Misunderstanding about nucleotide biosynthesis Some months ago, I asked what was a phosphoester bond, because I didn't really understand the following picture and explanations provided in the "Molecular biology of the gene" from Watson, Baker, Bell and al. (7th edition).

The explanation is the following:

We can think of how the base is joined to 2'-deoxyribose by imagining the removal of a molecule of water between the hydroxyl on the 1' carbon of the sugar and the base to form a glycosidic bond (Fig. 4-2). The sugar and base alone are called a nucleoside. Likewise, we can imagine linking the phosphate to 2'-deoxyribose by removing a water molecule from between the phosphate and the hydroxyl on the 5' carbon to make a 5' phosphomonoester. Adding a phosphate (or more than one phosphate) to a nucleoside creates a nucleotide.
Thus, by making a glycosidic bond between the base and the sugar, and by making a phosphoester bond between the sugar and the phosphoric acid, we have created a nucleotide.

What I didn't understand months ago was, to resume, "why is the bond between the phosphate group and the 2'-deoxyribose called a phosphoester bond since the phosphoester bond (which is, by definition, a P-O bond) already exists before the bonding between the phosphate group and the sugar?"
While this question is still bothering me (I was not entirely satisfied with the answers I got back then, because the synthesis of a single strand of DNA is something which is probably different from the synthesis of nucleotides themselves), the question I'm asking myself right now is: "why do general biology books always talk about condensation reactions, while this article and this book do not mention it in the biosynthesis pathways of nucleotides?"
What I mean is: it seems like the biosynthesis of nucleotides is far more complicated than just being two condensation reactions. Furthermore, when I look at the 10th step of this picture (which comes from the article I mentioned above), I see a condensation reaction at the end of the pathway, but it does not occur where the book from Watson and al. suggests it should:

So, after months of wondering and researchs about all this, my final question about this is, as mentioned above:
Why do biology books always mention condensation reactions while, apparently, it doesn't have a lot to do with the manner in which the nucleotides are synthesized?

A condensation reaction is defined on Wikipedia as

  a reaction in which two molecules or moieties, often functional
  groups, combine to form a larger molecule, together with the loss of a
  small molecule. Possible small molecules that are lost include water,
  acetic acid, hydrogen chloride, or methanol, but most commonly in
  biological reactions it is water.

It doesn't say anything about the number of steps required to reach the final compound, nor about the type of bonds formed. Following this definition, the nucleotide synthesis occurs via condensation reactions.


Why don't we have more cone cells (bigger fovea)? Background

Apart from being able to sense color, cone cells are able to perceive finer detail and more rapid changes in images, because their response times to stimuli are faster than those of rods.

The fovea centralis is where cone cells are most concentrated and is responsible for sharp central vision (foveal vision), which is necessary in humans for reading, driving, and any activity where visual detail is of primary importance.

Question

It is hard to imagine what it would be like to be missing the fovea centralis, and even harder to imagine what it would be like to have one the size of the entire retina! In any case it seems that having a bigger fovea centralis would be beneficial for survival, so why do we have so much peripheral vision?

We use central vision for a lot more things today than in the past. Peripheral vision is most important in navigation, so those who lose their central field retain the ability to navigate around objects. It is important that this is fast and sensitive in the dark as well as light. It isn't important for it to be in colour; this would mean it would be less sensitive in the dark and colour isn't important in navigation and also it would take longer. Navigation is of vital importance as it can be the difference between survival or death in the flight or fight response. Similarly it is important in the fight part, being able to see a foe.

Let's our foveas were bigger, well we would lose the above. What would we gain? The ability to see more at full resolution and colour. It's impossible for us to concentrate on more than we can see in our central field already. in fact we dart our gaze around to focus on many things because we can't focus on multiple things at once. By this I mean thinking about what we see not processing it. Of course we would also require a much larger brain to be able to process it all, processing the central field takes a lot of brain matter.

So in conclusion, it's not helpful.


Evidence against aging caused by loss of information in genome and epigenome in humans? After reading Lifespan by David Sinclair I'm curious if there is any evidence against aging being caused by loss of information in genome and epigenome of 3.7*1013 cells in human body.
Specifically has anyone compared the genome and epigenome of the same humans at different ages?

By loss of genome, I think he is referring to the shortening of telomeres. This
study compares the length of telomeres of human epidermal cells. The authors report that over time, the telomeres do shorten. They also report on the rate of loss of around 32 base pairs per year. Thus there is loss of some genomic information over the age of an individual.
However, the loss of epigenomic information is trickier. The primary reason for it being some regions of the genome have been shown to lose DNA methylation marks whereas others gain it. However, leaving that aside, there is comprehensive proof that DNA methylation changes with age. This study on female peripheral leukocytes shows that approximately 350 regions (known as CpG islands) which are differentially methylated with age. Of these 350, 250 loci become hypermethylated i.e. methylation increases with age while the opposite happens for the remaining 150 loci.


How do enzymes not change the overall energy change of the reaction they're catalysing if they lower the activation energy? Based on the Induced-Fit model of enzyme action, enzymes catalyse a reaction by lowering the activation energy of a single forward reaction over and over. But I read that enzymes don't change the overall energy change of the reaction $(\Delta H_{solution})$ they just speed up the reaction.
How can enzymes reduce the activation energy of every forward reaction but still not affect the $\Delta H$? $\Delta H$ is sometimes called change in heat because it is measured in Joules and it's either endothermic or exothermic (this bit is chemistry).
I'm a highschool student and I'm just trying to find out how the required activation energy doesn't affect the energy change for the whole reaction.

You're on a valley on one side of a mountain (representing some fairly stable state of your reactants), and you'd like to go to a town on the other side at a lower elevation (representing another stable state for your products, at lower energy than your current state: this is an energetically favorable reaction).
You can go over the mountain: high activation energy to climb up to the top, then you go down the slope to eventually get down to the town.
You can go through a pass between mountains instead: much lower activation energy to get over the pass, then you eventually get down to the town.
Whichever path you choose, you're at the same elevation (energy, $\Delta H$ compared to where you started), with the same products (your location in space), but if you took the pass you've gotten there via a different chemical route that was easier to achieve energetically at the peak.
Enzymes let you take the path through the pass rather than over the top of the mountain. They don't change where you started from or where you're going, so they don't change the overall energy of the reaction.


How to add oxygen to indoor air without opening windows? I'm not a biologist. I have read that low oxygen levels in the home can have a negative effect on health. I am interested in increasing the amount of oxygen in the air in my home.

To open the windows would be the most effective way but the air outside is cold and measurably polluted (PM2.5 usually greater than 30µg/m3) so I would like to find other ways.

I know that plants add oxygen to the air but I have read that an unrealistically large amount of plants would be needed to make a meaningful difference to the oxygen levels.

I am wondering what other methods I can use and also whether what I have written above is correct.

Please forgive me for my ignorance. If this is the wrong place to ask this question then please help me to find the right place. Also sorry for not knowing what tags to use.

You should also have in mind that, meanwhile plants produce oxygen through photosynthesis, they also carry out aerobic respiration. In short, this process requires oxygen which is normally not a problem during daytime as photosynthesis covers the oxygen needed. Nonetheless, during nightime, plants remove oxygen from the atmosphere and do not replenish it. This is why nurses normally remove plants from hospital rooms at night. So if you want to put plants in your room, have in mind that is best to take it outside during the night.

Refer to this link for more information: http://www.saps.org.uk/saps-associates/browse-q-and-a/453-do-house-plants-remove-oxygen


Why is the mechanism of inheritance for this disease autosomal dominant? An unrelated couple has a daughter and a son with the same rare condition. Neither parent has any obvious signs of the condition, but the father's mother (paternal grandmother) and her brother have the same condition. Select the most likely mode of inheritance:

  A. X-Linked
  B. Autosomal recessive
  C. Autosomal dominant
  D. Multifactorial
  E. Mitochondria

The correct answer is C. But I'm confused why it would be autosomal dominant when neither parent has the phenotype. I thought it might be autosomal recessive, even though this mode usually does not have a family history, just because of the fact that the paternal grandmother and her brother both had the disease, and this is consistent with the horizontal pattern associated with autosomal recessive inheritance. For it to be autosomal dominant, the disease would have to be incompletely penetrant, which seems like a less likely scenario than it being autosomal recessive.

Can someone explain why it is dominant, not recessive?

Thanks!

I think this question is not possible to answer without knowing the frequency of the deleterious alleles in the population.  There's no way to assess whether incomplete penetrance is more or less likely than an undetected mutation in the mother's side.  Since the question doesn't mention the mother's family at all, and only the father's, that suggests to me that the question writers don't want you to think that anything is wrong in the mother's side.  That would make it dominant with incomplete penetrance.


Why are eyes more sensitive to flicker in periphery — contradictory answers In terms of the perception of flickering by CRT monitors, This answer suggests that peripheral vision has faster response and is thus more sensitive to flicker due to being provided by rod cells.

But in another answer it's said that rods are saturated at daylight and even at twilight. These two answers are in contradiction, since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.

So, how to reconcile these two answers?

I think the most likely explanation is that ambient lighting conditions in the room where OP was sitting, as described in the original question, might not have been bright enough to saturate the rods. Under mesopic conditions, both rods and cones are active. Hence your statement that

  ...since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.

may not hold. Since rods indeed have quicker responses, the periphery may be more sensitive to the flickering of a CRT or light bulb.

Note, however, that cones have flicker fusion frequencies of up to 90 Hz (reviewed by Perz, 2010), and CRT screens and light bulbs flicker at frequencies following the mains (50 or 60 Hz). Hence, cones may still be able to pick up the flickering. Since OP reports on an anecdote, experimental conditions may have been suboptimal and their report might have been unreliable. So we cannot exclude OP was using photopic vision, regardless their report.

Reference
- Perz, Master's thesis, Eindhoven University


Why does this karyotype start numbering at 11? Here is some image I found for karyotyping a chromosome:

Why does the band numbering start at 11? When I count other things I usually start with the number one, and in some cases zero. Eleven seems random.

Why does the band numbering start at 11? When I count other things I usually start with the number one.

It does start with the number one!

What is happening here is clearly a small confusion. Looking at the centromere in this idiogram of chromosome 12 you can see two number 11, as you stated in your question, one above and one below the centromere:

An idiogram of a Giemsa-stained chromosome 12. © 1994 David Adler, University of Washington. All rights reserved.

However, those two 11 below and above the centromere are not, in fact, an 11 (eleven): they are just two number 1 together, 1-1 or one-one.

According to Nature (2017):

  This particular idiogram depicts the pattern of Giemsa staining at a fairly low resolution (i.e., it produces about 400 total bands in a karyotype, which is just above the threshold that is clinically useful). At this resolution, the long q arm of chromosome 12 can be subdivided into two main regions, which are designated 12q1 and 12q2. Region 12q1 can be further subdivided into five subregions, designated 12q11 through 12q15, each of which corresponds to a band detected by Giemsa staining. Orally, these subdivisions are referred to as "12q one-one" through "12q one-five" (not as "12q eleven" through "12q fifteen"). The more distal 12q2 region can be subdivided into subregions 12q21 through 12q24. In addition, subregion 12q24 can be further subdivided into regions 12q24.1 through 12q24.3, even at this relatively low resolution.. (emphasis mine)

Thus, those two 11 you see above and below the centromere are (or should be), respectively, 12p1-1 and 12q1-1 (remember that this is the chromosome 12).

The confusion here, therefore, is due to:

The omission of a 12p or a 12q before all those numbers.
The omission of some separator, like an hyphen or a comma, between those numbers.

A detailed PDF from the International System for Cytogenetic Nomenclature (ISCN) can be found here.

Bonus: In case you want to know, that number 850 in the top of the idiogram refers to the number of bands:

  At this higher level of resolution, approximately 850 bands can be distinguished in a karyotype

Source: Nature.com. (2017). Chromosome Mapping: Idiograms | Learn Science at Scitable. [online] Available at: https://www.nature.com/scitable/topicpage/chromosome-mapping-idiograms-302 [Accessed 23 May 2017].


How do caspase proteins kill a cell? Wikipedia just says...

  The active effector caspases then proteolytically degrade a host of
  intracellular proteins to carry out the cell death program.

Okay, but what parts of the cell do they cleave up? And what happens to the rest of the cells' internal components, especially the parts that don't get cleaved up?

Caspase do not directly kill the cell, but rather activate a process known as apoptosis, or programmed cell death. The programmed part is there to distinguish it from other types of cell death, such as necrosis, which are more aspecific death processes.

Coming back to caspases, they are a series of proteasis, that can activate in cascade in response to a pro-apoptotic signal.

To simplify matters a lot, the pro-apoptotic signal first activates initiator caspases, such as caspase 8, 9, 10 (plus a series of other proteins).

These, in turn, cleave other effector caspases, which are the ones who effectively do the dirty job: caspase 3, 6, and 7.

Now there are many things happening at the same time (see this PDF from AbCam to get an idea of the complexity of the system).

At the nuclear level you have, for instance:

activation of DNA cleaving enzymes, such as CAD (caspase-activable DNAse), which is normally inactive, due to binding to its inhibitor I-CAD. The latter is a target of effector caspases and its degradation causes CAD to go in the nucleus and starting fragmenting DNA.
cleavage of PARP (Poly(ADP-ribose) polymerase), a nuclear enzyme involved in finding and repairing single-strand breaks on DNA.
cleavage of lamins (by effector caspases + other proteases), proteins that are important for the formation of nuclear lamina, and stability of the cell nucleus
cleavage of U1, a nuclear protein necessary for processing of mRNA.

Very complex events also happen at the mitochondria level: here you have a series of protein, which belong to the Bcl-2 family that control apoptosis mostly by regulating the levels of Ca2+ in the cell. There are 25 members of this family, that can be divided into two "sides": pro-apoptotic proteins such as Bax, Bak, and BAD and anti-apoptotic proteins such as Bcl-2, Bcl-xL, and Bcl-w.

The functioning of the Blc-2 proteins is very complex and I am not up-to-date with the last literature but to simplify, essentially what happens is that when the balance between anti-apoptotic and pro-apoptotic proteins is shifted towards the pro-, there is:

liberation of cytochrome c from the mytochondria into the cytoplasm, which can activate effector caspases.
induction of MPTPs (Mitochondrial Permeability Transition Pores), proteins which increases mitochondrial permeability which causes all sorts of trouble, eventually leading to swelling of mitochondria and loss of their function

Different events also bring to an increase in cytoplasmic calcium concentration, which can, for instance, induce the activity of calcium-activated endonuclease or other pro-apoptotic calcium-dependent proteins.

This is far from being an exaustive list of what happens, but it gives you the idea of the complexity of the system.


What shows how healthy someone is by their heart rate? What shows how healthy someone is by their heart rate - how low it is at resting pulse or how low it is during exercise or how large the difference is between the resting rate and rate with load? Any ideas?

Clarification:
Essentially, how does the heart rate reflect healthiness and in which ways (is it the resting pulse, pulse during exercise, differences, etc.)

Thank you for your time and effort

A healthy heart and cardiovascular system distributes oxygenated blood more efficiently than a less healthy one. Therefore, for a given level of exertion, a healthy heart will need to pump fewer times than a less healthy one to provide the same quantity of oxygenated blood to the rest of the body.

It's pretty much that simple.

However, the whole patient has to be considered. A low heart rate in and of itself doesn't mean someone is fit since there are many drugs and medical conditions that can create a low heart rate. Person A sitting in front of you appears fit and healthy, is on no relevant medications, and has a heart rate of 50? Fitness almost certainly explains it. Person B sitting in front of you is overweight, on several meds and not very fit? Fitness almost certainly doesn't explain it.


Does a reproductively successful male have the same genetics as a reproductively successful female? Evolutionarily, using humans as an example, it would make sense that a successful female would produce successful male offspring. If a successful female produced male offspring that weren't successful, the female also wouldn't be successful by definition and would, through evolution, stop being desired by males. Therefore, females are selected for by their ability to produce successful males and thus successful male genes must be the same as successful female genes?

However, I've heard that in humans today, males don't like rich females while females like rich males. Also, from what I've read, lascivious females used to be looked down upon in the past while lascivious males weren't. Females and males also played very different roles in society. Also, successful males often don't spend much time taking care of children and spend more time making them, while successful females spend more time taking care of them. This suggests that successful males are genetically different than successful females? I'm an amateur in biology, so correct me if I'm wrong.

Evolutionarily, using humans as an example, it would make sense that a successful female would produce successful male offspring. If a successful female produced male offspring that weren't successful, the female also wouldn't be successful by definition and would, through evolution, stop being desired by males. Therefore, females are selected for by their ability to produce successful males and thus successful male genes must be the same as successful female genes?

That assumption is wrong. Of course the best thing for an individual's reproductive success is to have as many successful offspring as possible regardless of gender, but in the real world there are sometimes tradeoffs. If an individual had a trait that made, say, their female offspring a lot more successful but mildly impaired their male's offspring's success, the advantage to the female offspring might outweigh the disadvantage to the male and the trait might get passed on, even though it produced male offspring that weren't very successful.

Here is a paper apparently exploring the concept in seed beetles:
http://rspb.royalsocietypublishing.org/content/early/2009/12/21/rspb.2009.2026

  However, I've heard that in humans today, males don't like rich females while females like rich males.

You've heard that of humans, have you? Are you sure what you heard actually applied to all humans, and not the humans in one specific society? You say "humans today", do you mean "anatomically modern humans" or "people in the 21th century"?

You really ought to investigate this kind of thing you hear before drawing all-encompassing conclusions about biology or evolution from them. Maybe you were assuming that "in humans, males don't like rich females while females like rich males" was consensus biology; if so, well, it isn't. And given that it isn't, we can't answer your questions based on such a vague claim; you should give a source that explains more precisely what exactly is being said there.

  Also, from what I've read, lascivious females used to be looked down upon in the past while lascivious males weren't.

Same thing; I'll also highlight the "in the past" when your previous sentence talked about "today". Evolution works on the scales of hundreds and thousands of generations. Why would you assume evolutionary explanations for social trends that, by your own words apparently, have changed recently?

  This suggests that successful males are genetically different than successful females?

In order for those things suggest that, you would need: 1) to establish reliably that the differences you talked about exist, 2) to establish that they have a probable biological basis; one way of establishing this could be to show that they are universal across human cultures, geography and history. If they aren't then it's more likely the explanation is cultural than biological, and 3) to establish that the biological difference is related to individuals being successful, as opposed to being random variation (which happens a lot in evolution).


mRNA and Protein relation A and B are two different proteins:
1- can they have same mrna
2- is it possible that the gene types which encoding the synthase are same ?

my answer is yes to both .
because after protein synthased cell can remove aminoacids with  post-transcriptional modification etc.

1) Can two different proteins have the same mRNA?

This isn't clear enough to give you an answer:

Can two different proteins be made from the same mRNA molecule?

Yes, polycistronic mRNAs can encode several proteins which are translated separately (we can engineer this using internal ribosome entry sites, IRES).
Yes, different proteins can be translated from one open reading frame by failure of peptide bonding between two amino acids (we can engineer this using 2A peptide sites).
Yes, identical proteins can be translated from one mRNA and then modified differently after translation to yield different "final" proteins.
Yes, identical polypeptides can be translated from one mRNA and then incorporated in different protein complexes.

Can two different proteins be made from the same mRNA code?

No, not made in the sense of translated.
Yes, as above, identical proteins/polypeptides can be made and treated differently after translation.

2) Is it possible that the gene types which encode the synthase are the same?

Gene types? Do you mean genotype, i.e. allele? What synthase? Sounds like a homework question to me.


Can scientists "see" thought? Touching an object activates a nerve - something that can be observed by scientists.
Scientists can also trace the resulting "signal" through your nerves to your brain. They may know which portion of the brain is activated.
The next step is to think about the thing you just touched.
Does this process generate something physical that scientists can detect? Or is though, so far, "invisible"?
To put it another way, do scientists know what "thought" is made of?

Depending on the technique used, the short answer is yes.  For those of us who have been in the field for a long time, questions like this bring up memories of articles or seminars we have seen, but we really have to sift through a lot of non-digitized articles to find it. Although I will have to do some searching  to find it, there is a beautiful article using voltage clamping in very skilled fighter pilots where the author suggested (accurately IMO) a graphic representation of the formation of a thought. (I realize that without references, it is still hearsay, but perhaps someone else will recognize the details & be able to fill in the gaps more quickly.) But I will try to find the article and post the details.


Aquarium snail identification Many of these little snails suddenly appeared in our aquarium from nowhere.  I suspect that some snail eggs hitched a ride with some recently purchased plants.

Can anyone identify the species?  I am not having any luck with googling.

The photos show a baby snail of about 2-3 mm in size.  The shell is asymmetric, with one side looking completely flat (or concave).

These  are not pond snails.  We also have (uninvited) pond snails, but pond snails look different even when as small as these.  This new species has a lighter colour than pond snails, a more transparent shell of a different shape, and moves slower.

These are a kind of ramshorn snail, as Jestep correctly guessed.  Now they are grown up and they are clearly identifiable as ramshorn.

I will post photos of adults when I get the opportunity.


Sequence of ribosomal RNA Is it possible to sequence rRNA directly, that is, using the ribosome rather than the DNA from the nucleus? For example, this paper, Complete nucleotide sequence of a 16s rRNA gene from E. coli,  suggests that it uses DNA to find the sequence. Would it be possible to isolate the rRNA and derive the sequence from that?

Unequivocally, YES.

Before DNA sequencing was used to deduce the sequence of cloned or reverse-transcribed RNA molecules, slower and more cumbersome direct sequencing of RNA was performed using the method of Sanger et al.  (Sanger, F., Brownlee, G. G. and Barrel B. G. (1965) J. Mol. Biol. 13, pp. 373–398). This used ribonucleases in a manner somewhat similar to pre-Edmann protein sequencing.

Because of its abundance and ease of purification ribosomal RNA was a suitable species for this approach, and Carbon et al reported the complete sequence of E. coli 16S rRNA in 1978 (Carbon P., Ehresmann C., Ehresmann, B. and Ebel J.P. (1978) FEBS Letters 94, pp. 152-156).

Sigh! How little do modern molecular biologists know about the history of their subject.


The effect of 3D structure and solubility of the binding site of enzyme on its affinity Km and maximum activity Vmax? Could some one provide me with some resources or papers where I can read more about the following:

1- How can the 3D structure of an enzyme affect its Km and Vmax? (some papers, books or articles will be very neat).

2- How can the solubility of the amino acids of the binding site of an enzyme affect its Km and Vmax? (again some paper, books or articles will be very helpful).

Or maybe some description about that with some references? I spent some time in searching but unfortunately with no attractive results.

I just resay that I am inneed for some resources or papers about the two points in addition to some word explanation.

Thanks in advance!

Probably the big reason you were unsuccessful in your previous searches is that nobody quite knows exactly how enzymes' 3D structures lead to particular kinetic parameters.

It's wrapped up in the concept of "how the heck do enzymes work, anyway?" -- surprisingly, it's a question we don't really have a good answer to. The leading concept currently - influenced in large part by catalytic antibodies - is the transition state stabilization theory. That is, enzymes work by preferentially stabilizing the transition state, reducing the activation energy of the reaction. (A good overview of the theory can be found in Structure and Mechanism in Protein Science by Alan Fersht, one of the must-reads for anyone interested in enzymes.)

But that's probably not all of how enzymes work, or at the very least "bind the transition state well" is a rather coarse overview of the process. There's thoughts that the precise arrangement of active site sidechains are involved in a quantum mechanical interaction with the transition state. This is the "theozyme" concept put forth by Kendall Houk and colleagues.

The role of enzyme flexibility in catalysis is a highly disputed topic currently. The dynamics of proteins are an important concept for the understanding of the full reaction pathway, but there are some people who think that an important contribution of the protein is funneling vibrational energy into the appropriate bond motions for catalyssi. Nobel prize winner Arieh Warshel is (vocally) against it, though, favoring an electrostatic view of catalysis. (That is, enzymes work by stabilizing the charge distributions found in the catalytic pathways.)

So the long and the short of it is that we really don't understand how enzymes work, so we're rather far from being able to predict how the 3D structure changes the catalytic parameters. There are a number of efforts (particular from David Baker's lab) trying to use computational modeling of 3D enzyme structures to design enzymes, but the results have been rather modest. While such enzymes have been designed, their activities have been modest, and nowhere near the activity of native enzymes.

Doing the reverse - trying to predict the catalytic activity from 3D structures - is difficult, given the lack of knowledge. That's not to say people haven't tried. For example, there's been some efforts to use machine learning to predict catalytic constants from different mutants in a series. The problem with machine learning-type approaches is that the results tend to be only applicable for the particular system they've been trained on, and there's only limited interpretability of the results.


What are good sources of free-to-use images and diagrams I am looking for good image repositories for biology teaching. Photos and textbook-like diagrams.

I am interested  in images that can be used commercially without payment, or, at least, that require a small one-time payment. They would be used in videos, not only on lectures, hence the worry about copyright.

I'm guessing the videos are for a flipped/online course and posted on YouTube or Coursera?  I've done this. Biology is hard -- perhaps because I am picky and really want good images.

I used Wikimedia.com to search for many free images. I also contacted the publishers of the free online version of Molecular Biology of the Cell and asked if I could use up to 20 for my free online course, and they agreed.

My university was also able to work out an agreement with the textbook publisher to use 200 of the textbook images for the Coursera course as long as they were credited, and a link to purchasing the textbook was available on the site. They want to keep my university happy as our students buy a truckload of books every year.

I've also gotten somewhat decent at using a drawing tablet and powerpoint image (boxes, circles) manipulation to make some of my own cell processes and chromosomes and such.

Lastly, OpenStaxCollege.org has a wonderful collection of free textbooks for students, and they make their images available to faculty as free powerpoints. They aren't usually "good" enough to satisfy me, but definitely check them out.


Does physical exercise following lack of sleep increase the risk of sudden cardiac death (SCD)? Is there any scientific evidence supporting the hypothesis that physical exercise following lack of sleep increases the risk of sudden cardiac death (SCD)?

The only relevant research I could find is: Reddy PR, Reinier K, Singh T, et al. Physical activity as a trigger of sudden cardiac arrest: The Oregon Sudden Unexpected Death Study. International journal of cardiology 2009;131(3):345-349. doi:10.1016/j.ijcard.2007.10.024. However, it only points out that 5% of the SCD cases in the sample took place during vigorous physical activity, which does not directly answer my question.

I am not a biology professional, so please pardon me for any misunderstanding, and, when possible and reasonable, please avoid using too many biological jargons in the answer.

Sleep is an important aspect of our life. Sleep disorders are acute due to their effects in physiological and mental health of a person.Sleep occupies nearly 30% of our daily life and people were gradually decreasing the sleep time in order to adjust their busy schedule. According to the United States National Sleep Foundation, adults need to sleep 7-9 hours each night. The decrease in sleep time contribute mostly towards cardiovascular disease, including hypertension, coronary artery disease(CAD),risk of arrhythmia, stroke etc.
The circadian and dirurnal rhythms influence the neural circulatory control causing the changes in heart rate, vascular tone and blood pressure. The REM(Rapid Eye Movement)sleep and nonREM sleep affects the cardiovascular system. Researchers found it important that normal sleep is a complex and dynamic process with profound effects on cardiovascular homeostasis.
Insufficient sleep is a stress stimulator that acts through the sympathetic nervous system elicit changes in blood pressure, heart rate and barroreflex setpoint.
Sleep deprivation is a state of having less or no sleep which is a major reason for cardiovascular diseases.Which may cause
Inflammation
Cardiovascular disease is mainly driven by atherothrombosis, which is an inflammatory process. Increased levels of C-reactive protein(CRP) and interleukin-6(IL6) have been implicated as the predictors of cardiovascular disease risk.Both CRP and IL6 have been found elevated in both totally and partially sleep-deprived subjects.Inflammatory cells such as monocytes and neutrophils were also found to be elevated during acute sleep deprivation, supporting that sleep deprivation is an inflammatory process.
Endothelial Dysfunction
Endothelial Dysfunction has been reported after a combination of sleep deprivation and stress, also increased heart rate, blood pressure are reported in sleep deprived subjects may result in Endothelial Dysfunction.
Hypertension and Stress
Hyper tension and stress hormones are released by the body when lack of sleep occurs, this results in elevated bloop pressure and may lead to CAD.
CardioArtery Disease
The American Cancer Society , the Almeda County study and Partinen also showed an increased risk of CAD in subjects who reported sleeping 4-6 hours a day.
Diabetes Mellitus(DM)
Diabetes Mellitus is a major risk factor for CAD and it has been underlined from several studies across past decades that sleeplessness can result in DM.

A sudden cardiac death is highly probable for a person who follows increased physical exercise and decreased sleep durations. For a sleep deprived person the risk of cardiac diseases are so high, then for some one who spend lot of time exercising can cause chronic cardiac problems. Physical exercise and over training can cause more stress hormones and increased heart rates, these factors along with prolonged sleep deprivation can cause serious cardiac diseases or even sudden cardiac death.

Levels of cortisol (the "stress" hormone) are elevated for long periods of time.
The body spends more time in a catabolic state than an anabolic state (perhaps as a result of elevated cortisol levels).
Excessive strain to the nervous system during training.
http://en.wikipedia.org/wiki/Overtraining

References

Critical Care Nursing: Synergy for Optimal Outcomes - Roberta Kaplow
Sleep Deprivation and Disease: Effects on the Body, Brain and Behavior - Matt T. Bianchi


Can someone identify this bird? We recently found a nest in the back garden and a little bird inside. Can you help us identify it? The nest is quite small like the bird so we are wondering whether this is the parent or a baby chick. Is there anything we can do to help it or are we better off leaving it alone?

Update: I'm from the UK, currently in Oxfordshire to be more precise.

It looks like a passerine bird, but I can't really tell the species without seeing the whole body. As for what to do with it, your best course of action is to leave it alone. Trust me. Once placed tissue paper over a pigeon's eggs to keep them warm, and the mother crushed them when she landed on the nest because she didn't see the eggs.

If there are eggs in the nest, try noting down what color they are. Passerines have colored eggs.


Is there an example of a new species through mutation breeding? Is there a demonstrable species that went through mutation breeding and through successive generations it drifted so far away from its initial parent species that it can't breed with them anymore? (I assume it would need to be able to breed with intermediate generations though). Also by "demonstrable" I mean a case where we can directly demonstrate this process by starting from a parent species to a new species and not establish this relationship by looking back (like observing the connection between corn and teosinte through genetic information).
Edit: I'm mainly curious about postmating/post- zygotic reproductive isolation. As I understand, the timescale of us is not enough to observe that kind of speciation (we can either directly observe the start of the isolation or the end of it but not both), that's why I'm curious about whether induced mutation could speed up the process enough to directly demonstrate speciation by the most difficult to achieve definition.
I have checked the thread Have we ever observed two drosophila lineages that evolved reproductive isolation in labs? but it seems to me that those results only shows premating isolation.
I have checked: Sexual and postmating reproductive isolation between allopatric Drosophila montana populations suggest speciation potential article which says, that postmating barriers observed may be due to postcopulatory-prezygotic mechanisms.
Thank you for the corrections, Im reading into Examples of creating a new animal species by humans

Definition of species by the criteria of not being able to breed is problematic: e.g., some breeds of dogs cannot breed, due to the differences in their sizes, yet they are the sale species, as could be dhown by artificial fertilization.
Now, if we take any two closely related species and trace their genealogy deep in the past, we run into the same ambiguity: it turns out that at some point they could breed, and their separation into two dustinct species unable to breed was a process that lasted hundreds of thousands ir millions of years.
This brings us to another point: the characteristic evolutionary times for most animals are too long, compared to the existence of our civilization, for dustinc species to appear
This may not be true for faster evolving organisms, such as viruses or bacteria - e.g., HIV had diverged from SIV about hundred years ago. However we cannot define them as different species, except by saying that the dissimilarity if their genetic sequences exceeds certain threshold.


What happens to embedded membrane proteins after a vesicle is formed? When an animal cell is going through endocytosis it cell surrounds a food particle, and the membrane swallows it, creating a vesicle within the cell.

However, what happens to the embedded transmembrane proteins previously in the cell membrane? Do they shut down? Are they degraded? Or do they just not cause a problem that the cell just leaves them be?

Endosome formation.
For the sake of keeping this somewhat brief, I'm going to stay somewhat surface level.
When a vesicle is endocytosed, it is called a primary endocytic vesicle.
When multiple primary endocytic vesicles fuse together, they form a larger entity called an early endosome.
Early endosomes can also be called "sorting endosomes" because different portions of the vesicle are sorted into different destinations, including these things called "recycling endosomes."
Transmembrane proteins in endosomes
In my experience, transmembrane proteins largely get sorted into these recycling endosomes and are then re-inserted into the cell membrane.
To my knowledge and from some cursory review on the topic, this is a common outcome for transmembrane proteins; they are eventually recycled and placed back into the cell membrane via exocytosis after being sorted into a recycling endosome.
Further reading
I'm sure others can add more explanation and some of the alternative routes these proteins can take, but in the interest of brevity and clarity, I thought it best to just stick with what I've come to know as most common.
Also, if you'd like a helpful source, see if you can get access to the following paper through a school or library service: Elkin, S. R., Lakoduk, A. M., & Schmid, S. L. (2016). Endocytic pathways and endosomal trafficking: a primer. Wiener Medizinische Wochenschrift, 166(7-8), 196-204.
In a phenomenon that I think is really cool, some receptors are thought to actually keep functioning after they are endocytosed and form these things called "signalling endosomes" (search "signalling endosomes NGF and TrkA" to read more).


Why does it hurt when water touches cuts? Why do we feel a burning sensation when water touches cuts/wounds? People suggest applying oil over cuts while bathing to prevent water touching it, but water is heavier than oil so it shouldn't work, but it does, Why?

Water changes the local ionic concentrations and therefore induces an electric
signal at exposed neuron membranes.Oil is used to prevent entrance of water to the cut because it is hydrophobic i.e. repels water but attaches to the tissue.
Gravity plays no role here.


Why do we think chronic inflammation can cause cancer? Why do we think chronic inflammation can cause cancer? I know the pathway is not fully understood, but what makes scientists believe that inflammation causes cancer?

There are good epidemiological data for this.

Links between cancer and inflammation were first made in the
nineteenth century, on the basis of observations that tumours often
arose at sites of chronic inflammation and that inflammatory cells
were present in biopsied samples from tumours.
There are many triggers of chronic inflammation that increase the risk
of developing cancer. Such triggers include microbial infections (for
example, infection with Helicobacter pylori is associated with gastric
cancer and gastric mucosal lymphoma), autoimmune diseases (for
example, inflammatory bowel disease is associated with colon cancer)
and inflammatory conditions of unknown origin (for example,
prostatitis is associated with prostate cancer). Accordingly,
treatment with non-steroidal anti-inflammatory agents decreases the
incidence of, and the mortality that results from, several tumour
types.

Cited from Mantovani, Alberto, et al. "Cancer-related inflammation." Nature 454.7203 (2008): 436-444.
http://www.sld.cu/sitios/reumatologia/temas.php?idv=21500


Why do we dream while sleeping? Is there any specific reason behind why we dream? Why do we sometimes get weird and unusual dreams? Sometimes we can't even recall what we dreamt of. Why does this happen?

Disclaimer: the shortest answer still remains we don't know...yet.

Talking from the evolutionary perspective, I have found as many as 8 theories about the purpose of dreaming, some of which even contradict each other(!). But I'll describe them one at a time.

One obvious theory is that we dream about something we dream of. So, dream is basically a way of wish-fulfillment; what we are dying to achieve, we get that in our dreams. Though it has been made quite scientific by Freud et al, it still doesn't look much scientific, at least from evolutionary perspective.
Another idea, made popular mainly by Hobson et al, is that dreams are purely because of accidental firing of neurons. In what they call activation-synthesis theory, they claim that during sleeping, neurons in areas of brain, including brain stem, limbic system, secondary visual cortex, etc. fire accidentally. When the brain tries to interpret those signals, the result comes out as dreams.
Another theory, proposed by Zhang et al, is that dreams are our brain's way of converting short-term moemory into long-term memory. This quite explains why some people reommend a power nap after learning something new, it helps the brain in storing the knowledge as long-term memory. Also, recent studies have concluded that it is better to remain awake for hours after a traumatic experience rather than sleeping right off, if you want to forget that experience faster.
Another theory, popularly called reverse learning theory, basically says that we dream to forget things. Dreaming is a way for our brain to prevent information overload so that memorizing new things becomes easier. Seems the opposite of Zhang et al and most likely answers why Sometimes we can't even recall what we dreamt of.
Yet another theory, seemingly more sound from evolutionary viewpoint, says that dreams are just like the playing-dead response of our body. When we dream, the neurotransmitters related to movement are shut down, resulting in what seems like a dead body. So, our body preferred to retain this mechanism because it could've helped in a way like the freeze response did.
A theory, proposed by Revonusuo et al, says that dreams are to make people ready for real-life situations. According to it, people who often dream about being chased by a tiger will learn how to overcome that situation and eventually will be able to survive such case. Seemingly answers your question Why do we sometimes get weird and unusual dreams?
Barrett et al, based on Revonusuo's theory, proposed that dreams are a way for solving problems for humans, partly because dreaming mind makes connections faster than awake one. Though this explains how Kekulé predicted benzene's structure, it doesn't look very much scientific.
A yet another one, by Coutts et al, says dreams are a way for "natural selection" of best possible method to solve a problem, including emotional situations, and is called Oneiric Darwinism. A much similar idea by Hartmann et al is called contemporary theory of dreaming.

I will not discuss the mechanism of dreaming, not only because it will make the answer too long or because others have delved into that point in their answers, but because it will answer the How? part rather than the Why? part, and also because that part would be better suited for cogsci.SE.


Antibiotic resistance of Staphylococcus epidermidis and S. warneri I am looking for information regarding the antibiotic resistance of S. epidermidis and S. warneri, specifically against penicillin, ampicillin and tetracycline but to no avail. Are there any good websites with databases where this information is shared?

Here some studies concerning the antibiotic resistance of Staphylococcus epidermidis and Staphylococcus warneri:

Antibiotic resistance patterns of coagulase-negative staphylococcus strains isolated from blood cultures of septicemic patients in Turkey - Koksal, Yasar & Samasti [2009]

The abstract of the study above reads as follows:

  The aim of this study is to determine antibiotic resistance patterns
  and slime production characteristics of coagulase-negative
  Staphylococci (CoNS) caused nosocomial bacteremia. A total of 200 CoNS
  strains were isolated from blood samples of patients with true
  bacteremia who were hospitalized in intensive care units and in other
  departments of Istanbul University Cerrahpasa Medical Hospital between
  1999 and 2006. Among 200 CoNS isolates, Staphylococcus epidermidis was
  the most prevalent species (87) followed by Staphylococcus
  haemolyticus (23), Staphylococcus hominis (19), Staphylococcus
  lugdunensis (18), Staphylococcus capitis (15), Staphylococcus xylosus
  (10), Staphylococcus warneri (8), Staphylococcus saprophyticus (5),
  Staphylococcus lentus (5), Staphylococcus simulans (4), Staphylococcus
  chromogenes (3), Staphylococcus cohnii (1), Staphylococcus schleiferi
  (1), and Staphylococcus auricularis (1). Resistance to methicillin was
  detected in 67.5% of CoNS isolates. Methicillin-resistant CoNS strains
  were determined to be more resistant to antibiotics than
  methicillin-susceptible CoNS strains. Resistance rates of
  methicillin-resistant and methicillin-susceptible CoNS strains to the
  antibacterial agents, respectively, were as follows: gentamicin 90%
  and 17%, erythromycin 80% and 37%, clindamycin 72% and 18%,
  trimethoprim-sulfamethoxazole 68% and 38%, ciprofloxacin 67% and 23%,
  tetracycline 60% and 45%, chloramphenicol 56% and 13% and fusidic acid
  25% and 15%. None of the strains were resistant to vancomycin and
  teicoplanin. Slime production was detected in 86 of 200 CoNS strains.
  Resistance to methicillin was found in 81% of slime-positive and in
  57% of slime-negative strains. Our results indicated that there is a
  high level of resistance to widely used agents in causative
  methicillin-resistant CoNS strains. However fusidic acid has the
  smallest resistance ratio, with the exception of glycopeptides.
  Additionally, most S. epidermidis strains were slime-positive, with
  statistically significant (p<0.001) association between methicillin
  resistance and slime production.

The other two studies contain information on the aforementioned strains with regards to penicillin susceptibility.

Antibiotic-resistant Staphylococcus epidermidis in patients undergoing cardiac surgery - Archer & Tenenbaum [1980]

Clinical significance of Staphylococcus warneri bacteremia - Kamath, Singer & Isenberg [1992]

In addition, I would recommend to acquaint yourself with Google Scholar for these kind of questions. It normally makes for a good starting point.


Smallest viable reproducing population What is the smallest viable reproducing population, such as in a human population. By viable I mean a population which keeps genetic defects low (enough).

A very strongly related question: what is the expected number of generations a given population can survive?

The conservation biology literature has a great deal of information, particularly with reference to developing species survival plans (e.g., Traill et al. [2007] report a minimum effective population size of ~4,000 will give a 99% persistence probability of 40 generations).

Because the question specifically mentions human populations, I'll focus my answer on the genetics of small human populations, though considerably less information is available.

Hamerton et al. (1965; Nature 206:1232-1234) studied chromosome abnormalities in 201 individuals from a total population size of 268 from the small island of Tristan da Cunha. These authors report increasing chromosome abnormalities (aneuploidy; hypo- or hyperdiploidy) with age and suggest that it may result in decreased mitotic efficiency. This population is thought to have developed from a founder population of only 15. According to Mantle and Pepys (2006; Clin Exp Allergy 4:161-170) approximately two or three of the original settlers were asthmatic, which has led to a very high prevalence (32%) in the current population.

Kaessmann et al. (2002; Am J Hum Genet 70:673-685) present a more modern study of linkage disequilibrium in two small human populations (Evenki and Saami; ~58,000 and ~60,000 population sizes, respectively) compared to two large populations (Finns and Swedes; ~5 and ~9 million). The authors find significant LD in 60% of the Evenki population and 48% of Saami, but only 29% in Finns and Swedes.

Lieberman et al. (2007; Nature 445:727-731) discuss the potential for human kin detection to avoid inbreeding. Such mechanisms have been found in other species, "from social amoebas, social insects and shrimp, to birds, aphids, plants, rodents and primates." Lieberman et al. propose mechanisms contributing to sibling detection in humans, including "maternal perinatal association" and "coresidence duration." Beyond these behavioral cues, the authors also suggest physiological cues such as major histocompatability complex as playing a role.


Why do we blink instead of winking each eye independently? Question

Why do we blink both eyes at the same time rather than winking each eye as needed?

Why would winking independently be better?

The benefit would be a minor improvement whereby a person would receive continuous sight of the area of vision shared by both eyes.  I'd also assume that it would be more likely for the wink-as-needed mechanism to evolve than the blink-as-needed mechanism were there no benefit to blinking over winking.

Why then has evolution favoured blinking?

My guess at why is that the overhead on our brain of switching between binocular vision to monocular vision is more significant than the overhead of momentarily pausing our visual processing.

I also believe that some animals don't blink, but wink; e.g. chameleons.  This supports my theory as their eyes operate independently, so their brains would have to cope with the variance in each eye's information anyway.  That said, their wink is different; i.e. they roll their eye inside their head, rather than having an eyelid.

Research so far

I found a couple of Reddit posts:

https://www.reddit.com/r/explainlikeimfive/comments/2kzx4s/eli5_why_does_blinking_take_me_almost_no_effort/ - explains why blinking is easier than winking; but only based on how we are rather than how we got there (i.e. why evolution would have resulted in different muscles for winking vs blinking).
https://www.reddit.com/r/explainlikeimfive/comments/3mijgw/eli5_why_do_we_blink_with_both_eyes_at_same_time/ - doesn't have any hard fact answers; just discussion of opinion.

Looking at it completely in terms of evolutionary pressure:

1.1 The whole idea of binocular vision for humans, (and some other species) is depth perception. If you suggest continuous, alternate winking, the cognition of the individual would be seriously affected.
The 'wink as needed' mechanism (assuming all other visual processes are as they have evolved today) would be like continuously alternating between a pair of binoculars and a telescope while still trying to move forward.

1.2 If you are suggesting that there would still be an evolutionary pressure for winking, then its very likely that the evolutionary pressure for coordinated motion/ efficient cognition acting together with the evolutionary pressure for depth perception would be much higher as compared to it. (This would especially be true if eye-brain coordination evolved before the blinking mechanism, as is seen to be the case, which explains your point on 'how we are rather than how we got here'. Obviously fish have evolved some eye-brain coordination, but don't blink)

This link explains evolutionary pressure for depth perception/stereopsis to an extent
https://en.wikipedia.org/wiki/Depth_perception#Survival

2.1 As for the chameleon, the winking/ eye rolling mechanism might be very closely linked to the evolution of chameleon vision. It is seen as the link for studying evolution of binocular vision and stereopsis(depth perception) from monocular vision.

https://en.wikipedia.org/wiki/Chameleon_vision


Collective term for both exons and introns Is there a term I can use to refer collectively to both exons and introns? By collectively, I don't mean ligated as with an unprocessed transcription product. I'm just writing about exons and introns and getting frustrated that I keep on having to write "exons and introns", wishing there was a more concise term I can use in the place of that phrase.

For example, the term I am looking for would fill in the following blank perfectly.

  The gene has 5 exons and 4 introns, so it has 9 _____.

How about "splicing fragments"? It might be easier to refer to them according to the mechanism of production.


Can a vaccine or antidote be administrated via gases or sprays? On TV or in movies a gas or spray containing a vaccine/cure/antitoxin is released and everybody is saved. Is this something plausible in real life? Specific examples would be appreciated.

There are a number of currently used aerosolized vaccines throughout the world. Generally, these are studied and administered in single individual doses. There are advocates for the use of larger, sealed exposure chambers for rapid administration of vaccines to large numbers of people, possibly in the field, for example in a tent like this figure from the earlier linked reference.

The primary barriers for a general release of a vaccine or other medication as, e.g., an aerosolized spray, would be ethical (difficult to get consent from all potential exposed individuals) and dose related (difficult to ensure a specific safe and effective dose).

The closest natural experiment I'm aware of would be the use of live attenuated Sabin oral poliovirus vaccine. Unlike other currently used vaccines, the Sabin vaccine is transmissible. In developing countries, vaccine is transmitted from vaccinated individuals to un-vaccinated individuals through the fecal contamination of food and water, using the same route that wild type poliovirus is transmitted. This can result in extending immunity beyond those who directly receive the vaccine. You could conceptualize this as blanketing a local population with vaccine. It's not without problems, though, because in cases where the overall initial vaccine coverage is low, circulation of the vaccine can eventually result in reversion of the reservoir of previously non-virulent (attenuated) vaccine to a virulent type. This is how you get vaccine derived polio outbreaks, and one of the reason not to use transmissible viruses as vaccines.


Is there a vaccine against the plague (Yersinia pestis)? There seems to be recurrent events of infections of the plage (Yersinia pestis), from the well known Justinian plague to the Black Death and to recent years. In fact, two cases were reported in China in November 2019. However, it seems there is not an effective vaccine yet. At least until 2013 there was no vaccine approved by the US FDA. There seems to be on-going research about vaccines for the plage.

Is then no effective vaccine against the plague? If yes, does it mean humanity is still at risk of yet another pandemic of the plague?

There is little motivation right now for vaccination against plague because:

Human infections with plague are fairly rare. A vaccine administered to the general populace would have to be very cheap and extremely safe to make it cost-effective and have a net benefit given the risks of plague are so low, and because
Antibiotics are effective against plague - this makes the likelihood of a widespread outbreak fairly low. Antibiotic resistance could be a concern, but plague would not be one of the most concerning pathogens from that perspective - there isn't much exposure to antibiotics in the reservoir species that the bacterium lives in, so there is less selective pressure towards resistance compared to other bacterial pathogens.

Additionally, plague lives in reservoir species, so extensive human vaccination is not a plausible way to eradicate the bacteria entirely, unlike pathogens that have humans as a primary host.

That said, vaccines are available and can be used for certain individuals at high risk. However, they take a long time to show immune protection (>1 month) making them not that useful during outbreaks. From the same WHO report linked above:

  Worldwide, live attenuated and formalin-killed Y. pestis vaccines are
  variously available for human use. The vaccines are variably immunogenic
  and moderately to highly reactogenic. They do not protect against primary
  pneumonic plague. In general, vaccinating communities against epizootic
  and enzootic exposures is not feasible; further, vaccination is of little use
  during human plague outbreaks, since a month or more is required to
  develop a protective immune response. The vaccine is indicated for
  persons whose work routinely brings them into close contact with Y. pestis,
  such as laboratory technicians in plague reference and research laboratories
  and persons studying infected rodent colonies (23).

WHO plague manual:

https://www.who.int/csr/resources/publications/plague/WHO_CDS_CSR_EDC_99_2_EN/en/


How does motor nerve innervation determine type of muscle fibre? Muscle fibres are of two types - type I and type II. They differ from each other in various properties. Even the underlying biochemical processes are different to suit their function (slow vs fast)

In a normal muscle, on certain stains like ATPase and SDH, to differentiate between the types of fibres, a checkerboard pattern is seen. But in reinnervation following long standing denervation, there is a loss of the checkerboard pattern and fibre type grouping is seen.

This happens because, the the denervated fibres are reinnervated by other ones, which can change their type.

The question is, how can neural innervation lead to biochemical changes in muscle type?

'Slow' and 'fast' motor neurons differ in their firing patterns. This differentially affects intracellular calcium concentrations and energy usage of the innervated muscle fibers over time, and thereby influences their gene expression. The following review extensively covers this: http://www.ncbi.nlm.nih.gov/pubmed/22013216


Hardy Weinberg Clarification So I am taking an introductory Biology Course and I was recently introduced to the idea of Hardy Weinberg Equilibrium. I wanted to find out why exactly we calculate the frequencies of alleles in the next population using the law of multiplication.

For example,

In a hypothetical population of let's say 300 civets, 20% of the gene pool codes for blue eye color and the remaining 80% codes for black eye color. It is given that blue eye color is recessive.

300 civets = 600 alleles total
80% code for black eye color = 480 alleles
 20% code for blue eye color = 120 alleles

When we calculate the frequencies of the next population we basically say what is the probability a given offspring will this pair of alleles. Following the example above, I would argue that the probability an offspring has two blue eye color alleles is (120/600) * (119/600). However, my textbook says that it is (120/600) * (120/600) = 0.04 but doesn't that assume replacement of alleles! My only rationale is that as the population tends towards infinity the difference becomes negligible.

Am I right?

the population tends towards infinity

Well yes, Hardy–Weinberg principle is based on several assumptions one of them being "population size is very(infinitely) large". Another being "Mating is random".

However, even if the population is small your version of calculation does not make much sense biologically.
If we talk about civets (gonochorists) the probability an offspring has two blue eye color alleles is
(probability mother gives him blue eye allele copy)*(probability father gives him blue eye allele copy).

The two probabilities are not connected. What allele individual gets from mother has no influence over which allele they get from father. This is assured by "Mating is random" assumption.

To calculate the probability we should calculate:

(allele proportion in all possible mothers)*(allele proportion in all possible fathers)

In your example there is no information about sex of individuals, so the best approximation we have for allele proportion in females/males is the overall allele proportion in the whole population (20%) therefore the best calculation is 20%*20% = 0.04

  but doesn't that assume replacement of alleles!

It seems you think that there is some rule that each parent allele copy is used only once in next generation. This is not true. Under random mating some parents can produce many children and some have none. Some allele copies get replicated several times some don't get replicated at all. In large populations the resulting random changes to allele frequency even out. In small populations allele frequency drifts.


How are nutrients absorbed by a pitcher plant? I've read that pitcher plants thrive in nitrogen-poor soil, which is solved by dissolving insects and absorbing nitrogen that way.
I have a few plants, and when a pitcher start to rot, I cut it off and study the insects that've been trapped. I've never actually observed a dissolved insect. Both interior and exterior seems unharmed.

What digestive enzymes does the plant use?
What part of the insect gets dissolved?
What structures allows absorption and transport of nutrients into the plant? And how is it exploited?

Carnivorous plants use a variety of enzymes, including proteases which digest proteins to provide the plant with nitrogen. You might think that the hard exoskeleton would not be digested but pitcher plants (at least some types) produce chitinases which dissolve chitin (i.e. the exoskeleton), so there should be nothing left of the prey. The enzymes are secreted by tiny glands inside the pitcher.

  The enzymes that have been detected in carnivorous plants include amylase, chitinase, esterase, lipase, peroxidase, phosphatase, protease, and ribonuclease.

From the Sarracenia faq.

Aside from the enzymes secreted by the plant, there are micro-organisms present in the pitcher which will dissolve organic matter.

In my experience of growing Nepenthes and Sarracenia it seems to take a long time for the prey to dissolve and there is always some material left. Which type of pitcher plant are you growing?

There's a good description of CP digestion from the ICPS.
A more technical explanation about chitinase.

I can't find any specific detail on how the plant absorbs the nutrients, though even non-carnivorous plants can absorb nutrients through the leaf surface.


Why don't electric eels shock themselves? Why do electric eels not stun or pain themselves when they discharge their high voltage shocks? While it is known that they use those high voltage shocks to track their prey (as discovered by my professor Kenneth Catania [1]), and there is most likely some form of cage effect provided by the water (until they come out for a more powerful sting to scare predators), and that when curled less current might return through their own bodies [3], it is not clear why there discharges do not interfere with their own central nervous system (cage effect) or peripheral nervous system (through which current would flow in parallel to the water and target)?

[1] https://www.nature.com/articles/ncomms9638

[2] http://www.pnas.org/content/113/25/6979.full

[3] http://www.cell.com/current-biology/fulltext/S0960-9822(15)01147-1

Short answer, no one knows, there is some minor evidence they are do shock themselves but are resistant to it, (they react far stronger in air than in water to their own discharge), but it is not a high priority for research so no one has really tested it.


How is sexual selection evolutionarily stable? It seems like in any population subject to evolutionary pressure, sexual attractiveness will inversely correlate with other kinds of reproductive fitness. If you see a peacock with a small tail feather, this is information that it is likely above average in other areas, because otherwise its genes would already have been wiped out. So intuitively, you would think that it would benefit individuals to find less conventionally attractive mates.
So far, I have encountered two possible explanations for this. One idea was that the things that make an animal attractive correlate with evolutionary fitness. I'm not an expert here, but it feels like the correlation here will diminish over time as soon as there is direct pressure to increase attractiveness.
The other, more convincing, explanation was that it is advantageous to produce attractive offspring. So, there might be a feedback loop here where if members of a population care about sexual attractiveness more, then attractiveness would confer a greater advantage, making attractive offspring more important, increasing the evolutionary pressure for individuals to choose attractive mates.
Can someone give an intuition (or better, the relevant math) for why these two latter effects dominate my original intuition? Or are there other effects at work here?

first off you are talking about runaway sexual selection, run away sexual selection works because attracting mates matters MORE than individual survival. An immortal survivally perfect creature that cannot mate is an evolutionary dead end and might as well not exist where its genes are concerned. A bright red neon sign on your back that draws  the attention of potential mates is an advantage as long as it attracts mates more often than it attracts predators. Coincidentally this is why so many sexual displays are things you can turn off, even a peacock can fold its tail fan down. These displays often exploit existing attention  factors, like eye shaped objects, bright contrasting colors, loud noises, ect, things organisms are already predisposed to pay attention to.  Of course once neon sign displays exist your second idea comes into play, once neon signs are in play a female is best served if her own male offspring and descendants also have neon signs, which makes attraction to the  neon signs (and thus the genes making them) an advantage.
For normal sexual selection both your ideas also come into play, likely more often. common attractive features are things like size, symmetry, health, or excess energy, direct signs of fitness.
Most of the time displays reaches a point of stability where the cost is balanced by the attractiveness, this is how most displays work.  But sometimes runaway selection can drive it past the point of no return, where the cost of reducing it is so high (lack of mates) the only winning strategy is to invest more and more, on and on until the cost is so high you never get a chance to mate.


Can a person become addicted to tea? Can one become addicted to tea like coffee addicts or smokers? I heard there are some common substances in tea and coffee, do they cause addiction?

Yes, both tea (black tea at least, English speakers usually mean black tea when they say tea anyway) and coffee have caffeine which is addictive.

Apparently, being able to correctly reply to this question involves defining the word "addiction". My guess is that the negative connotation of the word "addiction" will cause some pressure to not use it.

Here's a recent review on caffeine addiction that says that caffeine is not addictive. I do not agree with their arguments but I'll leave it to the reader to judge.


Why does it hurt when you take sweets, if you have cavities in your teeth? When you have cavities in your teeth taking any sweetend drinks or food causes sensitivity or pain. What could be the reason?

The outer shell of a tooth is enamel, which is hard and dense so that not much can penetrate it.  Under that is dentin (or dentine), which is bony but has microscopic channels running through it to the center of the tooth where the pulp and nerve reside.  If the enamel is breached, as with a cavity, crack, or wear, the dentin is exposed to the environment of the mouth.  When sugar comes against the dentin, it draws fluid out of the microscopic channels (because sugar attracts water strongly).  The fluid flow causes pressure changes around the nerve of the tooth, which reports the change to the brain where it registers as pain.  Dentin is highly sensitive not just to sugar, but also to hot, cold, pressure, and other stimuli.  (This sugar response is a short term one; the influence of sugar on bacteria is a longer-term effect in which the acid generated by the bacteria eats away the enamel layer.)


Why do water molecules diffuse along axons direction? I am studying tractography technique which aims to reconstruct bundles of axons in brain by following the diffusion direction of water. It is very interesting because it is non-invasive. It exploits the difference between grey matter and white matter: in white matter (axons) we find an anisotropic environment since there is a preferential direction of diffusivity of water molecules that is along the axons direction, while in grey matter the environment is isotropic since molecules do not move with a preferential direction. The diffusion of molecules is generally given by a difference of concentration of molecules between two points but they should move even though this gradient is not present because of the temperature so because of the fact that they have a certain thermal energy. Therefore my question is: why do molecules move along the axons direction ? Is there a biological aspect that causes like a difference in concentration between the starting point and the ending point ? Maybe the answer is trivial but since I am not a biologist I do not know it :) and I am not able to find something on web . It seems that I find only explanations for diffusion of water molecules from outside the cell to inside... I would like to know the reason why they move in the same direction of the axon.

The movement is just the thermal energy motion you describe, not due to any concentration difference.
The anisotropy is due to the geometry. White matter tracts are effectively a dense bundle of thick, fatty hoses. Water can freely move in the tubes but cannot move as freely through the dense walls, so you see more movement along the axon length rather than perpendicular to them.
You can read more at https://en.wikipedia.org/wiki/Diffusion_MRI


Is there software or a website where I can browse extinct species? Is there any software/website where I can browse for extinct species? It must be based on real animals that are now extinct. It may be in animated versions.

You can search for species that are "Extinct" or "Extinct in the wild" at the IUCN red list website (International Union for Conservation of Nature and Natural Resources). That list currently includes 903 species, but some of the assessments might be obsolete (see annotations). From that list, you can click and get some basic information about each species.

Also note that many countries have regional Red Lists, where you can find information about regionally extinct species (i.e. species that have gone extinct in a particular country). For instance, 209 species are labelled "reginally extinct" in Sweden (http://artfakta.artdatabanken.se/, site only in Swedish), most of them insects, while still being present in other parts of the world.


Walk me through microsatellite markers and PCR Three polymorph microsatellite markers are used to try and narrow down the location of a disease locus, with the use of PCR with 2
  flanks on each side of the actual polymorphic area. The PCR product is
  then put on gel.

I need help understanding exactly what is going on here. I understand polymorph as "two or more phenotypes in the same population" as by wikipedia. I don't understand what they mean here.

How is the PCR different with 2 flanks from a normal PCR?

I do understand how the gel works.

It's actually very simple. You misunderstood the term polymorph in this situation.

A microsatellite is a sequence composed of a short repeated DNA motif. A polymorph satellite is then simply a microsatellite varying in length between individuals, i.e. composed of more or less repeats of the motif.

The flanks of the microsatellite are the DNA sequences targeted by the primers.

In essence, using two primers flanking the microsatellite you will amplify this specific DNA region and because it varies in length between individuals you can detect that by simple gel electrophoresis.

Note: Microsatellites can also change in sequence (also called polymorphic regions) as they are prone to a high-mutation rate but in this case you would need to sequence it to know how the sequence differs between individuals.


Name of this flower? i'd like to know the name of this flower.

It's a Dutchman's Pipe (aka Calico Flower); the genus has over 500 species, but I'm pretty sure this is it.


Cancer and Evolution Edit: just to clarify, I am asking what, if anything, the literature says can be gleaned about evolution by studying cancer, especially relating to how multicellularity evolved and the traits used to force cells under control of the organism.

Most of the original question details I had added were just my own thoughts on the topic.

Original question

Is there a sense in which cancer can be considered as a return to the unicellular "origin" of a cell?

It has always seemed to me like cancer is almost inevitable by the structure of the cell (its poor "design", essentially). The only thing standing in the way are the cellular controls: senescence/apoptosis (e.g. p53 pathway), immunosuppression (e.g. cytotoxic T lymphocytes), telomeres, etc...

So it seems like multi-cellularity did not evolve "ground-up", but was instead generated by slowly differentiating the functions of the various cells, while developing "top-down"controls against errant cellular behaviour.
Thus, cancer, which occurs when these protections fail, is in some sense merely a return to an ancient evolutionary root.

I suppose some arguments against this include the fact that modern cells are vastly different than their ancient ancestors (or even modern archaea/bacteria).
So the best we can perhaps say is that the core of the cell has been sufficiently preserved (ribosomes are still mostly RNA, are they not? :] ).
Further, it is hard to call some of the "micro-evolutions" of cancer (e.g. interleukin-8 production) as returns to primitive behaviour.
In these cases, I tend to see them as necessary occurrences to remove the "top-down" controls, rather than as integral to the destructive out-of-control growth characterizing oncogenesis.
But, debatably, perhaps not all of them are (e.g. extravasation in metastasis).

Obviously this seems very simplistic, but is there any literature thinking about it this way? Or directly debunking it?

Cancer and level of selection

Cancer results from the opposite action of different level of selection. There is selection on the population of multicellular individuals and there is selection on the population of cells within each multicellular individuals.

There is selection among cells within an individual for increase replication rate while there is selection among multicellular individuals in the population for controlled replication rate of their cells.

Major transitions

The passage from small unit of selection to bigger units is called a "major transition". Such transitions include the grouping of genes on chromosomes, the grouping of cells onto multicellular individuals, the grouping of multicellular individual onto colonies and, if there are several planets inhabiting life in the universe, then the grouping of life forms in every planet into a population of living planets. One can list other, more extreme or intermediate major transitions but there is quite a bit of debate on what really constitute a major transition.

Literature on the subject

  [I]s there any literature thinking about it this way?

The keywords that will help search further information are group selection, kin selection, major transitions.

I recommend having a look at Major Transitions In Evolution by Maynard Smith and Szathmary and also The Major Transitions in Evolution Revisited by Calcott and Sterelny which is a book made of many small parts, each written by a different author on these same questions of level of selection.

You might eventually have a look at Evolutionary Dynamics: Exploring the Equations of Life  by Nowak as well.

These discussions of level of selection include discussion of what an individual is and what level is most important. The extremely popular and well written books by Dawkins will also bring you some light on the subject. Consider The extended phenotype for example.

For more book recommendations in evolutionary genetics, please have a look at Books on population or evolutionary genetics?.

If you like the sensation of thinking of the entire earth as an individual part of eventually a larger group of living planet, then you'll maybe enjoy having a physiological / ecological view of this living planet earth with Gaia by Lovelock


Will a sandwich assay work with a GST 26 antibody/protein? I have a GST 26 kda antibody, and want to use it in a sandwich lateral flow assay. Are there enough epitope regions for both antibodies to bind to the protein?

This is completely dependent on the type of antibody you are using and the epitope specificity of that antibody (or antibodies). Because you haven't given any more detail, it's very hard to give you a definitive answer.

GST is known to dimerise, so even a monoclonal antibody might work in your sandwich assay, as long as the (identical) epitopes are far enough apart in the dimeric structure to allow two antibodies to bind.

If you're dealing with a polyclonal antibody mixture, then your chances are better. But even still, you won't know until you try it.


Visualising a subset of the tree of life I understand that many curated trees of life already exist (eg http://tolweb.org/tree/) but is there any website that allows one to input a list of organisms, and then produce the current best guess at their evolutionary relationships?

The best site I managed to find so far is http://itol.embl.de/itol.cgi, which allows you to select specific species from the main tree to plot into a sub-tree, but the tree itself is rather small, so more detailed comparisons cannot be made.

http://phylot.biobyte.de/ performs the requisite task (generating a phylogenetic tree based on the specific organisms provided, using the NCBI taxonomy tables).

For example, the input of tree elements

  Trichomonas vaginalis,Trypanosoma brucei,Homo sapiens,Fibroporia
  radiculosa,Paramecium tetraurelia,Tetrahymena
  thermophila,Cryptosporidium muris,Cryptosporidium hominis,Blastocystis
  hominis

generates the tree


Are both (partial) copies of DNA transcribed in S and G2 phases of cell cycle? For a little less than half the cell cycle, a significant number of genes are represented twice (just before dividing).  Does the cell differentiate between these DNA in any way or are transcription rates limited by the amount of polymerase anyway?

I can't unequivocally say, at least without further literature review, that both sister chromatids are transcribed equally everywhere, especially since the cell does have mechanisms to differentiate between the old and new DNA strands (such as methylation state). It would be conceivable to expect, however, that the same regulatory factors that were present before replication have the same effect on newly synthesized DNA as they did on the old. Here are some electron micrographs showing transcription from both chromatids at some locus.

McKnight SL, Miller, OL Jr. 1979. Post-replicative nonribosomal transcription units in D. melanogaster embryos. Cell 17:551-563

Here you can see RNA (solid line in schematic, b) of increasing length branching from both sister chromatids (dotted line):

A similar image but this time showing the replication fork (arrow):

This image shows RNA free gaps (arrows) in a single transcription unit, which are symmetrical between the two chromatids:

From which they conclude:

  The observation that fiber-free gaps often occur at symmetrical positions on sister chromatid transcription units suggests that the two identical transcription units respond similarly to the mechanisms that control RNA polymerase chain initiation. These cannot now be specified, but could include the local supply of RNA polymerase or other controlling molecules.


Picture of a camel's red blood cells I'm an art student in need of a little help. I'm looking for microscopic pictures of camel's red blood cells, I need their shape for an art project.

The pictures I find on Google seem a little sketchy as in "is it reeeeeally camel blood or is it from some other animal?" kind of sketchy.

I have tried looking further on the net and in books, but without any luck so far. I hope there is someone out there who can help, thanks for reading anyway!

Unlike humans and most of mammals, which have a biconcave (or "doughnut shaped") RBC, camels have oval shaped (or elliptical) erythrocytes.

The very first result in Google shows this:

That feature (which protects them from dehydration) is not unique to camels, but occurs in other Camelidae as well. This is an image of Llama blood:

Those are reliable sources of images (optical microscopy) of real cells.

However, for your project, I believe a scanning electron micrograph can better show the shape.

This is an SEM of elliptical camel (a) and alpaca, another Camelidae (b and c), erythrocytes:

For comparison, this is the biconcave human erythrocyte:

PS: There is this misinformation that camels' erythrocytes are nucleate. You can read this in several web pages. I have no idea who made this up, or why people keep sharing this wrong information: camels, like any mammal, have anucleate erythrocytes. See the post Do camels have nucleated RBCs or enucleated RBCs? for more information.

EDIT: The way your question is worded it really seems that you're just asking about the reliability of those sources. However, according to your comment below, it seems that you are indeed looking for better images. It's hard finding better ones than those indexed by Google, but since your goal is modelling those cells, here are two papers (about a protozoan parasite of camelids) which has some SEM that may suit you. The images are not high-resolution, but the cells are shown in several angles:

https://www.omicsonline.org/open-access/babesia-cameli-as-a-new-species-infecting-camels-camelus-dromedariusat-assiut-locality-2155-6156-1000700.php?aid=79911
https://www.ecronicon.com/ecmi/microbiology-ECMI-02-000040.php

In both papers the SEMs are at the bottom (just skip the optical ones, they are not good).


What are the criteria for determining the influence of epigenetic factors? Isolating a gene or sets of genes in diseases sometimes isn't enough to determine penetrance - epigenetic factors can have a significant effect. What are the criteria in determining whether epigenetic factors are significant?

First of all, the nature of penetrance is almost entirely unknown.  Likely it's a combination of epistasis and gene interactions, induced gene regulatory pathways, developmental noise, and other factors.  Epigenetics (imprinting, etc) may have little to do with penetrance, while chromatin structure may be a consequence of other things (most now regard histone modifications, etc, as consequence of transcription rather than heritable regulatory mechanism).  Currently, the field of epigenetics is undergoing a (long-overdue) reassessment.  Until that happens, anyone who wants to make claims of "epigenetics" is free to, so spurious claims are rampant.


Why do the proportion of predators increase at mass extinction events? Why does predation surge with mass extinction? It is caused by extreme selective pressures over resource competition that forces certain species to adapt to predatory niches?

The data used in the graph you posted seems to be from Bambach. 2002. Supporting predators: changes in the global ecosystem inferred from changes in predator diversity (in Kowalewski & Kelley. The Fossil Record of Predation) - see fig 19b - and, if so, is specifically dealing with marine predators.

I don't have time to look at that paper closely (it is quite long), and paleoecology is not my field, but a couple of relevant sections are:

  However, the diversity of predators and the proportion
  of total faunal diversity composed of predators have both increased over time, implying that ecosystems have
  increased their ability to support either more predators or more specialization among predators. Also, turnover
  in diversity dominance among predator groups, with more energetic predator taxa replacing or being added to a
  fauna of less energetic groups, implies that the energy available in marine food webs has increased.

and

  If
  the efficiency of energy transfer between levels in
  the food pyramid has stayed nearly constant (and
  there is no evidence that it has not), then a reasonable
  hypothesis for the increased proportional diversity
  of predators is that either the biomass of prey species
  has increased or the populations of prey taxa have
  become more stable (or both), permitting greater
  specialization by predators on more reliable food
  supplies. Thus, predators could increase their
  proportional share of total diversity by specializing
  on fewer prey taxa.

So according to the author, energetics, energy flow and predator specialization seems like likely reasons for the change. However, the paper also discuss factors such as rates of fossilization and also the fact that predators are generally rarer than prey means that there is probably more stochasticity in the fossil occurence process, which could affect estimated turnover rates and maybe also the proportion between predator and prey. You'll have to look at the entire paper for a fuller picture, and maybe somebody more knowledgeable can fill in later. I also think that you need to look at radiation patterns in certain taxa to fully understand these stepwise changes, and also to consider oxygenetion events as possible underlying reasons, but these are just my speculations.

The reasons given above also in one sense echoes the "biotic" explanation for the latitudunal diversity gradient (see e.g. Gaston, 2000 and Mittelbach et al, 2007), where high levels of primary production can support more specialized predators/parasites in more complex food webs, then leading to higher species diversity. So there might be interesting connections to contemporary patterns and processes of biodiversity as well. However, I haven't seen a compilation of %predators over different biomes or latitudes to match the graph in the question. Also, the "biotic" explanation for the latitudunal diversity gradient has been criticized and is not without problems (see papers above for more).


How do heredity and regression to the mean work with respect to intelligence? I am trying to understand the heredity of intelligence between generations in general, and how regression to the mean works in detail in particular. The answer I'm looking for should preferably answer some of the following questions.

When looking at the genetic basis for intelligence, it seems to me that the additive contribution of the genes should not be subject to regression to the mean, and that regression to the mean should rather be due to recessive genes and emergenesis. Is this correct? If so, what do we know about the extents to which these two mechanisms contribute to intelligence?

Towards which mean will a specific child be expected to regress? I have seen various suggestions here, ranging from the mean of the racial groups of the parents, to that of the child's grandparents.

Is it even possible to write down an (approximate) equation for the expected intelligence of a child, in terms of for instance the intelligence of parents, siblings and gransparents?

If someone coould answer these questions, that would be awesome!

I think the question mainly highlight either of two misunderstandings:

misunderstanding about the definition of heritability
misunderstanding why the slope of the regression line is equal to heritability (in the narrow sense).

Definition of heritability

Please have a look at the post Why is a heritability coefficient not an index of “how genetic” something is?.

Notation

Please note that, here I use $h^2 = \frac{V_A}{V_P}$ to designate the heritability in the narrow sense, where $V_A$ is the additive genetic variance and $V_P$ is the (total) phenotypic variance. If anything of what I just said is unclear, please refer to the aforementioned post.

Without any loss of generalization, we will set our scale so that the average phenotype in any studied case is equal to zero. From this starting value, we note X (with a subscript) the contribution of a given haplotype (or allele) to deviate the phenotype of an individual. We will note $E$ (with a subscript) the contribution of a given environmental state to deviate the phenotype of an individual.

An individual phenotype

Let's consider an individual O (stands for offspring, it will makes sense later). The phenotype of this individual is given by the addition of the contribution of each haplotype and of the environment. The expected phenotype of O (called $P_O$) is therefore

$$P_O=X_m + X_p + e_O$$

, where $X_m$ is the contribution of the maternal haplotype, $X_p$ is the contribution of the paternal haplotype and $e_O$ is the contribution of the environment.

Just a note

It might be worth skipping this note and coming back to it once you understood the below calculations (but I did not want to move this note to the end).

In the above calculation, one must assume absence of epistasis and dominance effect. I am not exactly sure how this might eventually cancel out later or whether results would then differ. I would welcome a follow-up in the comments to clarify this point but it might be worth its own post. As the question refers to the heritability of intelligence (assuming this term is defined), I would like to highlight that it is unlikely that we have much understanding about the exact pattern of epistasis underlying this trait as measure of epistatic interaction are often difficult to achieve.

Phenotype of O's parent

Let's note $P_P$, the phenotype of one parent of O'. The below notation applies to the mother but calculations would be the same for the father.

$$P_P = X_m + X_m' + e_P$$

, where $X_m'$ is the haplotype of the mother that has NOT been transmitted to the offspring and $e_P$ is the contribution of the environment experienced by the parent (mother).

Covariance between $P_O$ and $P_P$

The covariance between $P_O$ and $P_P$ (noted $cov(P_O, P_P)$ is just the sum of the covariances of all contributions, that is

$$cov(P_O,P_P) = cov(X_m,X_m) + cov(X_m,X_m') + cov(X_m,e_m) + cov(X_P,X_m) +\
 cov(X_P,X_m') + cov(X_P,e_m) + cov(e_O,X_m) + cov(e_O,X_m') + cov(e_O,e_m)$$

I let you take a few minutes to think about the values of each of these covariances.... They are almost all equal to zero (are independent). There are only two covariances that (under a simple model) can potentially be different from 0; $cov(X_m,X_m)$ and $cov(e_O,e_m)$. $cov(e_O,e_m)$ is teh correlation between the environment experienced by the mother and the one experienced by the father. For simplicity, we will make the assumption that these two environments are independent and therefore $cov(e_O,e_m)=0$. The above, long and hairy equation therefore reduces to

$$cov(P_O,P_P) = cov(X_m,X_m) = var(X_m) = \frac{V_A}{2}$$

Correlation between $P_O$ and $P_P$

By definition the correlation (which is the slope of the regression line) is just the covariance divided by the total phenotypic variance. Therefore the correlation between $P_O$ and $P_P$ (noted $cor(P_O,P_P)$) is

$$cor(P_O,P_P) = \frac{V_A}{2} \frac{1}{V_P} = \frac{h^2}{2}$$

Generalization to any correlation

Following the above logic, one can show that in general the correlation between any two individual phenotypes $P_X$ and $P_Y$ is

$$cor(P_X,P_Y) = r h^2$$

, where $r$ is the coefficient of relationship. For parent-offspring $r=\frac{1}{2}$.

Particular case of mid-parent vs offspring relationship

This is just a study case to show that when consdiering a made-up phenotype such as a hypoethetical mid-parent phenotype, then the math are just a little bit more tricky. If you consider the mid-parent phenotype $P_{mid}$, then you must consider that the total phenotypic variance is half the actual phenotypic variance. The correlation therefore becomes

$$cor(P_{mid},P_O) = \frac{cov(P_{mid},P_O)}{\sqrt{\frac{V_P^2}{2}}} = \frac{h^2}{\sqrt{2}}$$

Conclusion

All of the above mean that if you plot the phenotypes of a series of individual pairs, where each pair is related by $r$, then the slope of the regression line is $r h^2$. For example, if you plot the phenotype of the mothers with their offspring, then the slope of the regression is equal to $\frac{h^2}{2}$. If $h^2=0.4$ (which is a typical value of heritability), then the mother-offspring regression will have a slope of $0.2$.


what happens when you put enhancer and caat box in prokaryotes what happens when you put enhancer and caat box in prokaryotes

I do not think that enchancers do anything in procaryotes since there is no
chromatin spatial organization of DNA involved.