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In terms of differentiation, how many generations of asexual reproduction, will usually be equal to 1 of sexual?
As far as I understand, in sexual reproduction, there is a mix of 50/50 genes from parents. In how many generations of asexual reproduction, will offspring reach differentiation level that of sexual one ?

Welcome to Biology.SE!
Clarification of the question
It is unclear what you mean by differentiation? I will assume that the question is

For what value of $n$. is the number of pairwise differences between any two siblings under sexual reproduction is equal to the number of pairwise differences between any two $n^{th}$ cousins under asexual reproduction?

Answer
The answer to this question mainly depend on (1) the mutation rate and (2) the amount of genetic variation present in the sexual population (which itself is a function of the mutation rate).
Assuming a panmictic population of constant size $N$, assuming equal sex-ratio and non-overlapping generation (and a few other assumptions), we can make some estimations. Let's assume that the sexual and asexual populations that we are comparing have the same mutation rate $\mu$.
Sexual population
Using coalescent theory, one can show that the expected number of pairwise difference between any two individual in a sexual population is $4 N \mu$. It would be off-topic to explain why this is true. I let you open a population genetics book and/or open a different post.
Asexual population
Assuming an infinite site model (just like coalescent theory does), the number of pairwise differences between $n^{th}$ cousins is $2 n \mu$.
Comparison
Let's set the equation
$$2 n \mu = 4 N \mu$$
and solve for $n$, we get
$$n = 2 N$$
In words, $2N$ cousins in asexual populations have the same number of pairwise differences (on average) than two sibling in a sexual population of size $N$.
Remarks
Please note that the conclusion is drawn from important (but common) assumptions. Note also that drawing conclusions from the above calculation such as "sex helps retain genetic diversity" would be wrong, as we are comparing sibling to $n^{th}$ cousins and not randomly chosen individuals in the population.

excellent answer, thank you. The reformulation is good


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Assume the gene for freckles is dominant. A woman with freckles has a son that does not. What would have to be the genotype of the mother?
I need help understanding the question I guess. I have read the chapter in my book but still confused.

Welcome to Biology.SE. Please read about how to ask questions and take the tour. This is not a homework forum. If you want an answer, you should show attempts to answer the question yourself, or at least provide some background knowledge on the topic you are asking about. Also provide references and state your questions clearly.

@AlexDeLarge so why did you then give an answer? From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. Providing answers to crap questions like this just encourages more of them, and shows people we don't really care about or enforce the rules.

@MattDMo: Yes, that would be a never ending dilemma. Actually, i did not say this was a crappy question - I think it would be an appropriate one, if properly stated. Therefore, my comment was meant to be encouraging to improve the question according to the rules. Additionally, I tend to be very indulgent with newcomers - they might not know, they might want to learn. But fact is: they have a question and need help. So I took the 3-5 minutes to answer the question and tried to help T.Seevers out. But, of course, you are right in that this is a bit inconsistent and I will keep that in mind.

@AlexDeLarge like when dealing with children, consistency is key. (No, I'm not implying that all new users are like children.) "Being indulgent" is exactly the wrong attitude to take. Be welcoming, but firmly point them towards the help center and the various meta questions on common topics. If they want to learn, they'll know how. If not, they'll know our reasons. Read the entire help center yourself, especially what's on- and off-topic, how to write good questions, and how to write good answers. Use this for some good comment templates.

@MattDMo: Thanks. As I already said, I will keep it in mind.

The mother needs to have a heterozygous genotype. This means that she carries two different alleles at that gene locus. She needs to carry one allele for freckles (since she has them herself) and one recessive allele that does not.
Her son must have inherited her allele that does not cause freckles, otherwise he would have had freckles himself. Accordingly he is probably homozygous for that gene which means that he has two equal alleles, both not causing freckles. Alternatively, he could also be heterozygous but have two different alleles that both do not cause freckles (and therefore the allele he inherited from his father is different from both alleles his mother carries).

So would that mean the mothers genotype is Ff? And that the father doesn't have the same genotype?

Yes, the mother would be Ff (where f is any allele not causing freckles). No, the father does not need to have the same genotype. He could, but he could also be Ff*, where f* $\ne$ f but both f* and f alleles do not cause freckles.

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Is protein folding symmetric with respect to reversing the sequence order?
Suppose that I have two proteins, protein A and protein B, and suppose that the sequence of amino acids of protein B is exactly the reverse of the sequence of protein A.
For example (these are made-up proteins):
protein A = [G,A,L,G,M,F,R]
protein B = [R,F,M,G,L,A,G]

Will the 3D structure of protein B be somehow identical, or perhaps the mirror image, of the 3D structure of protein A?

Think about where the N and C terminals are with respect to "R" for example.

@AdamRadekMartinez — Correct usage is terminus (end) and termini (ends). Terminal is an adjective in this respect (even though in English it may be used as a noun in specific contexts e.g. Railway Terminal.

I suggest that you are in a little less hurry to accept answers that cite references to something other than the situation in your question. The wa SE works is that when people answer others can vote and comment on that answer to help you decide what is correct.

@David Thanks for the advice. If you happen to have more info regarding my question, or an alternative answer, I'm still interested and listening.

related: www.reddit.com/r/askscience/comments/34npph/if_you_reversed_a_proteins_primary_sequence_would/

No! Although there is a relationship, the protein would not fold properly since the C and N terminals are reversed consider the following:
H(NH)-A-C(=O)(NH)-B-C(=O)(NH)-C-C(=O)(NH)-D-C(=O)(NH)-E-(C=O)OH
as appose to :
HO(C=O)-A-(NH)(C=O)-B-(NH)(C=O)-C-(NH)(C=O)-D-(NH)(C=O)-E-(NH)H
These are completely different molecules!
http://www.ncbi.nlm.nih.gov/pubmed/1604320 http://www.pnas.org/content/95/13/7287.long http://www.pnas.org/content/111/32/11679

Although the two are different molecules, and you may well be correct, the two references you quote are not for reverse sequence proteins but for proteins of the same sequence built with D-, rather than L-amino acids.

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Why does the cloned cat, CC, exhibit mosaic fur color?
Since fur color in this cat is from a sex-dependent gene, I see how calico cats occur. However, I don't fully understand why it happens in cloned cats.
When the cat is cloned, the DNA is taken from a somatic cell in donor and put into the egg of a surrogate. Wouldn't the DNA from the donor already have one of the X chromosomes inactivated to a barr body? Since one of the X chromosomes are inactive, wouldn't there only be a single color expressed?

There are mechanisms through which the X-chromosome that has been turned into a Barr-body can be re-activated. This happens during cloning, but is also seen in some cells that turn into cancer cells. This paper discusses a lot of intriguing lessons we've learned from transplanting nuclei from one cell to another in frogs and mice.
Interestingly, though the succes rate of cloning is surprisingly low (see this paper), but it is equal for male and female clones. This implies that the failure to turn a Barr-body into an active X-chromosome does not contribute significantly to cloning failure.
Of course, if the Barr-body gets re-activated again and turns into a normal X-chromosome, that means that later in embryonic development it can get de-activated again (at random, as is normal in cats), leading to mosaic phenotypes such as the calico. The inherent randomness in this process (at least in some animals, such as cats) means that the calico pattern of the clone is highly unlikely to resemble the calico pattern of the original.

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Does the nuclear human exosome contain 9 or 11 subunits?
I'm currently reading about the nuclear human exosome, in particular, looking at the protein complex that was uploaded here; https://www.rcsb.org/3d-view/2NN6
According to the paper related to it, it mentions that: "The hExo9 structure reveals locations for each of the nine polypeptides in the complex (Figure 2). Human Rrp41, hRrp45, hRrp46, hRrp43, hMtr3, and hRrp42 form a PH-domain ring, akin to that observed for PNPase, RNase PH, and the archaeal exosome (Figure 3)."
However, the figures in the paper don't really show RRP44 and RRP6 but the supplementary shows 11 results under H. sapiens: https://ars.els-cdn.com/content/image/1-s2.0-S0092867406014279-mmc2.pdf
I'm just a bit confused, does the human exosome complex consist of nine or eleven subunits? And in terms of terminology, does each polypeptide chain equal to one chain as mentioned in the global stoichiometry?

Quotes from the paper:

While Rrp44 is an integral component of the yeast exosome, human Rrp44 (Dis3) is not present in human exosome preparations (Allmang et al., 1999, Raijmakers et al., 2004).

So there is a human analog of Rrp44 which is part of the yeast exosome but not the human exosome.

Rrp6 is associated with nuclear exosomes in yeast and human, although Rrp6 may not be restricted to the nucleus (Graham et al., 2006).

They say Rrp6 is associated with human exosomes, but do not state that it is a component of them.

The emerging consensus is that eukaryotic exosomes also form six-subunit PH-domain rings (Rrp41, Rrp45, Rrp46, Rrp42, Rrp43, and Mtr3) that are capped by S1 proteins (Csl4, Rrp4, and Rrp40). It has been suggested that Rrp44 and Rrp6 interact with the “bottom” of the PH-ring, surfaces opposite to those that interact with Csl4, Rrp4, and Rrp40 (Hernandez et al., 2006).

We next attempted to assemble yeast and human nine-subunit exosomes (yExo9 or hExo9). Human Csl4, hRrp4, and hRrp40 were mixed with hRrp41/Rrp45, hRrp46, and hRrp43/Mtr3/Rrp42 as above. Consistent with formation of a nine-protein complex, the apparent molecular weight (∼350 kDa) was consistent with the predicted mass, and SDS-PAGE analysis confirmed that peak fractions contained each of the nine proteins (Figure 1C)

Here they describe the nine-subunit human exosome that they build and list all the constituent parts.

The hExo9 structure reveals locations for each of the nine polypeptides in the complex

Again, clear they are talking about a 9 subunit complex.
I think overall it's probably of only moderate biological interest how many of these subunits make up the "complex" proper, if the other proteins are also there and interacting, it's just a matter of which "stick together" through the methodology being applied. Perhaps a bit analogous to the "lumpers and splitters" phenomenon in categorization, cellular and molecular biologists can choose to be more or less reductive in how they analyze protein function. Even the most solitary proteins interact with others, and at different levels of analysis it may make more or less sense to group subunits together into a complex or treat them as separate units with distinct activity.

wouldn't the components matter though? but if I'm comparing the ground truth against an AlphaFold-multimer prediction using the 11 associated proteins, then the prediction wouldn't be correct since two extra proteins have been included?

@Strider Depends what you're doing. Seems like you'd just want the 9 for what you want but it's quite possible the other two also interact and bind, just not tight enough to stay together.

I want to compare ground truth vs the predicted exosome. Do you think its because only the 9 subunits could only be crystallised?

I don't know, maybe you'll find out when you do your experiment! It's no fun to do an experiment when you already know the results.

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Activating smooth muscle tissue with electrical field
I see applying 20 mV to the smooth cell cell will make it contract/ relax, I wonder will it contract/ relax if i apply the same amount to a strip of tissue (I am asking this because people of applying 20V, 40V in organ bath type studies to intestine tissue while modeling studies involving Hai-Murphy type model use -70 mV as resting potential and -30-40mV as activation potential, doesn't that mean the rest of the voltage is an overkill?). Thank you!

20V or 40V over a bath isn't the same as that voltage over a membrane. Think from the perspective of some cell's membrane: what voltage is that membrane actually "seeing"?


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I have a ginger root that sprouted suddenly. What do I do with it?

Here is a ginger root that I have in my kitchen. I see that it has some sprouts, as seen on a picture. I would like to grow more ginger, however I'm not yet sure whether it's okay to plant it now that it has these sprouts.
Any guidance on what to do is appreciated.

Welcome Rusurano. Horticulture is more suited to our [gardening.se] site (afaik). I've grown them indoors on a sunny windowsill for decorative purposes, but if you want to know about conditions for cropping, best to check-out the other site.

@JiminyCricket. Thanks for the warm welcome and for the tip! It doesn't feel like too offtopic for Biology either, so let's see what other people have to say for that here, too :)

What I did: In a wide pot with sandy loam (well drained), I placed it shoots facing upward, then buried the body about 2 cm (an inch), leaving the tips poking through, then watered lightly. It took a few weeks for the shoots to get going. I watered infrequently. A bit like a grass, the leaves unwrap themselves from the stem as it grows. Multiple shoots followed from the root. End of season, I uncovered the root - if anything it was smaller than when I planted it, the stems too fibrous to eat. You need advice from someone who's had more success with it than I : )


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Why do lips heal fast
Whenever I have any cut in my lips ,it gets healed in 2-3 days so why do lips get healed faster as compared to other body parts?

According to this article:

Wet or moist wound treatment significantly reduces the time required for re-epithelialization

Since the lips are (normally) constantly being moistened by saliva, this could be the reason you experience accelerated cut healing.


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SNR for good MRI imaging
Resolution of MRI can be improved if FOV is reduced keeping other factors constant, but this reduces voxel volume, which in turn reduces SNR. How much SNR is enough for good imaging?

WTF are you talking about?

[Old question, but...]
There is an old adage in MRI:  High signal to noise, high resolution, short scan time... choose 2.
The question of "How much SNR is enough?" can't be answered without talking about specifics, primarily, what is the scan going to be used for?
For example, a typical MS diagnostic scan doesn't really need to be too high a resolution or signal to noise as typically the lesions are large and hyperintense.  BUT with higher field scanners one is able to see smaller and smaller lesions.
If one is doing quantitative work off of an MRI scan, then it will depend on the type of quantification, algorithm etc.
So, in some ways the question is very broad and it depends, significantly, on a lot of other factors.
Doing some Google Scholar / Pubmed searches for SNR and MRI might help with specific areas you are interested in (e.g., https://scholar.google.com/scholar?hl=en&as_sdt=0%2C9&q=minimum+signal+to+noise+ratio+in+magnetic+resonance+imaging&btnG=)


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What’s the evolutionary benefit of cats playing with their prey?
I just saw a cat playing and teasing a wounded bird for minutes, and I immediately started to wonder what the evolutionary rationale were. After all, it seems eating the prey as soon as possible should be the optimal strategy (as you can’t lose what you have already eaten.).

The cat is probably just having fun. So, we could ask "What is the evolutionary benefit for having fun?" Through play, animal learn (Fagen 1974, Spinka et al. 2001, Pellegrini 2007, Hirsh-Pasek and Golinkoff, 2008). This is particularly true for juvenile. Adults play is not uncommon though and might follow from the same principles (Bekoff and Byers, 1998). Note that playing is also associated with reduced stress in adult cats (Bekoff and Byers, 1998).
Whether or not, the cat actually learn much through playing with its poor little prey (it probably learns to be a better hunter) is not really relevant. Playful behaviour, as a general behaviour may have been selected for. There would be no need for "playful behaviour with a pink string" to have actually ever been under selection. Many behaviours have evolved as side-effects of evolution of related behaviours.

If the cat doesn’t learn much by this “playfulness”, I imagine a strong negative selection would render this specific instance of risking resources a non-behavior very soon. And your answer begs the question, why a general “playfulness” trait would evolve, and what “playfulness” even is.

Why doesn’t a dog do this kind of behavior? I find dogs satisfy your very broad “through play, an animal learns” criterion. And the cat also doesn’t play with random stuff (you don’t see cats playing with sticks or fire or ...).

@HappyFace I imagine a strong negative selection would render this specific instance of risking resources [..] You have too selectionist a view of evolution. You might want to have a lookd at this post or maybe this post.

@Remi.b can you add some references and clarify the answer a bit? I mean, are you sure that this behaviour can indeed be described as "having fun"? Can it be something else (analysing the prey, for example)?  If so, can you also link some articles that say talk about positive effects of "having fun" (which sounds quite reasonable)?

@WYSIWYG I added some citations (and some texts as I learned by going through these papers)!


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Will meat rot in alcohol below freezing?
I understand that freezing slows decay but I'm wondering what will happen if meat is kept in below freezing temperatures while submerged in a liquid that has a lower freezing rate, like alchohol?

The meat will still freeze

A chemist's perspective:
Ethanol and water are miscible, meaning they are perfectly soluble in one another in all proportions. So given enough time, the alcohol will likely seep into the tissues and cells of the meat, and some water will seep out into the surrounding alcohol bath. The liquids might not equilibrate very well on a reasonable time scale, that is, the bath surrounding the meat could remain mostly alcohol with some water, and the tissues of the meat could contain more water than alcohol. This is because the biological barriers of the meat interfere with the diffusion of the fluids to reach a mixture of equilibrium proportions. However, in theory, cell membranes are permeable to ethanol, so given enough time soaking we might build up a useful concentration of ethanol within the meat.
Note that it doesn't matter so much what happens outside the meat - being bathed in a substance that remains a liquid below 0 °C won't necessarily stop the meat itself (well, the aqueous solutions within it) from freezing. That is why the considerations of solubility and permeability are crucial. As I said, for ethanol we have perfect solubility with water (miscibility), and possibly sufficient ability to diffuse throughout the organic catacombs of our meat. So, assuming ethanol can sufficiently perfuse the tissues and enter the cells, what would happen?
Water has a higher freezing point (not "freezing rate") than ethanol (0 °C > -114 °C). When you mix some ethanol into water, the freezing point of the solution will be lower than the freezing point of the pure water. The freezing point of pure water is depressed by the addition of ethanol. Here is some data on the freezing point of water solutions with different amounts of added ethanol:

(Note that the freezing point at 100% ethanol seems to be -111 °C according to this data; this should technically be freezing point of pure ethanol itself, so we would expect it to be the -114 °C figure I quoted earlier. But that small discrepancy between this experimental data and the traditionally accepted number will not affect our analysis.)
So, as you lower the temperature, the water-ethanol solution in the meat will begin to freeze. It will freeze at some temperature lower than normal because of the ethanol present. Note that the normal freezing point of water in meat is already going to be lower than 0 °C due to all of solutes inherent in such a biological system (ions, sugars, metabolites, maybe a few stray amino acids, etc). As it freezes, the water will freeze first and leave the ethanol behind.
So, inside the meat, you will see the meat freeze at slightly lower than normal, with some liquid remaining in the tissues which would be the ethanol. Outside the meat, in the bath of ethanol which has drawn some water out of the meat, you will see that water forming ice on top of the liquid, which will become purer and purer ethanol as the water freezes out of it. The process I just described is fractional freezing, and you may be interested to know it is how "ice beers" (Keystone Ice, Natty Ice, etc) are made more alcoholic.
Now, if the proportions of ethanol and water are just right, something interesting happens. Instead of the water freezing first and precipitating out of the ethanol, a special eutectic solution is formed that freezes all at once. (Perhaps you've heard of fractional distillation and azeotropes, the the boiling point analogue to fractional freezing and eutectic mixtures). On the graph above, the eutectic mixture is achieved at the very minimum value, around -118 °C. Note that freezing point of the eutectic mixture is lower than the freezing point of pure ethanol alone. Unfortunately, for the specific case of water and ethanol, reaching that special point of bonus freezing point depression requires the solution to be almost completely ethanol (about 93%). That would be the holy grail of lowering the freezing point of your meat, but it's likely not feasible to replace that much water with ethanol throughout the meat.
So, in conclusion: It's what happens inside the meat that counts. If you bathe meat in ethanol, a useful amount of ethanol may permeate the meat. The freezing point of the meat (rather, the aqueous solution within it) will be lowered the more ethanol perfuses it. In theory, you could even drop that freezing point below that of ethanol itself, but it would require replacing nearly all of the water with ethanol.


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How to confirm pure-breeding parents
I was reading Genetic Analysis (Sanders, Bowman) and saw the following figure summarizing the 1909 work of Herman Nilsson-Ehle in describing the genetic control of kernel color in wheat:

How did Nilsson-Ehle determine that the original pure-breeding parents were in fact homozygous for each allele?

Welcome to Biology.SE. They were probably inbred lines for many generations.

If they are "pure-breeding", that means that they are homozygous.  If they were heterozygous, the offspring would not all have the same color as the parents.  But tree-breeding" means they all do.

These genes are additive. No dominance relationship is assumed to exist between allele $A_1$ and $A_2$ or between allele $B_1$ and $B_2$.

In Campbell Biology (2021) 12th edition it says that
"True-breeding" (or pure lines) can be verified over many generations of self-pollination. If they produce only the same variety as the parent plant, then they are homozygous.

There are more complicated situations, such as if being homozygous at a locus is fatal. You then end up with pure-breeding heterozygotes.


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What does "Pandercetes" (genus of spiders) mean?
"Pandercetes" is a taxonomic genus, and refers to certain Huntsman spiders (found in Australia/Asia).
It was named by Koch, a German entomologist, in 1875.
What does the name itself mean or connote? What are the defining characteristics of this genus?
I could not get a clue as to what roots the word is made of .. pander + cetes? pan + dercetes? My understanding leads nowhere this far.

Koch did write a book describing these and other species:
Die Arachniden Australiens nach der Natur beschrieben und abgebildet By Koch, Ludwig, 1825-1908 Nürnberg :Verlag von Bauer & Raspe,1871-1890.
Harvard apparently has scanned volumes: https://www.biodiversitylibrary.org/bibliography/121660
Perhaps the reasoning will be found there - should be fun hunt!

Cetus or cete means "whale" in Latin, and is the root of the English word "cetacean". Don't know how that refers to huntsman spiders, though...

biodiversitylibrary mentions highlight this genus' eyes "the eye area strongly raised in all directions" (as translated from Koch's German writings) .. and ..
Dercetes of Phyle is a character in Aristophanes' writings, whose name Dercetes itself means "looker", who ruins his eyes sobbing for his oxen.
Putting this together, I might conclude that Pandercetes can be broken into pan + dercetes, or "everywhere-looking" or simply "one with raised eye sockets in all directions"


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What is the animal in this video?
I made some research however there seems to be a conflict with this animal's translation to my language and the original. So I couldn't find it. Do you mind helping me out ?
https://static.59saniye.com/videos/2018/04/21/20180421080742-6014_720.mp4
Some resources say pufferfish or Porcupinefish. Are these the same thing ?

You can do a search by common name (possibly in your language) in http://www.fishbase.org/search.php This site also has images for species in a family, like here for tetraodontidae: http://www.fishbase.org/identification/specieslist.php?famcode=448&areacode=

This is a Northern pufferfish. It is called Sphoeroides maculatus.

  Source: https://www.flickr.com/photos/vims_photos/3570935564

You can confirm this on FishBase.

I'm no expert in the field, so I can't identify the fish in your video; but it seems that pufferfish belong to the family Tetraodontidae, while porcupinefish are of the family Diodontidae. So, no, they are not the same thing.


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What is the role of mesosomes?
Some guide books on biology continue to state that Prokaryotes respire through mesosomes. However, they don't exist in living cells. What is the stand now?

They are widely considered to be mere artefacts. If you are reading a book that stated otherwise, the book is likely outdated.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC408341/ --> Fairly recent, give it a go.

Thanks. The link states " accumulated evidence suggests that mesosomes are not strictly artifacts of chemical fixation...". However, Eli Korvigo commented that they were widely considered to be mere artifacts. It means the research for new evidences are still on.


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Sugar metabolism in preserved/cryopreserved livestock semen
I wonder how can semen use di/tri-saccharide (e.g. sucrose, trehalose, raffinose) for spermatozoa metabolism in preservation/cryopreservation of livestock semen, since the semen itself never bring any enzyme to breakdown those sugars and the extender used also don't contain enzyme needed?
Is there any other way to breakdown sugar without enzyme, or is there any component in the extender which can substitute the enzyme function?
Thanks in advance.

The sugars that you mention are primarily used as a "cryoprotectant" and thus to reduce physical damage to the cells while frozen.  The sugars are not used to provide energy to the sperm as the enzymes will not function in the temperatures and conditions of a frozen environment. The addition of sugars is typically used with other types of cells/tissues in their cryopreservation as well.  The abstract in the link below summarized this.
https://onlinelibrary.wiley.com/doi/pdf/10.1111/raq.12195


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Human ancestor reproduction after chromosome fusion
I read somewhere that human chromosome 2 is the result of 2 primate chromosomes fusing together somewhere along our evolutionary journey. This is why we have 23 chromosomes while other primates have 24. My question is this: for the first ancestor whose chromosomes fused to have 23 chromosomes instead of 24, how did he reproduce? Don't offspring receive half of their genetic makeup from each parent, so if one parent has 23 chromosomes and the other has 24, how would that work? I know that there have been animals with different chromosome counts being bred together, but the offspring typically have issues and are sterile, so even if the difference in chromosome count was not a problem, wouldn't the offspring between an organism with 23 chromosomes and one with 24 be infertile, thus leading to the end of animals with 23 chromosomes? Would there have to be two organisms of different genders experiencing the same chromosome fusion at the same time in order to avoid this problem? I'm just a bit confused as to how this would work exactly.

Related: Polymorphism in number of chromosomes?

Strangely enough we actually do have an answer for that.
There are a several examples of individuals who are born with two chromosomes fused together in all their cells.
We even have a few examples where these fused chromosome is in a diploid state, ie all instances of that chromosome are fused in the individual. Such individuals come from families in small isolated villages that are very inbred.
Chromosome number does not prevent fertility but it does reduce it in heterozygous state as it is now harder to get correct chromosome distribution during meiosis and thus fewer functional gametes are made. However in terms of function, as all genes are present in a somatic cell in the correct number, function is usually normal and the individual is alive.
If the population is inbred, it is possible to get an egg and a sperm that carry the same fused chromosome to meet. In which case you get a diploid individual with fused chromosomes. Fertility is now restored. And in an inbred population, a homozygote individual for the fused chromosome can meet another similar individual, and have offspring who are fully fertile.
AS you can imagine, over time there is a selection pressure for the population to separate. The homozygous state (be it fused or unfused chromosome) is more fertile that the heterozygous state.
So to put it short, chromosome fusion does not kill a cell. All gene are still present. However in the heterozygous state, where both fused and unfused chromosomes are present, fertility is dramatically reduced BUT is none zero. Fertility is restored in a homozygous state when an individual is diploid for either fused or unfused chromosomes. In small isolated populations, inbreeding allows for the emergence of diploid individuals which can reproduce with each other
http://genetics.thetech.org/original_news/news124

My question is this: for the first ancestor whose chromosomes fused to
  have 23 chromosomes instead of 24, how did he reproduce?

He or she reproduced the same way people today with balanced Robertsonian translactions reproduce.  During meiosis I, the separated chromosomes line up with the fused one, so the resultant cell gets either the replicated fused chromosome, or the replicated separate chromosomes.  Then meiosis proceeds as usual, with half the gametes having the fused chromosome, and half having the two separate chromsomes.  The fused chromosome has just about all the information the two separate ones have, so the gametes with the fused chromosome can go one to make a organism with all the required genetic information.


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Are there any benefits/disadvantages/traits from having a permanent lower core temperature?
My body temperature as far as I remember has always been around 35.6 degrees Celsius, that's a degree less than what is the usually quoted as the average temperature for humans.
Are there any known correlations such as a shorter/longer average lifespan or pronounced traits such as being more sensitive to warmer temperatures or later/earlier onset of hypothermia symptoms?
Or is it not low at all or low enough to have any noticeable effects.

There are many questions you ask, I would suggest revising to narrow it down. Temperature and 'its effects' is quite broad of a curiosity. What would you like answers to focus on? Have you tried searching online for some answers? Have you reached any conclusions? It appears that this information is readily available, and the data points in many interesting and sometimes conflicting directions, e.g. with respect to temperature-lifespan association: colder body temperature is associated with longer life, but women, who live longer on average, have higher core temperatures than men. It goes on!

I gave google scholar a quick search, and although longer temperature seems like an obvious one I coudln't find any paper easily that would point to that for either humans or animals. I was hoping someone might know some of top of the head, I understand my question my seem rather broad.

Are you asking about effect in general or for humans specifically.

Yes absolutely. Body temperature is associated with basal metabolic rate which is linked to life-span/body mass. Keeping your body at temperature is responsible for the majority of your caloric burden majority of your caloric burden, and having a lower resting temperature would mean you require fewer calories to survive. Higher body temps are thought to have been a defense against parasite infection, so reductions in body temperature might leave you more susceptible to disease, however a paper came out recently discussing falling body temperature in the US and its implications, and I think it addresses many of your questions in detail in the discussion.
Edit: To elaborate on that elife paper, they've identified a small reduction in average body temperature overtime using military medical records going back to the civil war. They postulate that the reductions they observe are due to improvements in healthcare and a potential decrease in chronic inflammation in the population which increases your body temperature.

Can you elaborate on the major findings of that linked paper? Link-only answers are discouraged.

Whilst it is possible that your actual core temperature is actually lower than the normally quoted average of 37.5 Celcius by a degree, it may also be the case that where you are measuring is below the average rather than your actual core temperature. For example, you might be measuring under your armpit, and perhaps due to low circulation in that area, it does not fully reflect your actual core temperature. Just a thought.
Mammalian enzymes have an optimum temperature range. Too low, and the rate of reaction is too slow to effectively support the organism. Too high, and the enzymes will denature (loose their tertiary and quaternary structure.)
So if your core temperature really is a degree lower, we might expect your metabolism to be slowed due to the effect on enzyme catalysed reactions. The rule for this is expressed as Q10, Q10 temperature sensitivity units in stack biochem.
Another possible effect is that a lower body temperature could mean being more prone to infection, as discussed in stack geneticsenter link description here. Temperature rise during infection (having a fever) is thought to be an attempt to thwart an infectious organism, so it follows that a lower temperature may aid teh infecting organism.

"Temperature rise during infection (having a fever) is thought to be an attempt to thwart an infectious organism, so it follows that a lower temperature may aid teh infecting organism." That doesn't follow at all. Successful pathogens are successful because they are adapted to the host organism. Their temperature optimum should be in agreement with the host organism's typical temperature.

So why do mammals have a fever? It is an attempt to get rid of the pathogen. It might not always be successful, but so far when I've had a fever, I have got rid of the pathogen each time.

Yes, of course. But decreasing the temperature below normal does not benefit the pathogen. On average, optimum temperature for a pathogen is aligned with normal body temperature.

Not so with fungi. Lower body temperature can benefit fungal infections.

Some pathogens will usually infect the peripheral tissue because the core temperature may be too high. If I recall, the bacteria that causes leprosy is an example.

Parainfluenzavirus is another pathogen whose growth is diminished at temperatures over 37 C.


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Effect of high temperatures on plant stomata
My biology textbook states that stomatal closure occurs at high temperatures to avoid water loss. Another stackexchange thread I can find (What is the effect of temperature and carbon dioxide on the opening and closing of stomata?) agrees with this, however most actual studies on the subject I can find talk about stomatal opening occurring at higher temperatures, but say the effect if the plant is experiencing water stress.
Does anyone know why there is conflicting info on this, and which source is correct?

I wondered the same. According to biology lectures I had stomata cells are opened by turgor (water pressure within cells). There are several depicted mechanisms. In some illustrations there is like a lid sitting on top of the stomata and turgor opens the lid by pushing it upwards. In other turgor deforms the cells so that they form a hole between them (a stomata). According to this theory as long as there is enough water available stomata should remain open, but probably other mechanisms exist.


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Are there comprehensive species descriptions on most species?
I was having a browse through Wikipedia and noticed how even the rarest, hardest to find species of bird have comprehensive articles and comprehensive descriptions, but other species like the 1400 Andrena species have next-to-no information.
I tried to do a search for resources on individual species of Andrena bees but found very little - at best a short description and the name of the entomologist who described it. Is there a place I could go to find comprehensive resources on these bees? If not, why are the available resources on these species much less comprehensive than those on other species?

To suggest a new species, someone must necessarily makes a rather thorough effort of description. A good solution to get some info could be to go to the original paper however, these papers can be very old and hard to find. Also, the standards at that time might be very different from today's. After all, K. Linnaeus managed to describe 13,000 species also maybe because the description were more simple than they are today (see this related post). Andrena hattorfiana was described by Fabricius in 1775 but I could not find the original paper.
Note that the english wikpedia article for A. hattorfiana is relatively decent.
The IUCN red list is also a good source (see here)
The page for the Encyclopedia Of Life is unfortunately a little empty.
Here are some amazing pictures on flickr
You can also just search papers that refer to a given species. Here are a number of papers on A. hattorfiana.

Most species (at least 80%), by virtually all estimates, remain undescribed. However, we have described the most visible and obvious species.


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Any known values of density for spinal cord (pig or human)?
Need to know the density of spinal cord tissue to evaluate the shear modulus from ultrasound elastography (shear wave velocity) measurements, but need the density of the tissue to compute this.
I am a physicist by trade so unaware of whether white and gray matter have homogeneous properties in the CNS as a whole or whether they are different in the brain and spinal cord.
Could do with density (g cm^-3 or equivalent) of white matter, gray matter or of the cord as a whole.
Also if there are any sources so i can cite this this would be most useful.


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Phototropism or Hydrotropism is a more important factor for trees beside the lakes growing bending to the water?
I see a lot trees beside the lakes are growing bending to the water and I wonder why. After reading this I think it might be a combined effects by:

Phototropism: the lake works as a mirror and sunlight are reflected
Hydrotropism: of course, Hydrotropism...

But which one is a more important factor? Phototropism or Hydrotropism?


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How long can swans hold their breath?
I’m curious if anyone has information or literature on the maximum duration that swans can hold their breath while submerged. Specifically, I’m interested in how long species like the Mute Swan or Whooper Swan can stay underwater during a dive. Any insights or references would be greatly appreciated!


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My fungal strain (ITS sequences) shows similarities with different species. How can I identify it?
I sequenced the ITS gene of my strain, but when I performed a BLAST without applying any filter, I couldn't easily identify it. My strain shows similarities with different species!

Welcome to SE Biology! It would be most helpful if you could show the actual data, like the % identity/similarity of your sequence against each species' sequence. Recall that you would expect BLAST to recover multiple species, because fungal species are related to one another by evolution. You would hope to find that one species has a higher similarity than another.


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Eddy currents caused by wind pollinated angiosperms to aid in pollination
dear biologists i hope everything is going well
as today i was reading angiosperm reporduction in my book campbell i came across a line
Wind tunnel studies
reveal that wind pollination is often
more efficient than it appears because
floral structures can create eddy
currents that aid in pollen capture. if some of you biologists do not know what eddy currents they are they are a topic of electromagnetic induction they are caused by changing magnetic fields which cause electric currents i could not find any research on this so if you all could please help me.

Most textbooks have a bibliography for their sources, usually broken up by chapter. Does Campbell? I'd also double check whether the book is talking about eddy currents in the electromagnetic sense, or whether they just mean eddies in the fluid dynamics sense. The later seems much more likely to me. (Though there is some cool research on pollinators using the electromagnetic fields around flowers).

Please take the trouble to divide your question into sentences starting with a capital letter and ending in a period/full stop. And as a new user finish reading the [Tour].


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What's the mechanism by which DHT affects hair pigmentation?
Is it based only in receptors, or is there more to it? How is it possible that under certain conditions terminal hair can grow without pigment?

Can you please not use abbreviations without introducing them?

And please expand your question making it independent of the title, and clarify: a mechanism “based in receptors” means nothing to me.


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What are some hypothetical pathways for generating ATP from glucose under anaerobic conditions?
I am very confused about how the steps of glycolysis relate to the generation of energy. From basic descriptions of metabolism, I would've thought that after opening the ring structure, the glucose might lose one oxygen or carbon at a time, and that these reaction would be coupled to the formation of energy carriers like ATP.
Instead, a lot of the steps involve rearrangement, and step 4 breaks glucose down without making any energy carrier. Steps 6 and 7 seem like a phosphate group is transferred on by having that reaction coupled to an electron transfer, and then the phosphate group is immediately taken off. This makes me think that maybe the glucose derivates are special (as compared to derivates of other plausible energy storage molecules) because they have electrons that really want to leave the molecule.
I’ve tried reading textbooks and looking a lot of different things up, but I feel like I’m not getting closer to understanding. I think an answer to these questions would be helpful:
What would be the most straightforward way for glucose to generate ATP in anaerobic conditions? If you had at your disposal any chemicals that a cell does, and you could create an enzyme that could lower the activation energy of any of your desired reactions*, what would you do to create one molecule of ATP from glucose with the fewest number of reactions? And, what is a series of reactions that uses the smallest amount of glucose’s energy to generate ATP? I’m curious if these sets of reactions will share the characteristics I’ve noted of glycolysis from above.
*I am assuming that the abilities of enzymes are not what constrains the evolution of metabolism, but maybe I am totally off.
Thank you in advance!

Welcome to SE Biology. Please finish the [Tour] and read the Help on asking questions. This is a Question and Answer site, not a discussion site and hypothetical questions are generally off-topic. If you do not understand the rationale for energy generation in metabolism, it is fine to explain precisely what your problem is and ask us if we can clarify. Assuming that it is somehow “wrong” and asking us to play God seems arrogant on your part and assumes arrogance on ours, even though I am sure that this was not intended.


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What is the primary function of the phosphorlyation of glucose in the first step of glycolysis?
Some textbooks emphasize that it traps glucose in the cell, but some sources mention glucose "activation." There is a response on Quora that claims that energetics are irrelevant and that phosphorylation solely about trapping glucose.


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MIT's Programming Language for Cells
I have read a lot about the programming language, Cello, that MIT created to program DNA; however, I cannot seem to find any sources online that shows you how to program with Cello. Are there any good sources out there with regard to this topic?
Thanks

Since this isn’t necessarily on topic I won’t make this a full answer, but I think this is what you are looking for: https://github.com/CIDARLAB/cello/blob/master/README.md

I’m not sure that this is on topic, as you really could have found this information yourself.

You don’t quote a source for your info about this, which doesn’t help you or anyone interested in this topic. Here is a Nature News article.
If you click on the link in that article you get to the Cello site. You need to choose a name and password to gain entrance, but are not asked for any personal information. All they will have is the IP number of your computer.

The info on this site will not mean much to anyone not involved in synthetic biology.


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is having more copies of gene better then having it less? if it's why is it ?
I was learning about elephants rarely getting cancer and learn that elephants have 40 copies of genes while human only has 2 copies of genes each from parents.
so I wonder if it's better to have more copies of the gene then having 2

I think you're reading that information wrong. They are referring to a single gene, not genes in general.

Here is one news article about the research. They are talking about p53 tumour suppressor. Rather interesting.

I also posted the equivalent article from Nature with Remi's answer @canadianer

It depends on the gene. Multiple copies of one gene in humans can result in Huntington's Disease, while multiple copies of TP53 in elephants is beneficial. Mostly, though, it's either benign or not a good thing. NB: Not a lot known about Copy Number Variations, but one article states: "Some CNVs have no apparent influence on phenotype, while as many as 40 others have been definitively linked with disease."

I was learning about elephants rarely getting cancer and learn that elephants have 40 copies of genes while human only has 2 copies of genes each from parents.

Where did you read that? Please always include your sources.
What you're saying is unclear but I suppose you are referring to ploidy variation among species and not to CNV (Copy Number Variation) for specific genes. It is also possible that you mistake alleles for genes but it is impossible to tell where your misunderstanding is without reading from your source. I will assume you talked about ploidy variation.
Elephants are diploids, just like humans. So, the claim appears flat wrong.

so I wonder if it's better to have more copies of the gene then having 2

There is no general rule. Because having a single working copy is often enough, high ploidy can be a pretty good defense against loss of function mutations but that's only valid for some time just after a recent polyplodization event as the relaxation of selection pressures against such mutations will lead these deleterious mutations to higher frequencies (at mutation - drift - selection equilibrium).
Note that doubling or halving the number of gene copies often yield to issues in dosage of mRNA and protein expressed. Related to that you might to read about dosage compensation

OP is almost certainly referring to https://www.nature.com/news/how-elephants-avoid-cancer-1.18534

(not sure where the downvote came from by the way, was not from me or related to my comment, I was just providing additional information)

Down vote solved :) I think it is good answer, and who down voted it is fool actually.

I think the OP is referring to CNV.


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how many copies of tp53 (p53) gene do we have?
I just started studying biology so I almost have no knowledge.
I learned about the tp53 gene and I just wanted to know how many copies of tp53 gene we have?

Humans have one copy of the p53 gene per set of chromosomes along with most other mammals (a notable exception being elephants with 20)[1]. Since it is located on an autosome (chromosome 17), each parent gives one copy of the gene[2]. Meaning two copies per human cell (and 40 per elephant cell).

A little extra information on p53 and the effects of only having 2 copies:
Since humans only have two copies per cell and p53 forms a homo-tetramer, it only takes one mutated copy to lose functionality.[3] This is because p53 needs to tetramerize to function, meaning only 1 out of 16 p53 proteins are effective if one copy is mutated (24 possibilities and only 1 combination has 0 mutated copies, ~6% are functional). This makes p53 a rare human tumor-suppressor gene with dominant negative mutations.
But with elephants, the more copies they have, the less and less one mutation affects the amount of functional p53. ($\bigl( \frac {39}{40}\bigr)$4 probability of having a functional tetramer = 90% functional, which is very high)


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What is this small brown spider?

Found in a doorway in eastern Tennessee. With its legs fully extended, it's about the size of a quarter.

I'd guess it's an orb spider by the habitus.

This spider has a roughly globular abdomen, (actually kind of egg-shaped, and pointed, which is a good clue), and is hanging upside-down in a 3-dimensional web which (if we could see it) would look pretty tangled instead of a nice, 2-dimensional orbweb.  It doesn't have any noticeable pattern other than the banded legs, and the greyish-brown abdomen looks like it has some darker blotches.  It's made its web near the top of a doorway in a house.
These clues all point to a very common Theridiid spider which goes by the name of House Spider.  It's not the House Spider that spins a flat sheet from a funnel retreat - that's the Tegenaria House Spider.  This House Spider is the Theridiid House Spider Parasteatoda tepidariorum.  It's a harmless (to us) spider that eats almost anything it can entrap in its web.  I've seen them happily eat Gypsy Moth caterpillars, centipedes and other arthropods that aren't very popular choices among household spiders.
Here's a link that you can browse to see the wide degree of variation that this spider can show - but always a kind of smudgy, blotchy greyish brown abdomen, banded legs and the tangled web in which it hangs upside-down.  You'll note that the legs of this Theridiid, like most of its relatives, aren't as burly and sturdy-looking as those of its cousin the Black Widow.  These Theridiids kind of totter along on their relatively spindly legs when out of the web, while the Widows go striding along like small Mecha-Spiders.  I always expect to hear the Imperial March from Star Wars when I see a Widow walking on the floor.
https://bugguide.net/node/view/6919

Nice answer! I've had the same kind of spider(s) at my back door every summer for years. They had/have much better webs, though, which they rebuild daily. I just assumed it was an orb spider because occasionally there was a zig-zag section in the web. She behaves just like this one. And this one. Now I'm confused. I think mine were orb spiders.

Yours probably were orbweavers - if they were hanging 'face'-down in a flat, circular spiral web, that would make it certain.  Look at these photos - see how the spider is hanging 'back'-down, with arched legs 'reaching' up?  Orbweavers hang vertically in the web (usually face-down, but some hang face-up), with their legs stretched to the sides.  You mention a zig-zag section in the web, which sounds like an Argiope, also an orbweaver.  Argiopes don't often make webs right at doors or windows, but sometimes they do.  Theridiid spiders, like this one, are different, though.

Thanks for the info! Yes, you're right on every point, including the direction she faced. But there is one every year in my back doorway, probably because the spot is good for insects (right next to a light). In fact, there is one at every floodlight as well.


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How does a glucose molecule enter the cell from blood vessel?
The transporters in the plasma membrane of the cells promote the entry of glucose molecules from the extracellular matrix to the cytosol of the cell. Could someone explain how does the nutrient molecule enter the extracellular space from the blood vessel?
For instance, in the context of the pancreas, the walls of the blood vessel is fenestrated. The literature also provides evidence for the presence of connexon in the endothelium of the capillaries.
My doubt is, the nutrient molecule that diffuses from the blood vessel reaches the cytosol of the cell through

Diffusing through connexon ?(or)
Does it reach the interstitial matrix(the fluid surrounding the cells) and then uptaken by the transporters present in the plasma membrane of the cell?

Connexons form gap junctions right? I am not sure because right now I don't have any appropriate literature to site for good answer but doesn't glucose transport involve solely GLUT? I mean if connexons were the option then why would diabetes even happen?Please do rectify me if I am going wrong.

@user33690 Yes, connexons form gap junctions.  GLUT transporters are involved in the active transport of glucose molecules from the extracellular space. For example, in the liver, the capillaries(sinusoids) are surrounded by the perisinusoidal space, the cells are found adjacent to the perisinusoidal space. Likewise, is there a layer, surrounding the fenestrated capillaries, from which the nutrients can enter the cell? My question is, which is the region in the pancreas that supplies nutrients to the surface of the cells? Any further thoughts?

I think I understand your question, Natasha. In short, your own answer #2 is correct.
There are 3 spaces, and 2 pathways for glucose to pass from one to the next:

intracapillary plasma
extracellular fluid
the cytosol.

Ways glucose gets into the cell:

(2->3) To get from the ECF to the cytosol , glucose always needs a transport protein. These are the GLUTs. In two cases, the small intestine and kidney, these are part of a secondary active transport system based on the Na/K-ATPase. In the pancreas, it's GLUT2.

(1->2) To get from the capillary plasma to the ECF requires filtration, the process of applying hydrostatic pressure to the plasma and literally squeezing it like a sponge. The boundary of the "blood sponge" is the basement membrane. The membrane holds in the proteins, and lets anything dissolved in the watery serum (like glucose) through.

The Filtration Constant Kf is proportional to the percentage of the BM that is exposed in a given capillary, which varies by the type and other factors like histamine release.

Type 1 (continuous) has the lowest exposure of the BM (only the intercellular clefts). Type 2 (fenestrated)has the clefts and the fenestrations to expose the BM. Type 3 (sinusoids) have huge gaps between the cells, and importantly, an incompetent BM that allows proteins and cells through along with the watery serum.
Dynamic factors that change filtration rates:

Histamine causes the post-capillary venule's endothelial cells to contract, and exposes more of the BM allowing more serum filtration, but it also allows neutrophil extravasation, during which the neutrophils punch holes in the BM through which white cells can squeeze, which is why you get a proteinaceous exudate in Type I hypersensitivity.

Increase in blood flow Like a water balloon increasing its surface area with more blood flow, skeletal muscle capillary beds (Type I) increase their volume and surface area when engorged with blood during exercise. This doesn't change the Kf (the only exit for serum is still the intercellular clefts, but they're bigger now).

P.S. A 1985 morphometric study of pancreatic capillaries shows that the idea that endocrine glands need a boatload of bloodflow (high serum filtration) is valid. Even within a single capillary that feeds both an exocrine acinus and and endocrine islet, the side facing the endocrine islet had more fenestrae.

From what I understand from the above explanation, the BM covers the endothelial layer .When the plasma is filtered out of the pores in the endothelial layer of the fenestrated capillary, how does it cross the BM? Will there be pores in the BM too?

Could you please provide references of studies that measure the Starling forces in the capillaries of the endocrine glands of the pancreas, if you have come across these studies in the past? I could only find the measurements of hydrostatic pressure and osmotic pressure in the intestine of cat.I have been looking for these measurements in the capillaries that pass through islets.

Terms to understand filtration. Blood = cells + plasma. Plasma = proteins + serum. Serum = water + ions + small-molecule solutes. Due to the transmural pressure in the capillary, the blood gets squeezed. Stuff that is too big to make it across the filtration barrier gets left inside (cells + proteins). The plasma gets filtered, like spaghetti in a colander. The proteins/spaghetti stay inside, and the watery serum gets through because it's small enough. The BM is made of Type IV and other collagens, laminins, and other adhesion PROTEINS. (more in next comment, ran out of room)

All proteins get their 3-d shape because they are dissolved in water. It is everywhere in the body. It surrounds each protein, and fills the space between them unless adjacent proteins have hydrophobic pockets for protein-protein interactions. So, even though there aren't pores you can see on EM, there are gaps to accomodate bulk flow (called convective flow). To answer your second question, that's a pretty specific study you're asking for, and I haven't read it. Have you tried a PubMed search?

+1 "The plasma gets filtered, like spaghetti in a colander".Couldn't have explained it better!! If my understanding is correct, in a fenestrated capillary, there is convection in the inner channel, filtration across the inner channel, and convection in the space between the inner channel and the BM.A silly doubt, is the fluid between the inner channel and BM referred to as the interstitial fluid? How do the cells get in contact with this fluid?

I tried a PubMed search and found values of pressure reported in the literature(a ref.).I'm yet to find a reference that provides measurements of the pressure gradient across the capillary channel.I could only find absolute values termed Capillary Blood Pressure or Hydrostatic blood pressure. I'm confused with these terminologies? Is the capillary blood pressure same as hydrostatic blood pressure?Could you please explain?

First, to your question about "capillary blood pressure" versus "hydrostatic blood pressure." Unless there is some very specific context in which the former is being used weirdly, I would take them to be synonyms if you are talking about intracapillary blood. You can also talk about hydrostatic BP in veins and arteries. The pressure gradient you talk about is the transmural pressure, a critical concept and part of the driving force for filtration explained well and briefly by the link I gave in my original answer at CVPhysiology.com. [1/3]

The wall (Latin: mura) of the capillary divides the blood from the tissue interstitial fluid (L: inter=between + statum=standing), the "fluid standing between the cells of the tissue." Since the fluid in the intercellular clefts between the endothelial cells is inside the BM wall, it's still plasma. Remember, the lack of albumin in the ISF makes it chemically distinct from the plasma in those clefts. [2/3]

I'm not sure what you mean by "inner channel." I infer that you mean the capillary lumen, as defined by the endothelium, because that's the only way I can understand your statements about convection and filtration. As stated in this book chapter on filtration, the BM has long been thought of as the filtration barrier, though studies released in 2010 suggest that it might be the glycocalyx of the endothelium. At a teaching level, it doesn't change the equations we use, as described in the first link I provided.[3/3]

Sorry for not using the appropriate terminology. By inner channel, as you rightly inferred, I was referring to the capillary lumen.Thanks a lot for the detailed explanations.


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When a muscle contracts, but not all the muscle fibers are activated, what happens to the remaining muscle fibers?
I understand how motor neurons work, but I would like clarification on what exactly is going on when a muscle contracts. For the sake of simplicity, let's just use the bicep as an example. If I do a bicep curl with a weight that is the maximum weight my bicep can lift, all the muscle fibers in my bicep will be activated and contract(more or less). If I remove the weight and do the same bicep curl, now only a small percentage of the muscle fibers in my bicep will be activated and contract, because that extra force isn't needed. But, the whole bicep muscle is still contracting! It must be, otherwise wouldn't the other muscle fibers staying at regular length prevent the bicep from contracting?
So the only thing I could think of is that the unactivated muscle fibers are pliant and DO contract, they just don't initiate the contraction, but instead go along for the ride. So if you looked at the level of sarcomeres, in the activated muscle fibers, the myosin heads pull on the actin, causing contraction. In the unactivated muscle fibers, myosin heads are NOT pulling on the actin, but the sarcomeres are still contracting, due to the forces from the activated muscle fibers. Is this a correct interpretation of what's going on or am I wrong?

I don't think the unused sacromeres will contract though because every time you contract, it requires ATP and so it will be really expensive if you contract when you don't need to. I believe the unused muscle fibre will just be compressed or bent, since cells have a certain degree of compliance. I am guessing that is also why you won't feel your muscle as hard if you are not doing MVC

If you define contraction, as the myosin heads pulling on the actin and engaging in the cross-bridge cycle, that requires ATP, so yes, that can't be happening. I agree with you and that's not what I was saying. Rather, I was talking about contraction as simply the shortening of the muscle fiber. I was describing would be what you said, compression. So if you were able to see the sarcomeres during contraction, the actin relative to the center of the sarcomeres would be in the same position in both the activated and unactivated muscle fibers.  But...

It would be due to the cross-bridge cycle in the activated fibers, and due to compressive forces in the unactivated fibers. Still, this is speculation on both our parts. I would like a reference that can verify this.

References please! To support your answer


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In a sarcomere, during contraction, is chemical energy turned into elastic energy and then mechanical energy?
I'm familiar with the cross bridge cycle and how the sarcomere contracts, but I have two related questions. I’ve read that when the myosin head cocks, it’s similar to a spring-loaded mousetrap. But is this actually true or just an analogy? In other words, is the chemical energy actually turned into elastic potential energy and then mechanical energy as the myosin head drives forward or am I misunderstanding this? And if this is correct, what is the evolutionary purpose for storing the energy as elastic potential energy? In other words, you could imagine a different configuration, where instead of the hydrolyzation of ATP to ADP + P being used to cock the myosin head into its high energy conformation, stored as elastic energy, and THEN driving the myosin head forward when the cycle is complete, you could envision a configuration where there is no intermediate step of storing the elastic energy. Instead the chemical energy is directly used to move the myosin heads and contract the sarcomere. So why does this intermediate step exist?

At such immensely small sizes, concepts like elasticity drastically change. The ability to "stretch" a molecule is nothing at all like elasticity in larger structures. As soon myosin moves, the rest of it moves virtually instantly.


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Is scalable growth the main reason why Darwinian systems select Fibonacci sequences?
The other day I was thinking about evolution of multi-cellular organisms, and why from the earliest onset of the development of communal cellular structure building, life may have selected a simplest possible strategy for building scale-able structures.
We humans employ relatively complex mathematics and measuring tapes to engineer structures, and we build them to full size, or modular so they assemble. We like proportionality, and there are strength and weight considerations associated with it, but we are not entirely ruled by these considerations. But it maybe that life is far more dependent on proportionality considerations. Life grows sequentially from a single cell, and each cell possesses both the building machinery, and what must be a relatively simple genetic program to govern growth. Because the generic programming operates on the basis of individual cells, there is conceivably a limit to the complexity of program you can expect life to be employing. And even if genetic coding is capable of tremendous complexity, life’s still going to select the simplest most effective approach. So how does lifes growth system achieve such consistently proportional results?
The answer may reveal itself, when you try to conceive of a building method that achieves the same outcome life does. That is to say, building a small scale structure, that will later scale up to full size through a growth cycle, and maintain a proportionality. If for example you build a small scale brick building, whereby the bricks can replicate and divide like living cells. Then so long as each brick does so at an overall synchronous rate, starts with select proportions and follows a very simple program governing growth that abides a proportionality which stays constant at all scales. Like the Fibonacci series rectangle does. Then the building can be scaled up through a smooth growth cycle while remaining structurally proportional. What you start with will determine your end result. And most importantly, having used a minimalistic coding system.
So what’s interesting, is that this is potentially a sound reasoning for why Fibonacci series emerges from such a fundamental level within Darwinian life. Life in the oceans subsisted as single celled organisms, but as soon as it started experimenting with multi-cellular structures, it needed to solve these issues of scale-able growth.
If this is correct, then it opens a fascinating window on a process of early life. Who knows what types of biological evolutionary insights might be derived from it.
Does this scenario sound plausible to more people than just me?

I didn't know there was something called theoretical biology! highly thought inducing!...I need to find some references for the answer in my head.

@KoustavPal I didnt know there was either. Here's a documentary which played a part in my realizing https://www.youtube.com/watch?v=h1qVloZKmdM

In any science there is theoretical side of this science. Theoreticians build hypotheses that can be tested. Theoretician also often build the necessary statistical tools. Btw, I am a theoretician

The question is very long and lack any kind of formatting. I am too lazy to read it. If you want people to make effort to read your questions, try to make them as appealing as possible. Also, by experience, long wordy question are often bad questions (but I can't tell for yours as I haven't read it but seeing expression like "Darwinian life" is not encouraging :)).

I have now read the question :) I still think it should be reduced in length. I know little to nothing in this field but it sounds worthwhile to me that you keep thinking about it! The fields of interest to you are system-biology and developmental-biology. You might want to have a look at plant mathematics: Fibonacci's flower.

TL;DR. There are some Markov processes that generate Fibonacci sequences. Perhaps that could be the reason why they are so common. I don't remember what exactly it was as I read this a while back in a relatively obscure (but good) book on Markov processes. And I lost that book unfortunately. I do remember that rabbit breeding was used as an example.

Okay. This is the book and it is not that obscure. I read an old edition which was in my university library.

I really wanted to put my thoughts into words as to why biological systems conform to Fibonacci's series.
What you say is entirely plausible and it does make sense. But what I wanted to address was why do these systems conform to it.
It is because of the interactions with the environment
Explaining this concept on multicellular organism first requires answering the same question in bacteria. Towards this end, I would like to point you towards this wiki page
It comes down to parameters such as medium concentration and hardness, parameters which we can influence. If we can extrapolate from this that cells, any cells will always follow a chemokine/nutrition gradient then we can start to understand why the system conforms to a fibonacci sequence.
Next, check out this video on a wound healing assay, what i would like to bring to your notice is that you'll find the cells replicate and move at the same rate.
If you follow a chemokine gradient, and move at approximately the same rate as your 2 billionth cousin, wouldn't you end up inevitably creating a symmetric structure?
Finally, I would, point you towards this article, where they explain a phenomenon called cell migration. This is particularly responsible for creating the symmetry which you see. And this is a similar article as the top one but it should be open access. Both support an idea which has been observed, I tried searching for the video but couldn't find it. The idea being that cells migrate collective, but there are some cells which are leaders and some followers. The leaders lead the collective migration (creating some sort of chemokine gradient) while the followers follow this gradient.
I attended a seminar last year by D Gilmour from EMBL. He showed us this particular video on collective cell migration and deposition of small clusters of cells which go on to establish the lateral line in zebrafish. You will find that a periodicity exists in this migration pattern. He relates it to a ligand activation. The related article to the video should be this one (I thought so after reading the abstract)

Thank you Koustav for your detailed answer. There's quite a bit here to think about, and follow up on. I'll go through everything you presented


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Determining the Value of Inhibition constant
I am trying to understand how the inhibition constant is calculated for competitive inhibition.
$\frac{K^{app}}{V^{app}} = \frac{1+I/K_i}{V/K_m}$.
But often in secondary plots, $\frac{K^{app}}{V^{app}} $ vs Inhibitor concentration is plotted and the inhibition constant , $K_i$ is obtained from slope $1/K_i$. How is the slope equal to  $1/K_i$ from the above equation?
Could someone explain?


text:
Where can I find the pZ189vector plasmid vector sequence?
I need this sequence since it was used in this paper https://onlinelibrary.wiley.com/doi/pdf/10.1002/em.1046. They say that the plasmid was prepared as in this paper http://www.jbc.org/content/271/16/9637/F1.expansion.html (see figure below)

However, they do not seem to be reporting the sequence of the pZ189 vector. Does anybody know where can I find this sequence?

Did a search on NCBI and found a list of nucleotides. Maybe you need one of these https://www.ncbi.nlm.nih.gov/nuccore/?term=pZ189

Turns out the sequence is not actually written down anywhere. I asked one of the original authors of the plasmid (not the paper above) and he said that nobody ever did it because at the time when the plasmid was used it would have been a laborious task with little utility. Bummer :(
He also said that plasmid pSP189 is sort of the same but much more efficient and what it does, and is also more studied, with the sequence freely available around the internet.


text:
What waste products do cells secrete in culture, and at what rate?
I am designing microfluidic chips for mammalian cell culture. One aspect I am interested in modeling is the rate at which I must renew media to ensure that:

Cells receive enough nutrients
Cytotoxic waste products are removed before they reach concentrations that would be detrimental to the cells.

Number 1 is fairly easy. Numbers for glucose uptake rate, for example, are available for many cell types. Number 2 is proving more challenging. I cannot find articles that detail secreted metabolites, including their secretion rate and the relationship between their concentration in media and toxic (or other) effects on cells.
Are there any resources out there on quantitative assessment of secreted metabolic waste?


text:
Immature lawn mushroom
These have been popping up all over our yard in South Western Australia. I have been digging them out before they mature as I have small children. But with 7 acres I can only check so much.
My question is: Is it possible to eliminate them as being harmful mushrooms from this picture before seeing them at maturity?
Some have been growing in isolation, others in clusters.
Note: a few weeks ago, from near this spot, I removed a white mushroom on a stem with its cap still closed and white gills when I opened it. I have also found a few different types of puffballs around

Are you able to obtain an additional photograph of the stipe (stem) of the fungus? If not, may you please describe the properties of its gills and hymenium - cells which eventually produce spores?

To get a good answer you will need to observe the growth of the mushrooms and post pictures at different stages. Puffball mushrooms will "pop" when poked releasing a cloud of spores. Some mushrooms look like a puffball when young but then open like an umbrella later.


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does order of genes in a chromosome matter?
does the order of genes within a chromosome matter? or is the main thing that the genes are there.
so for example, our DNA is very similar to that of apes not only by the genes themselves but also by the arrangement of those genes in the chromosomes.
is the order of this arrangement significant? Or if it were shuffled around, then the functional impact would be more or less the same?
Another example, an international study in the mouse genome has revealed that virtually all mouse genes have direct counterparts in humans, i.e. humans and mice contain virtually the same set of genes. is the difference between humans and mice due primarily to the different order of the genes or to the slight differences in the genes themselves?
This question was raised from a claim here which seems to imply it does not matter.

The chances are infinitesimal that human chr 2 were to resemble those
  of other primates at random. This is what you say in science when you
  mean 'impossible'. One simply doesn't see a segment of DNA the size of
  Chr 2A and 2B being so similar for such a length when we look at rats,
  dogs, worms or any more distantly related living thing.

is the difference between humans and mice due primarily to the
  different order of the genes or to the slight differences in the genes
  themselves?

The latter.

This question was raised from a claim here which seems to imply it
  does not matter.

You are talking about two different things.  Gene expression is often controlled by nearby DNA sequences that don't code for protein.  Moving a gene away from the DNA that controls it can change its expression a lot, and have huge consequences on the organism.  But in many cases, you can move a whole gene, including its controlling sequences, to another place, and nothing much will happen.
People were bringing up synteny as evidence of evolutionary relatedness, not as the cause for all primates looking similar.

Ye, the order matters. This can be seen in chromosomal translocations which can cause cancer.
A example for that would be the translocation of IRF4 which happens in a subtype of multiple myeloma. The translocation is permanently activating the transcription factor. See here for details:

Translocations activating IRF4 identify a subtype of germinal
center-derived B-cell lymphoma affecting predominantly children and
young adults.

The main reason for this is the regulation of the genes - when the order is changed, the regulatory elements which are important for regulating the expression are missing. A lot of these regulatory elements are located many kB away from the gene and are still important for its activation or silencing.
This can look like the image below (image from here):

Regarding the mouse question: On which chromosome a gene is located is not really important if you compare different species. The gene I worked on for a while is functionally equivalent between mouse and human (the human version works perfectly in mouse), but they are located on different chromosomes. It again comes down to different regulation and in some cases also a different amino acid sequence. Also mice (as other animals as well) have quite a number of genes which are unique for them and which make a difference between the two species. There are a few interesting papers on that topic:

Lineage-Specific Biology Revealed by a Finished Genome Assembly of
the Mouse
Comparison of the genomes of human and mouse lays the foundation of
genome zoology

That's kind of cheating though. Most cancer-causing translocations are either because their insertion causes frameshifts that disable other genes or because, as in your example, regulatory elements are left out. The modern definition of a gene tends to include its regulatory elements so here, you're not changing the order of the genes but breaking them up which is a whole different thing. I can't think of any cases where the order of the genes itself is important (in eukaryotes anyway, barring operons and the like) and would be quite interested to know of any.

authors: Юрий Евсюков


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Is a walnut a nut or a drupe?
We've been learning about fruits (and the various categories thereof) in class; among them we have the nut and the drupe.
My textbook differentiates between those terms as:

Nut: It is a single-seeded indehiscent, dry fruit.

Drupe: A fleshy fruit with a stony endocarp.

How here's the problem.
My textbook lists the walnut (fruit) as a nut. But Wikipedia disagrees on this point, calling it a drupe instead.

I'd like a second opinion, since both my book and Wikipedia have had reliability "issues" in the past.
Q- Is a walnut (fruit) a (botanical) nut or a drupe?

Short answer
Walnuts are classified both as nuts and drupes ('stone fruits').
background
According to University of Wisconsin - Madison, Department of Botany , hickory and walnut can be classified both as drupes and nuts, but are best classified as nuts.
Nuts fall into the class of indehiscent fruits: dry fruits that do not open when mature to shed their seeds. Many of this group are one-seeded fruits, such as the nuts. In addition, nuts have a thickened and hardened wall. Examples are beech, chestnut, oak, hazel, walnut and hickory. Because of extrafloral bracts, or "husk", the latter two fruits are sometimes called "drupes").
As opposed to indehiscent fruits, the fleshy fruits have a wall that becomes soft and fleshy as it matures. Drupes ('stone fruits') fall into this class. Drupes one-seeded, simple fruits developed from a superior ovary in which the innermost portion of the wall (endocarp) becomes hard and stony, the outermost part (exocarp) becomes a relatively thin skin, and the middle portion between the skin and the stone (mesocarp) becomes either fleshy or fibrous. Examples are cherry, coconut (the endocarp is the thick wood shell that surrounds the fleshy and liquid-filled seed), but also walnut and hickory. The latter two are, however, best called "nuts".
Indeed, according to a popular scientific article in the Guardian, many tree nuts are also drupes, including walnuts and pecans.

Some nut who thinks he's been duped, I suppose.

Then what's the fleshy part of the walnut?

@Rob The question's about the walnut (fruit), not the kernel (which is commonly referred to as the "walnut"). I had issues wrapping my head around that too at first :3

A true nut, botanically speaking, is a hard-shelled pod that contains
  both the fruit and seed of the plant, where the fruit does not open to
  release the seed to the world. Some examples of botanical nuts are
  chestnuts, hazelnuts, and acorns.
A drupe is a type of fruit in which an outer fleshy part surrounds a
  shell (what we sometimes call a pit) with a seed inside. Some examples
  of drupes are peaches, plums, and cherries—but walnuts, almonds, and
  pecans are also drupes. They're just drupes in which we eat the seed
  inside the pit instead of the fruit!

Source: http://www.seriouseats.com/2010/04/what-are-the-differences-between-nuts-and-drupes.html

I would opt against using culinary sources as the basis of an answer.

@AliceD:  I would normally agree.  However, in this case the author is known as the "Peanut Butter Guy" and Founder and President of Peanut Butter & Co.  I understand that peanuts are a legume, but I do value his opinion on nuts too.

I've never seen "drupe" figure in a purely culinary site/blog/book (I'm not much of a cook, but still...). That this source even mentions "drupe", and then goes on to discern between a drupe and a nut, adds to its credibility IMHO.

I wouldn't underestimate the knowledge that a culinarian has with foods.  Per wikipedia experts in this field need to have knowledge of food science defined as "the discipline in which the engineering, biological, and physical sciences are used to study the nature of foods, the causes of deterioration, the principles underlying food processing, and the improvement of foods for the consuming public"


text:
Human spine: Is the coccyx really fused?
Prologue: This post is about the adult (say, a 20 year old) human skeleton; I'm not particularly interested in infant skeletons.
The human spine has is composed of cervical, thoracic, lumbar, sacral and coccygeal vertebrae

 Image source

My school textbook (which has a history of possessing erroneous/outdated information) states:

The coccyx consists of 4 coccygeal vertebrae that are fused to become a single bone.

However, this Wikipedia article states:

Most anatomy books incorrectly state that the coccyx is normally fused in adults. In fact it has been shown that the coccyx may consist of up to five separate bony segments, the most common configuration being two or three segments.

Is Wikipedia correct?
If so, what is the (most common) number of bones that constitute the spine? Is the number of vertebrae that constitute the spine going to be different?

This other Wiki article appears to be particularly contentious:

A fully grown adult features 30 bones in the spine, whereas a child can have 33.

The cervical vertebrae (7)

The thoracic vertebrae (12)

The lumbar vertebrae (5)

The sacral vertebrae (5 at birth, later fused into one)

The coccygeal vertebrae (5 at birth, some or all of the bones fuse together but there seems to be a disagreement between researchers as to what the most common number should be. Some say the most common is 1, others say 2 or 3, with 4 being the least likely. It is counted as 1 in this article.)

I understand that there is little to no variation in the number of cervical, thoracic and lumbar vertebrae among humans, so they altogether constitute $\mathrm{7+12+5 = 24}$ vertebrae/bones (in this case, I believe "vertebrae" and "bones" are synonymous).
Assuming that the sacrum really is one fused bone (my question's regarding the coccyx, so I'm not going to question the anatomy of the sacrum in this post) consisting of five vertebrae (I think there's a bone-vertebra distinction here, so they aren't the same thing)
In that case, the cervical, thoracic, lumbar and sacral contributions are $\mathrm{ 24 + 1 = 25}$ bones, or  $\mathrm{ 24 + 5 = 29}$ vertebrae. (Right?)
According to the Wikipedia article I cited above (the second one), the adult human spine has 30 bones.
So the coccyx contributes $\mathrm{30 - 29 = 1}$ bone to the spine, or $\mathrm{30 - 25 = 5}$ vertebrae to the spine.
In other words, the second Wiki article implies that the coccyx is a single (fused) bone. However, the first article states that the coccyx is really composed of 3-5 (say, 4 on an average) bones.
This is horribly contradictory.

If the finer points of my question was lost, I'll restate them here:
1) Is the coccyx a single bone or multiple bones?
2) How many bones are there in the adult human spine?
3) How many vertebrae are there in the adult human spine?

Although from an academic standpoint these are critically important questions, the variability in human anatomy unfortunately renders the academic answers reasonably meaningless regarding the coccyx in any clinical circumstances. Although variability is much less, higher in the spine it is common to see a sacralized L5 or an S1 that failed to properly fuse, even more rare are the cervical ribs. Clinically, some of these items actually mean something, yet I have never seen a clinically significant issue related to coccygeal fusion.

@RudyB And that was the point I was making (with a different emphasis) in my comment below. Academically, the fusion (or lack thereof) of the coccygeal segments matters. Clinically (meaning practically), it really doesn't in most cases.

The wikipedia article links to two papers. The first article has data for 120 pain-free and 51 affected patients with data on the number of coccygeal segments in each. We can back-calculate a reasonable approximation of segment distributions from their percentages:

1 Segment: 7%
2 Segments: 51%
3 Segments: 38%
4 segments: 4%

So 2 or 3 segments makes up almost 90% of the population. Given that only 7% of the subjects had single element coccyxes, I think it's safe to call the coccyx usually made of multiple elements.
Whether you refer to those multiple elements a single bone if largely a semantic argument. Since there is variation, it seems reasonable to call the collection 5 of variably fused terminal vertebrae the "coccyx".
As a practicing anatomist, I would say that there are 29 vertebrae, as in 29 vertebral elements (but you can't say 29 ossification centers, because each is made of multiple centers). These fuse into 24 free vertebrae, the sacrum (5 fused vertebrae) and one coccyx, which is variably fused.

It is odd that you say you don’t trust Wikipedia for anything, but then base your entire answer on a paper that Wikipedia cites without analysis on whether that paper is accurate and up-to-date, which was really the question. Wikipedia can usually (though definitely not always) be trusted to accurately report the sources it cites, but whether or not it has the best source available is a much more difficult question—the kind of question you would bring to experts to get their opinion on.

@KRyan -- kmm's Bona Fides and profile/activity/awards rather makes this answer an "expert" opinion. -- Wikipedia can be edited by anyone and the "peer review" quality varies widely, as anyone with expert knowledge in a field who has used Wikipedia knows. -- I've had my own edits rolled back when I not only cited sources but cited the legally documented source that defined the very answer I gave. i.e. I literally proved my answer right outside of any matter of opinion and still my answer was rolled back. That was the last time I contributed to Wikipedia.

@user23715 I’m not doubting them, I’m saying that his answer does not so much as even assert that this is the right article to be looking at. “I am an expert and this paper is up-to-date and correct,” would be fine. But instead the answer is more like “the paper says this, which Wikipedia accurately reports,” which even I (who cannot name all of the major bones of the arms and legs) could have determined myself.

@KRyan -- I think he has that covered with, "As a practicing anatomist, I would say...", no? -- His disparagement of Wikipedia is founded IMO. Besides, if one has to "trust but verify" every time one uses Wikipedia why not bypass it to begin with and go straight to the sources? -- Something like Wikipedia made more sense when a search engine like Google did not exist. Now, failure to find appropriate sources is one's own fault. Using a squiffy source like Wikipedia as a first pass is rather redundant and their difficulties in getting funded lately means many others have figured this out.

To be fair, I do think it's incongruous that it wouldn't matter to you as a "practising anatomist". Anatomy is all about definining body structure. That includes variations, both common and less common. As a practising doctor, I've studied Anatomy in med school, and I know how important minutiae about spatial relations and variations are in the subject - I mean, that's the whole point of the subject! I bet this sort of thing is even more important to academic practitioners of Anatomy. What you said may have made more sense if you'd said "physician" (or even "surgeon") instead of anatomist.

lets answer in order.

Is the coccyx a single bone or multiple bones?

answer yes, A bone is not a concrete definition and can be used to describe the number of elements or the number of contributing elements. Bone is more a definition of material than object. My favorite example is the fused mammalian jaw which can be one or two bones (two fused dentaries one mandible) or two bones (two fused dentaries). Even using the word elements can get confusing. Like many things in biology nature doesn't care about our attempts to define and categorize.

How many bones are there in the adult human spine?

26 -35 depending on the individual and how you use the term.

How many vertebrae are there in the adult human spine?

this one is easy, 34-35 for most people. The variation is becasue not everyone develops all the coccyx vertebrae. Fused vertebrae are still counted as several individual vertebrae. This is why we have a seperate term for the fused element, the sacrum or attach the descriptor "fused".  This comes up a lot in paleontology since animals change the number of vertebrae they have and how they are distributed as they evolve.  Sauropods are particularly known for swapping vertebrae across segments.

I made a mistake on my math on question 3, I have fixed it, no stunning revelation I just added wrong. .

I suggest using >  instead of four spaces. It's HTML5-ly better, and looks nicer.

It isn’t just nicer looking—proper quote boxes are also vastly better for accessibility. Which is to say, they aren’t actively terrible for accessibility, which codeboxes can be. Please never use code formatting for non-code: quote boxes, or simple quotation marks, work quite well for quotation. When you use code boxes, you may see a gray box with monospace font, but others—say, those listening to the page because they are blind—may get something very different, which may be hard to understand. Reading letter-by-letter is not unheard of! So please, format properly.