biology.
The most fundamental mechanism, dating back to the evolution of stomata before they were even used to regulate photosynthesis, seems to be potassium regulation.  As a rule, water follows dissolved material (osmosis): if you enclose a bag of water and salt underwater in a membrane permeable to water but not salt, the particles of salt will push out on the bag with the same amount of pressure as if they were particles of gas floating in the bag and there were no water present inside or out.  Cells usually hoard potassium ions - they will also passively allow some negative ion, such as chloride or malate, to flow in to counteract the charge on the potassium.  Without those negative ions, a positive charge would quickly build up inside that would stop the potassium from moving in.  Thermal energy inside the cell gives every particle a random energy of motion (which leads to pressure at a boundary) that is equal on average, whether it is potassium, chloride, glucose, or a protein.  So when you double the amount of potassium in a cell, also doubling the corresponding negative ions, that is most of the particles in the cell - so the amount of water will also nearly double and the cell will get double the size.  In guard cells the amount of potassium can more than double to open stomata.
There is another mechanism to get to the same end: increasing the amount of glucose in the cell.  Normally, cells store energy as starch, which has a tremendous number of glucose molecules physically linked together.  These don't count as much more than a single particle for purposes of osmotic pressure, so starch isn't going to make the cell turgid.  But if you "mobilize energy reserves from starch" - split it up into glucose - those glucose molecules will all be moving around separately, each bashing against the membrane (and supporting cell wall) with its own random thermal energy.  Once again the guard cell will expand.
But everything I've described is relative.  A pile of dry salt or sugar won't exert any pressure at all, and a guard cell in a desiccated plant will not be able to expand.  Passively, a drying plant's guard cells will tend to close from lack of pressure.  However, the review explains that it would be dangerous for the plant to leave that to chance - it can't let air bubbles get into its water distribution network - which is one reason for all the active regulation described above.
Active regulation means "thinking" in some sense at the cellular level, so it is much more complicated than the physics of opening and closing.  People can tell a beautiful story that is pretty much wrong by trying to present the process without it.  You can see some of this complex regulation covered in the related question here about crassulacean acid metabolism plants, which open stomata only at night to conserve water.  Our review covers it under "Molecular evidence..." and it is quite complex; I would probably damage it in the retelling.  Key steps are abscisic acid production, H+-ATPase, and KAT/AKT-type Shaker channels.  But this is pretty much the on/off switch for a plant, so there could be quite a bit untold there, or unknown altogether.

thank you for the detailed explanation :)


text:
How could a water boatman bug get in a place with no water?
I built a pond in my backyard. Before I even topped it off, I started finding water boatman (Corixidae) swimming in there.
Note that the nearest body of water from my home is 30 miles away, and its about 1/2 acre in size. There are dry river beds, dry canals, and even a dry lake nearby, but I've never seen water there in 5 years being here.
So how is it that water boatman can show up so suddenly in my pond?

In animals some species migrate, some hibernate and some aestivate to
overcome the unfavorable conditions such as desiccation.
Some aquatic organisms enters into diapause during unfavorable conditions.

Source: toppr, also see Gemmule (in sponges)


text:
What is limiting the accuracy of genome sequencing today?
What are the current limiting factors of genome sequencing accuracy? By accuracy I mean a closeness relation between the sequenced genome and the finally assembled (I am not sure whether there is a proper name for this metric). I hope this way of measuring accuracy is useful since it also captures errors introduced during read-alignment (if short-read sequencing technology is used) and assembly.
As I understand it, there are two sources of errors limiting accuracy: errors in determining the correct bases and errors made in data analysis (read alignment, assembly, etc.). Which of these two sources is responsible for most errors in long- and short-read sequencing techniques? Are a significant amount of errors stemming from the data analysis?
As @David guessed correctly, I am a student (engineering) and wondering whether accuracy may be significantly improved by better algorithms.
As I currently understand it, short-read sequencing techniques are accurate but the repetitive regions are hard/impossible to align, while long-read sequencing techniques are more error-prone, and long-read & accurate sequencing (HiFi) is very expensive. Hence, my overly simplified perspective suggests that algorithmic improvements may continue to improve cheap long-read accuracy through hybrid approaches or improve the alignment and assembly of short reads. Is that correct?
The resources I used were:
https://www.pacb.com/blog/understanding-accuracy-in-dna-sequencing/
https://spectrum.ieee.org/tech-talk/biomedical/diagnostics/99-9-percent-accurate-genome-sequencing
and the paper recommended by @Maximilian Press

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. In addition, there is more than one method for doing genome sequencing and they have different limitations — this makes your question as currently written too broad. Under researched questions may be subject to down-voting and closure.

I notice that you have not completed the [Tour]. Doing so will help you understand how this SE works. The help on asking questions is a good follow up. More specifically, it is helpful to provide context and support for any assumptions in San question. What makes you think accuracy is a major problem? And the idea that it has to do with algorithms suggests that you have not researched the topic, but are data scientist or programmer looking for a problem. Are you?

On reflection, I wonder whether you mean "accuracy" or something else. "Accuracy" of genome sequencing relates to correct identification of a bases at a particular position: how frequently will a sequence contain a G (say) where there is really an A. However that is not a major problem in sequencing eukaryotic genomes, especially those of higher organisms. The main problems are closing gaps representing regions that contain long stretches of numerous, repeated gene copies, and mapping stretches of near-identical DNA called segmental duplications. This is not accuracy, but may be what you meant

One that isn't on your list: cost.

In the form of Oxford Nanopore data, we have extremely long reads of low accuracy. These are not too expensive but on their own they are probably not viable for many applications.
In the form of Illumina data, we have extremely abundant, cheap, high-accuracy short reads, suitable for "counting" approaches. This is great for some variant calling approaches, and also for some kinds of orthogonal measures. On their own, they are not viable for a lot of applications, though.
In the form of PacBio (specifically HiFi) data, we have long(ish) reads of high accuracy. These are the total package, and you can in principle use them pretty much on their own for any given application that I can imagine. The issue is that they remain quite expensive.

Here is a recent review as a reference that goes over these (I haven't looked at it in detail, but it seems to capture the tradeoffs accurately).
We have gotten extremely good algorithmically at using all of these various kinds of data, and at hacking them in various ways to complement each other, but we can't get around the fundamental constraints of contiguity (length) and accuracy.
The HiFiAsm assembler for example is at peak performance for the moment, and it combines PacBio HiFi data with e.g. Hi-C data (a hack of Illumina) to deliver pretty much whole diploid human genomes, which is really an astonishing technical achievement. It was also used to assemble the redwood genome, which is 10X the size of the human genome.
The issue is taking these technical possibilities and getting them to a scale and a technological refinement where we can generate this extremely high-quality data at-will and for all of the applications where we would like to use it.

Do you really accept the poster’s assumption that accuracy is a major problem? Massive over-sequencing seems to deal with it.

@David I do in certain narrow contexts. For genome assembly, an application that the OP brought up, inaccuracy (and relatedly, incompleteness) is a major issue in the final product. One could argue both sides about whether accuracy at the read-level base call is particularly an issue. It is one that is now being addressed by technology in the fashions that you and I mention, but "massive oversequencing" is prohibitively expensive with the technologies that actually address the relevant problems.

@David Massive over-sequencing also only helps with sequencing applications where you have sufficiently large and pure amounts of source material. There are many applications where this is not the case.


text:
Transposons and the net amount of DNA
The retrotransposons and certain DNA-transposons, are "jumping" sequences which may be incorporated elsewhere in the genomic DNA of an organism, through varying mechanisms. This insertion is almost random in case of retrotransposons and most DNA-transposons, but some transposing enzymes show specificity in selection of insertion sites. In either case, the "copy-paste" mechanism of transposition is essentially a random process(considering the frequency and place of transposition) and therefore, the extent of transposition should vary among all individuals, and all cells of a single individual. My question is,

Is the extent of transposition random and varied among the different
  somatic cells of an individual or is there a regulatory mechanism which ensures that
  there is not much difference in the net content of DNA (caused by unequal transposition) by equalizing
  the extent of transposition in different individuals or different
  cells of the same individual? If not, does this unequal c-value in different cell cause any troubles?

I'll have to find a reference before I can post an answer but I am pretty sure these will be independent processes in each cell. I would be fascinated to learn the opposite but I very much doubt it.

@terdon If it isn't equalized, will not the net DNA content(amount i.e. C-value) vary among different cells, and different individuals of the species?

for germ cells, I know that transposition is very tightly controlled.. most of the times transposons are heterochromatinized which reduces the rate of transposition. Will look up if there is any limit for the increased DNA content (or maximum observed expansion)

Transposition may occur at any given time in life, and in any cell. There are several cases known where transposition interests somatic cells (give a look here for reference). However, the frequency of transposition events is low, and the difference in amount of DNA between different cells in an individual is low. When you reason at the level of different individuals, however, the proportion of genome affected by transposable elements may be relatively high (give a look here for a reference)


text:
Disproportion in cranial nerve innervation?
The cranial nerve innervation is highly disproportionate, as far as humans are concerned.  I am not sure of the advantage of being innervated by cranial nerve versus being innervated by a normal spinal nerve branches, if any.
If there is any advantage to be innervated by cranial nerves, why is there such a largely disproportionate distribution of these cranial nerves?

Only the Vagus nerve (X) innervates parts other than the head of the
  animal. While there are 3 motor nerves just for the 6 eyeball muscles
  and the ciliary muscles (III,IV,VI), there is only one mixed nerve
  (X) innervating heart, gastro-intestinal tract and the respiratory
  apparatus and all smooth muscles therein. While there are three nerves
  for gustatory receptors, (VII,IX,X), one for retina (II), cochlea
  and vestibule (VIII) and the olfactory receptors (I) each, the
  entire plethora of intero-receptors in thoracic and abdominal viscera,
  aortic arch, external auditory meatus, tympanic membrane etc are
  carried by a single nerve (X). I am not sure if the disproportion is limited to the disproportionate area of innervation or even to the density of innervation in the target tissue.

Below are a few possible explanations that I came across while surfing the net, all without any strong arguments.

Is it because of the fineness of the senses in the head, i.e. the skin receptors in facial skin being higher than in the general body, providing a finer resolution of tactile reception? The special senses (vision, hearing, smelling and tasting) are also very fine in their resolution and might require more concentrated innervation and direct interpretation by the brain. But then the fingers and feet also have a high density of skin receptors, and the tactile sense can also be very fine (owing to several different kind of receptors) requiring dense innervation? Certain body movements (especially of hand) are very fine and detailed, requiring a very dense and co-ordinated motor neuron framework.
Is it because the cranial nerves, owing to some developmental restraint or functional trade-off, can only innervate areas close to its place of origin effectively? This might explain why 11 pairs of nerves innervate only the head region and only 1 pair innervates the remaining body. I have no idea about the validity and the reason of this claim.
Could it just be a random evolutionary outcome, there being absolutely no benefit of cranial innervation leading to random drift in the innervation patterns?

To me the third argument appears unconvincing. Talking about the first, it seems to be the most appropriate one as our special senses do put in a lot of efforts to collect every minute details of our surroundings. Also the final processing of the stimuli by these senses needs to be really very fast and accurate, whereas for the fine movements of our limbs the time duration in which a stimuli is to be analysed and responded to is comparatively more (as for quick responses the reflex arc comes into action).

So probably there was no need for our limbs and other organs to be innervated by the cranial nerves when the spinal nerves were just enough and did their job in appropriate time interval.!

I wonder to what extent 1) contributes to social communication (specifically, through a wider array of facial expressions).

We can somewhat rule out reason 1 because fingertips are also highly sensitive to sensory stimulus. Moreover innervation is not solely about sensory inputs but also motor functions, visceral control etc. All the nerves required for the motor function and a significant portion of visceral control nerves connect to spinal cord.
Therefore in my opinion reason 2 is the most appropriate which automatically rules out reason 3.
Spinal cord is an advancement of neural organization in the chordates. Spinal cord can be viewed as a central cable in which all power lines merge (they still maintain their individuality [the spinal tracts]; they just get clustered to form an organized bundle). Evolution of spinal reflexes must have been a secondary event.
The case of vagus nerve and cranioaccessory nerve suggests that this is an ancient pathway to control the heart. Heart with a closed circulatory system is found in molluscs as well. Apart from the functional significance of the heart (which might to some extent justify direct cranial innervation), it is decently proximal to the brain as well.


text:
Do RBCs need oxygen?
How do our red blood cells (RBCs) get oxygen? Do they even need it? They have no nucleus and no organelles, so I think they don't need it.

Their cytoplasm contains hemoglobin, a protein that carries oxygen. Here is a quote from wikipedia :https://en.wikipedia.org/wiki/Red_blood_cell                                  ..................   " Erythrocytes consist mainly of hemoglobin, a complex metalloprotein containing heme groups whose iron atoms temporarily bind to oxygen molecules (O2) in the lungs or gills and release them throughout the body. "............

the energy for RBC is from glycolysis, so I think they don't need oxygen. At least, for the energy they used.

Erythrocyte metabolism is unique in that the mature erythrocyte
  contains no mitochondria and therefore no Krebs cycle! Instead the
  energy needs of the RBC are met largely (95%) by anaerobic glycolysis
  in the two pathways: Embden-Meyerhof + Hexose-monophosphate.

+

Virginia University source


text:
What are these little creatures living inside a silk web?
They are found in Bangladesh. Some of my observations:

They are so small that their legs and appendages look transparent.
Their colour is brown and they have no wings.
My eye sight is not brilliant, but the don't look like spiders. Their head and mouthpart vaguely resemble that of the termite. When I tried to observe them closely, they looked bed-bug-shaped.
They are fragile: when I tried to grab them by pinching, they just squashed.
They seem like living in a big city made of silk strands. The can easily move in, out and within the structure which slightly bigger, potential predators could not.

Unfortunately my mobile camera is not good enough to capture a clear image of them. Click images for larger version.

Can you add where you took these photos? Also I can think of a couple of possible candidates but it would be purely speculative unless you can get a photo (or do a sketch?) of one. Any information on colour etc would also be useful.

it is from my backyard (Bangladesh). The silk structure is on old bamboo fence bordering a paddy field. Now it's raining so I can't go outside to make a stetch. so I'll try to describe it again. They are so small that it's legs and appedage look transparent. color is brown, has no wing. my eye sight is not brilliant but it didn't look like an spider. it's head and mouthpart vaguely resemble that of the termite,  my eyesight  is poor though so I can't fully gurantee this.
Please name all the candidate comes to your mind so I can compare with the images on the internet.

From the comments above (in particular, "it's head and mouthpart vaguely resemble that of the termite") it is possible that what is here is a Webspinner colony (Order Embioptera); if so you either have one of the few species in which the male is wingless, or the colony was without adults of that sex when your question was asked.  Webspinners are distantly related to termites, but have little or no economic importance (some species have been accidentally spread by man).  The Wikipedia article (https://en.wikipedia.org/wiki/Embioptera) has some basic information on the group (including photographs of both sexes and of nymphs), and references for further information; identification of species from Bangladesh will be problematic, as Edward S. Ross (the expert on this group from the mid-1940s, and not fully replaced--he has retired) had reportedly collected enough undescribed species to more than double the known diversity.

I didn't know this family so thanks for keying me into their existence. However...from the OP: "They looked like bed bug shaped" ; "They are so small that it's legs and appendage look transparent. color is brown, has no wing." The images of the embioptera I found do not match that description as they are too large and shaped incorrectly (even the wingless larva). Could you please comment about that in your answer. Thanks.


text:
Is there any math formula that can be used to describe shape of leaves?
There can be great variation in shape of leaves. Neverthless they are fairly simple shapes. How far are we in describing the shape of leaves in a mathematically rigorous way? Do we have a general formula that can be used to describe all shapes of leaves (or, at least, a reasonably large subset)?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419012/

L-systems.  Search on-line for examples, or read "The Algorithmic Beauty of Plants".  There's a freely downloadable PDF version online somewhere.

I don't think there is one equation that describes all leaf patterns. As the article linked by @CountIblis says, the mathematical description of the final forms using fractals or "golden ratio" can be biologically misleading. More accurate mathematical models would consider the developmental dynamics. L Mahadevan from Harvard works on pattern development in different biological tissues (not just leaves). Have a look at his site.

There are algorithms which can be used to describe leaves, if that is what you mean.
The following description takes into account that leaf shape is not solely a function of genetics, but is also effected by environment. It also models how different growth rates within the cells have consequences. Mutant, cloning cells are also factored into the description.
The mathematical model has interesting allometric implications.
Here is a very readable paper (PDF),which endeavours to describe differences using mathematics and for which for which we can thank Cornell University Library for hosting the paper and Lawrence Livermore National Laboratory.


text:
What is the point of toxins without remarkable coloring?
As far as I know, some toxic species (eg: some mushrooms) have no remarkable coloring. Therefore, what is the purpose of their toxins?
Toxic species often have colorful appearances to warn predators. Therefore, if a species has toxins but no vibrant coloring, this seems to me to not be beneficial for either this species or potential predators. But still, some toxic mushrooms (for example) have plain coloring.
What is the point of being toxic without vibrant coloring?

I think you got it wrong. Vibrant colors often attract animals (just think, would you like to eat a red apple or a green apple?), so plain color can be considered as that fruit (or anything) as not edible. That is (partly) why not many animals have pretty much no interest in eating sand as it doesn't have vibrant color. Obviously, sand itself is not alive ;)

why warn them, must mushroom are only a tiny fraction of the fungus's mass and dead animals make for good fertilizer. Also consider that toxic to humans or mammals is not the same as toxic to everything, there are still lots of critters that will eat toxic mushrooms without harm. so you have to weight dissuading some predators vs attracting others.

Also, the toxin might be incidental - e.g. it performs some role in the species metabolism.  Or it might have evolved in response to species with different visual capabilities, the way some plain to human eyes flowers have dramatic patterns when seen in UV, which the flowers' insect pollinators can see.

This is a really great question. To take a specific example, let's consider Amanita phalloides, the death cap mushroom. It doesn't advertise its poison; in fact, it resembles several edible species of mushrooms, including Caesar's mushroom and the straw mushroom. It contains alpha-amanitin, an extremely potent poison that inhibits RNA polymerase, shutting down protein synthesis. The estimated minimum lethal dose is 0.1 mg/kg or 7 mg of toxin in adult humans. The poison has a delayed effect, taking between 10-24 hours for significant effects to appear, so it's not like a poisoned animal can learn to avoid the mushroom in the future. None of the amatoxins appear to have any purpose except as a mammalian poison. They aren't specific to humans, and are capable of poisoning dogs. So what's the evolutionary advantage of this poison?
According to an essay written on the California Native Plant Society blog by John Chesnut, a horticulturist, the answer might lie in where the mushroom grows -- on tree roots as ectomycorrhiza (emphasis mine):

Death cap is an ectomycorrhizal symbiont. This means it forms connections on the root-tips of forest trees; in California, its typical (but not exclusive) partner is coast live oak. [...] Ectomycorrhizal (EC) fungi collect major nutrients, nitrogen and phosphorous, and exchange these with the host tree for sugars. Delicate hyphal strands extend outward from the root tip mass into the surrounding soil and mulch. EC also allows efficient active transfer of macronutrients, micronutrients, and soil water to the tree. The chronic phosphorous limitation in serpentine soils makes the EC symbiosis especially important for local forest types on this soil. Studies in Norway discovered up to 50% of a birch tree’s sugar is exchanged at the root tips with EC symbionts.

So the poison might not be intended as a way of preventing itself from being eaten, but as way of defending the tree it lives with from nematode pests (emphasis mine):

So why are Amanita so poisonous? It is an unlikely deterrence to vertebrate predation of the fruiting caps, as the effect is slow-acting (36-72 hours before the toxic crisis in humans) and the toxin is not concentrated in the cap. Evidence supports the hypothesis that the fitness obtained from synthesizing the toxin is secured within the hyphal network. Perhaps toxic Amanita obtain nitrogen from poisoned nematodes, or protect themselves (and their symbiont hosts) from plant parasitic nematode predation.
Perhaps the toxin suppresses the growth of competing fungal webs. It seems clear the toxic effect of death cap is intrinsic to its invasive success worldwide.

Interestingly, he points to some research suggesting that some mushroom flies might have co-opted this mechanism to keep themselves parasite-free (link and emphasis mine):

An evolutionary entomologist working in New York State, John Jaenike, has discovered four species of mushroom flies in the genus Drosophila that lay eggs in the gills of fruiting Amanita phalloides. The fruit fly taxa are related to ones that inhabit rotting skunk cabbage, but in New England have recently transferred to the recently introduced Amanita fruitings.
Jaenike discovered that Amanita phalloides is toxic to the damaging parasitic nematodes Howardula that reproduce in the stomach of fruit flies. The toxicity of the death cap to the parasitic nematodes results in much greater egglaying (fecundity) by the fruit flies. The fruit flies are affected by the toxic amanitin, especially the males, but the poison is more than offset by the increase in reproduction.
Janike also discovered that most other insects using mushrooms as egg laying sites (craneflies and forest gnats) shun use of the Amanita (due to its toxicity).

(in response to post by Gaurav) The concentration of toxins in Amanita phalloides IS highest in the cap and is basically zero in the hyphae (mycellium). This was found in 1996 and verified separately in 2015. Mycologia8, 8(6), 1996, pp. 909-921. Toxicology and Industrial Health 2015, Vol. 31(12) 1172–1177


text:
Genetic expression in interspecific hybrids
Referring to interspecific hybrids, I have the following two questions:-
Quoting from wikipedia:-

The offspring of an interspecific cross are very often sterile; thus,
  hybrid sterility prevents the movement of genes from one species to
  the other, keeping both species distinct. Sterility is often
  attributed to the different number of chromosomes the two species
  have, for example donkeys have 62 chromosomes, while horses have 64
  chromosomes, and mules and hinnies have 63 chromosomes. Mules,
  hinnies, and other normally sterile interspecific hybrids cannot
  produce viable gametes, because differences in chromosome structure
  prevent appropriate pairing and segregation during meiosis, meiosis is
  disrupted, and viable sperm and eggs are not formed. However,
  fertility in female mules has been reported with a donkey as the
  father.

1) The sterility of hybrids prevents interspecific gene exchange and is necessary in case the hybrid has odd number of total chromosomes (the hybridized species has odd and even pairs of chromosomes individually), where equal meiotic division would not be possible, and is also necessary to avoid sex determination problems that may arise from such hybridizations genetically. What is the molecular (genetic) reason behind the sterility? In other words, why is the expression of primary sexual organs and its further proliferation to effect reproduction not possible, although the genes required for it are already present in the hybrids? Is this due to epigenetic mechanisms or is the reason inherent in the hybrid nature of the genome?
2) This might probably sound a bit naive, but why are these hybrids viable? They have 2 non-homologous haploid pairs of chromosomes which have a huge variety(compared to two homologous pairs) of different non-allelic genes. Why are all the essential functions not hindered by the presence of such considerably unrelated set of chromosomes?
Probably related to the question is the fact that certain allopolyploids are viable and become an entirely new species, but others are not. Is it because here are 2 sets of each combining species' chromosomes (and hence allowing proper meiotic pairing) or is there some other reason pertaining to the nature of the combined sets of chromosome?

mitosis is not affected because there is no pairing of homologous chromosomes. Meiosis is possible affected because pairing is compromised. However, non-meiotic recombinations are possible.
Why are all the essential functions not hindered by the presence of such considerably unrelated set of chromosomes? Hybrids are not possible between totally unrelated species. The similarity of the genes and the genetic networks perhaps allows the cells to carry out normal functions.

Can you add a referece to support your first point? Hybrid introgression and hybrids with lowered fitness (i.e. not fully sterile) has been shown to be relatively common in natural populations.

@fileunderwater Please see the edit in my question.

@SatwikPasani Great! The relative prevalence of sterility probably differs dramatically between taxa (depending on e.g. how species concepts are applied, genomic differences within taxa and the strength of regulation).

i think it is not just about odd number of chromosomes. Pairing would be compromised if there are no homologous syntenic regions.

Mallett 2008 might be of interest to you. It doesn't answer the questions about genetic mechanisms, but is a good perspective on hybridization viability/sterility.

I've heard of mules producing offspring, but it's rare. It requires a gamete to be produced that just happens to get all of the horse chromosomes or all of the donkey chromosomes, making it equivalent to the hybrid's parents.

Davis et al. 2015 studied hybrid sterility in cats by identifying SNPs and transcriptome changes that are associated with hybrid male sterility.
They identified eight autosomal regions "involved in the function of the blood-testis barrier, gamete structural development". So it seems that the male hybrids have an altered testicular blood supply and sperm development.
More importantly, they have found a lot of altered genes on the X chromosome. It seems that a lot of regions on the x-chromosomes have duplicated. They also found "chromosome-wide upregulation of X chromosome transcripts in testes of sterile hybrids, which were enriched for genes involved in chromatin regulation of gene expression". This is a major hint that epigenetic regulation is the cause of hybrid infertility. I think this makes sense, since all (mammal) females have to shut down one x-chromosome by methylation of the x-chromosome, to prevent a doubling of gene dosage (Sex-chromosome dosage compensation). They mention that in their discussion (which is rather cryptic for my taste), too, and if I understood this correctly, males are also in need to methylate their X-chromosome (partially?). If they fail to do so, male hybrids upregulate X-chromosomal genes that in turn cause infertility. They mention a gene on the x-Chromosome called FMRP that is essential for spermatogenesis that seems to be altered in hybrids.
The focus on the x-chromosome might also answer your second question: I presume that the hybrids are viable since most genetic "damage" is concentrated on the X chromosome, while the autosomes seem to work fine. After all, autosomal damages don't carry as much weight as X-chromosomal damages, since autosomes come in pairs (in males). If one autosome has a dysfunctional gene, it is likely that his homologous partner carries the functional version. The X-Chromosome however is alone, so mechanisms like DNA-repair by homologous recombination is not possible and DNA damage can accumulate. But that is just speculation from my side (!).
They also talk about the "large X-Effect". I am no expert, but it seems that the X-chromosome is a 'hotspot for "speciation genes," that prevent genetic exchanges between closely related species' ref However I didn't understand what they were talking about, but maybe this throws your own research into the right direction.


text:
Why would there be a spike in coverage within a gene in RNA seq data?
I'm looking at RNA seq data in Geneious for Salmonella typhimurium and I occasionally see a spike in coverage for a sequence of RNA within a gene. Why is there a section of the gene that seems to be transcribed much more often than any other part of it? The name of the gene in question is ftsI which is an essential cell division protein that may link upstream cytoplasmic cell division proteins with downstream periplasmic cell division proteins.

Welcome to SE Biology. Your question seems potentially acceptatble, however it needs some modification before you are likely to get an answer. In the meantime it risks removal as "unclear what you mean". First, I had no idea what geneious was. You should capitalize proprietary software and state what it is. More important you should include an image of the peak you are seeing and indicate what organism it is. We cannot be expected to know what ftsl is, and CDS is not the name of a gene but an acronym for "coding sequence". Please edit it.

Without knowing how your libraries have been prepared and sequenced it is hard to tell if that is due to a technical or biological source.
However, there are a few bias sources in RNA-seq (which aren't an issue in DNA-seq)
One of them is that if you used a "random-hexamer" protocol, they're known to not be so random after all. See: Hansen KD, Brenner SE, Dudoit S. Biases in Illumina transcriptome sequencing caused by random hexamer priming. Nucleic Acids Res. 2010;38: e131.
You might also have a contamination from other species that would present a sequence identity for that part more specifically.

Some regions might be more present than others in the sequencing data because some exons might be more often included in the mature transcript (alternative splicing). Check whether the peaks matches with exons. Edit: This will likely not be the case since you are dealing with a bacteria: as far as I know, splicing is very uncommon in bacteria
Another likely explanation could be that there are biases during library preparation or sequencing.
In both scenarios, the biases would be post-transcriptional.
Yet another possibility would be that other transcription units are present within your gene of interest. This sometimes happen, especially when dealing with compact genomes.

Salmonella would not have exons/introns.

@emilliman5 Indeed, I hadn't taken into account the fact that the poster's question involved a bacteria.


text:
Do birds ever fly in clouds?
Do (some) birds ever fly in fog or clouds so that they would not be able to see either the ground or the sun? Assuming the visibility is good enough so they can see obstacles in time to avoid them.
If they do, how do they maintain straight flight?
Inner ear is inadequate in the air, because it can only sense the sum of gravity and acceleration, which is just the (reaction to) aerodynamic forces and those are always orthogonal to the wings. To an extent, it can also detect rotation, but this is not good enough to keep precision for minutes and hours in cloud. So how do birds know where is up?


text:
What DNA does a self-fertile plant's seedling have?
Some plants are said to be self-fertile. An example is Prunus tomentosa.
Assuming that no cross-pollination happened with other plants, if a self-fertile plant such as prunus tomentosa produces a seedling, what DNA will the seedling have? Is the seedling's DNA an exact copy of the parent plant's DNA, or do the genes get rearranged?

Selfing (aka self-fertilizing) differs from cloning. When selfing occurs, the offspring is not an exact copy of the parent. When cloning occurs, the offspring is an exact copy (except for a few mutations) of the parent.
Selfing implies that an individual will produce two gametes (typically a spermatozoid and an ovule but that might be a bit more complicated) and these two gametes are fusing to give the zygote (egg or offspring if you prefer).
As a consequence, when selfing, meiosis is occurring (and therefore segregation and recombination) so that the offspring is not an exact clone of the parent but rather some kind of a rearrangement of the parent genome (with a few mutations of course).

This question might be of interest: Peach pits with multiple seeds: Do the seeds have the same DNA?

This question might be of interest: Peach pits with two seeds: Are the seeds identical twins?


text:
Self-fertile PRUNUS: Approximately how much of the genome gets rearranged by meiosis?
I'll admit that I don't have a background in science, so this might be a stupid question. Suggestions and edits are welcome. The question is related to a similar question I had here: What DNA does a self-fertile plant's seedling have?

Some prunus plants are said to be partially self-fertile. An example is prunus tomentosa. I've been informed that through self-fertilization (a.k.a. selfing), meiosis occurs, which rearranges the genome.

...when selfing, meiosis is occurring (and therefore segregation and
  recombination) so that the offspring is not an exact clone of the
  parent but rather some kind of a rearrangement of the parent genome
  (with a few mutations of course). Source

Approximately how much of the genome of a self-fertilized seed is impacted by meiosis? Is a large amount of the genome rearranged, such as 25%? Or less than 1%?

It makes little sense to give a percentage of the genome impacted by recombination and segregation. I think you should read about segregation and recombination and that would be clear to you why giving a percentage makes little sense.
Segregation
Segregation causes that the two haplogroups of the parent can be rearrange at the among chromosome level. So, for example if, in this lineage, each individual has 3 pairs of chromosomes. Let's denote each haplogroup by a capitalize vs non-capitalize letter, we can represent the genome as
a|A b|B c|C

Without segregation (and recombination), a parent could only transmit either
a b c

or
A B C

in a given gamete. This results in the three possible zygotes
a|A b|B c|C
a|a b|b c|c
A|A B|B C|C

segregation allows the creation of gametes like for example
A b C

resulting in possible zygotes such as for example
A|a B|B c|C

Recombination
Recombination typically occurs at a rate of one recombination event per chromosome (that is 100 centiMorgan per chromosome as a rule of thumb; see here to understand what a centiMorgan is). Further rearrange creating new haplogroup from the two existing haplogroups. So for example, from the pair of chromosome
A|a

an individual could create a new haplogroup from recombining the end of A with the beginning of a (or vice-versa).
Related posts
There are probably a lot of related posts. Here are a few of them:

Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
Gene distance and Recombination Frequency: Mechanism
Is the discovery of dominant and recessive genes the only reason Mendel matters?
What is Mendelian Segregation and how is it related to the Hardy-Weinberg equilibrium?
Genetic linkage greater than 50 centimorgans
What are the exceptions of Mendel's laws?

As has been pointed out, it isn't so much a question of how much gets rearranged (because everything is potentially shuffled) but is really a question of how much is lost or changed, since any genes/alleles present are going to be subject to expression.  This is a simple Mendelian genetics problem, but to really answer it you need to know whether your alleles are in a heterozygous or homozygous state.  If you take locus A, for example and cross Aa x Aa, you will find the next 25% of the progeny will be AA, 50% will be Aa and 25% will be aa.  In essence, you lose 50% of your heterozygosity with each generation of selfing.  Why is this important?  If you are highly heterozygous to begin with, you will have difficulty recovering selfed progeny that resemble the parent.  The more homozygous the parent is, the more likely you are to recover selfed progeny that closely resemble it.  For crops like peaches, which are self-compatible and descended from a narrow genetic base, that means that lots of important alleles are more likely to be homozygous to begin with and less will be lost from each generation of selfing, whereas some other type of crop which might have higher levels of heterozygosity (an F1 hybrid strain or species that evolved as an outcrosser and/or has a wider genetic base) will be quite different.
For something like Prunus tomentosa my guess is that "domesticated" clones in circulation are probably all descended from one or a few individuals.  If they tolerate selfing it is quite possible that seedling strains have come about over the last Century (either intentionally or just because people found it easier to grow out seedlings than to propagate clonally on a large scale) since it was introduced.  Since each generation of selfing leads to loss of half of heterozygosity, you can very quickly reach a situation where alleles for major characteristics have become fixed in a small population.  Thinking about it this way if you start with a scenario where EVERY gene is heterozygous, in one generation only half will be, in two generations only 25% will be and with three generations of self pollination only 12.5% of your genes are in a heterozygous state.  At this point you can see that just 3-5 generations of selfing can lead to fixation of most of the alleles and that if only one plant is saved and moved forward from each selfing event as "the best" you will have something that will give progeny that are phenotypically very similar to the selfed parent.  This doesn't always work from the standpoint that many plants don't tolerate selfing and suffer from inbreeding depression, but this is usually related to the breeding systems that they have evolved with and species that evolved as self-compatible in the wild tend to be more tolerant than those which largely evolved as self-incompatible.

Can you please add sources?


text:
Do transcription factors need to undergo extensive post-translational modification?
Some proteins need additional processing to become fully functional, for example NiFe-hydrogenases need to be cleaved by endopeptidases for some of their subunits to be active.
Is it known whether transcription regulators could also, in some cases, need such extensive post-translational modification to be effective?
(I am not talking about possible conformational changes that by specific effectors, but rather an obligatory step in the maturation of the protein, that could also be necessary for other genes' expressions.)
To be a bit more precise, I am thinking about a metabolic system where the expressions of most of the involved genes are regulated by a master transcriptional regulator (SurR, an ArsR-type, redox-active regulator involved in Thermococcales’ (Archaea) energy metabolism).
I am wondering what kind of effects a change in the expression of the regulator-encoding gene could have on the whole system. And before getting to an effect on the regulon, I guess it is a good idea to start with the regulator itself: could it be theoretically fully functional in a greater concentration, if I would only consider overexpressing its gene for example?
One type of heavy post-translational modification is maturation by endopeptidase, which can hamper the correct activity of an enzyme if not considered adequately in a case of, let’s say, overexpression attempt. (this example is particularly important here since several enzymes of the regulon need to be importantly modified post-translationnaly)
Since there does not seem to be enough literature on the particular regulator I am interested about, and since a quick research for answers in other systems was not successful on my side, I am thus asking the SE community if anyone may have known about some kind of maturation-like, post-translational process, which could be needed for a fully functional transcriptional regulator. Would I need to worry about other genes than only the one coding for the regulator, to that extent?

Welcome to SE Biology. First, it would be useful to know why you are asking this question. As it stands it seems to me, at least, rather arbitrary. Potential responders would have more incentive if you told them why this is important to you. Second I have edited your answer so that it employs standard scientific English terminology. I appreciate this is difficult if you are not a native speaker, but the harsh reality requires all scientists to master this. My approach for other interests is to find a Wikipedia article in my own language and then switch to the foreign language version of it.

In addition to David's excellent advice, please note that this is a very broad question and could be closed due to lack of focus or insufficient prior research. Answers to a question like this are often unsatisfactory (tend to be superficial) because they require enough material for a review article or high-level textbook chapter to answer with any depth. This is not practical on this platform. If you can focus your question then a useful answer may be forthcoming — as it stands the answer is "Yes", which I suspect helps no one.

Thanks David and tyersome for your help and remarks. I have edited my initial post to give a bit more context, hope that’s better.

Notch signaling involves the cleavage of the transmembrane Notch protein. This releases the intracellular domain that then enters the nucleus and modifies gene expression. Does that count? Beyond cleavage reactions there are many examples of transcription factors that need to be phosphorylated (also a post-translational modification) for activation. But in your case you appear to be talking about a repressor, and at least LacI and TetR are both fully active repressors without any need for post-translational modifications. My guess is that it's quite general for at least bacterial repressors.

Your title seems to ask a different question (do [ALL] transcription factors...) than the body of your question (...in some cases...).


text:
Kansas Spider Identification
I live in Kansas (Pottawatomie County), and I found a spider crawling on a wall inside my bedroom:

I'm inclined to keep the spider in my house, but I just want to double check to see if it is venomous or dangerous.
The spider is approximately 3~4 cm long in size, and seemed to be in dark (possibly brownish) color. I saw it crawling on the walls once in the afternoon. And this time I saw it crawling at 10pm.
It doesn't appear to be a widow spider so I was a bit relieved. But could you please tell me what is the name of this spider species? And would it be dangerous to keep this creature in my house?
Thank you very much for your help!

That...looks like a brown recluse spider. The picture is a bit dark so I'm not 100% sure, but they can be identified by a violin-shaped marking on their back. Apparently they are very common in homes Kansas.

Illinois Department of Public Health
They are nocturnal:

Brown recluse spiders are mostly nocturnal, coming out at night to hunt for their insect prey. - TAMU

Assuming my ID is correct, they are venomous. Here are links to three government agency or university pages (hopefully reliable sources) on brown recluse spider control:

Illinois Department of Public Health
Kansas State University
Texas A&M

Thank you so much for your help!

I agree with Luigi - that is a Brown Recluse Spider (if you lighten the image, you can clearly see the diagnostic violin marking; that, plus the Recluse shape, size, legs and habits make me certain that this is what you have, even without seeing the eyes clearly).  By the way, this is an adult male, which is why you noticed it - right now, these guys are wandering around looking for love instead of hiding in some quiet, undisturbed area snacking on cockroaches and other delicious insects.
While these spiders are generally inoffensive, the venom is unpleasant in effect, and may rarely cause significant health effects.  In this case, I would consider calling in a pest control service, although you're in an area where Recluses are pretty common. You might also want to get used to taking some precautions like shaking out your shoes in the morning, laying down sticky traps around the bedroom walls and under the bed frame legs, etc.  I know that many people live their lives in close proximity to Recluses without problems, but once in a while unfortunate things can happen.


text:
Is there any way siblings could be related more than 3/4th siblings, but less than full siblings?
I couldn’t find anything on Wikipedia. 3/4th siblings are 37.5% related while full siblings are 50% related. Is there anything in between?

You may be confusing averages with the actual (genomic) relatedness of two given siblings. Two given siblings can in theory be anywhere from 0% to 100% related, but on average will be 50% related.

The International Society of Genetic Genealogy Wiki provides the following situations for which siblings may be considered $3/4$ siblings (a coefficient of relationship of 37.5):

a man has children with each of two sisters (the children are related    as half-siblings and first cousins)
a woman has children by each of    two brothers (the children are related as half-siblings and first    cousins)
a woman has children with both a man and his father (the    children are related as half-siblings and half-aunt or half-uncle and
half-niece or half-nephew)
a man has children with both a woman and    her daughter (the children are related as half-siblings and half-aunt    or half-uncle
and half-niece or half-nephew)

Note that the above situations assume that all grandparents are unrelated. If you consider a situation where either or both sets of grandparents are full siblings, then you have a coefficient of relationship in the sibling grandchildren that is intermediate between 37.5 and 50.

I edited my question, what I wrote was not what I meant.

I've extended my answer


text:
What does a typical, perfectly healthy vaccinium corymbosum (highbush blueberry) leaf look like?
What does a typical, perfectly healthy vaccinium corymbosum (highbush blueberry) leaf look like?

Colour (darkness of green, redness)
Waxiness
Veins

I'm guessing that soil ph, nutrients, and other factors play a part. Vacciniums seem to have very specific needs, and as far as I know, assessing the leaves is one of the best ways to determine plant health.

Vaccinium species are ericaceous plants (acid soil loving) so they will not do well in alkaline soils, and/or being watered with hard water. In fact they have a narrow optimum pH range 4.8 - 5.2 (Source http://www.westernfarmpress.com/management/blueberry-iron-chlorosis-has-multiple-causes)
The pH of the soil will effect the plants ability to access the minerals in needs from the soil, and mineral deficiencies will indeed show themselves in the leaves first.
Here is a photo of a healthy Highbush Blueberry leaves