text:
Why does eating saturated fat increase blood cholesterol?
I am interested in the biochemistry of diet and the way we have been advised to eat for the past forty years.
In researching an explanation for the relationship between dietary fat and blood cholesterol I came across the following: "It is clear that eating too much saturated fat increases the levels of cholesterol in the blood, especially our "bad" cholesterol which doctors refer to as LDL". This is from heartuk.org.uk.
"It is clear ..." - really?
I am mystified! I understand that dietary fat, other than very short chain fatty acids, does not immediately enter the blood stream but is transported via the lymphatic system as triglycerides packaged in protein assemblies called chylomicrons, finally entering the blood via lymph nodes under the armpits. Once in the blood the triglycerides are hydrolysed into fatty acids and transported to appropriate cells in albumin complexes.
Where does LDL feature in this transportation? And, by the way, why just saturated fats? Surely the small intestine doesn't differentiate between saturated and unsaturated fats, or does it?

Focus of your question seems twofold:
a. there is a missing link between chylomicrones/saturated fat going straight to adipose tissue on one side and liver producing bad cholesterol/LDL(VLDLP) on the other side - causality?
b. there is no reason to differentiate saturated from unsaturated fat: either unsaturated fats share the same fate or they pass over to the liver directly, and why should they not induce production of bad cholesterol/LDL(VLDL)

"Surely the small intestine doesn't differentiate between saturated and unsaturated fats, or does it?" - To formulate in another question: fate of saturated and unsatured fats in instestine/enterocytes?

In short: It may not be saturated fat by itself but high saturated/unsaturated fat ratio and high animal/plant fat ratio in the diet that increases the risk of heart disease.
A systematic review of the effect of dietary saturated and polyunsaturated fat on heart disease (NMCD Journal, 2017)

Reducing saturated fat and replacing it with carbohydrate will not
  lower cardiovascular events or CVD mortality although it will reduce
  total mortality. Replacing saturated fat with mono- or
  poly-unsaturated fats or high-quality carbohydrate [from whole-grain
  food] will lower cardiovascular events.

Saturated Fatty Acids and Cardiovascular Disease: Replacements for Saturated Fat to Reduce Cardiovascular Risk (PubMed, 2017)

Replacing dairy fat with carbohydrates from refined starches and added
  sugar was not associated with increased or decreased risk of coronary
  heart disease (CHD), stroke or total cardiovascular disease (CVD).
  However, replacing dairy fat with carbohydrate from whole grains
  reduced the risk of CVD, CHD and stroke. Relative to other animal
  fats, dairy was found to have less impact on CVD. When 5% of energy
  from dairy fat was replaced with animal fat from non-dairy sources,
  risk of CHD increased by 6%. However, when 5% of energy from dairy fat
  was replaced with an isocaloric amount of polyunsaturated fats, risk
  of CHD was reduced by 26% and CVD risk was reduced by 24% [41].

A basic explanation of the underlying mechanisms:
The liver produces low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Lipoproteins are composed of triglycerids, phospholipids, cholesterol and proteins.
LDL caries cholesterol from the liver to the peripherial tissue, including arterial walls, where it can accumulate and cause atherosclerosis. This is why LDL is called "bad cholesterol" (even if LDL is only a carrier for cholesterol). HDL clears excessive cholesterol from the blood and carries it to the liver for disposal, so it is called "good cholesterol. (Heart.org.uk)"
High LDL levels are associated with an increased risk of coronary heart disease (Bentham Open).
One possible mechanism by which saturated fats increase (LDL) cholesterol (PLOS):

Saturated fat is thought to increase LDL-C primarily through
  down-regulation of hepatic LDL receptor activity, leading to reduced
  clearance of LDL particles [from the blood].

Why is it saturated and trans fats are bad and unsaturated cis fats are good? The only difference between the two isomers is shape: saturated and trans fats are essentially linear whereas cis fats are bent. If indeed there is a causal link between linear fats and vascular disease then surely it can only be due to their conformation?

In medicine and nutrition, it may be enough to know what is the net result of high consumption of a certain nutrient without knowing the mechanisms. I'm sure, the exact effect of various types of fatty acids on LDL production is described in detail somewhere, but this is too much for this site, at least for me. They could know more on https://chemistry.stackexchange.com/ . The metabolism of LDL occurs in the liver, so you do not need to concentrate on what happens in the intestine and how fats come to the liver.

@adlibber Trans-fat are quite stable because the molecules are tightly packed due to trans structure. And saturated fats do not have a double bond (which makes the molecule reactive) , so they too are stable.

Interesting point user237650. So does stability = ‘bad’? And if so why so?

Fair criticism Jan but you could also say that all these questions relate to physics as well. This is a human physiological question and I felt that ‘biology’ was a more appropriate cover than ‘chemistry’. I’m not a biologist nor am I a biochemist so imagine the difficulty I’m having with this subject! i’m in fact an old retired systems engineer interested in all the noise about nutrition!

@adlibber, It can help tremendously if you say what is the exact goal of your research? Do saturated fats increase LDL? Do they increase the risk of heart disease? Or you are strictly interested in how all this happens on biochemistry level? I had a feeling that you are trying to find a direct connection between the structure of fatty acids and LDL synthesis. While this can make sense, it can be misleading, because you need to see the whole picture: the sum of effects of all fatty acids on LDL...

@jan, my goal is to find out whether eating a high fat low carb diet with lots of dairy etcetera is going to kill me. I am confident enough with my research thus far to have stopped taking statins after ten years of medication for high cholesterol. The subject is also of great importance in terms of the current obesity and associated diabetes epidemics. Getting into the available science helps to clarify the fog.

I edited my answer and the essence of it is in its first sentence. The risk of heart disease seems to increase with high sat/unsat fat and high animal/plant fat ratio. So, it's about what comes in and what comes out. Merely concentrating on the isolated effects of various fats and other nutrients on LDL alone can be grossly misleading.

@adlibber I can't say for sure but I think it will be hard to metabolize them. Also read this, but again I can't say if the claims are entirely true.

@user237650 many thanks for the link. Is Kendrick correct is the big question of course! If he is then he is in agreement with my understanding obtained elsewhere and hence my original question. The BMJ came out with this a few months ago illustrating the abject confusion on the subject. My gut (excuse the pun) tells me Kendrick is right!

re last quote. (PLOS): It's an empirical study, isn' it. However, in "Discussion" at the end of the paper there is some  theory on reasons for LDL being bad which I haven't  understood.

They asked about why increased saturated fat intake increases blood cholesterol levels, they did not ask about heart disease risks

"Why does eating saturated fat increase blood cholesterol?"
From your explanatory text I understand: ... as it is transported by chylomicrones and not by LDL which is commonly known as "bad" cholesterol.
I'm paraphrasing even more: How could eating saturated fat which is not transported by LDL (termed "bad cholesterol"), and for this reason should not lead to more LDL in the blood, be held responsible for "bad cholesterol"?
There are two common misunderstandings I think your question brings up (educating, to me):

Chylomicrones are not the only transporters of (saturated) fatty acids. There are the VLDL as well doing that job. The difference is termed "dietary fat" versus "endogenous fat". The liver is the body's biggest producer of (saturated) fatty acids (interestingly, the liver produces but saturated fatty acids!). This fat is transported from the liver to tissues  by VLDL (Very Low Density Lipoproteins). It is no trivial knowledge that LDL is not produced by the liver "as is", only the VLDL are. However, VLDL become "bad" LDL in the bloodstream.

Lipoproteins and Chylomicrones per se, as transporter molecules, incorporate cholesterol, in different amounts and percentages of total weight. From textbooks it may be easy to tell whether   cholesterol is a "part" of the transporter or being transported as  "package". Cp.Dr. Malcom Mkendrick (paragraph"re-cap")

What might appear as   some   "breaking news" AD Cooper · 1997 "Chylomicrons are formed in the intestine and transport dietary triglyceride to  peripheral tissues and cholesterol to the liver." Still another one: Enterocytes not only produce chylomicrones but VLDL, too.

Both Chylomicrones/chylomicrones-remnants and VLDL/"VLDL"(called LDL) resemble each other in their "later life" termed "remnant". What remains of VLDL after unloading fatty acid is termed LDL, and  packed cholesterol may  look like a building block of the lipoprotein (as the LDL receptor of tissue cell takes up LDL as is - no unloading).  Hint: my misunderstanding taken for typical learner's was to think of LDL being sent off by the liver - not correct: it's VLDL off from the liver, and "remnancy" after unloading fatty acid at the veins' walls. So VLDL become LDL in the blood stream. There is a special page in Wikipedia not easy to find:Remnant cholesterol
These preliminary remarks  are  practical hints, as you may search for "why does eating saturated fat increase VLDL (very low density lipoproteins) and get some clues and discussion via google -instead of searching for "saturated fat and LDL
Why is LDL held responsible for "bad cholesterol"? Among the lipoproteins it has the highest load of cholesterol; and  as a "remnant" transporter of cholesterol it does seem to unload cholesterol  at arterial walls just as that same transporter (named VLDL at that point)= does with fatty acids -  if tissue cells not in need of cholesterol do not express the LDL receptor (Nobel prize winners Brown and Goldstein's research on familial hypercholesteraemia).
That said, why then should reduction of dietary saturated food reduce VLDL and/or LDL (your question translated to that formula) as the only "clear" effect of saturated food is a higher production of chylomicrones which are very low in cholesterol?
Did you read my latest news up above?  I think it is no common knowledge that chylomicrons are  involved in cholesterol transport from the intestine to the liver.  Simple inference from that: more cholesterol input (combined to saturated fat) causes more cholesterol output (combined to fat, VLDL which becomes LDL "on deliverance").
However, searching  through literature, your question turns out  to be valid - nothing is "clear" and undebated, and that goes for the   following simple reasoning as well, recurring to basic knowledge (before I knew about chylomicrones delivering cholesterol to liver):
Effect of dietary saturated fat is that the liver will be able to synthetize and deliver to tissue cells more of  so called endogenous fat as it receives  more of fatty acids FROM tissues the more those tissues receive fatty adics from chylomicrones (see below about pathway from tissue TO Liver-Hint: it is not irrelevant in respect of your question that short fatty acids do not need chylomicrones for uptake from intestine, and it seems that in early scientific discussion the high amount of any kind of fat, saturated or not, was subject of debate).
Any surplus of fat the liver produces is transported to tissues (Stryer/Berg, Biochemistry)  by
VLDL, the Very Low Density Lipoproteins.
The important crossroad of those pathways is at  the arterial wall where VLDL unload endogenous fat from and made by the liver. VLDLs thus become "ILDL - Intermediate-Density Lipoproteins", half of which is returned to the liver for turnover, half of which,  however,  become LDL (how? By "unloading more fatty acids", cp. Berg/Stryer, Biochemistry).
So, this presumed mechanism is in favour of the quote cited: more saturated fat deliverd by chylomicrones will lead to more saturated fat in VLDL  which, after unloading fatty acids, become "bad" LDL transporting cholesterol (only). More saturated fat input is seen here as a "commodity" the liver replenishes its production of endogenous fat with.
Let me give you some quote describing the pathways, to see how the liver receives (saturated) fatty acids taken in by chylomicrones that have delivered to storage fat tissues (not to liver!). VLDL are only needed for transportation FROM the liver, not to the liver. How might liver input of fatty acids, leading to bad LDL, be heightened by chylomicrone input?
From:
[K.R. Feingold, Introduction to Lipids and Lipoproteins][1]

"...The exogenous lipoprotein pathway starts with the incorporation of dietary lipids into chylomicrons in the intestine. In the circulation, the triglycerides carried in chylomicrons are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids, which are subsequently metabolized by muscle and adipose tissue, and chylomicron remnants are formed (...) then taken up by the liver. The endogenous lipoprotein pathway begins in the liver with the formation of VLDL."
In Berg/Stryer,10ed., Fig. 26.16 depicts Fig 36.1 of Goodman/Gilman: The liver receives free fatty acids released into the blood by "adipose tissue", i.e.  tissue cells that have received saturated fats from chylomicrones.
So, if (saturated) fat input is transported to STORAGE tissue by chylomicrones high input of fat may lead to excess,  surplus storage of fat in adipose tissue, then to  free fatty acids input of   the liver which metabolizes to endogenous triglycerides(!) "re"-transported to storage and/or catabolic tissue. It may be a question of debate whether LDL from VLDL being turned to ILDL is a metabolic switch the aim of which is to "store as much as possible" - where, at the end of the line  fat broken down in liver and re-metabolized to cholesterol by the liver (via acetyl-CoA) can be stored as  cholesterol by any cell that is able to store away cholesterol,then not using cholesterol as building block of its membrane.
This point alludes to the second part of my answer that differentiates between animal and plant tissue: animal cells much more than plant cells might be able to STORE cholesterol which might explain why animal fatty tissue contains roughly 100 times more cholesterol thatn plant fatty tissue, see down below.
Quote continued:
"The triglycerides carried in VLDL (annot. see quote above: triglycerides made by the liver)  are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids and IDL are formed. The IDL are further metabolized to LDL, which are taken up by the LDL receptor in numerous tissues including the liver, the predominant site of uptake."
Surpringly, the liver emits LDL, but does have LDL-receptor.
These LDL-receptor of the liver are said to take receive "chylomicron remnant", see, for instance, Dr. Malcom Kendrick
Assuming those LDL-receptor of the liver also take up LDL that has been refused by tissue cells however,  seems coherent to some basic principle of "store ("can"..) as much as you can": fat non used or stored in tissue being receivevd by the liver (free short fatty acids in blood!), liver handing its surplus back to tissue on VLDL; surplus fatty acid in liver metabolized to cholesterol, delivered to cells, cholesterol not taken up by cells  returned to the liver.
Thus, deposition of bad cholesterol in veins can be seen as some last resort of storage activity, in case the liver does restrict LDL-receptors as presumably tissue cells have done before.
Thus, excess (saturated, but, as you suggest: same should apply to unsaturated) fat in food might lead to excess storage activity by bad LDL.
Refering to the distinction between saturated and unsaturated fat your question seems to focus on  see, for instance,  Palm Oil Consumption Increases LDL Cholesterol Compared with Vegetable Oils Low in Saturated Fat in a Meta-Analysis of Clinical Trials
Ye Sun et al.,  This digest of empirical studies speaks in favour of saturated fat in contrast to unsaturated fat increasing "bad" (LDL) blood cholesterol. Doing quick research I did not find any explanatory theory. Here is  hint: Among unsaturated fatty acids there are some that are "essential" (as vitamins are). That is mentioned here:  [bmj.com] 5https://www.bmj.com/content/361/bmj.k2139 Maybe metabolism of essential unsaturated fatty acid signals a situation where there seems to be less need to turn fatty acids into cholesterol and send it to tissue cells (because those are signalled to be able to synthesize enough on their own). That's one idea.
Even if there is somehow "clear" causality in
dietary fat - chylomicrones - liver production of endogenous fat - VLDL - VLDL remnants - LDL
it seems to be debated on if there is a  difference between saturated and unsaturated fat in that respect. "You're right."
In the following, I would like to show that the statement "less fat, less cholesterol" your question refers to  might still be correct, in its statement of a rule of thumb, in its empirical result, especially in what regards differentiating unsaturated and saturated fat.
Content of cholesterol in food may be considered as   proportional to content of saturated fatty acids.
If you exclude saturated fatty acids from your diet according to the rule quoted in question you end up with zero input of cholesterol, and you end up as a vegetarian.
This is because

food from plants does not contain saturated fats - with a few exceptions: coconut and palmoil, nuts..., and

food from plants does not contain cholesterol in form and relevant quantity as animal food does.

"While cholesterol averages perhaps 50mg/kg total lipid in plants, it can be as high as 5 g/ kg(or more) in animal."
This is a factor of 100!
Quote is from a paper advocating the opposite point of view (no bias):
Journal of Chemical Education  J. Behrman* and V. Gopalan, Cholesterol in plants
However,
"There is a widespread belief among the public and even among chemists that plants do not contain cholesterol. This error is the result (in part) of the fact that plants generally contain only small quantities of cholesterol and that analytical methods for the detection of cholesterol in this range were not well developed until recently (1). Another reason has todo with the legalities of food labeling that allow small quan-tities of cholesterol in foods to be called zero (...). The fact is that cholesterol is widespread in the plant kingdom although other related sterols, such as β-sitosterol (henceforth referred to as sitosterol), generally occur in larger quantities. No current biochemistry text that we have examined provides an accurate account of cholesterol in plants.  Here is a suggested paragraph for the next generation of biochemistry texts: More than 250 steroids have been described in plants (3).Of these, perhaps sitosterol, which differs ..."
I think it's legitimate to inversely defere from this quote that food derived from plants, at least, does not contain cholesterol in  amounts relevant to nutrition.
See also Athel Cornish-Bowden
From  Wikipedia:
"Plants make cholesterol in very small amounts.[...] In larger quantities they produce phytosterols, chemically similar substances which can compete with cholesterol for reabsorption in the intestinal tract, thus potentially reducing cholesterol reabsorption." Wikipedia, Cholsterol
From Biology online
"Because of cholesterol that provides cell membrane structural integrity and fluidity, animal cells need not to have cell walls such as that in bacterial and plant cells."
Refering to point 2 of reasoning above:
"Most animal fats are saturated. The fats of plants and fish are generally unsaturated."
Wikipedia, Unsaturated Fat
Thus, avoiding saturated fat means avoiding animal fat, thus avoiding cholesterol.
Again, this reasoning is not what the quote  cited in your question seems to refer to or be based on. As an empirical rule it might be correct for the reasons stated.
To sum up: Even if it must be admitted that there are relevant amounts of saturated fat in plants, reducing saturated fat in diet in any case reduces cholesterol input (even if that'd mean the exclusion of coconut, palm oil and peanuts, from the diet - in that way you'd sure still end up a veggie).

No references are cited to support this answer.

@Bryan Krause I added some reference and am sure to be able to add many more references. However, I have become some suspicious mind with you - personally! - and I am begging you to either withdraw comment or downvote, explain what's wrong, or - best - delete this anwer that moreover I guess is not politically correct. Can user delete answer on his own? thanks.

Yes, users can delete their own answers. The references you've included do not seem to support the main conclusions in this answer. The first includes a quote but the citation is not sufficient for a reader to find the source of the quote, and therefore invalid. The second is also insufficient for a reader to find the source of the quote.

Hi, Bryan Hi,  Thank you for your criticism, I tried to amend accordingly, and very much expanded my answer according to what the question seems to focus on.  Let me know if you want me to delete the answer. There will be others.

I gave you an upvote for trying so well to support your answer. (I didn't read the sources, so I won't comment on their appropriateness.) I can't remove downvotes; only the downvoters can do that. To notify Bryan, you need to "ping" him by using the @ character before his name (he didn't get notification of your comment.) I'll do that for you: @BryanKrause - Is this answer improved enough for you to remove your downvote? Thanks.

Upvoted your answer for the amazing effort. It is definitely educative to me. Please don't delete it. The SE community behaves too protective. I have always felt with most SE sites that curiosity is not welcomed by the SE community. There is sadly always an attitude of "you should know better" or "how can you ask such a foolish question" or "how can you write such an amateurish answer". I have always faced unnecessary and unexplained mass down-voting.

I think you are right to question this "wisdom". In my opinion the statement from the web site that you linked is simply wrong. The idea that eating fat would make you fat dates back to the 1960s and was originally published by an MD just as offhand speculation, not any kind of science. Since then many others have just mindlessly repeated this incorrect idea.
First of all, it is physically impossible more or less for fats to be transported through the intestinal wall (see http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_lipids.html or Heinemann, T & Axtmann, G & von Bergmann, Klaus. (1994). Comparison of intestinal absorption of cholesterol with different plant sterol in man. European journal of clinical investigation. 23. 827-31.) Dietary cholesterol has to digested into more basic lipids and then transported through the intestinal wall by special molecules to be absorped by the body. So, the idea that eating eggs or whatever would give you "high cholesterol" is just an irrational idea.
Note that you will find papers with statements like 30% of dietary cholesterol is absorbed or 50% of dietary cholesterol is absorbed by the body and so forth, but these papers are either just observational papers that have no real controlled science behind them, or they are misleading. For example, it is true that 50% of dietary cholesterol gets DIGESTED and absorbed, but what gets absorbed is not cholesterol but monoglycerides and other small lipids that are the product of digestion. There are a lot of nutritional papers out there that just gloss over this and falsely imply that because cholesterol is being digested, that it is being absorbed whole, which is not true.
Virtually all serum cholesterol is synthesized by the body in the liver. The liver synthesizes cholesterol from fructose, a simple sugar that can be derived from complex sugars like cane sugar or from carbohydrates, such as wheat. Carbohydrates are first broken down into starch, then the starch is converted into sugars and the fructose component is circulated to the liver where it is converted into cholesterol or other things, such as triglycerides.
Concerning transportation of LDL: LDL is insoluble in water and cannot be transported across epithelial membranes. It must be digested into small lipids like monoglycerides with a watersoluble shell and then be transported by micelles. In the blood, triglycerides or LDL cholesterol manufactured by the liver can be transported for storage by special molecules called lipoproteins which emulsify the LDL and allow it to be transported in an aquaeous medium (the blood). In this form the LDL cannot cross any bodily membranes, but can only be placed in storage areas with direct blood contact. To be utilized as food for cells, LDL and triglycerides have to be circulated back to the liver where they are further broken down into COA, glucose and other types of molecules that cells can use as food.

Please add some (simple textbook) reference to "LDL is insoluble in water..." - that can't be true, as the function of the Lipoproteins is to make water insoluble fat soluble in blood, in water for transportation purposes. Please add some reference for tissue taking up cholesterol by "micelles", not by LDL-receptor (not to mention Nobel prize winners Goldstein/Brown). Did I get you wrong?

@PeterBernhard All lipids are insoluble in water. Very first sentence in this book: https://www.ncbi.nlm.nih.gov/books/NBK305896/. LDLs are not and cannot be transported across the intestinal wall for various reasons including their size. "Cholesterol is only minimally soluble in an aqueous environment and thus must be partitioned into bile salt micelles prior to absorption." direct quote from this book: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2692399/. I am aware there are papers claiming dietary cholesterol can be transported across the intestinal wall whole (continued)....

The intestinal wall has a paracellular pore size of about 10nm and only hydrophilic molecules smaller than this can traverse it. Micelles fit these restrictions. LDL, triglycerids and other large lipids are at least this large and are NOT hydrophilic, so they have no way to pass through the intestinal wall, unless they have been digested to smaller molecules and then attached to or enveloped by hydrophylic carriers such as micelles.

My first impression of your answer was that it might be a comment to my answer, rightly questioning the premise of its second part, ie.e. more cholesterol in food  means more bad cholesterol transport to cell.  Actually, the question here - there are several others on Stackexchange - focuses on "more fatty acids", and even more: on saturated fatty acids input.  - More fat does not mean more VDHL? Didn't you mention fat being stored away before it gets to the liver? Then "insuline" might be a worthy word.

Highly enlightening I find "The intestinal wall". Bluntly: LDL has got anything to do with the intestinal wall, as you mentin LDL in that context. I'd be interested in your textbook or even internet reference for LDL not soluble in water or blood.  How could LDL be a transporter of fatty acids? The word "acid" has it: any acid is hydrophilic. Can it be? The fat renders the LDL soluble? That is amazing and should clearly be emphasized in any textbook. Are you sure?

@PeterBernhard Did you not read my comment? "All lipids are insoluble in water. Very first sentence in this book: ncbi.nlm.nih.gov/books/NBK305896." Maybe read my entire comment before making snarky remarks? Do I have to link this book a third time?

I'm no good at snarkiness, please apologize. You want me to delete my comment, that'd be ok with me. Your reference is useful to anyone, however, it does not cover "LDL". These Lipoproteins are proteins, after all, so to say, and should be soluble. Snarkily: "...LDL, triglycerids and other large lipids" not soluble - not correct! Please falsify me. Is it okay for me to read and "digest" my lengthy comments into some list or so, to shorten what might be considered small talk by webmater and peer?

Let us continue this discussion in chat.

Again, your answer focuses on uptake in intestine, and that is 50 percent maybe of what the question is about. No "snarkeyin'": please explain more what your understanding of LDL is.

"Low Density Protein" is a protein, thus soluble in blood and water
Nowhere it's written that LDL gets closer to the intestine wall (pun: it's written on any wall of textbooks that LDL gets close to the arterial walls). You seem to state that LDL is a transporter from the intestine. That's not correct.

From Wikipedia: "Chylomicrons transport lipids absorbed from the intestine to adipose,  ... and  ... muscle tissue, where their triglyceride components are hydrolyzed by the ... lipoprotein lipase, allowing ... free fatty acids to be absorbed .... When a large portion ... s been hydrolyzed, chylomicron remnants are formed and are taken up by the liver, thereby also transferring dietary fat to the liver."
I'd be interested in knowing if "pancreas lipase"    breaks down unsaturated, not saturated fat, within intestine for "easy uptake", similarly: enterocytes, in stead of muscle/adipose cells.

From 2nd paper : "major lipoproteins secreted by the intestine are VLDL and chylomicrons." Surprising to all I bet. Enterocytes and liver cells so similar.   However:  LDL not mentioned in text.   LDL, in evolution, might have started as you appear to wrongly assume: as an uptake instrument. It wouldn't be surprising if you'd be right assuming enterocytes shedding LDL into the intestine... what for? For uptake of triglycerides - it's just the inverse of VLDL converted to LDL by un-loading. In evolution LDL might once have up-loaded. Please accept moving to chat except you want me to stop "it".


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Number of alleles' variations in a mushroom that has over 20,000 sexes
I am trying to understand the mating behavior of a particular species of fungi known as Schizophyllum commune, or the split-gill.
I found a blog post that explains the mechanisms that define the mating types (or sexes) of this species (there are about 28,000 sexes):
http://www.creativewi.re/2017/11/this-fungus-species-has-more-than-23000.html
The post says that the fungus' mating type is defined by a set of two genes that are present on two loci on the chromosomes. Each of these two genes has two alleles. Again, each allele has a number of variations. For example, a fungus with the A1 allele at locus A, and the B2 allele at locus B has the A1B2 mating type. This is a simplified example that doesn't include the alleles' variations.
Now, my question is as follows:
what is the number of these alleles' variations at each locus, and how did the scientists count the total number of sexes?
Thank you!

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Is the composition of the Cerebrospinal Fluid (CSF) in the first two ventricles different than that in the third and fourth ones?
We know two things. The first is that Cerebrospinal Fluid (CSF) flows from the first and second ventricles down to the third and then fourth ones https://en.wikipedia.org/wiki/Cerebrospinal_fluid#Circulation . And the second is that the Blood–Brain Barrier (BBB) only protects the two first ventricles https://en.wikipedia.org/wiki/Blood%E2%80%93brain_barrier#Structure , because part of the blood vessels around the two lower ventricles aren't covered with the BBB.
From this it seems to follow, that certain molecules enter the lower ventricles and never arrive in the first two. The first two ventricles are more protected.
An example of a theoretical consequence would be that if there is some reason to deliver some medicine to the third ventricle, and that medicine won't pass through the BBB, it could still be used because it would get there. But if the medicine needs to get to the first ventricles, it won't make it there.
Am I correct?

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text:
What is the proper quick freezing /snap freezing protocol for pancreatic tissue?
I would like to do a quick freeze on pancreas from mice. I want to then make sections (30 µm thick).  The idea is to preserve a fluorescent staining done in vivo.
I do not know if I should place my fresh tissue directly into liquid nitrogen, then embed the tissue in OCT, and then freeze everything in cold isopentane?
Or do I have to embed the fresh tissue in OCT first, prior to putting everything in nitrogen?
Or is there another protocol to do quick freezing in order to do sectioning?

Embed the tissue in OCT first (roughly cut to remove everything what is not needed) and the flash freeze it. Then you can cut your sections.
The first protocol describes it in detail, the second gives some additional information:

Protocol for Preparation of Frozen Tissues for Sectioning
Tissue freezing methods for cryostat sectioning

do not place it directly in the N2 unless it's clean. and high grade liquid N2 costs an arm and leg. put the tissue in the oct in a conical vial and that in the N2. don't use polycarbonate it may crack. check with the OCT manufacturers suggestions first though. I've followed this BD protocol before
http://www.bdbiosciences.com/resources/protocols/frozen_tissue.jsp

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Organ donation compatibility based on DNA
As far as I know, multiple tests are made before organ transplant to determine matching. Would it be possible to do the matching based on the DNA of the patients, rather than the actual serum antigen/antibody? If yes, is it any better/cheaper/easier?

Since the DNA is not recognized by the immune system (in contrast to surface molecules), this wouldn't make much sense.

@Chris but the these molecules are coded by the DNA, aren't they? I know there are post translation modifications (including immune cell maturation), but I was wondering how important/predictable are they

@Zeller If you are trying do test if a chair exists, why would you look for a carpenter rather than a chair? Sure there might be DNA markers, but whilst it's cheaper and (presumably) quicker to do the more appropriate method, why would you need/want to do a DNA test? (That is not necessarily a rhetorical question)

I'm trying to find a better solution for organ transplant matching based on genetic data instead of immunology. Assuming that if all the genes are know for both the donor and the acceptor, it is possible to determine the match. I haven't researched too much as the idea came up today, but I'd like to know if it is theoretically possible. Maybe going to the gene level, you can avoid multiple tests, predict/prevent chronic rejection and so.

@zeller
The better answers are being sought in a field called Regenerative Medicine.
A number of techniques have been tried, among them 3D printing of organs and dissolving the cells from a donor organ leaving the collagen scaffolding, then reseeding the organ with a patients stem cells in a bioreactor.
Most of these technologies, unfortunately, are in the proverbial 20 years from now category, which means that there are an incredible number of technical and biological challenges to overcome, but the ideal result would be organs with the patient's own cells and therefore no rejection or need for immunosuppressant therapies post transplant.
A nobel prize was awarded a few years back to Shinya Yamanaka for creating Human Induced Pluripotent Stem Cells. A technology like this would be the likely source of the stem cells necessary to seed these organs, however there have been problems with these cell lines including their tendencies to become neoplastic and form cancers.
So for at least the near and medium term the best alternative is to find organs that are as close a match as possible for Major Histocompatibility Complexes, and as Moderator Chris said, the best way to do this matching is to test for the cell surface proteins, as these are what will be the targets of immune cells. Also an organ has a very short life span after the donor dies to be usable. Sequencing is much slower than the protein screening that is in place today. You run into ethical questions regarding keeping someone on life support for the sole purpose of harvesting their organs.
And we still wouldn't be 100 percent sure that even people with the same alleles for these molecules express them in the exact same way as there may be slight differences in the post translational modifications that are made. The human immune system has evolved to detect small variations and as such we would still need to test the proteins, even if we found allelic matches. People get autoimmune diseases all the time, so there is no guarantee that even allelic matches would not be rejected.

It's not really (directly) related to this question as such, but you have listed a lot of different approaches & you do appear to still be active in here, so I just wanted to ask if you know of any suggestions of this approach in any available literature? https://biology.stackexchange.com/questions/79881/could-bone-marrow-transplants-be-used-to-prevent-tissue-rejection-of-trans-speci

The human genome is 3 billion letters long.  Most of that sequence has nothing to do with tissue rejection.  Only a handful of genes relate to tissue rejection, so those are what one might want to sequence, but even having the sequence doesn't necessarily tell you how the proteins are shaped, and it's protein shape that determines how they interact with each other.

But the different alleles of each protein, or gene, is what determines compatibility. That could be easily tested. The thing is it is cheaper to analyse serum than Next Generation Sequencing.

The SHAPE of the proteins is what determines compatibility, and that can't be predicted now from sequence alone. Anyway, next generation sequencing takes a week, PCR and sanger sequencing of 10 genes would take 48 hours.

It is the shape, sure, but the alleles are already known. If we look for compatibility we just have to identify them, not predict their structure. And I don't know where you got that NES takes a week. NES takes about half a day depending on jow much you have to mount and sequence (providing you have the equipment in your lab).

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


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Is there a biological reason for spreading food intake into breakfast-lunch-dinner?
I keep hearing over an over how humans can satisfy their entire daily caloric need in one sitting at a fast food restaurant. At the same time I'm looking at the kitchen plates, cups, etc, and they also seem to be getting bigger.
This makes me ask the question - was breakfast-lunch-dinner a concept invented because people:

Could not make enough food?
Could not make food fast enough?
Could not make food with high enough caloric intake?

I'm thinking along the lines of: you can make only so much tasteless porridge and stuff it in your mouth before it gets cold. At the same time I know that gorillas and some other primates have a very long (8 hours?) feeding session of eating raw vegetation throughout the day.
Is there a biological explanation why human food intake should be spread into X distinct sittings?

A biological reason? I don't think so. I think this is more a cultural thing. It is before, during and after work.

In stone age I dont think it would be beneficial to have a fixed schedule.

The three meals a day seems to be a cultural trait. Then what is the optimal number of meals a day? It is not known. Here are the results of some studies:
Reduced meal frequency:
It was found that the body can adapt to a single meal a day by modifying circulating hormone levels and glucose tolerance [1]. However it does not modify lipogenesis rates [2]. It may support cardiovascular disease risk factors [8].
Increased meal frequency:
Although there are studies that claim 5-6 meals a day help in maintenance of weight loss [3], others claim this habit increases hunger and the desire to eat and has no significant effect on fat oxidation [4]. A higher number of daily meals is recommended to the elderly suffering from cardiovascular diseases [5] because less but square meals lead to a redistribution of blood to the gastro-intestinal tract to increase absorption, which causes reduction of blood pressure [6].
Conclusion:
Energy balance is more important than meal frequency. As this study says [7]:

... there is no evidence that weight loss on hypoenergetic regimens is altered by meal frequency. We conclude that any effects of meal pattern on the regulation of body weight are likely to be mediated through effects on the food intake side of the energy balance equation.

References:

Carlson O, Martin B, Stote KS, Golden E, Maudsley S, Najjar SS, Ferrucci L, Ingram DK, Longo DL, Rumpler WV, Baer DJ, Egan J, Mattson MP. Impact of reduced meal frequency without caloric restriction on glucose regulation in healthy, normal-weight middle-aged men and women. Metab. Clin. Exp. 2007 Dec;56(12):1729-34. doi: 10.1016/j.metabol.2007.07.018. PubMed PMID: 17998028.
Jones PJ, Namchuk GL, Pederson RA. Meal frequency influences circulating hormone levels but not lipogenesis rates in humans. Metab. Clin. Exp. 1995 Feb;44(2):218-23. PubMed PMID: 7869919.
Bachman JL, Phelan S, Wing RR, Raynor HA. Eating frequency is higher in weight loss maintainers and normal-weight individuals than in overweight individuals. J Am Diet Assoc. 2011 Nov;111(11):1730-4. doi: 10.1016/j.jada.2011.08.006. PubMed PMID: 22027056.
Ohkawara K, Cornier MA, Kohrt WM, Melanson EL. Effects of increased meal frequency on fat oxidation and perceived hunger. Obesity (Silver Spring). 2013 Feb;21(2):336-43. doi: 10.1002/oby.20032. PubMed PMID: 23404961.
Ortega RM, Redondo MR, Zamora MJ, López-Sobaler AM, Quintas ME, Andrés P, Gaspar MJ, Requejo AM. [Relationship between the number of daily meals and the energy and nutrient intake in the elderly. Effect on various cardiovascular risk factors]. Nutr Hosp. 1998;13(4):186-92. PubMed PMID: 9780751.
Westenend M, Lenders JW, Thien T. The course of blood pressure after a meal: a difference between young and elderly subjects. J Hypertens Suppl. 1985 Dec;3(3):S417-9. PubMed PMID: 2856754.
Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. Br. J. Nutr. 1997 Apr;77 Suppl 1:S57-70. PubMed PMID: 9155494.
Stote KS, Baer DJ, Spears K, Paul DR, Harris GK, Rumpler WV, Strycula P, Najjar SS, Ferrucci L, Ingram DK, Longo DL, Mattson MP. A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am. J. Clin. Nutr. 2007 Apr;85(4):981-8. PubMed PMID: 17413096.

The answers to your 3 questions are no, no and no. The 3 meal concept is more of a recent concept when you compare that Ancient Romans used to frown upon eating more than once a day. You can read a brief history of how food habits evolved in this article. Food habits have been variable all throughout history and it still varies by culture. Food habits divided by different eras can be read in this article. In the current age and time, I think we just try to spread our calorie intake over the day and that is why we try to stick to the 3 meal concept.(reference). There is no biological reason as far as I could see (reference). Just a matter of improved health consciousness and understanding of the human body. This article contain some interesting thoughts on meal timings and optimal intake.

could you perhaps share/summarize an important quote from some of these sources? I ask because if any of your links go dead (which is surprisingly common) your answer loses much of its value. Just want to make sure posts remain helpful for as long as possible :). Thanks!


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Is greed an evolved trait?
I am not a biologist, but I am fascinated by evolution.
I was watching the news this morning and, as so often is the case, there was a news story about a corrupt politician who was accepting bribes.
This started me thinking about how greed can become such a strong factor in one's life that it cancels out empathy for your fellow human beings.
So I was wondering--is greed an evolved trait?  Maybe some result of an evolutionary pressure to hoard food for example?

I doubt that human behaviour can be biologically explained. Something that might appear greedy to someone might not be so for others.. It is opinion based I would say...

@TheLastWord I think that many evolutionary psychologists would disagree with you. I'm not saying that I necessarily would, but there's at least a lot of scientific discussion on the topic.

There's some connection to this question, although of course 'cheating' in social insects and in human societies could be a very different thing (or, perhaps, very similar): http://biology.stackexchange.com/questions/5076/modern-reference-for-kropotkins-lazy-bees/9478#9478

@Oreotrephes So maybe then this question was better suited for http://cogsci.stackexchange.com/

I think that Sociobiology should be considered enough of a science to discuss it on biology stackexchange.  It gets published in Science, hopefully that's good enough in general.

The whole point about your question is to define what is an "evolved trait"? The concept of "evolved trait" does not exist in evolutionary biology. Here are various definitions I can think of that could apply to the expression "evolved traits".
Heritable Traits
Does evolved traits mean heritable traits?
A trait may be heritable or not. See for example my answer to this post to understand what heritable mean. You may want to understand the difference between the narrow and broad sense of heritability. Greed is probably heritable as several studies showed that many personality traits are heritable. This post will maybe give you more info.
--> Greed is probably a heritable trait
Traits that evolve
Does evolved traits mean traits that can evolve?
Any (existing) biological trait evolves. Not necessarily because they are selected for or against, neither even for genetic reasons, but traits change through times. Culture changes.
--> Yes, greediness can evolve
Traits that are adaptations
Does evolved traits mean traits that are adaptations?
The concept of adaptation is not always easy to define and its definition may vary from authors to authors. Simply speaking, an adaptation might be defined as a trait that is now fixed in the population (meaning that all individuals in the population carry this trait) but when it was not fixed yet it was beneficial. Such definitions would not fit the concept of greediness if we assume there is some genetic variance for greediness. But while I am not aware of any study on the subject, a level of greediness very probably influence the fitness  (=~ reproductive success) of its carrier. If someone is extremely greedy, he might not find a mate and may fail to reproduce. On the other side, someone that is extremely generous may give everything it has up to its life and would definitely fail to reproduce. Therefore, it seems at first though that there is what we call stabilizing selection on the level of greediness.
--> It depends on the meaning of adaptation. But yes, it seems intuitive that greediness is a trait that undergoes (stabilizing) selection.

Social traits
Greediness is the kind of trait that are particularly interesting because it influences not only the fitness of its carrier but also the fitness of other individuals in the population. We say that it is a social trait and the field that study such traits is called social evolution. You'll need to get in touch with Hamilton's rule (Kin selection) and evolutionary game theory to understand more about the evolution of social traits. This post may eventually help you.

Really nice answer - I think this is a perfect example of a great response to a "I'm not a biologist, but I just wondered..." question.

this is a better answer, but would love to see a full answer to the question here on the site


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Can wasps see under moonlight?
It appears that the best time to attack a wasp nest is in the middle of the night. Their venom might terrorize us (my five-day old sting remains swollen and is starting to have red bumps in an area the size of a tennis ball), but at least our eyesight is superior. If we attack while they are asleep, or at least resting, we have our best chance of escaping unscathed—or so the online pundits claim.
The nest in question is at the edge between the wall and the roof protrusion. Because it is 8 feet off the ground rather than on the ground, it would appear to be a paper wasp nest. But because it is covered with paper and the individual cells are occluded, with the entrance at the bottom the only visible path leading inside, it may well be a yellow jacket nest.
Maybe it's futile to attack the nest in September. One might as well let them be. The nest will anyway be deserted in October when the temperature starts to freeze overnight. But it's never too early to prepare for next Spring.
I could choose a night when there is absolutely no light—not even moonlight—but then I myself would need to use a flashlight, providing them with the means of pursuing me. Or I could choose a full-moon, or near full-moon, night, and then I can see and they can, perhaps, not see.
Can wasps see under moonlight?

The false assumption here is that all animals are as dependent on vision as humans. Insects, in particular, make great use of chemical senses. The reason people say attack at night is not so they can't target you. It's to get as many of them as possible on the first strike so they have fewer to retaliate with.

From my experience in the field, they are pretty adept at flying around in pitch black abandoned farmhouses.

No.... probably not... wasp cannot see at night... their scotopic vision{dim light vision} is not well develop so before sunset they return back to thier nest... so at night.. probably you can get them all together... rather then hunting for each indivisually...for reference https://sciencing.com/how-to-identify-wasps-bees-13406632.html hope it helps..

Welcome! Thanks for providing an answer. Whilst the information may be correct, we prefer answers to have some kind of citation or reference to back up statements made. If you could add something like that, it would be great. Thanks.


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What software can be used for simulating human meiosis, taking linkage and recombination into account?
I want to study the nature of genetic variation in offspring from the same set of human parents. To this end, I would like to take two (male and female) complete genomes, generate gametes from them, combine pairs of them at random, and analyze the distribution of the resultant offspring’s genomes (calculate variance of polygenic risk scores, etc.).
In the absence of recombination, this is trivial; I just duplicate gamete DNA and segregate the vectors representing tetrads. However, I want to take recombination and linkage into account. Of course, I could randomly generate crossover sites and even encode interference in the algorithm I write to perform this, but I want things to be as similar to observed human recombination dynamics as possible.
I can’t seem to find any software packages (preferably in Python, but I’m not picky) that would allow me to do this, but I figure I must have overlooked a standard library for this purpose as this seems like something people would have wanted to do long before now.

I believe that this is an application of the ms program, which is widely used in population genetics.
More recent programs also exist (here is another; here is another, here is another) that may be more applicable directly to human genomes.
I'd suggest looking at those various options and deciding which of them fits your application. This is certainly not exhaustive, there are plenty more!


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Why is this oxoglutarate dehydrogenase and not oxoglutarate decarboxylase?
I was looking at the oxoglutarate dehydrogenase complex and saw the reaction mechanism for its E1-TPP mechanism, which results in the formation of a stabilized carbanion intermediate.
The mechanism begins with a protonation, but since the "goal" of the enzyme is to form the carbanion intermediate, it seems to me that the decarboxylation is the key part of the reaction. So why is this a dehydrogenase-catalyzed reaction and not a decarboxylase-catalyzed one?

I'm new to citric acid cycle and I'm judging this question based on my previous knowledge of biochemistry and organic chemistry.
I've looked into several protein databases and shockingly it seems oxoglutarate dehydrogenase is the correct name for it.( See :Uniprot , PDB 1 , PDB 2 )
Although the nomenclature of biological enzymes sometimes does not sound right to me , I believe this naming is appropriate for this molecule. First take a look at these definitions:
(Definitions from Oxford Languages / Google)

Dehydrogenase :  an enzyme
that catalyses the removal of hydrogen atoms from a particular
molecule, particularly in the electron transport chain reactions of
cell respiration in conjunction with the coenzymes NAD and FAD.

(Wikipedia)

Dehydrogenase (also called DH or DHase in the literature) is an enzyme
belonging to the group of oxidoreductases that oxidizes a substrate by
reducing an electron acceptor, usually NAD+/NADP+ or a flavin coenzyme
such as FAD or FMN.

(Wikipedia)

Decarboxylation is a chemical reaction that removes a carboxyl group
and releases carbon dioxide (CO2). Usually, decarboxylation refers to
a reaction of carboxylic acids, removing a carbon atom from a carbon
chain

Here is why the usage of "decarboxylase" in the name of the enzyme is incorrect :
Recall amylase (Amylase-Wiki) . That enzyme consumes amylose as substrate and produces maltose out of it. It sounds weird if one calls it "Demaltase" just because it gives out maltose. Instead, in this case , consumption of amylose plays a more important role in digestion.
According to above definitions , the "goal" here is simply the movement of H+ and the electron to FAD (to generate FADH2) and then to NAD+ (To generate NADH), Not the removal of CO2. That is just a by-product resulting from the mechanism. see :Reaction
Here's why the usage of "dehydrogenase" in the name of the enzyme  is correct :
Take a look at this  .
The whole process involves the movement of one proton from thiamindiphosphate and one from CoA-SH and also 2 electrons from two S-H bonds (I've traced the Hydrogens for you. Trace the electrons yourself ! :) )
Recall the concepts of carbonyl functional group from organic chemistry. One way to perform any reactions on carbonyls is to use an acidic catalysis which is most of the times H+ resulted from H2SO4 or HCl.Take a look at this. Also see Morrison-boyd organic chemistry or Vollhardt's This H+ Activates the carbonyl functional group , allowing it to participate in nucleophilic substitution more easily. The addition of H+ to Carbonyl oxygen is reversible and thus it is important to optimize this equilibrium. The indicated enzyme operates on this equilibruim to gain the maximum yeild. Plus it may induce TPP to lose a H+ . These two processes (the removal of H+ from TPP and the addition of H+ to oxogultarate ) can not be done with the help of the enzyme , hence the name Dehydrogenase for the enzyme.

Your first mention of dehydrogenase is  missing the de.

@Polypipe Wrangler , Thank you for that . Actually the title of question is missing the de too!


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Sextuplet corn (Zea mays with branched ear)
In 2019 I planted some sweet corn next to some Hopi blue flint type corn. Of course my mistake was apparent once I started to see the ears. The closer the two types were to each other, the more they were mixed. So this year, not realizing what might happen, I planted the solid blue seeds that I had saved. I don't know much about corn, clearly, and assumed that if I planted blue seeds, I'd get all blue corn. Not the case. Most was all kinds of different colors, shapes, including some kernels that were clearly sweet corn, with most being a field corn, some with a dent, most without. Then some plants had some nice large ears of large blue kernels.
Okay, so that is just the backstory in case it will help. I ended up with this one 'cob' that is actually 6 small cobs all on one stem. Very bizarre, and I can find nothing like this online. I am curious if anyone can tell me how this happened, and perhaps if planting those same seeds would result in more of this. I took a video to get the best look of this oddity. https://youtu.be/xIAYaRwgQ-k

Welcome to Biology.SE! This sounds very interesting, but please [edit] one or more clear photos of the unusual cob into your post — the standard for questions (and answers) on this site is that they must provide enough information without requiring users to go to external sites. For example you could upload stills captured from your video. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

Thank you, I was unable to upload before due to your size restriction and I didn't have an easy way to resize.

This looks a lot like a ramosa mutant (for example see the ears in panels A,G,H - taken from Figure 2 from Gallavotti et. al. 20101).

Ramosa mutations affect the branching pattern of the inflorescence (i.e. the ear and tassel in maize - aka. corn in the US) and are typically highly variable.  These are thought to be partial reversions to the phenotype of teosinte, which is the putative ancestor of maize2,3.
The unusual ear you collected may have resulted from a spontaneous mutation (possibly transposon driven), but also could be due to infection by a fungus (these sometimes secrete hormones that create developmental effects), or even insect damage to the developing ear.
If this phenotype was due to a heritable mutation you may notice an effect on the tassel (more densely branched), but IIRC this can be quite subtle. The best evidence for this being genetic would be seeing this phenotype recurring in subsequent generations. If possible plant kernels from the strange ear in an isolated area. It is also possible to do controlled crossing in maize — if you go this route I would suggest that you try to self pollinate (i.e. take pollen from each plant's tassel and put it on that same plant's ear).
You also might find this short video to be of interest.
If you get plants with similar phenotypes in this or a subsequent generation I can put you in touch with someone working on ramosa genes who might be interested in having some of the seed if you're willing to share ...
References:
1: Gallavotti, A., Long, J. A., Stanfield, S., Yang, X., Jackson, D., Vollbrecht, E., & Schmidt, R. J. (2010). The control of axillary meristem fate in the maize ramosa pathway. Development, 137(17), 2849-2856.
2: Iltis, H. H. (1983). From teosinte to maize: the catastrophic sexual transmutation. Science, 222(4626), 886-894.
3: Bennetzen, J., Buckler, E., Chandler, V., Doebley, J., Dorweiler, J., Gaut, B., ... & Walbot, V. (2001). Genetic evidence and the origin of maize. Latin American Antiquity, 84-86.

Thank you very much! I do hope to try some hand pollinating the next time I have an opportunity to garden. I would certainly be willing to share seed if it seems that they would pass this phenomena along to their progeny! I'd love to see what a capable person could do with this, if it is genetic. Being in the Pacific Northwest, it would not surprise me if fungus played a role. ha


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Stomata during night (respiration)
How does carbon dioxide from respiration diffuse out of the leaf during the night?
Do stomata close completely during night?

Salt water macro algae ( calurpa ) discharge CO2 at night , but I don't know if it is from stomata.  I had a 75 salt tank with a lot of calurpa and few fish ; the pH would drop impressively each night considering the high buffering capacity. as I remember 8.7 to 8.3.

Land plants might do better to keep their CO2 to use in the morning, unless they produce way too much of it.
CO2 is present in air at concentration around 0.03%. (In recent years it's gone up to 0.04%.) That's a low concentration to work against.
Remember, in the daytime those plants are sending water vapor and O2 OUT the stomata. It's a pressure gradient. Why let CO2 out at night and then  depend on it coming IN against the flow the next day?
Plants have ways to grab onto CO2 so it won't just drift away. They convert it to things that aren't gases -- oxaloacetic acid or malate, or 3-phosphoglycerate, or possibly others that haven't been noticed yet.
These compounds can be stored. Then restore the CO2 precisely when and where it is needed.
Some CO2 gets this treatment at the roots (where CO2 concentration can sometimes be as high as 8%) and the storage compounds then get sent toward the leaves along with water and minerals.
CO2 from roots

Carbon dioxide is gas and can easily diffuse out through epidermal cell following concentration gradient. As during night respiration is going on, lot of Carbon dioxide accumulates inside leaf to form a concentration gradient which is sufficient to cause diffusion.


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Albino elephants
How many albino elephants are there across the world? There is no information on the total number of albino elephants across the world except for the few albino elephants captured by people.

According to this howstuffworks.com article who itself poorly cite a paper with a broken link (!), albinism in mammals occur in typically about 1 in every 10,000 births. The claim is quite definitely not trustworthy but that's all I found!
There are an estimated 450,000 - 700,000 African elephants and between 35,000 - 40,000 wild Asian elephants. So, if we believe that about 1 birth in 100,000 is an albino, then there are between 30 and 100 albino elephants in the world.
See also this quora post

This is the website/magazine howstuffworks.com is referring to. They don't cite anything but "some researchers".


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What is the type of conservation in which seed banks are an example?
Firstly I think this question is quite ambiguous (I did not come up with it) so sorry.
I have only come across 4 'types' of conservation: environmental, animal, marine, and human conservation.
I am aware that animal conservation includes their habitats, so perhaps keeping seed banks is a way of preserving habitats.
I may generally say that seed banks are a way of preserving biodiversity but I don't know if 'biodiversity conservation' is even a thing.

I don' t really get what your "types" are referring to (do you have a reference to these specific four types?) and they are clearly not covering all cases in conservation biology. They are also not mutually exklusive, and can overlap. Also, by "seed bank"I assume that you are referring to human conservation of seeds (as genetic material, see eg the Svalbard Global Seed Vault) and not the soil seed bank that some species has.

@Mesentery could you expand?

I agree with @fileunderwater. The "types" you list are unclear. The question is based upon a series of issues of terminology and semantics and therefore cannot be answered. Anyone could just say random things like "agriculture conservation", "plant conservation", "economic conservation", "field conservation", "forest conservation", "private-sector conservation", etc... and there is no way to judge what would make sense or not. I am voting to close as unclear.

@Remi.b I am simply rewriting the question that has been set as homework. Any ambiguity is therefore not at all down to me. Part of the reason I asked here is because I did not really understand the question. I also "shared my previous  attempts" at the question and therefore have met the question asking guidelines.

@BenHughes Is there a certain book your homework/lectures is based on? Or did you get any definitions during the lesions regarding the terms you used in the question?

@Marzipanherz no it was amongst a bunch of past paper questions he set us

@BenHughes You might want to link to this series of paper. Maybe one of them attempt to do this kind of categorization.

Seed banks are a part of "plant conservation" efforts which is missing from your list.

IMO the question makes no sense and an answer to a senseless question cannot make any sense (unless it starts by redefining the question). -1

I do see your point.  But, one of the problems that I've seen on one other SE site is that questions go unanswered because they are somehow viewed as unworthy.  I choose to answer if it takes less energy than many of the comments. IMO.


text:
What limits the speed of human perception?
I'm writing a novel in which the main character's perception and thought processes are sped up considerably, in essence slowing down the world around him. To others, it seems like his reactions are far faster than normal. Of course, there's a fantasy explanation for this in the story, but it led me to wonder exactly what limits the speed of human perception and reasoning in the real world.
From what I know, the speed at which we perceive events appears to be a constant. What exactly determines that rate? Is it possible to change it? Is it possible that different people perceive things at different speeds?

Actually there is a movie on this concept- Limitless..
You can check this post. You may find it useful.

The vertebrate photoreceptors may have a certain speed threshold, so you can give him mutant fly photoreceptors. Chimpanzees can see 10 different objects on a screen and choose one of them much faster than a human, perhaps it's to do with peripheral vision. you can have mutant connections between the old and new areas of the brain which can learn reflexes perfectly.

Flicker Fusion Threshold:
The wikipedia definition:

It is defined as the frequency at which an intermittent light stimulus appears to be completely steady to the average human observer.

Background
In 1824, Peter Mark Roget (who also wrote the famous Thesaurus) first presented the concept of "persistence of vision" to the Royal Society of London, as the ability of the retina to retain an image of an object for $\frac{1}{20}$ to $\frac{1}{5}$ second after its removal from the field of vision.
A second principle - the $\phi\ phenomenon$ or stroboscopic effect is closely related to flicker fusion. It was first studied by Max Wertheimer and Hugo Munsterberg between 1912-16. Wertheimer and Munsterberg found that subjects can perceptually bridge the temporal gap between two consecutive displays, so that a series of static images appear as continuous movement. The discovery of flicker fusion became the perceptual basis for moving pictures, television, and all media based on stroboscopic presentation of stimuli.
The minimal frequency at which flickering stimuli appear continuous is called the critical flicker frequency.

Perceptual factors affecting the critical flicker fusion threshold
This critical flicker fusion threshold depends on the stimulus’

Luminance (the Ferry-Porter law),
Size (the Granit-Harper law),
Color,
Retinal eccentricity,
Background Luminance, and other factors.

Biology Behind it:

Physiological evidence in humans and monkeys shows that flicker rates
  above the perceptual critical flicker frequency threshold can
  nevertheless generate cortical and subcortical visual responses.  Thus
  the temporal integration underlying flicker fusion does not occur at
  the level of the retina,  but must take place later in the visual
  hierarchy. Single-unit recordings in the primary visual cortex of
  primates suggests that,  for two brief-duration targets presented in
  close succession, the after-discharge to the first  target interferes
  with the onset-response to the second target (Macknik, 2006) (see
  Figure 5). The onset-response to the second flash is absent for
  inter-stimuli intervals of 30 msec or shorter (equivalent to 17 Hz
  periodic). If the flashes are separated by more than 30 ms, the
  after-discharge to the first flash and the onset-response to the
  second flash begin to recover (i.e. equivalent to <17 Hz flicker).
  These intervals roughly coincide with the critical flicker fusion
  threshold in humans for 100% contrast stimuli in the fovea .
This suggests that perceptual flicker fusion may be due to the lack of
  robust transient responses to the flickering stimulus.

http://images.scholarpedia.org/w/images/thumb/8/8b/Flicker_fusion_fig5.png/360px-Flicker_fusion_fig5.png

Source:

Bartley (1939). Some effects of intermittent photic stimulation. Journal of Experimental Psychology 25, 462-480.
Bloch, A. M. (1885). Experience sur la vision. Comptes Rendus de Seances de la Societe de Biologie, Paris 37, 493-495.
Brücke, E. (1864). Über den Nutzeffect intermittierender Netzhautreizungen. Sitzungsber k Akad Wissensch Math-naturw Cl, Wien 49, 128-153.
Di Lollo, V., and Bischof, W. F. (1995). Inverse-intensity effect in duration of visible persistence. Psychol Bull 118, 223-237.
Ferry, E. (1892). Persistence of vision. Amer J Sci 44, 192-207.
Fukuda, T. (1979). Relation between flicker fusion threshold and retinal positions. Percept Mot Skills 49, 3-17.
Flicker Fusion

What is the Different speeds of Visual Perception?

First-order motion
Experiment: A moving sinusoidal grating with bright peaks and dark troughs is seen through a window.
Result: Even when its velocity is so high that 30 of its bright peaks pass each location per second (30 Hz), observers still perceive its direction of
motion.

Depth from binocular disparity
Experiment: Two identical gratings, one in each eye, are viewed through identical windows.
Result: One is spatially shifted relative to the other, introducing a binocular disparity that is perceived as depth.
Even when they move at a 30 Hz rate, the depth is still perceived.
If the input to depth mechanisms were blurred at a >30 ms timescale, detecting the depth would be impossible at this rate.
Edges and texture boundaries
Experiment: Against a gray background, a field of white dots is adjacent to a field of black dots.
Result: Both fields are set in rapid alternation between white and black, but out of phase – when
one is white, the other is black. The conspicuous boundary between them is perceived even at fast
rates of 30 Hz, whereas at faster rates the black and white are averaged by the brain into the same color as the background.
http://ak.picdn.net/shutterstock/videos/3139525/preview/stock-footage-retro-geometric-dot-background-in-black-gray-and-white.jpg
Binding of color and orientation sharing a spatial location
Experiment & Result: If a red, right-tilted patch is alternated with a green, left tilted patch,
it is easy to distinguish from the complementary pairing of red left alternating with green right, even at
fast 20 Hz rates.
Binding of form and color across space
Alternating color-shape pairings can only be reported at rates below ~3 Hz.

source: http://www.psych.usyd.edu.au/staff/colinc/HTML/dynamics.htm
Binding of global form with color
Two specially constructed dot patterns that form distinct shapes alternate, with all the dots of one red and all the
dots of the other green.
At alternation rates faster than several a second it is very difficult to determine the shape color pairing even though the shapes and colors themselves
are easily identified.
Direction change and acceleration perception
A moving stimulus alternates between two speeds (acceleration) or two directions. When the alternation occurs
faster than several per second, these changes are unperceivable.
Its limit is 8-10 Hz.
Word perception
Certain pairs of words (such as ‘jump’ and ‘pink’), when alternated in the same location, cannot be distinguished
from another matched pair at rapid rates as one perceives only the sum, which is the same for both pairs.
They can be distinguished only at rates slower than several items per second.

Source: http://www.psych.usyd.edu.au/staff/alexh/research/words/
Source:

Holcombe AO (2009) Seeing slow and seeing fast: two limits on perception. Trends Cogn Sci 13:216 –221.
http://www.psych.usyd.edu.au/staff/colinc/HTML/dynamics.htm

Hi, nice response! but I'm still wondering which part in your response shows the limiting factors/reasons behind the human perception speed limitation. You have a very nice list of perception/cognitive limitations but not the underlying reason. Are there explanations for these limitations that can be elaborated through neurophysiology or molecular biology perhaps?

Definitely some interesting material that you've shared here, Devashish Das, but I also would be interested in the underlying reasons that the human perception rate is limited. You don't seem to have talked about that too much here--looking forward to hearing more from you.

@Bez: Oh Sorry!! You were asking about Flicker fusion threshold!!!

Here's a paper on the link between perception and reaction time. The general theme in biology is that the greater number of neurons an animal has in series, the more latency that animal will have in that pathway. This can partially account for organisms which have tiny nervous systems and very quick reflexes.
In our own body, we have reflex pathways which entirely circumvent our brain. These help us maintain our posture and remain upright. These are muscle spindles and spinal reflexes. They are among the quickest response mechanisms.
You might want to look up synaptic pruning and synesthesia. These are two phenomena on opposite ends of the spectrum of synapse count. Synesthesia is an excess of sensory pathways in the brain and synaptic pruning is the natural deletion of pathways in the maturing brain.
Most of our movements are variations on muscle memories, mediated by the cerebellum. You can start your research on muscle memory here. Developing muscle memory is a rigorous process, but is a fundamental learning tool for musicians and those in martial arts.

The limitations are of several natures: cognitive once the signal has arrived in the brain, but also physical within the eye e.g. for vision.
For vision, the crucial bit is to transform changes of incoming light into an electrical signal. It is not completely elucidated. Recent research shows e.g. that for some flies, there may be a mechanical intermediate stage: the light-sensing cells react by contracting, and this would modify the electric resistance of their membrane. I don't think it is known whether the human, who have less need for a fast response but want more detail of what they're looking at, have the same mechanism or not: maybe your hero has something of the fly that we don't have?


text:
T7 phage promoter action in mammals
Does anyone know if the T7 phage promoter is efficient in mammalian systems?

Amazingly, yes.
See High level gene expression in mammalian cells by a nuclear T7-phage RNA polymerase. The authors recognize that the T7 RNA polymerase tends to work only in the cytoplasm thus is unable to transcribe genes in the nucleus. To remedy this limitation, the T7 polymerase was fused to a nuclear location signal peptide to localize the polymerase correctly.
Promega sells a T7 expression system for RNAi production.


text:
To understand Second messenger signalling in I/c and E/c
I found this picture in my study materials.
I think it is too schematic and ignores the big pictures.

I think the thing connected to the hormone is receptor.
The second messanger is then connected to the receptor which stimulates the effector cell in the cytosol.
The cell then response both to cytosol and to extracellular space.
How do you understand this picture?
Do you know any similar pictures which present the same thing but clearer and more exactly?

I think the schematic you have there and the one that @Masi posted are pretty good.  A better way of getting a grasp of intercellular signaling would be to study a specific hormone and understand how each of the elements in the block diagrams here could vary.
For instance take a look at this diagram from a journal article where they are tinkering with yeast mating factor, one of the first discovered extracellular signaling pathways.

alpha factor and 'ligand' (I assume its not known at this point) bind to their receptors Ste2 and hGPCR respectively.  They then activate G protein complexes and both activate the same kinase cascade Ste4/18 -> Cdc42 -> Ste20 -> MEKK/MEK/MAPK/Ste5 which then may activate Far1 (or not) and Ste12.  Far1 and Ste12 are migrated into the nucleus to activate genes for cell reproduction.
By actually filling out the boxes in your diagram you can see dozens of different paradigms for how cell signaling may work, and why the diagram you have needs to be so simple.  Hope this helps.

Glad it makes sense!

I found this picture from my old study materials which I edited little to show the I/e and E/c spaces.

I think some arrows are missing. Probably, some arrows should go from specific modifications of enzymes or proteins to I/c and E/c. What do you think?


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How does the MMR vaccine affect lymph nodes in preventing measles?
I am trying to understand this statement about the Measles part of the MMR (Mumps, Measles and Rubella) vaccine

Measles prevention: MMR (AB protect during primary and secondary viremia)

Measles enters from respiratory tract, through mucosa of the upper respiratory tract. The virus passes into cervical lymph nodes. Now, starts first viremia (MMR somehow helping here) which lasts about 5 days. Then antibodies are secreted during 15 days which leads to rash lasting about 3 days.
I think this second viremia refers to the possible dissemination of the virus to other lymph nodes by blood.
This suggests me that the vaccine primarily have a mechanism that affects in the lymph nodes or generally in the lymphatic circulation.
How MMR vaccine affect lymph nodes in preventing measles?

Lets define viremia first: The primary viremia occurs in the cells which the virus enters first in the body. There it replicates to high titers before it leaves this cells, spreads through the body and infects other cells. This is then the second viremia.
For measles the primary viremia occurs in the respiratory epithelium and in the local lymph nodes. The second viremia then occurs in skin, conjunctiva, respiratory tract, and other distant organs. In this phase also the characteristic rash occurs due to a hypersensitivity reaction of the skin. For details see here and here.
The measles vaccine works like any other vaccine: By raising an immune response against the vaccination virus. This leads to a normal immune response which leads to the production of specific antibodies against the measles virus and also to immunologic memory. These antibodies are available to fight the virus when it enters the body of a vaccinated person. This also triggers the proliferation of virus specific memory B cells which then differentiate into plasma cells and produce vast amounts of protective antibodies. So there is no special mechanism involved here beyond immunologic memory.

Thank you for your answer with appropriate sources! I think similar immunopathology exist also for Rubella (German measles); the MMR vaccine seems to affect similarly as for measles.

You're always welcome. It is the same for rubella, the antibodies protect effectively against the virus.


text:
How host defends against S. pneumoniae capsule?
The host response involves at least phagocytosis and probably localised acute inflammatory response at least after the colonisation.
I am thinking how the host can defend against pneumolysin which helps the streptococcus pneumoniae invasion.
How can the host defend against Streptococcus pneumoniae capsule?

According to the two papers listed below, this is mostly done by a neutrophilic inflammatory response. The response is regulated by mechanisms of the innate immune system and is mediated by receptor like TLR2, TLR4 and SIGN-R1.

Role of Dectin-2 in the host defense against Streptococcus
pneumoniae infection
Dectin-2-dependent NKT cell activation and serotype-specific antibody
production in mice immunized with pneumococcal polysaccharide
vaccine.

There are a few papers which go deeper (reviews, so you will probably have to go through the reference lists):

Mechanisms of host defense against infection with Streptococcus
pneumoniae.

This paper mentions specific antibodies later on in the reaction and finally the opsonization by immune cells.
These two papers tal specifically about pneumolysin:

Pneumococcal virulence factors and host immune responses to them.
Pneumolysin as a vaccine and drug target in the prevention and
treatment of invasive pneumococcal disease.

This seems to be localised acute inflammation what they describe. Probably, first fibrous type of acute inflammation.

@Masi I expanded my answer.


text:
Pathogenesis of chronic venous congestion in skin?
I think CVC cannot lead to heart failure primarily.
So let's think its pathogenesis in skin now only.
I think the pathogenesis is like this

dilation of veins and capillaries due to impaired venous drainage
reduced outflow of blood from a tissue
passive process
$\to$ local increase in blood volumes
$\to$ local increase in venous pressure
pathological
$\to$ shortage of oxygen and built-up metabolic waste
$\to$ structural changes in microvasculature
$\to$ increased venous permeability % hallmark of acute inflammation
$\to$ increased size of venous caliber
$\to$ emigration of leucocytes
$\to$ accumulation at site of injury
activation of acute inflammation
$\to$ protein into extravascular space
$\to$ increased viscosity of blood
$\to$ deoxygenated blood blood stasis
$\to$ congested tissue
$\to$ leucocytes move to endothelial wall (selectins)
$\to$ roll
$\to$ adhere (integrin to stop)
$\to$ migrate
$\to$ dysky reddish-bluish skin (cyanotic)
$\to$ healing via fibrosis
$\to$ scar
Causes: venous thrombosis; venous compression; heart failure;

I am not sure about the role of leucocytes exactly in this process.
I am not sure if they play a big role in the formation of cyanotic skin.
I think the outcome is mostly because of increased vascular permeability and its deoxygenated blood in extracellular space.
What is the right pathogenesis of chronic venous congestion in skin?

I extended this question to lungs to understand CVC enough well: http://biology.stackexchange.com/questions/15874/pathogenesis-of-chronic-venous-congestion-in-lungs/15875#15875

Probably so simple answer is enough

acrocyanosis (manifestation of heart failure) which lead to distant (acro - distant) cyanosis, bluish skin.


text:
How does HIV know to attack specific immune system cells?
I'm no biologist, but curious of the answer to which I could not find online.
How are Human Immunodeficiency viruses able to detect and distinguish immune system cells with a CD4 receptor on the surface from other cells in the body, in particular other immune system cells without the receptor?
If I have asked the question on the wrong platform, please inform me otherwise.
Thanks

It's not really a matter of "knowing", it's simply a complex chemical reaction.

@jamesqf could you recommend me some reading in this topic?

This paper, specifically the sections titled "HIV Entry Fundamentals" and "Discovery of the HIV Receptors", is a good resource.

@acvill Thankyou very much!

The CD4 receptor is a protein complex that harbors very specific chemistry. A virus is able to bind with the receptor if it harbors a particular protein/set of proteins that are able to interact with the receptor. The virus is basically disguised as something the CD4 receptor recognizes, and from there it is internalized within the cell via a process called endocytosis. You can google viral endocytosis to learn more.


text:
How does glucose uptake happen in the various tissues of the body?
I know that the GLUT4 transporter allows for insulin-dependent uptake of glucose in skeletal muscle, liver and adipocytes. I also know that GLUT2 transporters are present in the liver and allow it to absorb glucose in the absence of insulin, and GLUT1/GLUT3 allow glucose to cross the blood-brain barrier and enter neurons.
However in my research I could not find the mechanism for glucose uptake in the remaining tissues of the body (Ex. epithelial tissue, connective tissue). Are there other types of transporters for glucose in these tissues? Surely these other cells also need glucose to survive.

As far as I am aware, all tissues have glucose transporters, but there are many different types with varying tissue distribution. A short review in Biophysical Reviews (2016) by Navale and Paranjapei is freely available and provides a summary with links to original papers.
In short, there are two types of glucose transporter, those involving sodium symport (SGLTs) and those operating by facilitative diffusion (GLUTs). The review lists six SGLTs and mentions thirteen GLUTs, belonging to three different structural classes.
The tissues specifically mentioned in relation to one or more of these transporters include:
For SGLTs — small intestinal cells, proximal tubule of nephron, intestine, testes, uterus, lung, brain, thyroid, kidney, liver, uterus, pancreas.
For GLUTs — pancreatic beta cells, liver, kidney, brain, heart, skeletal muscle, adipose tissue, small intestine, testes, placenta.
I reproduce below a table from Chapter 6, Insulin and Sugars, in Gerald Litwack
Human Biochemistry (2018). The chapter is available if you belong to an institution with a subscription to Springer publications.


text:
Is it possible to spread vaccine through air?
I am not a biology people. But this question has been bothering me for months.
I read the news that, even if an effective vaccine (for Covid-19) successfully created, the transport of the vaccine and its acceptance might still be a big problem; some vaccine need to be kept at extremely low temperature prior to using.
But then, what if the vaccine could cause one recipient to fall sick and the recipient spreads the mild disease to other people? This might sound bad, but then the community will develop immunity against the notorious Covid far much faster, more effectively and possibly free of charge for most of us. Instead of injecting the recipients one by one, just spread the vaccine like how Covid-19 spread.
Maybe the vaccine contains only part of the virus but not living virus, but considering those infected by mild cowpox will develop immunity against small pox, can't we just synthesize the cowpox-analogue for Covid-19? (Cowpox might not be spread through air, or from people to people, I am just saying, use highly contagious living virus that cause mild symptoms as vaccine)
Or is it because deliberately spreading viruses might be labelled as immoral so no one attempted this?

Hello. This may interest you. This question explains how the vaccines for Covid. Also note covid vaccines are not attenuated viruses. Also think about this - you have no control on the dosage each person will receive once you release a virus into the air. That does not sound ethical and healthy.

I’m voting to close this question because it is primarily a medical question and so would be more appropriate on [MedicalSciences.SE], but please do not crosspost, instead request migration. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

I don't see how this is a medical question. However, it is poorly phrased and displays some misconceptions.

First: This is ethically completely out of question.
Then: You could of course think about a attenuated virus, but these are designed to not spread like the disease, as they might mutate back and cause problems. This was a problem with the oral polio vaccine which is not used anymore for this reason.
This virus would need a higher transmissibility than the original virus to outcompete its spread. Creating a virus that spreads more easily but is less dangerous always harbours the danger that this virus mutates into something ways more dangerous than the original SARS-CoV-2 virus. Would you want to risk this? Also: We barely know the long-term consequences of COVID, what about another virus?
So, no, this is not a possible way.

Live attenuated poliovirus vaccines are still in use in various parts of the world. And yes, I agree it is an ethical concern, resulting in (rare) polio cases from vaccine derived polioviruses, particularly in immunodeficient children.

@user1136 Yes, to clarify, the ethical issue isn't that it's a live vaccine, it's that it is a live vaccine that is transmissible, and therefore exposes people who (a) haven't consented to receive the vaccine and (b) may be harmed by the vaccine (e.g., those with certain  immunodeficiencies). For modern vaccines, transmissibility is only an issue with certain oral poliovirus vaccines.


text:
Are there special pairs present in the RC of both photosystem I and photosystem II?
I am confused regarding the existence of special pair (primarily regarding PS2). Do both, P680 and P700 have special pair?
I have checked various sources online and have come across conflicting information. For instance wikipedia article on Photosystem (https://en.m.wikipedia.org/wiki/Photosystem_II) says:

Unlike the reaction centers of all other photosystems which have a special pair of closely spaced chlorophyll molecules, the pigment that undergoes the initial photoinduced charge separation in PSII is a chlorophyll monomer.

This is hyperlinked to a study by AW Rutherford which says:

It is proposed that the key event in the evolution of PSII was a mutation that resulted in the separation of the two pigments that made up the special chlorophyll pair, making them into two chlorophylls that were neither special nor paired.

However, Voet and Voet 4ed says that there are two Chla molecules that are analogous to the special pair seen in Photosynthetic Bacteria Reaction Centre (PBRC).
Additionally, I found this (http://www.life.illinois.edu/crofts/ahab/psiistrc.html)

The nature of P680 (the primary donor Chl) is still controversial. The dimeric special pair expected from bacterial centers has not been unambiguously demonstrated, although H198 of D1, and the equivalent in D2, are conserved as putative ligands, and the near IR band of P680+ is diagnostic. Several suggestions have been made that P680 might be monomeric (8-10), and more equivalent to the ancillary Chls of the bacterial reaction center.

The article is not dated unfortunately but I checked that all the citations are prior to 2000.

@Martin Klvana - what is that? What do you want to say. I dont get it. Why'd you post that? Doesnt answer my question.

Hello Gerardo, please take look at the question again. I have made the required changes.

Thanks so much for the edits, Gerardo. You made the question neat.