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What are the structural factors affect enzyme's Km?
Is there any rules (should not be exact), to estimate the kinetic changes in an enzyme if I did any mutation on it?
If I cannot estimate the new kinetic values, is it possible at least to clarify or suggest any explanation for the new kinetic after mutating an enzyme depending on the point mutation I did on it?
So I want to explain the changes in the kinetic parameters (Km / Vmax) in my enzyme after mutating it, maybe depending on the 3D structure? or the charge/size of the new amino acids? Or any other factors I may use to suggest anything logical how and why those changes happened to my enzyme after mutating it?
I need that for my dissertation and I am still totally lost, any ideas (with the proper references) will be great. I really appreciate any help.

Any mutation affecting the interactions between the enzyme and the substrates, intermediates and products will change the enzymes behavior.
I suggest reading some structural biology books and papers... Also please don't call it structural factors, that term is already used in crystallography. Finally you may want to add structural biology as a tag and possibly also ask the question at the chemistry stackexchange.

Computationally by molecular dynamics simulations coupled with free energy calculations (free energy perturbation or linear-approximation-based methods: linear response approximation and linear interaction energy. Visit PubMed and search for the relevant works by Arieh Warshel and Johan Aqvist. https://www.ncbi.nlm.nih.gov/pubmed

Computationally, using molecular dynamics (MD) simulations, it is difficult but not impossible, to quantitatively reproduce the effect of mutations on ligand-binding free energies, and activation and reaction free energies of enzymatic reactions. The most useful MD simulation methods for such a purpose are: free energy perturbation (FEP), linear interaction energy (LIE), linear response approximation (LRA), empirical valence bond EVB), and their combinations---developed by Arieh Warshel (The Nobel Prize in Chemistry 2013).
Mechanistically, mutations affect short- (van der Waals and electrostatic) and long-range (electrostatic) interactions with the surrounding environment, which comprises the rest of the protein and the solvent. Note that free energy is an attribute of an ensemble, not of a single 3D structure---which is why exploring a single structure of the mutated protein is unlikely to reveal the effect of the mutation qualitatively, not to mention quantitatively. One has to sample the conformational space of the protein---and MD simulation is the most efficient computational technique for such a sampling.
In summary, the effects are simple, but the system is extremely complex . . .
Klvana et al. (2012) Biochemistry 51: 8829-8843.
Klvana et al. (2016) J. Phys. Chem. B 120: 13017-13030.

What you are asking is not completely clear: do you want to predict the effect of mutations? Or do you want to make sense of experimental kinetics data comparing the wild-type enzyme to point mutants?
To predict the effects of mutations, ideally you need a three-dimensional structure of the enzyme in complex with a substrate analogue. Is there such a structure in the PDB for your enzyme? This would help you reason about the potential effects of point mutations. If there is no such structure, you can only rely on sequence alignments (and possibly structures of homologous enzymes, if they have been solved) to figure out which residues are important for substrate binding and catalysis.
KM is related to the binding affinity of the enzyme for its substrate. So, any mutation that for example disrupts an H-bond between the enzyme and its substrate would increase KM.
Any mutation that targets a catalytic residue (say, an amino-acid side chain acting as an acid-base catalyst) would affect kcat (and therefore Vmax as well), and could make it larger or smaller depending on the mutation.
If you are trying to make sense of experimental kinetics data, then ask yourself why you chose these mutations in the first place. One usually mutates residues to test an hypothesis. Or are you trying to understand the effects of naturally occurring mutations?

do you want to predict the effect of mutations yes. Is there such a structure in the PDB yes. any mutation that for example disrupts an H-bond between the enzyme and its substrate would increase KM. why? that does not make sense for me. Without referencing any study which proves that I cannot rely on it.

Km is different than Kd (see textbooks for the precise definitions and meanings of both), but close enough so we can approximately consider Km as the binding affinity for the substrate. What causes binding? Well, any interaction between the enzyme and the substrate, including H-bonds, salt bridges, hydrophobic pocket on the enzyme that can accommodate the hydrophobic part of the substrate, etc. Disrupting any of these interactions will give a weaker binding affinity, therefore higher Kd and Km values.

Regarding the available 3D structure of your enzyme: have you tried using it to figure out the potential effects of mutations? If so, how did you proceed, and what difficulties did you run into? Helping you would be easier if you told that.

My problem is understanding how these factors you mentioned (H-bonds, hydrophobic pockets, etc.) may effect Vmax and Km differently? tighter binding (more bonds) between enzyme and substrate stabilizes the transition state, and that increases the Vmax, but I cannot get how Km will be impacted differently. In other words, I cannot distinguish which changes in the structure may change the Vmax, and which may change Km.

To the best of my knowledge (I am not an enzymologist), this is really hard to predict. Ultimately, the predictions you make from a structure need to be tested experimentally. The structure is a useful guide to narrow down the potential interesting mutations to only a few residues, because it clearly shows which ones have nothing to do with the catalytic site (i.e. most of them).

Here actually comes the problem of energetically coupled residues (distal amino acids, may play a role in the catalytic activity, even they appears to be far and not important on the 3D structure). In my PhD. dissertation I discussed that, but that was really not so simply, and they are still somehow not very clear.


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Fish Carcass Identification
Can anyone identify the species of this fish carcass?
This photo was taken in Brooklyn, NY. The fish would have presumably been in Gravesend Bay.

The large lozenge-shaped scales suggest me it could be some sturgeon species. The location is compatible with what Wikipedia says:

In North America, they range along the Atlantic Coast from the Gulf of Mexico to Newfoundland [...]

Specialists may be able to refine a little more the identification, based on location and visible features.

I asked on reddit too and got the same answer, so I think you’re right. Thanks!

source: Stack Exchange

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

sort: votes


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What’s the term used to define a terrestrial being that moves by using six limbs?
I know that Bipedal locomotion would describe how beings like humans and ostriches get around.
Quadrupedal locomotion describes how beings like dogs and cats move around.
What about insects, specifically, a cockroach? I believe a cockroach has six “legs”, what would be the term used to describe that type of locomotion?

Hexapedal. From wiki > Hexapedal

Having six legs

Note that Hexapoda is a taxonomic group including insects and the smaller groups that are Collembola, Protura, and Diplura.

Thanks. I actually searched that before the post. Based on the feedback from google, the subject must be A.) Highly complicated B.) Lacks much interest, or C.)All of the above.

What is the subject in your comment? I don't really understand your comment. Do you think 'hexapodal' is the word you were looking for?

Well, the subject is “Hexapedal Locomotion “. Not much data

Oh do you just men the term is rarely used? Yes, I am sure it is very rarely used!

I’m an electronics hobbyists, and I’m enthusiastic about robotics. Wanted to know how much man understood about hexapedal motion. Doesn’t seem like much so far.

Right.... I'm sure there's quite a bit on the subject though. But anyway.... did your question got its answer? If yes, you can click on the checkmark next to the answer.

I have seen a couple programs where professionals from universities were demonstrating big-like robots...now that I think about it, I think their “bugs” only had four legs. Hexapedal locomotion must be a complicated concept.

Searched for six legged robot on youtube and found quite a few examples. None of them are particularly fast. Anyway... talking robots is not the point of your post.

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


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Identification of a caterpillar from NY
I recently camped at Harriman State Park in Southern New York, in early October.  Upon returning home, I noticed that I had a passenger with me.
The caterpillar in question is an almost translucent, pale green color with a single reddish stripe running down the center of the back.  It is approximately 1.5 inches long, with a reddish face as well.
I tried using a caterpillar identification book, but the closest one I could find also had a split tail, which this one does not.

Based on this picture, I'd say it's a Macrurocampa marthesia. I realize your specimen lacks the split tail, but I note that the "tails" of the larva of this species are longer in earlier instars. I wonder if this one is just an older caterpillar, getting ready to pupate? The image is a very good match otherwise, and this species does occur in the appropriate range.

That sounds fairly reasonable.  Doing a search for it gives me a picture that looks even more similar to mine.  The diamond shapes on the mid-back seem quite distinctive.
I wouldn't be surprised if it was an older caterpillar, it did seem quite pudgy.


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Evolutionary uselessness of the male nipple
The Male nipple serves no evolutionary function, yet it remains in the Genomic code. Is there only one Gene for the human nipple?

Perhaps the answer is that there are not two entirely different genomes, male and female, but a genome which is at least 25/26ths identical.  So (simplistically!) the basic "make a breast" machinery (and pretty much everything else) exists in both males and females, but is only switched on in females, at puberty.  But hormones can activate breast growth in males, either through disease or deliberately, as part of a sex change.

A small percentage of males today are able to lactate like the female.  Maybe at some point in the past, the male species were also capable of feeding offspring in case the female perished.  Also, in some males the nipple is an area of sexual stimulation.  So, it does serve a purpose.


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Why Interracial couples always give birth to colored one?
Whether couple is White male and colored female or White Female and colored Male
but they always give birth to colored one.
Why Interracial couples always give birth to colored one?

I feel you haven't looked into the matter enough.

This isn't really a biology question. It's a matter of law and politics. In some polities, a racial classification of people was carefully tracked, and children of mixed race parents were defined by law to be "colored". See for example South Africa during Apartheid, and some US states during the Jim Crow period. Children of mixed race parents may or may not inherit characteristics would lead to them being characterized as one race or another by casual observation. See the Wikipedia article on "passing".

Anecdotally: They don't.


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How do people actually find codons in a DNA transcript just by looking at it?
I was looking at this transcript of a DNA sequence, and the article kept referencing what the first codons are, but a codon like AUG isn't in the sequence...there's no "U" in any sequence. What am I missing?

In DNA, the first codon would be "ATG"

as far as i know genomics, you can align your transcripts (mRNA) to your peptide, as well as align mRNA to genome and cDNA, to detect first codon. Also, starting sites are conserved and have canonical sequences (on average)

Codons refer to sequences of nucleotide triplets that translate to amino acids. As you know, polypeptides are translated at the ribosome using a messenger RNA (mRNA) blueprint produced by RNA polymerases from the DNA.
DNA consists of four nucleotides: adenine, guanine, cytosine and thymine. Thus, DNA sequences read, for example, ATAAGC. RNA, however, replaces thymine with uracil. So to transcribe the above DNA nucleotide sequence into mRNA would result in UAUUCG.
The mRNA may also get spliced into various isoforms coming from the same gene. In short, it may be difficult to determine the gene product from the DNA sequence.
Does that make sense?

There are also start codons other than AUG.


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Which one is true about sunflowers, "follow the sun across the sky" or "always face east"?
Which one is true :

Sunflowers follow the sun across the sky.

Or...

Sunflowers always face east.

Or are there 2 kinds of sunflowers with different behaviours?

Here at biology we like to see some effort to solve a question yourself. So: What have you found out?

@Chris : Hello chris, I was a bit surprised, when I open http://list25.com/25-science-facts-that-were-proven-wrong/2/ which stated that sunflowers do not follow the sun across the sky, so I surf the web and find out 2 different answers. so I asked about it here.

Both are correct.
The issue here is the developmental stage of the flower, that is, if it is a immature or a mature flower (actually, not a flower but an inflorescence instead).
Immature or young flowerheads do display heliotropism. However, as the flower matures, it stops showing heliotropism and becomes "fixed", always facing east.
This is a photo of the sunset. If the mature flowers (or inflorescences) still displayed heliotropism, they would be facing the sun (at the west). However, they face the opposite side (east):

Also, to be honest with the sources, the first link (Science ABC) you provided does make that clear. You can read next to the end:

Mature sunflowers finally stop displaying heliotropism.

So, there is no contradictory information here.
A good source of information, with videos, can be found at this page of Berkeley University, which says:

As the sunflower matures and the flower opens up, overall growth slows down and the plants stop moving during the day and settle down facing east. This seems to be because, as overall growth slows down, the circadian clock ensures that the plant reacts more strongly to light early in the morning that in the afternoon or evening, so it gradually stops moving westwards during the day.

Source: https://nature.berkeley.edu/news/2016/08/sunflowers-move-clock


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Evolutionary advantage of consciousness
What possible theories are out there, regarding the evolutionary benefits of having consciousness? Why is not all information processing done subconsciously?
Can it have something to do with language and communication? But then, a lot of animals can be considered to be communicating without "qualia".
EDIT:
Some background. Philosophy student here. Recently ventured into reading a bit of genetics. Every aspect of life seems to be slowly evolved out of need, either survival or atleast survival till reproduction occurs.
Consciousness, according to me, would be the constant "subjective experience" of our lives, the inner movie as they would say.
My question, then, is why would a part of the brain be dedicated to generating an integrated coherent experience when zombie-like information processing could suffice? Did the ability of movement, along with certain cognitive skills, really make the upper mammalian habitat so unpredictable that genes had to adapt to "every-situation-might-be-a-new-situation" level of brain capacity?
Has any biologist written about the evolution of intelligence (which is a precursor to the consciousness I'm talking about) corresponding to early humans?

I find it hard to disantangle evolutionary advantage of counsciousness from the ones linked to other cognitive abilities especially the social ones such as for example cooperative hunting, Machiavellian intelligence or advanced communication. I think a big part of the issue in this question is in the exact definition of consciousness. Can you please try to explain in what way is your question different from just asking What are the evolutionary advantage of high cognitive abilities in humans??

Although there is no mention of consciousness, you might want to have a look at wikipedia > Evolution of human intelligence.

Machiavellian intelligence and advanced communication can be categorized as reactions to situations. Or tools for problem solving. But the "subjective nature of experience" develops in the more advanced animals. I suppose the constant self awareness in conscious stream of thought, is what I meant by consciousness.

To me, it feels either too complicated and inefficient or just a chance byproduct of "useful intelligence"

This has the possibility to be a very good question but it needs to be fleshed out a bit. Your first problem is defining what you mean by consciousness.

DISCLAIMER
I know little on the subject. I want to first express my personal views of the existing difficulties at answering this question and then I will attempt to give a short overview of the potential answers I could find.
ISSUES WITH THE QUESTION
Consciousness vs higher cognitive abilities
I personally find it hard to disentangle evolutionary advantage of consciousness from the ones linked to other cognitive abilities especially the social ones such as for example cooperative hunting, Machiavellian intelligence or advanced communication. I think a big part of the issue in this question is in the exact definition of consciousness.
So, a very important issue with the question is that 'consciousness' is not well defined.
Only few peer-reviewd papers on the subject
While there are a number of ressources in the non-peer reviewed literature (mainly books or popular articles) on the question, I could not find a lot of papers in the peer-reviewed literature. I suppose again that part of the issue that prevents much discussion in the subject is the absent of a commonly agreed upon definition of consciousness. Some of what I'm about to quote is not peer-reviewed and some are not written by biologists but philosophers.
Evolutionary psychology remains very theoretical
One would note as well that most work in evolutionary psychology remains mostly theoretical as it is often hard to perform meaningful empirical testing for the existing hypotheses.
Quoting for safety
As I often failed to make sense of what I just read(!), I will try to quote quite  a bit to avoid misinterpreting other authors.
ANSWER
Definition of consciousness
I recommend having a look at Perlovsky (2007) for a semantic discussion (and opinion) on the concept of consciousness. Quoting their full abstract

The knowledge instinct is a fundamental mechanism of the mind that drives evolution of higher cognitive functions. Neural modeling fields and dynamic logic describe it mathematically and relate to language, concepts, emotions, and behavior. Perception and cognition, consciousness and unconsciousness, are described, while overcoming past mathematical difficulties of modeling intelligence. The two main aspects of the knowledge instinct determining evolution are differentiation and synthesis. Differentiation proceeds from and unconscious states to more crisp and conscious, from less knowledge to more knowledge; it separates concepts from emotions, Its main mechanism is language. Synthesis strives to achieve unity and meaning of knowledge; it is necessary for resolving contradictions, concentrating will and for purposeful actions. Synthesis connects language and cognition. Its main mechanisms are emotionality of languages and the hierarchy of the mind. Differentiation and synthesis are in complex relationship of symbiosis and opposition. This Leads to complex dynamics of evolution of consciousness and languages. Its mathematical modeling predicts evolution of cultures. We discuss existing evidence and future research directions.

Consciousness as a by-product
To my personal experience, consciousness is in general viewed as a by-product of the selection for specific cognitive abilities. Again, without much of a definition of consciousness it feels to me that selection for specific social skills, such as those requiring the Theory of Mind (ToM) would yield to increase consciousness.
If consciousness and ToM (and other related cognitive skills) are the same thing, then we got our answer, otherwise, the standard view is to consider consciousness as a by-product of the selection for those higher cognitive skills.
On the topic, see for example Judd (1910) (did I really cite such an old paper?) or Dennett (1980) (Dennett is a philosopher, not a biologist).
In the comments the OP said

To me, it feels either too complicated and inefficient or just a chance byproduct of "useful intelligence"

I would note that, if taken as an argument, then it would be a logical fallacy called argument from incredulity.
Consciousness as a result of higher social abilities
This opinion seems quite related to the previous one. Quoting from Ingold (2005)

Becoming a person is thus a matter of gathering social relations into the structures of consciousness: the movement in development, as Vygotsky put it, is ’not from the individual to the socialized, but from the social to the individual’
[..]
as relationships unfold in the course of purposive social action, they are
  enfolded in the consciousness of persons, that is, in the structures of the self.
  The connection between social relations and consciousness should thus be
  understood in terms of unfolding and enfolding, rather than in terms of cause
  and effect
[..]
This view of sociality, and the theory of direct perception on which it is
  founded, suggests that it is possible for persons to engage with one another on
  the basis of shared perceptual experience prior to the objectification of that
  experience in terms of collective representations encoded in language and
  validated by verbal agreement. Thus sociality is possible in the absence of both
  language and the kind of objective self-consciousness that (probably) depends on language

Conscioussness as result of the logistics of decision making
Quoting from Merker (2003)

Consciousness will be interpreted as a biological
  function evolved by mobile animals as a solution to neural logistics problems inherent in the
  control of orientation to their surroundings. The interpretation is motivated by the conspicuous
  absence from the contents of consciousness of two significant classes of information known to be
  present in brains, one on the afferent and the other on the efferent side of neural function. In fact,
  the thoroughness of their exclusion from consciousness suggests that their absence represents a
  design feature of consciousness providing important clues to its nature and biological function.
  This in turn helps constrain conceptions of its neural implementation as well as the search for its
  origin in the phylogeny of life forms

The problem with the question is that 'consciousness' is not well defined. +1

I'd note that the way most neuroscientists use the term "consciousness" it has little or nothing to do with theory of mind. Theory of mind requires consciousness but not the other way around; theory of mind is a much higher bar to achieve.

You put a lot of effort into answering a terribly unclear question!

I agree. However, 1) this type of question has already popped up several times in the past (and having said somewhere on an SE post that a big part of the issue lies in the definition of consciousness may be helpful in the future) 2) there is some literature on the subject 3) the question has already received 3 upvotes (non of them being mine).

Also, I have received this question twice myself and it is always unsatisfying for someone asking a question to just get a "your question is unclear" kinda answer especially in a personal setting so I thought I would give it a shot, also to educate myself a little bit. But.... I agree with you @anongoodnurse


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Manipulating phylogenetic trees
I am looking to manipulate manually constructed phylogenetic trees (adding bootstrap values, markers to indicate trate loss/gain etc.) I came across a paper that used Macclade, however, this no longer appears to be a program that will run on almost all computers. Is there a useful alternative software package? I have tried Mesquite, but it does not appear to have the same functionality (although, I have probably just missed understood how to use it effectively).
Any help/recommendations would be appreciated

If you have some knowledge of python, you can do a lot of things with the ETE toolkit.
Disclaimer: I have used an older version of it, but in a very limited manner.

The MEGA software package is the most comprehensive software I have used, if you don't want to rebuild your tree I have used FigTree in the past but it seems to be unsupported now.


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Why is there extreme itching when we touch a hairy caterpillar? What are ways to stop itching?
I mean there are lot of caterpillars or hairy caterpillars to be more precise when we touch those hairs we get extreme itching on that area i want to know why we got that itching? Ok i know that it must be some chemicals but which? And if one has got itching how to remove it?

Google search caterpillar sting, the hairs themselves cause itching. http://www.wikihow.com/Treat-a-Caterpillar-Sting

how to remove it? makes your question more of either a medical question (should be asked on health.SE) or a life hacks question (should be asked on lifeHacks.SE).

It would seem that you're referring to caterpillars that have urticating hairs, such as the goldtail moth caterpillar.
Erebidae similis

.. when we touch those hairs we get extreme itching on that area i want to know why we got that itching?

In this case, the itching sensation is the effect of a hair-specific, soluble protein known as Thaumetopoein. According to this publication, in where they studied the urticating hairs of the Thaumetopoea pityocampa moth caterpillar when applied to guinea-pig skin:

The hairs are hollow inside with sloping spikes toward the distal end. There are no holes or pores on the hair and the irritating factor can only be obtained by crushing the hair. This suggests that when stinging occurs the hair is broken in the skin and the substance [Thaumetopoein] is released.

More information about this immunological reaction begins on page 5 (numbered 350).

And if one has got itching how to remove it?

Remove all caterpillar hairs by first using tweezers to extract any embedded hairs, then the sticky side of tape to remove surface resting hairs. Do not use your bare hands, as this will only spread the caterpillar hairs.
Rinse the affected area with warm water & soap.
Apply some kind of hydrocortisone cream.

Poison.org - Caterpillar Stings


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Myopia & the Blur Effect
I know myopia is caused by elongation of the eyeball. When the eye is too long, light entering the eye balls falls in front of the retina instead of on it.
However I do not quite understand how this leads to the "blur" we observe. If part of the light entering the eyeball "misses" the retina shouldn't the observed effects simply be a reduction in the brightness of the object - as if I were standing in a less illuminated place? For example, if I take off my glasses in broad daylight my retina is getting a far greater dose of light than when I'm indoors (wearing my glasses) under artificial lighting. Yet the world still looks blurry outside (without glasses) and clear indoors (with glasses).
What causes the blur effect? If less light is hitting the retina it should simply look less illuminated, not blurry.

You have some misconceptions about visual acuity. You need to understand how lenses work to understand why objects up close are blurry in myopia.
Sure, if one elongates the orbit, blurring will occur, but that's not usually the cause unless it's in childhood. As we age, the elasticity of the lens has more to do with it.
Light comes in through the pupil. The amount of light is what determines brightness; too little, and we can't see, too much and we look away. In between we "see". Being able to focus doesn't have any effect on brightness; the size of the aperture does, however (the aperture in this case being the pupil.)
Blurriness is caused by where the light rays striking the object we're looking at come into sharp focus in out eye. Sharpness falls within a very small range, then once the range is exceeded, the image becomes progressively blurrier because the rays scatter again. This is why looking through a pinhole improves our vision: less scatter. If your pupil could constrict down to a pinhole, that would be pretty amazing, but it can't.
The purpose of the lens is to focus the image. It can do so (with the help of ciliary muscles) by changing shape. But it can only change shape within a range. If it cannot change shape enough to focus the image where it needs to be - on the retina itself - you have blurry vision.
That's why additional lenses (or changing the contour of the cornea) help.


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Hardy-Weinberg for triploids
Problem:
A certain species has somatic cells with ploidy 3n (the organism inherits
three sets of homologous chromosomes from each of three parents). At a certain locus, there are three possible alleles A 1 , A 2 , A 3 , which are
completely dominant in the order A 1 > A 2 > A 3 . The proportion of organisms
exhibiting traits A 1 , A 2 , and A 3 are respectively 0.614, 0.306, and 0.08. In
addition, the proportion of organisms that are completely heterozygous
(genotype A 1 A 2 A 3 ) is 0.18. Which of the following are allele frequencies of A 1 , A 2 , and A 3 , respectively?
Answer Choices:
A. f(A 1 ) = 0.5, f(A 2 ) = 0.3, f(A 3 ) = 0.2
B. f(A 1 ) = 0.3, f(A 2 ) = 0.5, f(A 3 ) = 0.2
C. f(A 1 ) = 0.3, f(A 2 ) = 0.4, f(A 3 ) = 0.3
D. f(A 1 ) = 0.6, f(A 2 ) = 0.2, f(A 3 ) = 0.2
E. f(A 1 ) = 0.7, f(A 2 ) = 0.2, f(A 3 ) = 0.1
Correct Answer:
A
Solution:
No clue. I'd guess that the solution follows a hardy-weinberg model for polyploids. For simplicity, I will refer to A1, A2, and A3 as x, y, and z, respectively.
(x + y + z)^3 = x^3 + 3x^2y + 3xy^2 + y^3 + 3x^2z + 6xyz + 3y^2z + 3xz^2 + 3yz^2 + z^3
Given that z^3 = 0.08, shouldn't z (A3) equal the cube root of 0.08 = 0.43?
That doesn't match any of the answer choices, so I will assume that my steps were incorrect.
Any suggestions?

First, although it only speaks about cases of diploidy, you might want to have a look at Solving Hardy Weinberg problems.
Information given to us
The question gives the same names to the phenotypes than to the alleles which si rather confusing. Let's call the three possible phenotype $P_1$, $P_2$ and $P_3$. We know that the frequencies of these phenotypes are
$$f(P_1) = 0.614$$
$$f(P_2) = 0.306$$
$$f(P_3) = 0.08$$
Compute phenotype frequencies in terms of allele frequencies
Let, $x$, $y$ and $z$ be the frequencies of the three alleles, $A_1$, $A_2$ and $A_3$ (I chose those names to fit with the equations you wrote). The whole difficulty now is to express $f(P_1)$, $f(P_2)$ and $f(P_3)$ in terms of $x$, $y$ and $z$. You should try yourself before looking at the result. Start with $f(P_3)$, it is the easiest.
Here is the solution for $f(P_3)$

 $f(P_3) = z^3$

Here is the solution for $f(P_2)$

 $f(P_2) = y^3 + yz^2$

Here is the solution for $f(P_1)$

 $f(P_1) = x^3 + 3x^2 (y+z) + xyz + xy^2 + xz^2$

Once, you have done that, you have three equations with three unknowns and you just have to solve them. Make sure at the end that $x+y+z = f(P_1) + f(P_2) + f(P_3) = 1$.

I've tried to do that. z^3 = 0.08. z = 0.43, which isn't correct. Maybe f(P3) should equal 0.008 instead of 0.08?

Indeed. Something is wrong in the possible answers or we misinterpreted the genetics basics as the explanation of dominance is a little unclear. If $f(P_3) = 0.008$, then some other phenotype frequency must be adapted so that that sum up to one. In any case, the other phenotype frequencies are made so that the corresponding allele frequencies don't match! So, I very much think I did not interpret the genetic basis correctly. Stating  completely dominant in the order A 1 > A 2 > A 3 is not sufficient unfortunately. IMO, the question is undefined.

Well that's a shame! Thanks for the help, regardless.


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Onion Cells or Pear Cells?

I am researching different cells under a brightfield microscope for homework and am having trouble determining whether or not these cells are Onion cells (Allium cepa) or pear cells (Pyrus) under a light microscope. I am pretty sure they are pear cells, but I just wanted to be sure!

Pear has loosely arranged spherical cells and some cells are sclereids cells. Onions cells are rectangular and almost transparent.
Honestly I'm about to vote for closing, because I don't see how this question can be important.

@MaximKuleshov No question should be closed solely because it is unimportant, but this question doesn't show any effort at in researching the question before posting. What were you expecting the difference to be? Where did you previously try to answer this question and what didn't you understand about those answers? Why are you pretty sure it's a pear cell? I think this question is close to being a very nice question.

You are correct, those are pear cells.
Onion skin cells (popularly in slide sets)

source and a hommge to onion skin cells
Pear Cells

source and also several other neat pictures of pear cells


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What does the total membrane current vs time plot of an action potential look like?
What does the total membrane current vs time plot of an action potential look like? I see that there are voltage vs time plots, but I can't seem to find the current plots.
Thanks

Check out panel b for total current, panel c for K+ and panel d Na+ currents separated...

This is from this website: imageWebsite

Could you please also provide a link to your source in case someone wants to read more about how these currents are measured?


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How frequent are selective sweeps?
Introduction
Selective sweep is the most famous genetic signature of selection. We know of a number of classical examples of selective sweeps, some of them in humans. See the classical example of the sweep on a sequence relgulating the lactase gene in the post Are humans the only species who drink milk as adults?.
Question
I do not have a good intuition about how common such sweeps are. Are there constantly 5 to 10 sweeps happening in a species genome or is there a sweep every 1000 generations only?
How frequent are selective sweeps?
Clarification
Of course, the answer will vary (and will probably vary greatly) among species. I would welcome empirical estimates and/or theoretical expectations coming from any species (I would prefer an estimate coming from a eukaryote species though).

Check out these papers: one / two / three

I know this question is a bit old, but I read a paper recently which (claimed) to answer this question.
I think the answer to this question is suprisingly controversial. I don't really have a formed opinion yet of which answer is correct, but I will try to discuss the different viewpoints here.
Argument 1: Sweeps are rare
On one hand, we have the people who are sceptical of how common sweeps are. This, in my understanding is most researchers. Many people believe that polygenic is the predominant form of selection in humans.
There is the paper by Hernandez et al (2011), who find scant evidence of selective sweeps in recent human history. Essentially, they looked at the reduction in diversity (something which is associated with sweeps) around amino acid substitutions and synonymous substitutions and found that the two were statistically the same. They say it's probably more likely that this is caused by strong purifying selection at linked sites rather than sweeps.
Szpak et al (2019) suggested that most of the time, the criteria for designating something a sweep in human populations was probably too lax, and many of the previouly claimed sweeps were probably artefacts of some kind. In fact, they only find compelling evidence for 2 sweeps in recent human history.
Argument 2: Sweeps are more common
Alternatively, there are some studies which have apparently discovered a relative abundance of sweeps in human history. Some might make the argument that sweeps are likely to be common, since humans have a relatively small effective population size (~20,000) and low mutation rate.
Souilmi et al (2020) claimed to have discovered 57 (fpr<10%) sweeps using genomes from ancient Eurasian individuals. 35 of these 57 were inferred to have occured before 35kya. The reason they claim to have found many more sweeps than previous studies is because they used ancient DNA. It is well established (Hellenthal et al 2014) that admixture is virtually ubiquitous within modern and ancient human populations. Admixture likely obscures the signal of sweeps by introducing non-selected haplotypes from the admixing population, making hard sweeps look like soft sweeps, or perhaps not even sweeps at all. They confirm this using simulations and show the power to detect sweeps is massively reduced when you are looking at admixed populations.
However, their method uses ancient DNA, which is highly prone to various artefacts, which they didn't appropriately test with simulations. It also hasn't been peer reviewed, so there may well be other potential issues.
References
Hernandez et al 2011
Szpak et al 2019
Hellenthal et al 2015
Souilmi et al 2020

Good job! You might want to add Booker et al. (2019) who make back-of-the-enveloppe calculations and estimate that over its whole genome and at any time "D. melanogaster has approximately [..] 80 incomplete sweeps of alleles that will ultimately reach near fixation."

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Could removing non-functional parts of coenzymes improve enzyme function?
As pointed out here, many important co-enzymes (essential enzyme cofactors) such such acetyl-CoA and vitamin B12 contain nucleotide portions that do not function in the enzyme catalysis. They have been suggested to be relics of the RNA world, so it would appear to me that they are redundant. Suppose we were to remove these nucleotide portions of the co-enzymes, would that improve the working of the proteins (and perhaps our health) or wouldn’t it make any difference?

Those aren't enzymes but rather coenzymes, and the nucleotide moiety is necessary for function.

@canadianer — I agree that this question is based on a fallacy. Surely that point should be made in an answer or the question should be voted to be closed. The only point of a comment to the poster would seem to me to be to ask the poster to withdraw the question, which he is unlikely to do if he doesn't understand that the nucleotide part of coenzymes interact with proteins rather than provide the functionality.

@David Surely the point should be made in an answer. Actually I think this question is a duplicate but I cannot find the other post.

@canadianer —  Don't know about the duplicate. But, yes, probably best as an answer. Are you going to answer or me. In any case I think I'll edit it so it's more accurate and explains the problem in more detail. (I've a little time to kill while waiting for a program to run.)

@David I don't have the time; feel free.

The video cited in the question is to be commended and presents a number of points relevant to questions about DNA and RNA posted here previously.
The problem with the question sems to be an incomplete understanding of the role of these coenzymes/cofactors in the function of the enzyme. (The original question implied that acetyl-CoA and vitamin B12 are the enzymes.) In contemporary protein enzymes, these non-protein cofactors are bound to the protein part of the enzyme and complement it in its function. Typically, the protein will have binding sites for the substrates (the reactants) and the coenzyme will provide the sophisticated catalysis or other essential function.
The coenzyme must obviously interact with the protein, and in a way that leaves its catalytic or functional part free to operate. This is what the nucleotide portion of the coenzyme does — in fact it is performing the same role as has been suggested it played in the RNA world, but instead of interacting with an RNA enzyme (ribozyme) by base pairing, it interacts with amino acid side-chains by a variety of weak interactions. An example of this is shown for coenzyme-B12 in the enzyme, methylmalonyl-CoA mutase (my annotations in red and brown).

To quote from the figure legend in the paper: “The lower axial ligand to the cobalt is histidine HisA610, which is in turn bound through AspA608 to LysA604. The pseudo-nucleotide tail is bound in a pocket between the sheet and the C-terminal helix.”
The situation for coenzyme-A (CoA) is slightly different, in that it is involved in the transfer of acetyl and other groups, rather than catalyis per se. However the principle is the same — there is a chemically functional portion and a nucleotide portion that binds it to the protein.
Thus, the nucleotide portion of coenzymes is not redundant and without it they could not bind to the enzyme and enable it to perform its function.


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Cnidarian life cycle, a case of ontogenetic polymorphism?
Cnidarians have a complex life cycle which usually goes as follows:

Egg hatches larva.
Larva settles on sea bottom and transforms into a sessile polyps.
Polyps undergoes strobilation and asexually buds off juvenile, free-swimming medusae.
Medusae eventually mature and reproduce sexually to beget new eggs.

Given the morphological and physiological disparity between the three forms (larva, polyps, medusa), and how each form comprises a distinct stage in the cnidarian's development (i.e. ontogeny), would it be accurate to say that the cnidarian life cycle is an example of "ontogenic polymorphism"?

The question has a feel to me like an invertebrate biology class question, though I have given a brief answer below anyway.

Sure it would.  I would usually use holometabolous insects as an example of this (egg, larva, pupa, adult), but Cnidarians certainly fulfill the basic requirements encapsulated by the phrase "ontogenic polymorphism." It appears that the pressures of finding/establishing food sources and escaping predation in competitive environments has driven both Cnidaria and Insecta toward this evolutionary strategy, though that is a field of active study still (at least in insects).


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Is a DNA molecule a single strand of polynucleotide or two of them linked together?
Our molecular biology teacher told us that a double helix of DNA was composed of two DNA molecules linked together by hydrogen bonds. The thing is, until now, I always thought a DNA molecule was composed of two strands, those being polynucleotides, both of them being linked together. I can't find a link which is saying the same as my teacher, even if it seems technically correct to call a double helix a dimer of two DNA molecules.
I was curious to know what was the exact terminology.

I have provided an answer to this question, but would stress that there is NO "exact terminology" provided in any of the answers because, as far as I am aware, the terminology in molecular biology is based on usage rather than definition.

As you pointed out, though this may be basic biology, seeking clarification when receiving conflicting information is a good thing. Don't feel embarrassed for asking. :)

.. our molecular biology teacher told us that a double helix of DNA was composed of two DNA molecules linked together by hydrogen bonds.

Respectfully, your teacher is incorrect. A single, double-stranded DNA molecule is comprised of two helical shaped polynucleotides, and are connected together via hydrogen bonding.

Highlight of each polynucleotide

Highlight of hydrogen bonding

And just for further validation, according to Molecular Biology of the Cell, 4th ed., by Alberts B, Johnson A, Lewis J, et al.:

A DNA molecule consists of two long polynucleotide chains composed of four types of nucleotide subunits. Each of these chains is known as a DNA chain, or a DNA strand. Hydrogen bonds between the base portions of the nucleotides hold the two chains together.

So, it would seem that your teacher is referring to each polynucleotide, a.k.a. DNA strand, as a DNA molecule. Instead, she should use the verbiage: a single DNA molecule is composed of two DNA strands, which are helical-shaped polynucleotides.

the easy way to remember this to think of RNA which is a single stranded polynucleotide.

@John Well, there's double-stranded RNA too, so... ;)

@paracetamol on the flip side, there is single-stranded DNA too, so... :P

It is easier to understand if we consider RNA. It has higher structural diversity in nature compared to DNA and can form hairpins/stem-loops, double helices, triplexes, quadruplexes and single strands (and a complex containing all these forms). DNA can also form all these structures, BTW. In such cases we do use the terms inter/intra- molecular interactions/hydrogen bonds to distinguish between the double helices and hairpins/stem-loops.

"double-stranded DNA molecule is comprised of two helical shaped polynucleotides, and are connected together via hydrogen bonding".. This is wrong. Polynucleotide can be a polyribonucleotide or a polydeoxyribonucleotide and DNA is the latter. This definition also asserts that there are helical and non-helical PN and only the helical ones come together to form a dsDNA. Your description of the biophysics is misleading. ssDNA is also considered and called DNA. Plus, a "strand" is not a proper chemical term.

@WYSIWYG No, the asserted definition isn't wrong. This is a biology SE and not biophysics or even chemistry. The terms are relative to the context of the site. If the OP wants more objective definitions and explanations of everything going on in DNA then Biology.SE isn't the place to look for it.

@Charles and why do you assume that to be the scope of this site. It is a site for biology researchers, academics and students; it is not a popscience site.

@WYSIWYG If you're going to even contest the usage of strand then you're on a whole other level, and if you feel strongly enough about it then please, by all means, spend two hours posting your own answer and explain everything down to the IUPAC definition of it all.

@Charles I'm just saying that the way you used the term "strand" is not appropriate. Your statement sounds as if strand is a defined entity by itself. And please pay attention to my first comment. What would you call a ssDNA? Some viruses have ssDNA genome.

Hmm, I think that the teacher is actually correct and that the previous explanation, although very nicely referring to text book diagrams, is a little misleading.
The issue here is the nature of a hydrogen bond within the DNA structure. Within a chemical context, generally a molecule is a collection of atoms primarily bonded together via covalent bonds. Hydrogen bonds, by their very nature are transient - if they weren't then the double stranded DNA wouldn't be able to opened for reading! So, a strand of DNA, from the 5' end to the 3' end is one molecule. The reverse complement strand to this is another molecule of DNA. This is important as if you were carrying out a PCR reaction (for example), you would use single, stranded DNA as primers - so this would be a molecule of DNA. Also, if we were to use hydrogen bonds as a means of defining a molecular species, then water would only be one molecule - all of those H2O molecules interact via hydrogen bonds with each other!
But what about the double helix structure? Well this is a consequence of the chemical structure of each nucleotide (and the chemical properties of those atoms), aided by the hydrogen bonding to tightly pack the atoms together - it's a form taken by the thermodynamics of the inter-molecular interactions between the two molecules of DNA.
So, a strand of DNA is a molecule. Two strands (two molecules) of DNA give us the natural, stable, helical form.

Biologists can be pretty lax when it comes to chemical definitions. Technically it's not a molecule at all but rather a polyatomic ion.

I don't see how my answer is misleading, and at no point did you directly identify the portion(s) of my response that you then claim to correct. It would be nice if you could do this.

The IUPAC definition of molecule is "An electrically neutral entity consisting of more than one atom (n > 1). Rigorously, a molecule, in which n > 1 must correspond to a depression on the potential energy surface that is deep enough to confine at least one vibrational state. " https://goldbook.iupac.org/html/M/M04002.html So unless the two strands are held together too weakly to confine at least one vibrational state (which is not the case) the two hydrogen-bonded strands are one molecule.

"Hydrogen bonds, by their very nature are transient .." -- although generally true, there are many opposing examples, with the first to mind being HF. ". This is important as if you were carrying out a PCR reaction (for example), you would use single, stranded DNA as primers - so this would be a molecule of DNA." -- PCR methods don't match how DNA behaves naturally, specifically in that PCR separates both strands entirely all together, whereas naturally occurring separation involves a replication fork, meaning that a great portion, if not almost all, of the DNA remains double-stranded.

"So, a strand of DNA is a molecule. Two strands (two molecules) of DNA give us the natural, stable, helical form." -- Notice how you keep saying "molecules of DNA", and not "DNA molecules". The OPs teacher didn't use this verbiage, which is important because the two have quite different implications. Additionally, nobody has claimed that the single strands of DNA couldn't be considered as molecules in and of themselves, except perhaps @canadianer =P. No offense, but with respect to you singling out my answer, I believe your response presents a straw man's argument against it.

@DavePhD There needs to be more rigourous definition I believe because if we just consider the cited IUPAC definition, liquids and solids can also be possibly considered one single molecule. That is definitely not the case. Moreover, in case of RNA (which has higher structural diversity in nature compared to DNA) can form hairpins, double helices and single strands (and a complex containing all these forms). In such cases we do use the terms intra/inter- molecular interactions/hydrogen bonds to distinguish between the double helices and hairpins/stem-loops.

This has come up again recently, so let me summarize my own arguments on what I believe is a purely semantic question.

In strict chemical terms, according to the IUPAC definition, neither double-stranded DNA (dsDNA) nor its individual separated strands is a molecule but, as stated in the Wikipedia article, a polyatomic ion.

If one extends the term ‘molecule’ to ions and considers only the historical criteria of covalent chemical linkage and indivisibility (as applied to small chemical species) one would conclude that the individual separated strands of DNA were molecules, but dsDNA was not — the complete opposite to the assertion in the accepted answer!

In practice, however, many authors refer to dsDNA as a molecule, presumably because they regard it as conceptually different to the two (different) single stands. I accept this as usage, but emphasize that it is not based on any formal re-definition of the term ‘molecule’ for molecular biology that I am aware of.

Although some text-book authors avoid using the term ‘molecule’ for the individual strands of dsDNA — presumably for clarity in explanation — this use by others is widespread (e.g. in Lakowicz, DNA Technology).

It seems absurd to argue that the single stranded DNA genome of, say, SV40 virus is a molecule, but an individual strand of a circular dsDNA plasmid is not. The situation is compounded in the comparable question for RNA. Consider dsRNA viruses, where one strand is synthesized in large quantities: what is being synthesized if it is not an RNA molecule?

But likewise it would seem to be absurd to argue that dsDNA is not a molecule but becomes one after, say, chemical cross-linking.

In my opinion this question would only be of practical importance if ambiguity could arise from applying the description ‘molecule’ to both dsDNA and its single strands. I see no such ambiguity, per se, and maintain that this is a purely semantic question.

I therefore conclude that assertions that the term ‘molecule’ be restricted to either dsDNA or, conversely, to its individual single strands are both pointless and unjustified.

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Recording policies in functional magnetic resonance imaging
Assume that the areas in a single-subject's brain that are involved in solving a task are supposed to be visualized with fMRI. The dynamics of the task solving process shall not matter (which areas are active first, which second?).

How, i.e. by which policy, are the data collected to give the final image?

I believe to have understood that data are collected per slices (of some millimeters thickness) and later postprocessed to give the final image.
For the sake of definiteness, let $T$ be the overall time it takes to complete the task (e.g. 10 seconds). Let $t$ be the time it takes to simultaneously take the BOLD data of one slice (e.g. 100 milliseconds). Let $N$ be the number of slices to be recorded (e.g. 20). Let $n$ be the minimal number of recordings of one slice that is necessary for statistical analysis ($n=?$). So there are $N n$ recordings of slices necessary which takes $N n t$ milliseconds, if only one slice could be recorded at once. If $T$ is too short, the experiment would have to be repeated $N n t/T$ times to get all of the required $N n$ slice recordings.
If $m$ slices could be recorded simultaneously, a single run of the experiment would suffice, when $m > N n t/T$.

In any case: In which order are the slices to be recorded chosen (in
  case they cannot be recorded all at once)?

Possible policies:

always from top to bottom (along the z-axis) in time $T$?
repeatedly from top to bottom in some time $T'=T/k < T$?
alternating between top-bottom and bottom-up in repeated experiments?
in a random order?
in an order informed by knowledge of the stages of the task (when different slices are primarly active at different times during the task)

Or is my picture of the recording process all too naive? Or is the question somehow meaningless (for reasons I do not see, but would like to learn about)?

@Remi.b I'm not a big fan of the question, but I strongly, strongly disagree that it belongs on Health.SE because 1) fMRI is used primarily as a research, not medical tool (it is not the same as "MRI" used for diagnostics), and 2) although this question oddly refers to "policies" which might imply healthcare, that isn't what it is asking at all.

@BryanKrause Ok, thanks for your light. I am retracting my close vote (and associated comment).

If I recall correctly, in BOLD fMRI an echo-planar imaging (EPI) sequence is typically used. In one example:

44 slices were acquired, every 3 seconds, 96 times in a row, leading
  to a total number of 4,224 images acquired in 4 minutes and 48
  seconds.

— https://www.imagilys.com/functional-MRI-fMRI/
You can read more about EPI here. I think you will find the zig-zag pattern in this link interesting. See also this link for a description of EPI.
fMRI is slow and has a low temporal resolution, because the hemodynamic repsonse of the blood is around 6 second long. This is perhaps a limiting factor for fMRI, which is why there is a limit to optimizing the sequences. However, one real impact of faster sequences is to capture head movement artifacts more accurately. Other sequences are used in anatomical MR imaging, such as FLAIR.


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What if we blend hydras to form a soup. will they still regenerate to form new individuals?
Hydras can regenerate if cut into pieces. But if we take a pound of alive hydras in a blender/grinder and blend/grind them to form a jelly like liquid made of hydras where we have finely blended them, then will this soup turn into millions of hydras or they will die and rot

depends some on if you're doing damage on a cellular level, which you probably are.

Based on this article, the answer is probably no. Quote (emphasis mine):

Small tissue pieces were excised from wild-type polyps of Hydra magnipapillata, allowed to regenerate, and the size-dependent characteristics of head regeneration were examined. The excised tissue piece was initially a square flat sheet. This piece gradually rounded up and, within 24 hr after excision, turned into a "spherical shell" which had a continuous ectodermal layer outside, a continuous endodermal layer inside, and an empty cavity at the center.
The smallest spherical shell that could be produced had a diameter of 0.2 mm and contained 270-300 epithelial cells. A tissue piece too small to form a spherical shell always disintegrated, presumably due to lack of an osmotic harrier between the tissue and the environment.

In short: any piece of hydra tissue with a diameter less than 0.2mm or that contains less than 270-300 whole epithelial (skin) cells is incapable of surviving and regenerating. It is highly unlikely that any hydras would survive being blended because the pieces would probably be too small or too damaged to be viable. Of course, if you had a chopping machine that cut hydras into large enough pieces without causing any significant cell damage, you could probably manage to create a large number of hydras in a very short time span. (I'm not sure why you would want to, though.)


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Do Alzheimer's patients have spaces in their brain with low interstitial space?
Lulu Xie et al write in their paper Sleep Drives Metabolite Clearance from the Adult Brain:

Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep.

Given that Alzheimer's patients have more β-amyloid in their brains, do they also have less interstitial space?

It's hard to judge whether interstitial space changes are due to beta amyloid accumulation or because the Alzheimer's brain has suffered such profound cell loss and neurodegeneration as a result.
The Nedergaard paper you quote is more about a daily cycle of increase/decrease in interstitial space related to the sleep/wake cycle [Ref 1]. Specifically, that during sleep, there is more space to flush out the brain including beta-amyloid.  One interesting hypothesis from that being that perhaps the accumulation of these aggregates is actually due to inefficient sleep -> inefficient flushing of plaques which go on to give symptoms.  So even if the interstitial space in what's left of the Alzheimer's brain remained the same as a healthy brain, the problem of beta amyloid clearance could still be present.  It remains to be seen if one could restore normal clearance whether degeneration could be slowed and symptoms abated.
[Ref. 1]: Paper from Nedergaard group


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Are porins on the inner or on the outer membrane of mitochondria?
I've looked at multiple resources and they are saying different things.

This is not my field, but The Transporter Classification Database would appear to be a reliable source and states that:

The best characterized members of the MPP family are the voltage-dependent anion-selective channel (VDAC) porins in the mitochondrial outer membrane.

Searching through the Protein Data Bank one can find a crystal structure for human voltage-dependent anion channel 1 and the associated paper also states that it is in the outer mitochondrial membrane, so you would imagine that they should know.


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A grey water bird with brown head

A greyish bird, with brown head and relatively long, pointy beak.
Size comparable to mallard.
Spotted in central Poland, on small, artificial pond, populated by mallards and Eurasian coots.
Photo has been taken today (late September).

I'd be grateful for any information that could be used to identify this bird.

It is a goosander

Based on the location and picture I believe this a Goosander (Mergus merganser) which is the European name, the North American name is the Common Merganser.
You can find more information about them here.

They undergo two main molts, breeding plumage in December and eclipse plumage in May. Here is a description of the eclipse molt by Bent, 1923:

In May the adult male goosander begins to assume its eclipse plumage.
  The adult male in August has the crown reddish brown, with a gray
  tinge; chin white, and the rest of the head and upper neck rich red
  brown.

By the looks of your photo, you either have 2 females during the breeding plumage phase (January - May) or either sex during the eclipse phase (June - December). It will depend on when the photo was taken.
Here is an image with a breeding plumage male (left) alongside some females:

References:
Bent, Arthur Cleveland. 1923. Smithsonian Institution United States National Museum Bulletin 126 (Part 1): 1-13. United States Government Printing Office

Thank you so much for the answer. It looks like a good match, and I've already heard about goosanders in the area - just haven't seen one. This year somone introduced fish, to keep the pond clean -  I guess it become a nice dinner plate.


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Why do house geckos take so long to react?

This is the Common house gecko found abundantly where I live.
I've been observing this for quite long and I used to ignore it after thinking on it for a short while. Today I decided to write this here on Biology SE.
So in my lawn there's this large wall on which there are usually around 3-4 geckos foraging for their favorite insects in night. Everytime I walk towards them some of them instantly go into their hiding spots (within 1-2 seconds of my arrival) with lightening speed. But most of them initially look cool and not actually bothered by my presence. Not only that -I can even wave at them; go closer towards them and nothing happens. But suddenly after all of my actions they also run towards their hidings as they were daydreaming. (Though not instantly)
Just curious-
Is there any real lag between their signal reception and processing?
Are there some other animals which show such behavioural responses?
(Maybe they are just kidding with me :P)

This is entirely behavioral and is quite widespread.
If they ran away everything something large passed by they would waste a lot of energy, many animals wait first to see if you are just moving through, and thus can be ignored, OR if you are going to hang around and thus are a potential threat (and in the case of camouflaged organisms have a much higher chance of spotting them).
It is seen in many animals gazelle are known for it for instance.  This paper on the behavior in other lizards should help with understanding the evolutionary pressures behind it.


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What is functional dissection?
Reading [1] I found the sentence:

Consistently, functional dissection of mouse and human wild-type and mutant RAS isogenic leukemia cells demonstrated induction of methotrexate resistance but also improved the response to vincristine in mutant RAS-expressing lymphoblasts.

I did not find a definition online yet. What is the meaning of functional dissection in this context?
[1]   K. Oshima et al., “Mutational landscape, clonal evolution patterns, and role of RAS mutations in relapsed acute lymphoblastic leukemia,” Proc Natl Acad Sci USA, vol. 113, no. 40, pp. 11306–11311, Oct. 2016.

That means that you dissecting the functions not the elements.

The term 'functional' in this context implies a type of analysis that is able to provide a mechanistic understanding.
The authors first describe their exploratory approach, by which they identified some genes and their mutations that are associated with patient relapse in acute lymphoblastic leukemia. Then they proceed to intervene in the system, by expressing mutated KRAS in mice. When they did that, they observed several hallmarks of relapse in those mice. Hence they can conclude that a mutation of this gene is involved in the mechanism that underlies relapse.
Thus the way these authors use the term 'functional analysis'/'functional dissection' is in contrast to a correlational approach.

The underlying assumption is that by isolating parts of the system and studying their properties and their effects we will be able to understand the physical world. This is a philosophical (metaphysical) thesis called reductionism, which is arguably the prevailing view in the natural sciences.
The first use of the term "functional dissection" I could find is in a 1971 paper on the immunological response of small molecules. Their goal in that paper was to dissociate (or dissect) the effects of small molecules, such as a bovine glucagon, on antibody specificity versus antibody production. They have found that different parts of this molecule were responsible for antigen specificity (all antibodies recognised the N-terminal) and cellular immunity (mostly the C-terminal of the molecule was associated with DNA synthesis).


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Focusing your attention on an area within your body, what effect does it make?
When I focus on tactile signals from a certain part of my body for a while (e.g. for one minute), this part of the body will usually become warmer. For example I can do that with a certain finger or with my palm, or with a certain spot on my forearm or on my leg, etc. Basically any part of the body.
From what I heard, when you focus on a spot within your body, the blood flow increases there. But what is the mechanism exactly? How does it happen? From what I found in neuroscience, sensory system only sends signals in one direction, from receptors to the brain. Attention is something happening within the cortex. What processes exactly take place when you focus on a certain body area? Is there a "response" signal from the brain to the area? How does it increase the blood flow?
My interest actually comes from my discovery that using my attention I can do surprising things within my body. I can relieve pain in most cases, it only takes 5-15 minutes of deep focusing. Once I successfully used this technique to relieve itching sensation from a minor skin inflammation on my leg, and after that the inflammation has gone away completely by the next morning. So I assume that focusing attention initiates certain processes in the body. I'm researching to find out what exactly these processes are.

Welcome to Biology.SE. Are you sure it is getting warmer? Did you rigorously measure it with a surface thermometer and comparing before and after focus? If not, then it is possible/likely that the question "why" is based on a false belief that the focus increase the temperature. Without an evidence for the claim, the question should be closed as based on a potentially false belief.

Hmmm ok I'll have to get a precision surface thermometer to make sure the temperature actually increases and not only my feeling of temperature.
Another my suggestion is that the blood flow increases because of deep relaxation of the muscles in the area.
If the temperature doesn't change though (which is still a subject to test), there is still a way to relieve pain by concentrating on the source of pain. How is that working at all? And does it only turn off the pain or also helps healing? Has there been any research on this subject?

You are all in the field of subjective experience here. If you are already convinced that concentrating on a wound helps reduce the uncomfortable feeling, then it probably will work for you (via the placebo effect). Most of the time people rather attempt to divert their mind from the pain to reduce the uncomfortable feeling. You might get better answers to your questions from a psychologist (see CognitiveScience.SE) than from a biologist.

Remi.b, psychologists focus on non-bodily aspects, I'd rather focus on the biology of the process here. Actually that's one of the main reasons I started studying neuroscience half a year ago.
So from your answers I would assume that your opinion on the subject is that nothing is happening in the body in response to the person's attention, right? Or at least nothing like this has been reliably observed/researched/proved.


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plant crossing for creating breeding population
I read some material about plant breeding. For a self-incompatible plant with high heterozygosity, it said that after selecting the plant population based on phenotype/desired trait, a cross was done among plant with the desired trait to create the breeding population. However, as far as I know, the breeding population was usually phenotypically selected for desirable traits. I'm not experienced in this field, could you please kindly explain to me why crossing is conducted for creating breeding population?
Thanks in advance

Here, self-incompatible here means that the plant has both anther and pistil, but need pollen of another plant for pollination.

A cross was done among plant with the desired trait to create the breeding population. The breeding population was usually phenotypically selected for desirable traits.
That phrase is confused. To phenotypically select from a breeding population, you first have to generate the breeding population, which requires an initial cross of desired plants. The generations are generally labelled as F1 F2 F3 and checked for statistics. They can back-cross the mother plant onto herself. The selection refines itself as the number of crosses of the most desirable plants increases in generations.
Hybrid populations are often stronger and have a wider gene base, so if you want big fruit for a tree, you can cross an asian one with a european one, it might be more resistant and vigorous, gain stronger roots, better low N performance, and better structre from one plant, which is then mixed with the desirable traits for example of yield or mould resistance. The wider the gene base, the more potential diversity of individuals can be chosen which also contain the alleles from the desired traits, and the selections start with more options. The goal is to maximize the desired pheno's.
http://www.nature.com/nature/journal/v537/n7622/full/nature19433.html?foxtrotcallback=true

What do you call a gene base? Note that definitely not any cross result in hybrid vigour. Some causes hybrid depression.

And in OP it was already said that the initial population before breeding had a high level of heterozygosity?


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Why are the no bioluminescent plants?
There are bioluminescent creatures and some fungi too. As far as I can see there are no bioluminescent plants. Why is this?
I imagine it would make a good attraction for night pollinators, or even for carnivorous plants so there must be some reason why this hasn't evolved somewhere on our planet. My guess would be that it takes too much energy for the chemical reaction involved and it's not worth the pay out but that's just a guess.

you can perhaps buy some here: https://www.kickstarter.com/projects/antonyevans/glowing-plants-natural-lighting-with-no-electricit/description

Overall, bioluminescence has arisen over forty times in evolutionary history.[25]
There are bioluminescent funghi and bacteria.
Phosphorus is the 2nd most important nutrient for plants, so perhaps it's too expensive to use for bioluminescence, most plants don't live in phosphorus rich environments.
Bioluminescence also uses quite a lot of nitrogen, and most plants can't fix nitrogen.
there are 71 species of glowing funghi, perhaps to distribute spores, so plants with spores could have had the same strategy.
If two species of plants used light for night time insects, it can confuse the insects if they are plant specific, light is more confusing than scents.
A tree can potentially produce a lot of light, and it would turn into a forest lamp-post attracting lots of insects. It could be ecologically hazardous. perhaps a carnivorous plant could benefit from it.
It seems like plants and algea easily could have evolved bioluminscence easily, if bacteria and protists have, and that it wasn't profitable to the plants.
A crowdfunded project to make some failed because it was too difficult to put 6 animal genes into the plant.
land animals use light as an indicator of fitness, and plants don't need to indicate their individual fitness to others, and most bioluminescent animals have the option to switch things on and off very effectively, which difficult for trees.

the same reason there is no bioluminescent mammals or birds, the benefits are too small to make up for the cost in calories, in plants it might even have a bigger cost because it might interfere with some parts of photosynthesis.


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How do cells become differentiated using epigenetics despite having the same genome?
How is epigenetics used in the differentiation of cells and is this the only thing that is used? I've seen that transcription factors play a role but are these simply proteins that initially write the epigenetic code or something different altogether?
I've written this explanation of how I understand it currently. Please tell me if this is right or wrong.
How do our cells become specialised if they have the same genome? The answer lies in the fact that gametes have most of their epigenetic information taken off at fertilisation, (apart from small sections like at IAP retrotransposons) so it’s like a clean slate. The zygote cells divide to form many identical cells that have the capacity to become any cell in the body.
Proteins in the egg then bind to certain genes and regulate their expression by adding epigenetic markers like methyl groups and histone modifications. The proteins created from these genes then go to control the regulation of other genes and so on, until all the cells have different epigenetic markers put on them that mean they produce different proteins in different quantities to serve different functions in the body.

Have you had a look at wikpedia > Cellular differentiation?

@Remi.b Yes I have and that's how how I wrote that explanation but I don't know if it's correct


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Why do neurons lose the potential to regenerate and reproduce in adult animals?
I have read in several books that neurons in the central nervous system lose the power to regenerate after some developmental stage but why do they? Can we artificially induce regeneration?

There's roadblocks to stop nerve regeneration, perhaps the organization of the brain means that making new brain cells would re-wire you and make you confused. Most vertebrates that have a damaged spine or brain would be dead anyway, given the force required to damage a fish or a lizard spine, it's not that useful for vertebrates, it's in the most protected, tough, defended zone of the animal, so structurally the animal wouldnt have the time to heal for food and drink and defense while the nerves also mend themselves. afterwards the knee and hip nerves might have swapped round left and right.

Neurons do not regenerate! If we could regenerate neurons, we would be able to help paralyzed patients regain their movement and help people with dementia and Alzheimers regain their memory and cognition. Neurons can regenerate axons if the cell body (soma) is intact, but otherwise, they cannot. There is more info on this site, and a few things on wikipedia as well. https://askabiologist.asu.edu/regeneration Hope this helps!

To answer the first part of your question: In order to regenerate, the neurons need to divide. In order to do that they need to round up so that they can form a mitotic spindle that sorts the chromosomes and makes sure that each daughter cell gets exactly one copy of the genome. For most animal cells this genome sorting only works in rounded cells, which is why neurons need to round up before they divide.
However for a Neuron, rounding up would mean that the neuron needs to retract its axon as well as all its dendrites. To do so is physically impossible for most neurons simply because of the length and complexity of the axon and dendrites (the axons of human motor neurons can be more than a meter long). See also the image below.

Even if retracting the axon and dendrite network was possible, this would mean that the neuron would lose its function completely because it would lose all connections to other neurons and with them all information it has stored. Thus, from an evolutionary standpoint it does not make sense to regenerate a neuron once it has matured and started to form connections with other neurons.
That being said, despite the fact that matured neurons cannot divide any more, our brain and our nervous system retain a lot of regenerative potential:

Provided that there is little scarring at the wound, a nerve fiber (consisting mainly of axons of neurons) can regrow because the neurons don't necessarily die when their axon is cut and they can regrow a new axon. The main difficulty for regeneration in this case is for the axon to find the path to its destination. Therefore it is important that there is minimal scar tissue (glial scar) because scar tissue prevents regrowing axons from finding their path.
The brain retains some neural progenitor (stem) cells that are able to differentiate into new neurons even at old age (but not as many stem cells as other tissue).
When parts of the brain are damaged, other regions can often take over that functionality (for example by by rewiring their axons and dendrites) a process called neuroplasticity. For example, people can often re-learn to speak after a stroke.

As to the second question: Using stem cell technology it is possible to grow fresh neurons in cell culture. In principle, these neurons (or rather their progenitor cells that mature into neurons) can be implanted in order to regenerate nervous tissue in the central nervous system. However, this cannot solve the problem that once the neurons are dead, even a new neuron that replaces the dead one cannot recreate all the connections that the old one had.
Replacing neurons is like replacing the hard disk of a computer. All information is lost. Therefore, current research on the therapy of spinal chord injury focuses on the prevention of scarring in order to help the existing neurons to regrow the axons and reconnect the body with the brain.
Edit: added references.


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Where in the digestive tract are melatonin pills dissolved? Same question for gelatin capsules
I want to do a blind controlled experiment on myself to learn whether melatonin pills have any effects on me. I bought some empty gelatin capsules. I am going to fill some of them with rice and put pieces of melatonin pill in others.

Melatonin pills instruction says I should take it 30-40 minutes before going to bed. Now I wonder if the timing is the same when stuck inside gelatin capsules. Also is it possible that melatonin pills stuck inside capsules will get to a later stage of the digestive tract than they should and thus will not work.

Unless specially coated or formulated, most pills break apart in the stomach. Note: "break apart", not necessarily absorbed.
Take a gelatin capsule with rice or melatonin and immerse it in warm water. Massage gently with your fingers. Watch the clock.
When the rice is fully exposed, or the melatonin starts to break apart and dissolve, add that amount of time to the instructions. Be sure to take it with at least 4 ounces of water.

Doesn't acid in the stomach help the capsule break apart faster?


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Is there any evolutionary significance of downward facing nostrils in human beings?
The nostrils in apes and monkeys are almost at the front, but in humans nostrils (external nares) face downwards. Also a lot of non-primate mammals like goats have nostrils at the front.
Is it the increased cranial capacity in humans which pushed the nostrils downwards?
Is having a pair of downward facing nostrils, an advanced feature? If yes, then why?

I think you're right, there's a lot of articles here: https://www.google.fr/search?q=evolution+of+human+nose&oq=evolution+of+human+nose&aqs=chrome..69i57j69i60.3832j0j7&sourceid=chrome&ie=UTF-8 Some people do have quite upturned nostrils, it seems that dust, aridity, cold, long distance running, checking food, swimming, diving, and talking to people who have caught a cold are good reasons to have discreet nostrils and longer nares.


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Plasticity between excitatory and inhibitory neurons?
All that I've learned about synaptic plasticity only concern the synapses between excitatory neurons. For example, all pyramidal neurons (excitatory) in the cortex have plastic synapses between them, but as far as I know there are no plastic synapses between pyramidal neurons and their inhibitory interneurons.
So I am curious, are there any plastic synapses between inhibitory and excitatory neurons?

Various forms of plasticity has been reported for inhibitory-excitatory synapses as well. See below figure from [Woodlin et al. 2003].

Holmgren CD, Zilberter Y (2001) Coincident spiking activity induces long-term changes in inhibition of neocortical pyramidal cells. J Neurosci 21: 8270–7
Woodin MA, Ganguly K, Poo MM (2003) Coincident pre- and postsynaptic activity modifies GABAergic synapses by postsynaptic changes in Cl- transporter activity. Neuron 39: 807–20


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Are there any creatures that will eat their own limbs or body parts to survive?
I'm curious if there are any insects, bacteria or perhaps even large animals who would bite off their own limbs or body pieces to chew on in the desperate times of hunger.

What you're describing is actually a well-documented occurrence in individual cells and single-celled organisms. The phenomenon is called autophagy, and Wikipedia has a page about it here. The basic gist is that when cellular components stop functioning or need to be removed for some other reason, the cell essentially digests those components and reuses their parts to make something else. Cells can also consume themselves to prevent the spread of disease or in the case of extreme starvation, when the extra energy might be needed to keep the organism alive.
Self-cannibalism on the macro scale (larger than single cells) is significantly rarer, but it can and does happen. For example, leopard geckos (and maybe some other lizard species? I'm not sure) regularly eat their own shed skin pieces to conserve energy and nutrients. Sea squirts (a type of marine invertebrates) literally digest their own brains as a part of their life cycle, and apparently, some crickets have been known to consume their own wings. Generally, though, unless the limb in question is already damaged and/or rendered unusable, it would be a waste of energy for its owner to consume it, as the energy spent repairing the damage would likely outweigh the energy gained from its consumption in the first place. That is why it's a relatively rare behavior in multicellular organisms.


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Why do animals use glycogen for their polysaccharide storage whereas plants use starch?
The polysaccharide storage form of glucose in animals is glycogen, whereas in plants it is starch. Both of these are polymers of α-glucose with α-l,4 glycosidic linkages and α-l,6 glycosidic branch points (Wikipedia article on polysaccharides). The only difference that most sources mention (e.g. Berg et al.) is that glycogen contains more branches than starch.
It is not clear to me from this information what effect the different branching would have on the structures of the polysaccharides, nor why one rather than the other would be preferred in animals and plants.

It is surprisingly difficult to find a proper answer to this question on the internet — my own answer was only found after consulting specialized reviews. I therefore think this is an important question and have therefore edited it, tightening up the wording, avoiding the implication that polysaccharides are the only storage form, and spelling out the chemistry. If the original poster is still active on the list I hope he will accept these changes.

What about fungi? Do they even have storage polysaccharides and if so, what kind?

Summary
The key difference between glycogen and amylopectin (the main constituent of starch) is not the number of α l,6-glycosidic branches, but their arrangement.
In glycogen branches are successively subdivided, producing a relatively small globular structure that is unable to grow further. It is soluble in an aqueous environment and, with its numerous exposed ends, can be metabolized rapidly — appropriate for animal cells in which energy reserves must be mobilized in response to immediate demands, e.g. for muscle contraction.
In amylopectin there is a long central polysaccharide chain from which branches of limited size extend at intervals. This produces much larger semi-crystalline particles (starch grains), a form especially suited to long-term bulk storage in seeds and tubers.
The Chemistry

This is the common feature of glycogen and the amylopectin portion of starch. (The amylose portion is unbranched.) In glycogen there is approx. one branch point per 10 glucose units, whereas in amylopectin the figure is 1 per 24–30 (source: Wikipedia).
The Topography
The contrasting branching topography of the two polysaccharides, mentioned above,  is illustrated diagrammatically below:

This is a two-dimensional representation. In three dimensions the glycogen spreads out in all directions from a central point — actually the primer enzyme, glycogenin. In three-dimensions the amylopectin strands mainly lay side by side.
The Macro-structure
The illustration below, modified from Bell et al., shows the different shapes and sizes of the macromolecular structures. It should be mentioned that semi-crystalline nature of amylopectin is aided by the helical conformation of the chains.

Rather than providing a précis of the review of Bell et al. (Journal of Experimental Botany, Vol. 62, pp. 1775–1801, 2011) I shall quote from them directly (omitting their citations).
As regards glycogen they write:

Each chain, with the exception of the outer unbranched chains,
  supports two branches. This branching pattern allows for spherical
  growth of the particle generating tiers (a tier corresponds to the
  spherical space separating two consecutive branches from all chains
  located at similar distance from the center of the particle). This
  type of growth leads to an increase in the density of chains in each
  tier leading to a progressively more crowded structure towards the
  periphery.
Mathematical modelling predicts a maximal value for the particle size
  above which further growth is impossible as there would not be
  sufficient space for interaction of the chains with the catalytic
  sites of glycogen metabolism enzymes. This generates a particle
  consisting of 12 tiers corresponding to a 42 nm maximal diameter
  including 55,000 glucose residues. 36% of this total number rests in
  the outer (unbranched) shell and is thus readily accessible to
  glycogen catabolism without debranching. In
  vivo, glycogen particles are thus present in the form of these limit
  size granules (macroglycogen) and also smaller granules representing
  intermediate states of glycogen biosynthesis and degradation
  (proglycogen). Glycogen particles are entirely hydrosoluble and,
  therefore, define a state where the glucose is rendered less active
  osmotically yet readily accessible to rapid mobilization through the
  enzymes of glycogen catabolism as if it were in the soluble phase.

Regarding amylopectin they write:

Amylopectin defines one of, if not the largest, biological polymer
  known and contains from 105–106 glucose residues. There is no
  theoretical upper limit to the size reached by individual amylopectin
  molecules. This is not due to the slightly lesser degree of overall
  branching of the molecule when compared to glycogen. Rather it is due
  to the way the branches distribute within the structure. The branches
  are concentrated in sections of the amylopectin molecule leading to
  clusters of chains that allow for indefinite growth of the polysaccharide.
  Another major feature of the amylopectin cluster structure
  consists of the dense packing of chains generated at the root of the
  clusters where the density of branches locally reaches or exceeds that
  of glycogen. This dense packing of branches generates tightly packed
  glucan chains that are close enough to align and form parallel double
  helical structures. The helices within a single cluster and
  neighbouring clusters align and form sections of crystalline
  structures separated by sections of amorphous material (containing the
  branches) thereby generating the semi-crystalline nature of
  amylopectin and of the ensuing starch granule. Indeed the crystallized
  chains become insoluble and typically collapse into a macrogranular
  solid. This osmotically inert starch granule allows for the storage of
  unlimited amounts of glucose that become metabolically unavailable.
  Indeed the enzymes of starch synthesis and mobilization are unable to
  interact directly with the solid structure with the noticeable
  exception of granule-bound starch synthase the sole enzyme required
  for amylose synthesis.

Coda
The paucity of information on plant starch metabolism would seem to reflect  a combination  of their being less is known about plant biochemistry, and less general interest because of a general focus on medical and animal biochemistry. Although an animal biochemist myself (and, thus, previously ignorant of the information in this answer) I feel that it is time to redress this imbalance.

Your labels for the alpha 1>4 and alpha 1>6 linkages in the first diagram are the wrong way around.

well glycogen can be broken down into sugars a lot faster, many more branches means many more ends to clip individual sugars off of, that's how you mobilize the sugar for use, it is clipped of the end of a strand. With many more branches glycogen can mobilize more sugar more quickly.  This is not important in plants but in animals that need to be able mobilize lots of energy in a hurry, glycogen works better. Additionally glycogen is a smaller molecule and easier to make, not surprising since glycogen is the ancestral condition for plants and animals.
As for why plants switched to starch, or more precisely gained it through symbiosis, starches folded crystalline structure makes it a higher density energy store but also slows its release, it is however more stable, which is important if you are going to be storing it for a long time. Animals would likely switch to starch too if they did not have to break it down to digest it, just because they take in so much of it. But since they have to break it down there is no real incentive the build it back into starch when glycogen has some advantages and quite frankly since the pathway is already there and evolution has a lot of "eh good enough".

Any references for either of the claims?

Added, and good thing to my old notes were wrong about ancestral condition.

Some interesting ideas, but seems speculative. (1) It's true that glycogen can generally be mobilized faster than starch, but I'm not sure it's due to higher branching -- I would rather think it's due to the soluble nature of glycogen granules vs. the crystalline form of starch, which you mention later.  (2) What exactly do you mean by glycogen being "easier to make"? (3)  You seem to contradict yourself in saying that for animals "glycogen works better", and then that animals "would switch to starch too" if they could?

Sorry, (1) I meant  evolutionarily speaking animals probably would just use starch as it is if they did not have to take it apart then rebuild it to get it inside, since the advantage of glycogen is nominal. (2) Glucose is a simpler molecule with a shorter synthesis pathway. One step in starch synthesis involves producing amylopectin a molecule very similar to glucose. (1)the branching and the solubility are related and both definitely contribute, but starch is also a more complex molecules which requires multiple enzymes and must be unwound to be broken down into glucose.

There would seem no reason that animals could not have evolved to synthesize starch as a variety of bacteria do just that and the chemical bonds in starch and glycogen are identical. There is every reason that they did not evolve to synthesise starch, given its unsuitability for rapid release. Energy storage in animals is divided into two functionally distinct molecules: a limited amount of glycogen for rapid release and provision of glucose, and a larger supply of fat for slower release and which cannot provide glucose (except from the glycerol component).

@David  please read the full exchange you are basically restating what I already said. The reason  they never evolved it is they gain nothing by rebuilding glucose into starch instead of glycogen, the bonds are identical but the finished molecule and there properties are not.

I think you may not quite appreciate how SE is supposed to work. What matters is the questions and the answers. The comments are primarily to allow users to ask for clarification or query the content of these, after which, if appropriate, the question or answer can be modified, thus improving it. So the content of your exchange with Roland is not what is important; it is the fact that your answer still contains the unsupportable speculation “Animals would likely switch to starch too if they had the ability totsynthesise it.” Your answer would be improved by deleting this.

@david,  I thought you were referring to my comments, that's a good catch I will fix that.

What is your basis for saying glycogen is a "simpler molecule" and "easier to make"? Also, your mention of storage of starch in plants "for a long time" is fine for seeds and tubers, but more problematical for starch in leaves, which is apparently formed during the day and broken down at night.

@David the fact it is a simpler molecules and easier to make. I included links to justify each, glycogen can be large but  starch can be much larger molecule glycogen is self limiting in size due to its branching pattern. its production pathway is also shorter. I will clear that up a bit. for the second part some starch is broken down at night, not all, plants have slower metabolisms which makes stability more of an issue, now there is a bit of chicken and egg quality to this.

I don't see that one molecule is simpler than the other. Both include the same chemical bonds. Starch granules are larger on average, but size is not complexity. The differences I can see are (1) initiation — it is known how this works for glycogen with glycogenin, is it known how this operates in starch? Is the plastid membrane involved? (2) control of topology of branching — is anything known about either process? (3) packaging of starch in seeds etc. — is there some surface layer? Is this the same in leaf starch? Interesting questions, but I don't think they have simple or easy answers.

by looking at mutant plants we can tell a lot of the sugar produced is never converted into starch in the first place. this source from my answer actually answers a lot of your questions, https://www.ethz.ch/content/dam/ethz/special-interest/biol/plant-sciences/plantbiochemistry-dam/pdf_Dokumente/Publi_nr_37.pdf