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Why do simulations of dichromatic color vision portray medium wavelengths as yellow rather than green?
Please take the time to read & answer this at your own convenient pace.
Is this even the right way to put this?
Do you think this post better belongs in the Physics or Philosophy forums?
This must be part of the old philosophical question of whether you see the same colors as I do.
This is a simple question really, but the description may get a bit technical if your not familiar with the basics. If you find this complicated to read then I can write it more basically if you desire.
It’s important to bear in mind that we shouldn’t equate or compare other animals’ senses & perceptions with our own, such as ‘modified’, ‘enhanced’, ‘dehanced’, ‘reduced’ or ‘increased’ human senses.
We can form educated estimations about how the perception of other animals is through study of their nervous systems, brain & sense organ anatomies & behavioral tests, but have little way of proving how they actually experience things.
The same applies to other humans, only that we have more ways of proving how other humans actually experience things because we have language, but even that’s still very subjective.
It’s a basic fact that unlike shape, dimension & location, sensations are not matter & energy itself, but our brain & mind’s representation of them. For example, how do we know for sure whether other animals even perceive gradients of light as shades of black & white? It could turn out to be something totally different, even uncomparable or unimaginable for us.
This is common sense when mentioned, but many people forget or aren’t aware of this basic fact to keep in mind.
Nevertheless, what I’m wondering is whether the short-medium wavelength dichromats of most mammals & some humans & New World Monkeys, which have two kinds of opsins sensitive to short & medium visible EM wavelengths in constrast to having the extra opsin sensitive to long visible EM wavelength for most humans & anthropoid primates, actually see green or yellow as their primary color representating the middle EM wavelength?
Simulations of dichromatic color vision usually portray them as seeing the primary colors blue & yellow, with the rest being combinations of those primary colors & shades of black, grey & white.
In fact I’ve never come across a dichromatic simulation using green to portray the perception of the middle wavelength color for them.
Its always yellow.
Could it be because we’re not exactly sure whether short-medium dichromats actually see either green or yellow as their primary color for middle wavelength peak, if they even do see those colors for that matter?
However, yellow is not a primary color. It may be in art & design, but it’s not in biology & physics.
Yellow is the extreme end of red & green, & a mixture of red & green.
In biology & physics, red, green & blue are the primary colors.
So what I’m wondering is why do simulations of dichromatic color vision portray the perception of the medium visible EM wavelengths in gradients of yellow rather than green, the actual primary color for middle visible EM wavelength, & how can we know or give the best answer to what color dichromats see as their perception of middle wavelength of Visible EM?
So which color is it? Yellow or green?
& is it the same for all short-medium wavelength dichromats?
How would we know? If we can’t, then what is the best evidence & way to give the best educated guess?
Like why is the dichromatic simulation of the frog & parrots below using yellow & blue to represent their primary colors? Wouldn’t using blue & green be more honest to biology & physics? Isn’t yellow not a primary color but the extreme end of & mixture of both red & green?

which kind of dichromates are you talking about, there are more than one.

Opponent color processing.
https://en.wikipedia.org/wiki/Opponent_process
Studies have shown blue and yellow are opponent colors, as are red and green. We process the colors in opposition, as in perceiving one requires perceiving less of its opponent, equal amounts of both (minus other colors) yields no color in your final visual perception. If you cannot differentiate red and green, than the only two colors you can differentiate reliably are yellow and blue. As a side note this is also why in image processing programs these colors are on paired sliders, it is the simplest way to manipulate color images.
The most common forms of color blindness in humans, and the one all non-primate mammals have prevents them from differentiating red and green.
If you cannot differentiate red and green, and if I show you blue and yellow, you see no color, if I show you red and green you see yellow, becasue your blue cone is not being activated.
The image below is our opponent pairs in our vision.

I just wanted to ask what you mean when you say ‘no color’? Do you actually mean no color at all, or do you specifically mean white, grey or black?

no color would be white, grey, or black, those contain no color at all. Greyscale a colorless scale.


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denovo 2Gb whole genome sequencing on a small sequencer
What are the limitations of using Illumina's smaller sequencers (e.g., iSeq100, miniSeq) to do de novo whole genome sequencing on an organism with a larger genome (~2Gb)?
Naively, it seems even if I am only able to do 5Mb worth of sequencing per 24 hour run on these sequencers, after about two years of running the thing continuously, I should be able to have enough reads to be able to assemble a de novo genome sequence of a larger eukaryote (downstream bioinformatics concerns aside). Yet clearly the sequencers are never marketed like this and I'm struggling to understand why.
I am interested in GWAS on non-model vertebrates if that matters. That time frame doesn't seem crazy, as some field experiments take several years before something is publishable.

Yet clearly the sequencers are never marketed like this and I'm
  struggling to understand why.

You don't see why two years of instrument reagent costs for a single project might be considered prohibitive?

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Energy coupling between two spontaneous reactions?

This diagram describes energy coupling between a nonspontaneous reaction (the formation of glutamine from glutamic acid and ammonia) and a spontaneous reaction (the hydrolysis of ATP). I can see that if you add reaction 1 ($\ce{Glu + NH3->Glutamine}$) and reaction 2 (ATP hydrolysis), then the overall ∆G will be negative, and this reaction will be spontaneous.
My question is this: why can’t you add the reverse of reaction 1, which would on its own be spontaneous, to reaction 2? Would that not make an overall ∆G that is even more negative (more spontaneous)? This would be even more favorable than what we got from the energy coupling shown in the diagram. Yet it seems that energy coupling can produce the reaction presented in the diagram. How does the universe know to add the nonspontaneous reaction to the spontaneous reaction rather than the spontaneous reaction to another spontaneous reaction? It seems to me that the latter would be more probable.

Hi lightweaver. Is it you who down voted my answer below? If so, I would be interested to know why. Thank you.

@TheQuark It wasn’t me, sorry.

Points to bear in mind

That the biological coupling of an energetically favourable and unfavourable reaction (I would avoid using the term spontaneous†) is done through a composite reaction involving all the components of the two separate reactions. The reactants and products are the same as in the sum of the separate reactions — so it is valid to calculate the overall free energy change from the separate reactions — but we are talking about a different reaction or serious of reactions that occur on the enzyme. For example in the glutamate synthetase reaction that you mention there are the two reactions shown below. Gamma-glutamyl phosphate can be considered as an activated intermediate to which the free energy of hydrolysis of ATP has been transferred, rather than dissipated in heat, as would occur in the isolated reaction with inorganic phosphate as the product.

Such coupled reactions are no different from non-coupleld thermodynamically favourable reactions in a cell in that they require an enzyme to catalyse them. They do not proceed spontaneously† because there is an activation energy barrier.  If you regard this as “forcing” a reaction, then the answer to the question you pose in your comment to @VonBeche is ‘yes’. However I would describe it as an enzyme having evolved to ‘permit’ or ‘facilitate’ a reaction. It does this by providing binding sites for the substrates and (often) a different reaction pathway that involves a lower activation energy.

So why no reaction Gln + ATP ➞ Glu + NH3 + ADP + Pi ?
This can be regarded in two ways.
(1) Why hasn’t an enzyme evolved to do this sort of thing?
Either there is no selective pressure on an organism for an unneccesary enzyme to evolve, or (in this case) if the organism needs an enzyme to deaminate glutamine one evolves, but this enzyme (glutaminase) doesn’t need to involve ATP as the reaction is already thermodynamically favourable.
(2) Why doesn’t the glutamate synthetase enzyme catalyse this reaction
From your comment, this seems to be your concern. There are three binding sites on the enzyme, one for glutamate, one for ATP and one for ammonia; and I presume you are thinking why can’t glutamine bind to the glutamate site (after all it leaves from there) and react with ATP to form γ-glutamyl phosphate. The answer to this is the chemistry of the reactions shown above. The mechanism of the glutamate synthetase reaction is complex, but at the simplest level the first stage is the nucleophilic attack of the negative acid oxygen (yellow) of glutamate on the γ-phosphate of ATP:

In glutamine there is an amino group instead of the negative oxygen, so the reaction will not occur.
Furthermore, you should be aware that the enzyme is an active participant in the reaction, and the various substrates and products are oriented specifically in relation to residues at the active site of the enzyme to allow the reaction to proceed. To give a flavour of this I reproduce a portion of the summary of a paper by Liaw and Eisenberg on the mechanism of action of glutamine synthetase. I don’t expect you (or anyone else) to digest this — it merely serves to illustrate that enzymes are highly sophisticated machines in which many components participate in producing a specific product.

I still don’t understand how an enzyme can specifically couple two reactions in those fixed directions—the nonspontaneous with the spontaneous ATP hydrolysis. What is it about the enzyme that doesn’t couple the spontaneous reaction with the ATP hydrolysis? Enzymes can recognize both the reactants of a reaction and the products, so what gives it their specificity to couple the formation of γ-glutamyl phosphate from glutamate with the conversion of ATP to ADP, rather than the formation of glutamate from γ-glutamyl phosphate with the conversion of ATP to ADP?

@lightweaver — I've now modified my answer to try to deal with the question you ask in your comment. I didn't include a 3D model of the active site as the answer is already rather long, but I can add one if it will help.

Interesting. I’ve learnt that enzymes can always catalyze reactions in both directions. Sucrase can break down sucrose into glucose and fructose or it can build sucrose from those two. It is a catalyst, after all, and catalysts usually speed up both forward and reverse reactions so as to not alter the equilibrium position of the reaction. Is my conception wrong, then? Your answer seems to indicate that enzymes catalyze only the forward reaction.

@lightweaver  Not at all. Enzymes do catalyse reactions in both directions. But what you are proposing is not the reverse reaction. The reverse reaction is Gln + ADP + Pi ➞ Glu + ATP + NH3, whereas you are asking why Gln + ATP ➞ Glu + NH3 + ADP + Pi does not occur. That is a quite different reaction! (And of course the reason that the true reverse reaction does not occur is thermodynamics — the coupling will ensure that the reverse reaction has a positive deltaG.)

Ahh. I think that was my main source of confusion. Thanks for clearing it up!

Keep in mind that there needs to be an enzyme present to "couple" two reactions. You can imagine it like the energy from the ATP hydrolysis pushing the enzyme to a high energy state, and from that high energy state the enzyme can push the secondary reaction against the equilibrium.
You could do this, and there might even be examples (maybe for some reactions that are just barely exothermic), it's just that enzymes coupling two spontaneous reactions did not evolve that often as there's not much pressure to do that. A spontaneous reaction could just be sped up by a single enzyme, no need to build a big coupling enzyme for that. Coupling this to ATP hydrolysis would just lead to useless energy consumption and extinction.

So it is the enzyme that forces a reaction to occur the way it does?

There is just no point to consider the reverse of reaction 1 if the goal is to synthesize glutamine. The coupling with reaction 2 is just that: to make favourable the synthesis of glutamine from glutamate and ammonia by "encapsulating" it in an overall favourable reaction.
Now, theoretically, nothing prevents in principle that two spontaneous reactions be used concurrently to make spontaneous a 3rd reaction that would require more free energy than each could provide. In "practice" it is probably evolutionary (and mechanistically) easier to obtain a similar result by using a mechanism in two steps (two successive coupled reactions) and by passing through an intermediate (provided such an intermediate can be formed).
A case where two ATP molecules are hydrolysed simultaneously has recently been shown for the dimeric human alcool dehydrogenase enzyme (ADH1A):
Energy transfer along Müller cell intermediate filaments isolated from porcine retina: I. Excitons produced by ADH1A dimers upon simultaneous hydrolysis of two ATP molecules, Igor Khmelinskii  and Vladimir I Makarov, Spectrochim Acta A Mol Biomol Spectrosc. 2021 Apr 5;250:119361.

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When is Water Produced During Photosynthesis?
The formula for photosynthesis is: $$6CO_2+12H_2O \rightarrow C_6H_{12}O_6+6O_2+6H_2O$$
I can count the carbons, the waters on the reactant side, the oxygens, and the glucose, but I cannot seem to locate where in either light or dark reaction 6 water molecules were produced again. Where and when were they produced?

why can't you just reduce $6H_2O$ on both sides? Do you have source of that equation?

@aandreev Googling photosynthesis formula "12h2o" gives multiple sources quoting the "12h2o" version. While it may not be correct, it is at least widely spread.

oh i love when biologists do physics/math

@aandreev  You can't think of this reaction as a math formula, the water on the right is actually produced by the reaction, it is not left over. While green plants use $H_{2}O$, some bacteria use $H_2S$ instead and they also produce water on the right. Also, this shows the net reaction which has many, many intermediate steps. The basic reaction is $CO_2+2H_2O \rightarrow (CH_{2}O)+O_2+H_2O$. However, to produce glucose ($C_6H_{12}O_6$), you need 12 water molecules and 6 of carbon dioxide. I love it when physicists try to do biology.

I realize that several steps are folded into one equation. And that is what the answer should contain, chemical equation where water appears as a product, or those where water is taken from environment.

Some of the water that's split is regenerated when the hydroxyl radicals (reactive oxygen species) are converted to hydrogen peroxide, water, etc. by superoxide dismutases and antioxidative mechanisms in the chloroplast (peroxisomes/catalases, etc. take care of this). There's also some evidence that the presence of mannitol, ascorbate and glutathione protect against ROS produced in chloroplasts as well. So you input water, and in an effort to avoid oxidative damage, you do get some water generated. However, the balanced equation doesn't reflect this because it's not an actual product of photosynthesis.
About ROS and protective elements
Extra Reading on ROS in photosynthetic systems
I think that's a very obscure fact, and despite the reality of things, it's actually difficult to query the literature. Good question.

So the water produced isn’t actually part of photosynthesis? Then wouldn’t the actual equation for photosynthesis be $6CO_2+12H_2O \rightarrow C_6H_{12}O_6+6O_2$? (Not balanced, but it reflects the reality of it, doesn’t it?)

In addition, when 18 ATP are hydrolyzed, should 18 water molecules also be included in the equation on the reactants side?

So you hydrolyzed 18 ATP, and if you look at the calvin cycle, for each CO2 that enters the cycle, you use up 2 ATP in the formation of G3P and 1 ATP in the regeneration of rubisco. So 18/3 = 6, and that would coincide with the entry of 6 CO2 into the cycle, or the normal photosynthesis equation. Someone correct me if I'm wrong!
As for convention, we'd say that yes 12 water molecules went into forming sugar and oxygen in reality, but had we not noted the regeneration of water somewhere in the formula, we'd have to assume the buildup of reactive oxygen species!

Short Answer
The short answer is the the six water molecules on the left-hand side come from CO2, as a by-product of reduction. That is, carbon dioxide may (formally) be though of as the source of the oxygen atoms in the six RHS water molecules (with the protons coming from 'the environment') 1†.
In photosynthesis, only half of the oxygen atoms of CO2 are lost to reduction.
The balanced equation given by the OP (Eqn 1 below) acknowledges this, and envisages that the other half remain as part of the synthesized hexose.
In photosynthesis, reduction of carbon dioxide is incomplete. If we reduce CO2 all the way to methane (an 8-electron reduction) both oxygen atoms are lost, and (in the simplest case) end up as water.
By inclusion of 12 water molecules on the left hand side, the balanced equation also acknowledges that the 12 reducing equivalents (24 electrons) required to make glucose from 6 CO2 all come from water and give rise to 6 dioxygen molecules (that is, oxygen is 'split').
In short, the six waters on the RHS result from the reduction of carbon dioxide, whereas the twelve LHS waters provide the necessary 12 reducing equivalents.
We need to add here that Eqn (1) applies to green-plant and cyanobacterial photosynthesis: not all photosynthetic organisms use water as electron donor, or produce O2 as a by-product.
Equations of Photosynthesis
The equation given by the OP (Eqn 1) is the overall balanced equation for green-plant and cyanobacterial photosynthesis (see Abeles, Frey & Jencks, 1992, p 635, for example) 2†:
$$\ce{6 CO2 + 12 H2O -> C6H12O6 + 6O2 + 6H2O \tag{1}}$$
We may summarize as follows:

12 reducing equivalents (24 electrons) are required to reduce 6 carbon dioxides to 1 glucose. These are supplied by water.
Water is the source of the oxygen released in green plant photosynthesis (not CO2)
In the reduction of CO2, six carbon-carbon and six carbon-hydrogen bonds are 'made' (thus accounting for the requirement of 12 reducing equivalents).
The reduction of 6 CO2 produces six water molecules as a by-product.
The reduction of 1 CO2 requires 2 reducing equivalents (four electrons). Or, 2 water molecules are required to reduce  1 CO2
CO2 is 'fixed'

In addition, we may add the following:

The reaction is thermodynamically unfavorable, where the free energy necessary (about 600 kcal/mol) being supplied by sunlight (Abeles, Frey & Jencks, 1992).

But green plants and cyanobacteria are not the only photosynthetic organisms, and  not all photosynthetic organisms use water as a source of electrons (or evolve oxygen).
Some photosynthetic bacteria use hydrogen sulfide (H2S) and 'make' elemental sulphur rather than oxygen.  The balanced equation may be written as follows:
$$\ce{6 CO2 + 12 H2S -> C6H12O6 + 12S + 6H2O \tag{2}}$$
It can be seen that although no water appears on the right-hand side of the equation, water is still produced as a result of CO2 reduction.
A balanced equation describing photosynthesis in general may now be given, where H2A is any substance that can be oxidized to A (Abeles, Frey & Jencks, 1992):
$$\ce{6 CO2 + 12 H2A -> C6H12O6 + 12A + 6H2O \tag{3}}$$
Other examples of H2A are H2, isopropanol and lactate.
The Reduction of a Single Carbon Dioxide
We may note first of all that the oxidation of two water molecules to a single O2 is a four electron (two reducing equivalent) oxidation.
$$\ce{H2O + H2O <=> O2 + 4e^- + 4H^+ \tag{4}}$$
The photosynthetic reduction of a single carbon dioxide may be represented as follows (Abeles, Frey & Jencks, 1992) and we may note that this is  a four-electron reduction:
$$\ce{CO2 + 2H2O^* ->[$hv$] (CH2O) + O2^* + H2O \tag{5}}$$
The asterisk indicates that if oxygen atom in water is labelled (using an isotope of oxygen, for example), the label is found in the oxygen 3†.
In green-plant photosynthesis, the (incomplete) reduction of 1 CO2 requires two reducing equivalents which are supplied by 2 H2O, and this four-electron results in the formation of 1 O2 and 1 H2O.
Oxidation and Reduction
I suspect that most readers of this post will know all of what follows in this section. Nevertheless, what is and isn't oxidation/reduction seems to sometimes cause confusion and some examples may help to clarify.
Oxidation is the loss of electrons. Reduction is the gain of electrons.  A hydration is neither an oxidation or a reduction, and neither is an ionization.
Some examples
The reaction shown in Eqn (6) is an oxidation (ethane is oxidized to ethanol). (Electronegative oxygen has 'taken' a pair of electrons from the second carbon atom, which is oxidized)
$$\ce{CH3-CH3 +\frac{1}{2} O2 -> CH3-CH2OH \tag{6}}$$
The  reaction shown in Eqn (7) is neither an oxidation nor a reduction, but a dehydration (the dehydration of ethanol to ethylene). The oxygen atom has not been  oxidized or reduced. It 'owns' the same number of electrons in ethanol as in water. (A good example of a hydration/dehydration reaction from the world of biochemistry is fumarase. The formation of malate from fumarate is not an oxido-reduction in any sense). This is an important one.
$$\ce{CH3-CH2OH  ->  CH2=CH2 + H2O \tag{7} }$$
The reaction in Eqn (8) is a reduction (the reduction of the carboxylate group of acetic acid to the aldehyde (acetaldehyde)), but note that the oxygen in water has not changed its oxidation state.  When water is eliminated, it leaves 'taking with it, in terms of electrons,  what is already owns'. But, unlike the previous example, the tetravalency of carbon is 'maintained' by the 'acquirement' of a pair of electrons (reduction).
An example from the world of biochemistry, is the aldehyde dehydrogenase reaction, where NAD+ acts as electron acceptor.
$$\ce{CH3-COOH + 2H+ + 2e- ->  CH3-CHO + H2O \tag{8} }$$
Eqn (9) is also a reduction (the reduction of acetaldehyde to ethanol). An example is the alcohol dehydrogenase reaction.
$$\ce{CH3-CHO + 2H+ + 2e- ->  CH3-CH2OH \tag{9} }$$
This final example (Eqn 10) is an ionization (the ionization of acetic acid), and may not under any circumstances be considered either an oxidation or a reduction (all the electrons 'stay put').
$$\ce{CH3-COOH ->  CH3COO- + H+ \tag{10} }$$
(When dealing with oxidation and reduction, protons are 'free'. We may add them in or take them out without changing the oxidation state).
Rant
Failure to distinguish between hydration/dehydration and oxidation/reduction has led to claims that water in the Krebs cycle is a source of reducing equivalents. Racker, for example, claimes in  A New Look at Mechanisms in Bioenergetics that electrons from water are transported down the respiratory redox chain, and Wieser claims that water provides 'the additional reducing equivalents needed to transform the chemical energy of one molecule of glucose into that of 36 molecules of ATP'. Both of these claims, IMO, are  nonsense (see here).
A Final Look at CO2 Reduction
Let's take a final look at the reduction of CO2 (where carbon is 'fully oxidized'), and reduce it by adding reducing equivalents (pairs of electrons) one-at-a-time until carbon is fully reduced, that is until we reach CH4. (We will also need to add a pair of protons at each step, but as far as oxidation and reduction is concerned, as stated above, these are 'free').
Adding a pair of electrons to CO2 gives formic acid, adding a further pair gives formaldehyde plus a molecule of water, adding another pair gives methanol, and adding a final pair gives methane plus another water molecule
This is summarized in Eqn (11).
$$\ce{CO2 ->[2H+, 2e-] {HCOOH}->[2H+, 2e-]{HCHO} + H2O->[2H+, 2e-]
 CH3OH->[2H+, 2e-]CH4 + H2O }\tag{11} $$
The oxygen atoms in the water molecules eliminated in steps 2 and 4 have not changed their oxidation state.
To fully reduce carbon dioxide to methane requires 8 electrons, and the two oxygen atoms are eliminated as water. To reduce six carbon dioxide to one gluc ose requires 12 reducing equivalents (24 electrons).  If nature had decided to make hexane ($\ce{CH3CH2CH2CH2CH2CH3}$) the photosynthetic storage product, this would have require 19 reducing equivalent (38 electrons), and if methane was the final photosynthetic product, then 4 reducing equivalents (eight electrons) per CO2 oxidized would have been required.
Footnotes

In the 'real world' of green-plant photosynthesis, the oxygen is 'lost' as phosphate, not water, in the glyceraldehyde-3-phosphate dehydrogenase reaction (see here), a key step in photosynthesis where reducing equivalents enter the carbon skeleton (see here). The electronegative atom (oxygen) 'eliminated' to 'accommodate' the incoming reducing equivalents does not  have to be part of a water molecule (or, in a more general sense, have to be oxygen at all).
In the case of aerobic respiration, the general equation may be given as follows, which emphasizes that 6 O2 atoms give rise to 12 H2O (six 4-electron reductions), and that (formally) 6 waters are consumed in the production of 6 CO2. Subtracting 6 waters from both sides, as is sometimes done (see here), only leads (IMO at least) to confusion.

$$\ce{C6H12O6 + 6O2 + 6H2O -> 6 CO2 + 12 H2O \tag{12}}$$

This experiment was done by Kamen and Ruben (1943), using 18O as tracer. Martin Kamin and Sam Ruben are credited with the co-discovery of  14C, that great gift to biochemistry and science as a whole. Sam Ruben died of phosgene poisoning, which he was preparing for the war effort during WW2. The story of his death is poignantly told by Martin Kamen in Radiant Science.

References
Abeles, R H.  Frey, P. A., Jencks, W. P. (1992) Biochemistry Jones and Bartlett
Kamin, M. D. (1985) Radiant Science, Dark Politics. A Memoir of the Nuclear Age.  University of California Press. Google Books

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Why does the direction of endolymph flow oppose direction of body motion?
In the semicircular canals, the endolymph always flows in a direction that is opposite to the motion of the vestibular apparatus itself. I’m having trouble grasping why this is, and I would greatly appreciate it if anyone could give me some physics insight into this.

Perhaps it would help to think of the endolymph as trying to stay in the same place while your ear moves around it?

The endolymph inside the ear, like any kind of matter, has mass and so is subject to inertia.  This means any change in speed and direction will be resisted.  The ear and semicircular canals themselves are fairly solidly connected to the rest of the body and so accelerate smoothly.  But since endolymph is fluid, it cannot be brought up to speed as fast, so it lags behind in moving.  So, as the ear moves forward, the endolymph stays behind and so in relation to the ear, flows backward.
This is like what you experience when a car or airplane accelerates: you "flow" backwards into your seat as the vehicle surges forward.

Does this cause dizziness after twirl? (am I using the right word? :D)


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What separates gene loci?
Introns are sections of noncoding DNA that separate exons within a gene locus. However, between different gene loci, I also would assume there to be noncoding regions of DNA. What are these regions called? (And if my assumption is wrong, then please correct me.)

These regions, if unannotated, are simply called intergenic regions.
Sometimes, if a large section of chromatin is regulated by an enhancer/silencer/locus control element, then there are boundary elements that demarcate this chromatin region and prevent the spread of the chromatin state to neighbouring regions.

It would be valid to call them "intergenic regions", but this is just another way of saying that they are the regions between genes. I don't think you can do much more because they are not homogenous in nature. Some may be short and perhaps lack any other function than that described by @WYSIWYG, others may be very long and have enhancers and regulatory elements for proximal or distal genes, simple repeated sequences, pseudogenes, replication origins etc. etc.


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Growth factors vs. mitogens
According to Campbell Biology,

A growth factor is a protein released by certain cells that stimulates other cells to divide.

and according to Wikipedia,

A mitogen is a chemical substance that encourages a cell to commence cell division, triggering mitosis.

What’s the difference between them? I suppose a mitogen specifically refers to mitosis, but if something is stimulating mitosis, isn’t it stimulating growth? Are mitogens all growth factors? Are all growth factors mitogens?

There is a lot of confusion and conflicting / imprecise definitions of these terms. It's biology after all :)
A mitogen is an agent that causes a cell to enter mitosis. This definition is pretty clear, and there is a good consensus about it. (Well technically, mitosis is not the same as cell division, but we will gloss over this distinction.)
The term growth factor has at least two different definitions: (1) a factor that causes growth of tissues, organs or entire individuals; or (2) a factor that causes growth of cells (increase in cell size). These two versions are often mixed up, and this causes no end of confusion. Let's consider them both in turn.
Definition (1) is more common and probably older. Since growth of whole tissues usually (but not always) implies both cell growth and division, according to this definition, a growth factor is also a mitogen. But the reverse is not true: there are cases where cells divide without growing, for example the first few cell divisions of a fertilized egg. But note that, since this definition concerns the level of tissues or individuals, it's meaning is not entirely clear in terms of cell growth and division. Muscle growth in the adult stage usually does not involve cell division, for example.
Definition (2) is better suited to cell biology (in my opinion), because it actually concerns cells, not tissues. This definition is more common when studying cell growth and division; see for example this review. Cell growth is a separate phenomenon from cell division: cells can grow without dividing (fat cells, muscle fibers and neuron do this, for example), or divide without growing (as mentioned above). So with this definition, growth factor and mitogen are two completely unrelated concepts. Now, it is certainly true that many proteins can act both as growth factors and mitogens; Matej Pribis gives some nice examples in the other answer. But that is an empirical fact, not a question of definitions.

What about PDGFs? Are they both mitogens and growth factors?

Yes, most of the classic proliferation-promoting proteins are both growth factors and mitogens, since in most cases cell growth and division go together. But to be precise, it depends on the target cell as well: a given protein may be a growth factor for one cell, a mitogen for another, and have no effect on a third. Not all cells respond to PDGF. Nerve growth factor is a good example of a "pure" growth factor (for neurons).

You can find a great article about this here.
basically, these two groups are very similar in their effects, however they work through different pathways.
Mitogens directly promote cell to get through G1 checkpoint through highering the activity of cyclin D/cdk4 (the complex needed to get through the checkpoint.) and according to the article above, also the cyclin E/cdk2 complex (which helps cell to get into S phase). By activating the MAPK (mitogen-activated protein kinase) pathway leading to production of transcription factors (Elk-1, jun, fos), which then promote specific transcription of proteins needed to get through cell cycle.
The mitogen pathway also causes phosphorylation of Rb (Retinoblastom) protein, which then dissociates from E2F transcription factor. This activates the E2F, which in turn helps synthesise proteins needed to promote S phase.
Growth factors usually stimulates mTOR receptor, which is a "serine/threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, autophagy, and transcription." Source
mTORC complex generally promotes translation. It plays role in "cell growth via the modulation of protein synthesis in yeast and mammals, it and its yeast homologs strongly stimulate transcription from all genes involved in ribosome biogenesis, transcription of rRNA genes by RNA polymerase I (Pol I), transcription of ribosomal protein genes by RNA polymerase II (Pol II), and transcription of tRNA and 5S genes by RNA polymerase III" and many other effects. Source.
Although all of this, in practice, I've seen many people use this categories interchangeably or referring to mitogens as a subgroup of growth factors.
I hope this helps.

Nice with some examples, but I think you miss the point of the classification as growth factors or mitogens. These terms do not refer to individual proteins, it's a theoretical classification of function. And they are not "very similar in their effects", on the contrary they are completely unrelated, by definition --- cell growth and cell division are very different things. That some people use the two terms interchangably is just wrong.

Please note that mTOR is not a receptor, it is just a kinase, and also that it can signal through the MAPK pathway as well.

@Roland I definitely agree, and I might have misstated what I meant. These processes (cell growth and proliferation) are distinct, but I wouldn't say completely unrelated. They can affect each other e.g. the progression of cell cycle inhibited by too small cell size. Moreover, GFs (or rather the mTOR) have some effect not only on growth, but also on proliferation and cell cycle progression. According to this article


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When does lactation occur?
High levels of estrogens and progesterone antagonize prolactin’s effect on the mammary glands, and it’s only after the placenta has been removed and the levels of estrogens and progesterone has decreased that prolactin effectively stimulates milk production in the alveoli. However, I’m also aware that many hormones cause the maturation of the breasts and mammary glands during pregnancy—is anything produced then? When does lactation really occur—before birth or after birth? I ask this because I’ve heard things about milk leaking out of breasts during pregnancy, and there’s also the fact that the breasts seem very heavy and laden with milk during parturition.

See prolactin..

@WYSIWYG - don't forget estrogens, progesterone, adrenal corticoids, insulin and growth hormone... it ain't just prolactin.

@anongoodnurse I was just giving a hint.. Not answering the question because I feel it is a bit broad. Hypothalamic control etc is also important.

@WYSIWYG It's not too broad at all. Geez, we get questions about why we didn't evolve wheels, wings, etc. This one is a walk in the park comparatively.

Stage I lactation occurs from midpregnancy onward; stage II is the onset of substantial milk secretion associated with having given birth.

In humans, stage I occurs at approximately midpregnancy... the gland is sufficiently differentiated to secrete milk, but secretion is held in check by high circulating plasma concentrations of progesterone and, possibly ...estrogen.

You ask,

...is anything produced then?

Yes. The mature primed breast produces colostrum, containing sodium, chloride, immunoglobulins, lactoferrin and other substances.

I’ve heard things about milk leaking out of breasts during pregnancy...

Not at all common that I know of. I'm sure one can manipulate the breast to get a small amount of milky discharge, but that's a big leap from leaking. More common (again, that I'm aware of) is galactorrhea associated with early oral contraceptive pills, prolactinomas, and other conditions.

the breasts seem very heavy and laden with milk during parturition.

The breasts mature during pregnancy in preparation to make milk; that's why they get bigger. They can get even bigger when they are actually full of milk. It may not be as obvious in a human, but in milk animals (goats, cows, etc.), well, a full udder is pretty obvious.
Different researchers divide lactogenesis into a different number of stages; this is a simple two-stage approach.
Lactogenesis: The Transition from Pregnancy to Lactation


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How does Organ Transplant work well despite having Foreign DNA
My question is little bit related to this one Why does organ transplant work although it seems organ's motor neuron isn't connected to recipient's CNS but only little bit.
Problem
Suppose the case in which person A got his kidney transplanted (and person B is donor). Now both A and B have different DNAs and how come lung (organ) transplant works well for person A and how does person A's DNA going to "accept" the lung's DNAs and how is replication going to work across the foreign lung?
Question
Will person A's lung contain:

Person A's DNA
Person B's DNA
DNA of both Person A and B (will convert to person A's after some-time having a certain half-life for it)
or
Forever contain both DNAs

Thanks in advance and kindly provide reference for your answer. Thanks

The DNA plays no direct role in organ transplant acception (or rejection), since it is not recognized by the immune system. It is 99.99% identical anyways. Replication works in the normal way it always does.

Replication works in the normal way... So predict the DNA of the transplanted organ after lets say 1 day: Will it have all the DNA (DNA of all the cells I mean) converted into the person A's DNA?

Why should the DNA in the transplant be changed? And how should this happen? Technically you are chimeric after an transplantation.

Chimeric?? Any reference for this point kindly?

After a transplantation you contain the DNA of two different humans.

4. Forever contain both DNAs
Yes, the donor kidney still has (and will remain to have) the donor's DNA. That is irrelevant to the acceptance and continued functioning of the organ, though.
The thing that could make an organ transplant fail is the recipient's immune system. If it detects the organ as "alien", it will attack it like any other foreign particle, and the body will reject the transplant.
To avoid this, two things are being done:

A donor is sought whose organs have similar protein markers to those of the recipient. (Those markers, and not the DNA, are what the immune system looks for when trying to tell friend and foe apart. DNA is inside the cell, the protein markers are on the outside.)
Similar protein markers are usually found in people with similar DNA, which is why close relatives are tested for this kind of compatibility first.

The recipient recieves special drugs that partially suppress the immune system.

If the recipient's body does not reject the organ, it can continue to function normally despite its different DNA. If, for example, there is a genetic defect in there that will lead to some kidney-related issues at a later time, it will be the donor's defect. If there has been a defect in the recipients kidneys that would have led to issues later in his life, that defect would be gone with his kidney. Other cells in his body would still carry the same defect, but those cells are not kidney cells, and thus that particular issue will not manifest itself.
Replication of cells will follow the same pattern: Cells from the recipient will replicate the recipient's DNA, cells from the donor's organ will replicate the donor's DNA.

In case this question was inspired by any novel / movie depiction of "his DNA was changed" and suddenly a person undergoing significant changes in appearance, capability, and / or personality (as in e.g. Star Trek or similar franchises), those are (largely) unscientific. Of course a donor organ could produce a very different mix of hormones, by- and waste products, with all the effects that could have -- but any "change" would be slow, gradual, and basically indistinguishable from naturally occurring changes in a person. With the exception that, without a donor, the recipient would be dead.

(ctd) Also, given that similarity in DNA / protein markers and healthiness of the organ is a basic requirement for organ transplantation, radically unbalanced organ functions are unlikely.

No this question came totally in my mind by chance (as these days all I think about is DNA).


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Does the arrangement of amino acids in a protein matter for nutrition?
Let's say there are two diets, consisting of entirely different proteins. If you split up all of the proteins from one day of each diet, you'll get the same set of amino acids and the same count of each. Assume everything else about the diets is the same.
Would these diets have the same effect on the protein composition in your body? Different polypeptides, but overall the monomers are identical. Does your body break down proteins entirely, or will it reuse some chains of amino acids?

I'm thinking this question would be better suited to the Biology exchange, but it's not clear to me what "same effect on your nutrition" means and I'm guessing the folks in Biology will have the same problem. Can you clarify that aspect of your question?

I changed "the effect on nutrition" into "the effect on the protein composition in your body" to make it clear what you are asking. During digestion, proteins are not necessarily broken down into individual amino acids but, to some extent, also into di- and tripeptides or even larger peptides that can be absorbed. This question would better suit in Biology SE or maybe Chemistry SE - they discuss about biochemistry there a lot.

Arrangement of amino acids determines the protein structure which in turn can determine how easy it is to digest the protein. I cannot think of an example right now; never really checked if two entirely different proteins have identical composition. However, it is not really surprising. In chemistry, it is known that different isomers have vastly different physical properties.
So if the two proteins have different digestibility then they will have different nutritive values.
Regarding, protein digestion and nutrition. New proteins are built from individual amino acids and not pre-formed oligomers. Read about translation. So at some point the ingested protein has to be completely broken down into amino acids.

It's your last sentence that's crucial. It is known that some, even large peptides, can be absorbed, so it's not necessary for a protein to be digested into a single amino acid in the intestine in order to be absorbed into the bloodstream. You are suggesting that all body proteins can be created only from individual amino acids, so any dietary peptides/proteins may need to be broken down at some later point...Translation is about single amino acids, but can some pre-formed (dietary) peptides find the way into body proteins...This would answer a lot of related questions...

@Jan "can some pre-formed (dietary) peptides find the way into body proteins".. Not in my knowledge.


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Do there exist enzymes that can take up multiple cofactors to do different reactions?
I was thinking about enzyme catalysis, and it seems like enzymes can only catalyse one kind of forward/reverse reaction (please correct me if I am wrong). Does there exist an enzyme that can catalyse multiple reactions with different cofactors? For example, an oxidoreductase that has $Fe(III)$ as a cofactor for one reaction and $H_2O_2$ as a cofactor for another reaction.

Can you name an enzyme for which hydrogen peroxide is a cofactor, rather than a a substrate? How much do you know about enzyme catalysis?

@user1136, thank you!

@David, I am not very familiar with enzyme catalysis-just the basics. I was just curious if there existed such an enzyme.

But what you mean by “such” an enzyme is unclear if you are confusing substrate, cofactor and catalytic mechanism. Until you clarify your question it is valueless in relation to the objectives of this site.

It sounds like you are asking about what are commonly referred to as "multifunctional enzymes".
For a reasonably recent article covering this subject — see:
Cheng, X. Y., Huang, W. J., Hu, S. C., Zhang, H. L., Wang, H., Zhang, J. X., ... & Ji, Z. L. (2012). A global characterization and identification of multifunctional enzymes. PloS one, 7(6), e38979.

A specific example of such an enzyme is the fatty-acyl-CoA synthase from yeast — this enzyme catalyzes multiple reaction steps that use both NADP and Coenzyme A and also uses a third cofactor, FMN.

The enzyme from yeasts (Ascomycota and Basidiomycota) is a multi-functional protein complex composed of two subunits. One subunit catalyses the reactions EC 1.1.1.100, 3-oxoacyl-[acyl-carrier-protein] reductase and EC 2.3.1.41, 3-oxoacyl-[acyl-carrier-protein] synthase, while the other subunit catalyses the reactions of EC 2.3.1.38, [acyl-carrier-protein] S-acetyltransferase, EC 2.3.1.39, [acyl-carrier-protein] S-malonyltransferase, EC 4.2.1.59, 3-hydroxypalmitoyl-[acyl-carrier-protein] dehydratase, EC 1.3.1.10, enoyl-[acyl-carrier-protein] reductase (NADPH, Si-specific) and EC 1.1.1.279, (R)-3-hydroxyacid ester dehydrogenase. The enzyme differs from the animal enzyme (EC 2.3.1.85) in that the enoyl reductase domain requires FMN as a cofactor, and the ultimate product is an acyl-CoA (usually palmitoyl-CoA) instead of a free fatty acid.

Source: https://www.ebi.ac.uk/intenz/query?cmd=SearchEC&ec=2.3.1.86

But my reading of the question is that the poster is not thinking of what are in effect multi-enzyme complexes. I suspect from the mention of cofactors in the question that the poster is quite naive. I seem to have heard of enzymes that can change the reaction catalysed in certain circumstances, but two cofactors — unlikely, given their need for specific binding sites.

@tyersome, that is interesting! I understand that multiple functions would need multiple domains. Thank you for your help!


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What slope do I need to prove a hypothesis?
I am conducting an experiment for school in which I am measuring people's heart rates as music plays at different tempos. My hypothesis is that as the tempo of the music increases, so will the subject's heart rate. After recording data from many subjects, I will use linear regression to find the overall function to represent my data.
What slope would I need on my function to prove my hypothesis correct?

As your hypothesis states: relating the tempo of music and the heart rate, the slope must be greater than zero.

I'm voting to close this question as off-topic because it belongs at SE-Cross validated (https://stats.stackexchange.com/)

I would worry less about the slope, and more about the p-value of the correlation.

It seems like you need to calculated a correlation ; It varies from 0 to 1.

Hi, welcome to Biology.SE. It seems like this question isn't quite about Biology, you seem to be asking a much more general statistics question. However, there isn't nearly enough here to motivate a migration to CrossValidated.SE. The general area you are looking for information in is called "power analysis" - I hope reading about power analysis can either help you directly or help you formulate a better question for CrossValidated.

You will get a much more complete answer on a statistics forum, or by simply consulting some basic tutorials on linear regression.
But a little intuition should tell you that setting a cutoff on the value of the slope does not make sense. For instance, suppose you measured heart rate in beats per second instead of beats per minute. All the y-values would be 60x lower, your slope would be 60x lower, but intuitively, nothing should change about your interpretation.
When you calculate your linear regression, you'll be able to obtain a correlation coefficient and a p-value, which tell you how well your data fits the line and the probability of obtaining such a result if there was no relationship between the data. These will be based not on the slope, but rather on how well your data fit the line and the number of points you have (the more data you have, the more confident you can be of the effect).
But you will never prove your hypothesis. The best you'll be able to say is "if my hypothesis were false, the probability of obtaining the result I got is less than X%". The clearer your data, the smaller X will be.
You would also do well to consider sources of systemic bias, not just statistical power. For instance, could the music affect the accuracy of the measurement? Do you always gradually increase the tempo of the music, or do you randomize the order? Just some examples off the top of my head, I'm sure you can think of others more relevant to your setup.

Sorry, the word I meant to use was "accept" I asked this question on stats.stack exchange( https://stats.stackexchange.com/q/435803/265532) and posted some more details on it


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Why have ground beetles never evolved the ability to get back up?
This may seem like a funny question, but I've seen so many ground beetles upside down on the floor and wondered why they've never evolved the ability to get back up. Wouldn't something like this drastically increase their survivability?

Welcome to Biology SE! This is a variation of a more general question that is often asked in this site: Why do some bad traits evolve, and good ones don't?.

By "floor", I'm assuming you mean a smooth floor like that inside a house or building.  I imagine that these beetles are actually quite good at flipping themselves over when they have something to grab onto -- e.g. a blade of grass, a fallen leaf, etc.  The detritus-free environment that is the modern indoor floor (or smooth path, or paved road) is not part of the natural niche of these organisms, and encountering such surfaces was uncommon in their evolutionary history.  Rare encounters are weak selective forces.

Normally, if a healthy bug is knocked onto its back, it can use its legs to rock on its sides until it rights itself. If, however, the bug can't roll back onto its abdomen because it has become too weak or because its nervous system isn't functioning properly, it remains stuck on its back.
An injury, a compromised nervous system due to pesticides or a lack of food or water can also reduce a bug's ability to right itself. Or the bug could simply be at the end of its lifespan and its strength and coordination abilities are declining.
references:
https://www.livescience.com/33334-dead-bugs-lying-on-back.html
https://www.thoughtco.com/why-do-bugs-die-on-their-backs-1968414


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Acrosomal enzymes and the female reproductive tract
My textbook wrote that the reason why acrosomal enzymes are so securely contained within the sperm (thus needing capacitation to facilitate their release) is to prevent any premature release in the male reproductive tract. If they were released, they would start digesting the male organs. However, wouldn’t this apply in the female reproductive tract too, once capacitation has occurred? Does the female reproductive tract have some sort of protection against this? (I’m assuming that the sperm has been capacitated but has not fertilized the egg yet.)

The acrosome reaction does not take place till the sperm reaches the zone pellucida of the ovum, which causes the acrosome to rupture. Thus the female reproductive tract does not get exposed to the enzymes.
Links:
https://en.wikipedia.org/wiki/Acrosome_reaction


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Advantage of GCPRs over RTKs or other receptor protein kinases
My book lists two important differences between GCPRs and receptor protein kinases:

GCPRs do not directly activate a signal transduction pathway. It only does so indirectly, via a G protein. On the other hand, RTKs directly activate a signal transduction pathway, bypassing the mediation of a G protein. (Any G proteins involved with RTKs act as relay molecules in  themselves and are part of the signal transduction pathway.)
GCPRs only activate one signal transduction pathway, while RTKs can activate many pathways.

From what I can tell, receptor protein kinases are faster and more versatile than GPCRs. They do not require as many intermediate steps and can activate many pathways at once. However, GPCRs make up the most largest class of ligand receptors in human cells. This leads me to think there is a great advantage GPCRs have over RTKs that I’m not seeing.
If RTKs are more advantageous than GPCRs, why are there more GPCRs than RTKs?

I think GPCRs are evolutionary more older since tyrosine kinase signalling is relative recent evolved system. This could be one explanation for why their is more diversity in GPCRs
By the way GPCRs can actually signal g-protein independent, for example via B-arrestin. Also their are many types of g-proteins witch can all induce signaling via different signaling pathways. So GPCRS are actually quite versitile.
And then their is also a lot of crosstalk between GPCRs and RTKs

Since both systems are widely distributed, they are both evolutionary pretty old. I would rather say "RTKs are evolutionary newer than GPCR" and not that they appeared relatively recently.

Thats is indeed what I ment


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Ions in Stomatal Opening Mechanism
When a stoma’s guard cells try to swell and open the stomata, they actively pump out protons outside of the cell. This causes a membrane potential, where the inside of the cell is negative with respect to the outside. This then causes potassium ions, which are positive, to rush into the cell, mitigating that potential. However, my texts say that anions such as chloride and malate ions follow potassium into the cell as well; their rationale is that positive ions must be balanced by the presence of negative ions. I do not understand why this is the case. If you extruded positive ions (protons) out of the cell and allowed positive ions (potassium) back in, there would be no ionic imbalance to draw the anions from where they’re idling. Could someone clear this up for me?

The ion concentrations are different inside and outside of the cell, allowing a potential.  The cell becomes even more polarized by the pumping out of H+ ions, making the cell even more negative (potential difference). Then this negative potential happens to cause voltage-gated channels to open and the uptake of potassium occurs. This will depolarize the cell (return it to the base potential difference).  It is usually very important for the cell to maintain the negative potential after it recovers. To combat the uptake of potassium, negative charges can be used to balance the increased positive ion influx so the resting potential is stabilized.
These mechanisms are usually mediated by special proteins that are regulated by actual electrical changes in the membrane.

You may find it an interesting sidelight that in many plants with potassium deficiency, we see necrotic leaf spots or leaf tip or marginal burn. The plant can't adequately close the stomates, so you get localized dessication in the leaf and therefore necrotic leaf spots. In this way, drought stress and potassium deficiency are somewhat related.

do you have any references that one can read for more information on your answer?


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What’s wrong with a shriveled cell?
When you place a cell into a hypotonic solution, water rushes into it and it bursts/lyses. Thus, the cell dies.
However, when you place a cell into a hypertonic solution, water rushes out of it and it shrivels. The membrane is still in tact and all the organelles are still held inside. Why is having a shriveled cell a problem then?

Just as a comment at the moment: Water is the most important substance for the function of a cell. Without it, no reactions will take place etc.

@Chris Is that the only reason, though?

@lightweaver An interesting read if you're really interested.

Just to elaborate a bit on @Chris's answer - the protons and electrons that come from the disassociation of H2O are very important for reactions.  Also the hydroxide ion has some important applications as well in organic reactions.

Adding on to @MG_MD's answer: a lot of metabolic reactions and cellular processes require water as a solvent and medium. Transport of electrolytes and dissociation of compounds into ions also requires water

Plant Cell
In the case of plants, shriveled cells are a huge problem. When plant cells are put in a hypertonic solution, the cell wall remains turgid and stays that way but the plasma membrane doesn't, it shrinks as you already know with the other organelles as well. This is known as plasmolysis. If this situation continues it causes death.

Shrivelling  causes the plant to wilt too.

Animal Cells
Well it does have affects overall and at cellular level

It changes the RMP(resting membrane potential) across the cell because of change of sodium ions outside the cell
-It decreases rate of metabolism

Perhaps you may want to elaborate here. For all cells, exosmosis will increase the concentrations of solutes inside the cell. This would affect all cells not just electrically active cells. You may also want to explain how metabolism is affected. Moreover, this question is general (not pertaining just to humans); so you can remove the perspiration and fatigue part and explain what happens at the cellular level (as you started your answer).


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How can the following data regarding flower phenotypes be explained?
$$\begin{array}{c|c|c} \hline
\text{Parents} & F_1 & F_2\\ \hline
\text{Blue}\:\times \text{white} & \text{All blue} & \text{196 blue, 63 white} \\
\text{Blue}\:\times \text{pink} & \text{All blue} & \text{149 blue, 52 pink} \\
\text{Pink}\:\times \text{white} & \text{All blue} & \text{226 blue, 98 white,
77 pink} \\ \hline
\hline
\end{array}$$
From the above data, it is likely that this is more complex than simple Mendelian inheritance. My guess is that there is epistasis at play here, but I can’t figure out what is really happening. What are the phenotypes of the parents? What genetic loci are involved and which traits are dominant?
(I was thinking blue ($B$) was the dominant epistatic flower color allele—$BB$ or $Bb$ would give blue regardless of the other color allele, and $bb$ would allow the expression of color dictated by the other gene, which has pink ($P$) as its dominant allele. This doesn’t work, as seen in the third row.)
Can anyone lend their aid here?
(The data was taken from here, question 32 in the sample multiple choice.)

Because it seems you might be studying for a test, I will try to not answer directly but show the beginning of a chain of logic that might be more useful.
Let's review the very plain evidence. blue crossed against other colors leads to 3:1 ratios of blue:other. So it seems that blue is dominant in those cases. But when you cross those colors against each other, you get silly nonsense, a 3:1.2:1 ratio or something.
So, based on the linked answers, you are justified in thinking that genetics determines flower color, just because of the simple Mendelian pattern of the first 2 crosses. But things don't work for a straightforward monogenic trait in the pinkxwhite cross.
Let's now analyze your explanation. You say: "I was thinking blue (BB) was the dominant epistatic flower color allele—BB or Bb would give blue regardless of the other color allele, and bb would allow the expression of color dictated by the other gene..."
But look at the parents and offspring of the third cross. You say blue is dominant- but it is in fact expressed in the offspring of non-blue parents! So blue can't both be dominant and be the "controlling" epistatic gene. So now: let's consider some other similar possibilities:
1) blue = dominant and is controlled by another locus (recessive or dominant?)
2) blue = recessive and controls another locus (recessive or dominant?)
Do any of those hypotheses match the data?
A final observation: I find it always helps to add up all the combinations of phenotypes (if possible; for example the ratio of (blue+white) : pink, etc.) to see if anything looks like a familiar ratio.
I hope that is useful (and not too late to be helpful in studying, if that is your goal).

This is an example of recessive epistasis
In short, flower color is controlled by two genes. A recessive mutation can happen in either of those genes. In one gene, the recessive genotype (pp) results in pink flowers. In the other, the recessive genotype (ww) results in white flowers. If neither of genes are homozygous recessive, the resulting phenotype is blue.
When you cross a white flower (ww PP) with a blue flower (most likely WW PP) you get offspring that are homozygous dominant at one locus and heterozygous at the other (Ww PP) and the resulting phenotype is blue. The next generation will have 1/4 white offspring (ww PP) and the rest are blue (1/2 wW PP, 1/4 WW PP). The same pattern is seen for pink flowers.
When you cross a white flower (ww PP) with a pink flower (WW pp), you get offspring that are heterozygous in both genes (Ww Pp) and the resulting phenotype is blue. The second generation shows all possible phenotypes and genotypes.
You do not need to know this much detail to answer that multiple choice question, however. All you need to know is that this is a genetically controlled trait, even if the pattern of inheritance is complicated.


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Can Chilopoda "vocalize" or produce sound for the express purpose of communication, as opposed to sound as a byproduct of other movements?
Is there any species of Chilopoda that can "vocalize" or or otherwise produce sound for the express purpose of communication, as opposed to sounds it might create  as a byproduct of other movements and body functions?
An example of non-communication sound in other arthropods would be insects wings causing "buzz" sounds while in flight.
An example of a communication sound in other arthropods would be crickets (and others) rubbing their legs together to "chirp".
Do any Chilopoda intentionally create sound for the purpose of communication?

We are starting a Bioacoustics Stack Exchange for people interested in the studies of non-human animal sounds and the impacts of sounds on animals. Please join us! https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

@ASimonis Can you please stop to write your comment under each seamingly fitting question? In this frequency this can be seen as spam. Most of these questions (if not all) are old anyways and your comment will be useless.

I have been trying to help the Bioacoustics community grow and thrive, and I am sorry if the comments were inappropriate. I recently learned about the Chat space, so I'll try to direct some recruitment effort over there.  :-)

@ASimonis Unfortunately I cannot, in good conscience, indicate that I will commit to use that new Bioacoustics Stack Exchange, as I don't believe I would use it for anything other than attempting to get a single answer to this same question I've posted here.  My interest in bioacoustics is limited to this one specific use case.  If the stack exchange does gain enough support to be fully created, I will likely repost this question there, but that will likely be the full extend of my use of it.


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Predatory animal tracking methods
As far as I know, humans are the only animals that use visual references to track prey that is not immediately visible to them.
Do any other animals do this?
I'm not referring to stalking prey that the predator already has in sight, like many big cats do, and not tracking prey, that is out of sight, by scent or other means, before switching to visual before the final attack.
Are there any other animals that primarily use visual information, such as tracks, shed fur, broken foliage, disturbed earth, etc., to follow or approach a prey animal that they can't already see?

This is a really interesting question. Based on what I'm reading online the answer is no, not as far as we know. Bears, mountain lions, and other species have been noted to follow tracks but this is commonly thought to be due to following the smell an animal leaves behind, not the visual cue itself. This similar question on Quora has a discussion of this phenomenon.
As is pointed out in that discussion, the best candidate for this would likely be birds, particularly corvids. This article discusses a study in which ravens could not only tell when someone was looking at them, but could remember areas in which they'd previously been observed (i.e., they can tell when someone is 'spying' on them). This is a bit different than what you're asking here, but you can imagine that an animal that was capable of this level of cognition might also be able to connect seeing footprints --> find human if they were incentivized to do so (possibly by the potential to gain food or other resources). However, it doesn't look like that has been specifically studied.

-1. Please avoid citing Quora as a source -- Quora answers are rarely cited, not peer reviewed, and often FALSE. It's really a low quality site. We try to hold higher standards here on Bio.SE by requesting that all answers provide reputable support. (For the record, MentlaFloss is not really a whole lot better than Quora in terms of quality). These types of sources are best fit for sites like reddit. Here, please elevate your citation game as we are striving to compile expert answers to questions for biology researchers, academics, and students. see our site [tour].

noted. I included this one only because the primary response to the question in Quora was knowledgeable and answered by an Ms in a relevant field. But I will avoid this in the future.


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Which animal has the smallest percentage of their body mass made up of water?
It's a "well known" and interesting "fact" that the human body is made up of "mostly water".  With percentages from 65% to 90% often being repeated as if they were exact and proven amounts.
Obviously the exact numbers will vary from one individual to the next, and from one measurement method to the next, and from one to the other definition of which water is included in the measurement, etc.  And it will even vary within the same individual over time depending on water intake and excretion (in all its forms).
Moving on from humans, water is also going to be a significant component of the body mass of animals as well.  And the variations in percentages here is likely to vary even more, when you add different species in to the mix of factors to compare.  One obvious example is jellyfish, with an extremely high (compared to humans, at least) percentage of their body mass composed of water.
But which animal is at the lower end of the spectrum, with the smallest percentage of their body mass being made up of water?
In my attempt to research this topic, I was unable to find any documented information that was not behind a pay-wall, such as this article.
For clarity and simplicity, please limit answers to multi-cellular animals, assume a normal healthy adult specimen, averages and estimations are acceptable for measurement comparisons, as avoid answers that include grey areas in defined classifications (e.g. are viruses alive), and answers need not be reduced to a specific individual species if a genus or even family is enough to identify the animal to a layman, etc.

I'd guess Australian marsupials probably have pretty low water content, but can only find papers on water conservation in the marsupials.

@bob1 That line of thought was my first intuition as well, but the more I think about it, the more I find that I can't directly correlate "the ability to prevent moisture losses" to "total moisture content".  Just because they're exceptionally good at maintaining their hydration level doesn't necessarily translate to a lower overall water content.  They might still be the winners, for other reasons, but the retention ability alone isn't convincing enough for me.

I had that thought too. I suspect all mammalian animals will have similar water content, but its actually a hard question to find answers to because not many people take a dead animal and do the science by properly weighing and reducing it to ash under controlled conditions.

the only real variation is the amount of nonliving tissue present, things like shells otherwise animal tissue is all but identical under living condtions,esspeically for things like vertibrates which have basically no noticable variation here.

A Tardigrade, when exposed to extreme conditions, can suspend their metabolism and reduce water content to 1% of the normal; from 85% to 3%. Although this may not count, because it is only under extreme conditions.

Good answer, and good information.  But I'm not sure that suspended metabolism in an attempt to maybe survive (no guarantees, despite their much higher likelihood of success compared to most other animals) those extreme conditions qualifies as 'normal' or 'healthy' ...


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How did migrations evolve?
Disclaimer: I know nearly nothing about biology.
I was wondering how did the migratory behaviour of birds evolve. Assuming that evolution/natural selection works slowly and gradually (at least most of the time) I don't understand how some birds decide to fly thousands of kilometers once a year and then fly back.
How does a bird species start it's migrational behaviour? The first generation flies close by, then the next a bit further and so on up until the migration distance is thousands of kilometers? Or do they randomly fly in small groups until they find nice land (abundant sunlight and food) and only the small group which find the nicest land reproduces succesfully?
If evolution works gradually and migration distance increases also gradually, how did, for example, the artic tern evolve to migrate from pole to pole? In the gradual increase of distance, some generation of artic tern must have migrated to a tropical latitude and be unable to survive there. Obviously this must be very wrong.
Can someone explain the evolutive mechanism behind migrations?
Thanks!

This may help. https://www.thespruce.com/types-of-bird-migration-386055#:~:text=Nomadic%20birds%20tend%20to%20stay,abundant%2C%20or%20when%20crops%20ripen.

Here is an article discussing bird migration that you might find interesting, although it doesn't really discuss the original evolution (it discusses convergent appearance of migration in many different groups but in ways that suggest it's a latent trait reappearing by mechanisms maybe different from the very first migratory behaviors) https://academic.oup.com/bioscience/article/57/2/165/228565

John and @Oosaka maybe post as answers (if this question doesn't just get closed).


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Why do the eyes of this cat have different colours when viewed from different angles?
Why do the eyes of this cat have different colours when viewed from different angles?

Both of the eyes of this cat appear yellow when looking straight at the camera.

However, when the cat looks at an angle to the camera one eye appears green. Unfortunately, the cat is not mine and I don't have many more pictures of it.
I have also noticed that my own eye which appears dark brown from straight on, looks lighter when viewed from an angle.
Why does this happen? Is there a special property of the iris that lends itself to such behaviour? In this website, it is mentioned that the colour of the iris varies with the angle at which it is viewed but no explanation is given.


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Are “tremors” and “ tetanic contractions” the same thing?
Do these two expressions have the same meaning?
1- Tetanic contractions in the skeletal muscles
2- Rythmic shaking of the hands
(These two expressions are supposed to be two symptoms of Parkinson’s disease ,however I am told that this is repetition)

I think both for the purpose of convincing your instructors, and for the purpose of asking a well-researched SE question, it would be better if you started with trying to make your case. Why do you think they should be considered distinct? What have you learned about these symptoms yourself? Telling a test grader "these should be considered distinct!" is less convincing than "these should be considered distinct because A, B, C, D". I worry that giving you an answer here that you use to debate a test grade is similar to doing homework for you.

I really appreciate your point of view and admit I have to do better research . But I wish you would at least answer this question :  do you consider them distinct?

No, I won't, for the reasons I've stated.

Tetanic contractions and tremor are different phenomena.
Tetanic contraction (or tetanus) refers to sustained contraction of a muscle subjected to high-frequency stimulation. With this high frequency, a new contraction begins before the previous one has ended. Thus the contractions get 'summed up'. You could see this interesting video for a demonstration.
Tremor is an involuntary shivering movement which is caused by alternating contractions of opposing muscle groups. The causes are many, ranging from physiologic tremor to degenerative disorders of the nervous system (such as Parkinson disease).
Note that tetanic contractions are not a symptom of Parkinson disease. In fact they are not a symptom of anything at all, inasmuch as they are a physiological property of isolated muscle. Tremor, on the other hand, is a phenomenon seen in muscle groups, and is one of the core symptoms of Parkinson disease.

What about “rythmic muscle contractions” ? As it is stated here  (https://g.co/kgs/Pvd27p) as a symptom.

@user261947 The Google page is probably referring to myoclonus, which is sometimes seen in Parkinson disease.


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How can I search through literature databases for words containing a * when the asterisk is read as syntax and not part of a query?
I'm exploring the literature on microRNA, where it is common for the less utilised strand of the miRNA duplex to be referred to as the miRNA* strand.
However, I am experiencing some issue searching for literature sources, as the databases I use for my searches (Web of Science, Google Scholar) utilise an asterisk as part of the search syntax rather than part of the query itself. This leads to any search for "miRNA*" yielding every paper on miRNA in general.
I am getting by for now using alternate search terms and other papers references, however it would be excellent if someone knows how to tell these databases that the asterisk is part of the query and not syntax.

Regarding Google Scholar this answer  should be relevant. Regarding WoS, this support document. In short: no luck.

I have not tried this (and it isn't really my field), but it should be possible to save search results to a file with a tool like this https://www.seoquake.com/index.html to give you a file of URLs.  Then you could search for "miRNA", save those results, then write a program to check those sites for "miRNA*" using something like wget and grep.  One of the programming sites might get you better info, since it's more a programming/web use question than specific to biology.


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How to build SEG in your personal environment?
I'm trying to implement SEG (Wootton & Federhen,1993) in my MATLAB and Python environment. From this oriinal article I cannot figure out what I need to build my script. Are there any related article that explains the various steps to build this algorithm (from the mathematical point of view)?

Your question seems to relate to software rather than biology. You are likely to have more luck in SE Bioinformatics.

Yes I know that it seems like that. But I do not want anyone to explain me the code. I want to know if any of the users of this blog know the related articles. From a certain point of view it could be related to the biology context since we all have to study and we all can share our experience!

That paper isn't open access, so many potential helpers (including me) can't read it...


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what kind of dinucleotides can be considered important from a mutational point of view other than CpG islands?
CpG islands are regions with an high frequency of CpG (Cytosine-phosphate-Guanine) sites. The usual formal definition is that of a region with at least 200 bp, a GC percentage greater than 50% and an observed to expected ratio grater than 60%. In colorectal cancer, these regions have been found drastically methylated with respect to the normal mucosa tissues surrounding the tumor (Illingworth et al. 2010). This brought to speculate a role in the cancer onset. My question is: are there any other kind of dinucleotide rich regions that represent important cases of study in literature?If yes, can you suggest me some papers and references?Than you
Illingworth RS, Gruenewald-Schneider U, Webb S, Kerr AR, James KD, Turner DJ, Smith C, Harrison DJ, Andrews R, Bird AP (2010). "Orphan CpG islands identify numerous conserved promoters in the mammalian genome". PLOS Genet. 6 (9): e1001134. doi:10.1371/journal.pgen.1001134. PMC 2944787. PMID 20885785.

In some types of cancers like breast cancer, APOBEC3 cytidine deaminases can become upregulated and enhance mutagenesis. As shown in this mutational signature from cancer tissue data the enzymes prefer TC motifs.

Source: https://cancer.sanger.ac.uk/cosmic/signatures/SBS/index.tt

Are there signatures in protozoans or in micro-organisms (Eukaryota)?By your experience, to find a huge proportion with respect to the gene length,of TC motifs or TT motifs, could be representative of the proclivity of a protein coding gene to undergo cross-linkings or, in general, sufficient to speculate such a tendency?Given the degeneracy of the genetic code I am restrained to assume such a conclusion (a lot of codons with TC and TT in their first and second codon position)and I am asking for that

This particular signature no, unless you introduce an APOBEC3 gene into that species and there are labs that have recreated this signature in yeast using mammalian genes. There are other signatures with no known etiology or suspected to be environmental (UV, reactive oxygen species, etc.) that one would expect in other eukaryotes and there are labs that study this. I don't know about your gene question. Mutation signatures are created from genome wide sequencing and I don't know if anyone has looked at local chromosome structure.

Anyway, your suggestion are greatly appreciated.

The obvious answer (to me) is dinucleotide microsatellites, though it may not make sense to restrict to dinucleotides unless you had some particular reason; other motifs (e.g. mononucleotide repeats) have higher mutation rates. It also depends to some extent on the organism.
While the particular motif may have only a modest effect on mutation rate (e.g. Figure S9 here), microsatellites in general have very high mutation rates and certainly have a nonrandom distribution pattern throughout genomic regions that have functional effects.


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Name of dominant dinosaur
I seem to remember reading some time ago about a dinosaur appearing very prominently in the fossil record, with continent-wise distribution. The layer is known specifically for having so many fossils of this dinosaur and might be named as such. Terms "cow-sized", "vegetarian", and "near to extinction event" come to mind. Does this ring a bell?
My memory might be so faulty that it could be an early amphibian, reptile or even mammal!

The closest example I can think of is Lystrosaurus, which was one of the most common animals in the early Triassic period. It was distributed across many modern continents, and was roughly the size of a pig or cow, depending on the species. Lystrosaurus was not a dinosaur, despite its name.

Excerpt from the Wikipedia page (emphasis mine):

Lystrosaurus is notable for dominating southern Pangaea during the Early Triassic for millions of years. At least one unidentified species of this genus survived the end-Permian mass extinction and, in the absence of predators and of herbivorous competitors, went on to thrive and re-radiate into a number of species within the genus, becoming the most common group of terrestrial vertebrates during the Early Triassic; for a while 95% of land vertebrates were Lystrosaurus. This is the only time that a single species or genus of land animal dominated the Earth to such a degree

Note that Lystrosaurus was not a dinosaur; it was a dicynodont therapsid.  However, it may well be the answer to the question anyway.


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R/Bioconductor query for a gene?
I'm fairly new to bioinformatics, so please be gentle ;0
Is there a way to query a particular gene using a script in R/Bioconductor? I'm particularly interested in Gene Ontology terms. There are many websites that, given the gene name, will return relevant GO terms. My question is, can it be automated?

Please ask questions about Bioconductor on the Bioconductor support site.
Bioconductor also distributes 'annotation' packages with curated information. These don't rely on a web service, so are always available, and are fixed at each (6 month) Bioconductor release, but are less comprehensive. Choose your organism
BiocInstaller::biocLite(c("org.Hs.eg.db", "GO.db"))  # first time only
library("org.Hs.eg.db"); library("GO.db")

Query for GO ids
symbols = c("BRCA1", "BRCA2")
df = select(org.Hs.eg.db, symbols, columns="GO", keytype="SYMBOL")

Symbol - GO mappings are 1:many, so
> dim(df)
[1] 149   4
> head(df)
  SYMBOL         GO EVIDENCE ONTOLOGY
1  BRCA1 GO:0000151      NAS       CC
2  BRCA1 GO:0000724      IDA       BP
3  BRCA1 GO:0000724      TAS       BP
4  BRCA1 GO:0000794      IEA       CC
5  BRCA1 GO:0003677      TAS       MF
6  BRCA1 GO:0003682      IEA       MF

Use the GO.db package to gain more insight into the GO ids
> head(select(GO.db, df$GO, "TERM"))
'select()' returned many:1 mapping between keys and columns
        GOID                                                    TERM
1 GO:0000151                                ubiquitin ligase complex
2 GO:0000724 double-strand break repair via homologous recombination
3 GO:0000724 double-strand break repair via homologous recombination
4 GO:0000794                            condensed nuclear chromosome
5 GO:0003677                                             DNA binding
6 GO:0003682                                       chromatin binding

See the vignettes on the AnnotationDbi landing page, the annotation-related work flows, and the training material on the Bioconductor web site.

Take a look at the biomaRt package. This package allows you to access some databases in R directly. Quote from the user's guide:

The package enables retrieval of large amounts of data
  in a uniform way without the need to know the underlying database schemas
  or write complex SQL queries. Examples of BioMart databases are Ensembl,
  Uniprot  and  HapMap.   These  major  databases  give  biomaRt  users  direct
  access to a diverse set of data and enable a wide range of powerful online
  queries from R.

In the user's guide you will find anything you need, i.e. description and example tasks, for doing queries on HGNC symbols, GO terms, and more.


text:
How to feed bacteria out of lab
I want to take a sample of skin infection bacteria (I suppose combination of staphylococus, strep, etc) and give it to the doctor for analysis but the appointment is in two weeks. The bacteria will be dead by then, right? Is there any home-made nurturing solution that I can put them in to preserve them until then?

Depends on the bacteria. You can inoculate the bacterial cells in a sterile isotonic solution like saline and store the sample in the fridge (4⁰C). The cells will survive for 2 weeks.

Do you have sterile swabs with which to take the sample? Just a regular cotton swab won't work.

The problem that stands out the most is will a clinical lab even bother running tests on a patient-procured sample, and second to that, would the results be valid?

Thank you everybody for your answers. Then I can give it a try by extracting the crust that contains liquid on the inside with sterilized tweezers and try to preserve it in saline in the fridge. I hope that the lab will accept it cause the alternative is no sample or me going to the emergency for a pimple since I will never manage to synchronize the doctors appointment with the random moment that it decides to re-appear every time :P

In a lab there are so many ways of doing this. However, at home is a little tricky. This is what I would do:
Keep your bacteria in a liquid media.
Liquid Media: make the media out of NaCl and AS CLEAN AS POSSIBLE (distilled if possible) water (concentration 18g NaCl / L). Place a sample of the bacteria into the solution. Freeze solution with bacteria (-20 degrees C if possible). Take out when wanted.


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The Collagen Triple Helix
In the amino acid sequence X-Hyp-Gly (where X can be any amino acid) of the triple helix can the Hyp residue be both hydroxyproline and hydroxylysine? In our textbook it says that the Hyp residue is hydroxyproline but "hydroxylysine also occurs in the collagen".
Thank you!

Welcome to SE Biology. We can answer this question for you, but you will learn more by thinking about the structure of the amino acids and of collagen, and WHY every third residue might be hydroxyproline, and whether the structure of lysine would allow it to perform a similar function. (This is also what we expect of people who post questions.) Look at one of the online texts at NCBI bookshelf — Lodish, and perhaps this article. Come back and tell us what you found.


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Is recapitulation theory correct?
Most school books still say that recapitulation is an evidence of evolution but as far as I know it has been proved wrong so why is it being still taught? Has it got any sort of relevance?

It is not correct and is outdated. However, it is a compelling hypothesis and was formulated based on interesting pieces of evidence. It has been discussed on this SE before, please use the search function. See e.g. this answer of mine, and the rest of the thread or this excellent article from 30 odd years ago.

Welcome to SE Biology. Your question has a couple of problems. First, you should explain breifly what recapitulation is. I don't know. Then you should cite an actual modern text book that still presents it. Then you should explain the basis that it is thought to be incorrect so that your question is about a clear and specific biological idea, that can be answered objectively. Don't ask questions in terms of "why it is being taught" — an answer may well be out of the realms of biology. Ask, instead, whether a scientific argument against the idea is correct.


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What causes the elongation of Genome down the evolutionary time line
Theory of natural evolution says that complex life forms arose from simpler ones e.g. starting from Eubacteria to modern day multicellular eukaryotes. {If we try to reduce these changes happening at molecular level, it should be like, from Eubacteria like E.Coli. (20 kilobasepair genome/DNA strand size ) evolving, over time, to Multicellular Eukaryotes ( 3 Gigabasepair genome size) e.g. (humans and other hominids.)}
Now if we see molecular changes happening inside cells, the molecular changes are within nucleus as extra nuclear changes are largely function of nuclear information (and a smaller extent external stimuli). For biochemical changes to take place inside cell Nuclear information is the major guiding force. But according to Central Dogma elongation of DNA shouldn't have happened as there is no scope for it in either doubling, translation or transcription. But actually it is not so according to evolution. So what allows changes to be imbibed in the DNA that also increases it's length ?

Your question is unclear. One interpretation is that you think there is some principal of nature that would prevent DNA elongating, and you perhaps also think this is Crick's mistakenly-named Central Dogma. There is no such principle, and Crick's Central Dogma was that molecular genetic information transfer could proceed from DNA to RNA to Protein, but not from Protein to RNA or DNA. Regardless of what Crick said, gene expansion is known to occur and the mechanisms involved are understood and can be found from an internet search. Or did you mean something else?

@iayork — You can say that the word Dogma was ill-chosen (Crick admitted he misunderstood the meaning of the word) and that it is dangerous to give students the idea that there are dogmas in science. Or you can say that the concept is so obvious now that we know the mechanisms of gene expression that it is difficult to justify teaching it as such. However the expression "outdated concept" suggests that it is incorrect. It is not. Suggestions about the nationality of the OP and the teaching of science in India are not relevant, and I suggest you think about withdrawing them.

Yes exactly if information flows from DNA to RNA to protein and in no way from protein towards DNA than how come the changes that happened in external environment (that should mostly affect cellular cytoplasm and not nucleoplasm) went to the DNA and made such changes that started getting reflected in offsprings of the organism (as adaptation to the environmental change that happened). More intriguing is the fact that Nuclear DNA in modern primates have genome size of up to three gigabase pairs but there is no mechanism described that elongates the DNA.

DNA misreplication events can lead to accidental duplication of DNA (even the entire genome), misalignements in recomibination events, integration of DNA from extracellular sources e.g. viruses. All these events can lead to large scale changes in the genome size of an organisms, smaller scale changes can be insertions and deletions in the DNA from repair pathways such as non homologous end joining.


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Will obligate aerobic bacteria die if placed in a buffer solution even in the presence of oxygen?
The electron transport chain in aerobic bacteria functions by pumping H+ out of the cell to establish a concentration gradient.
So if the bacteria are placed in a buffer solution having pH equal to the cytosolic pH of the bacteria, will they still be able to establish the required concentration gradient? Will the increase in pH of cytosol(due to loss of H+) alone be enough to drive ATP synthesis even in the absence of a pH change in the medium? i.e.Will obligate aerobic bacteria die if placed in a buffer solution even in the presence of oxygen?

Answer
No. There is ample evidence that:

Most non-extremophilic bacteria grow over a broad range of external pH values, from 5.5 – 9.0, and maintain a cytoplasmic pH that lies within the narrow range of pH 7.4 – 7.8.

The explanation for this is another matter, but, before discussing that question there are two points of possible misunderstanding in the question that require a note of clarification.
Clarifications

What the electron transport chain establishes is an electrochemical proton gradient, or proton-motive force (PMF). This consists of two components§: the hydrogen ion concentration difference, ΔpH, and the electric potential gradient, Δψ.

The source referenced in the question shows hydrogen ions being pumped from the cytoplasm, across a membrane, to a space labelled “outside”, which, according to the figure legend represents hydrogen ions “pumped out of the cell”. This is incorrect. The hydrogen ions are pumped into the space between the inner and outer membranes of gram-negative bacteria, or the space between the inner membrane and cell wall of gram-positive bacteria. It cannot necessarily be assumed that this space has the same pH as the external milieu.

How is the proton motive force maintained?
A possible explanation of why a constant or, more striking, alkaline pH does not destroy the proton motive force relates to the two-component nature of the latter. Bacteria appear to be able to compensate for any decrease (or even inhibition) of either ΔpH or Δψ by a reciprocal increase in the other (Bakker and Mangerich,1961). One mechanism that illustrates how this can be achieved in certain cases is the use of an alternative terminal oxidase, cytochrome bd:

Cytochrome bd generates a PMF by transmembrane charge separation, but
does so without being a proton pump.

However there is a complex set of anion co-transporters involved in cytoplasmic pH homeostasis which may influence the membrane potential. The situation is neither simple nor, as yet, completely resolved, as far as I am aware (but it’s not my field).

§ The treatment of electric potential gradient, Δψ, tends to be downplayed in biochemistry text books. This may be because the generation of a hydrogen ion gradient is easier to understand than that of a membrane potential, or because the texts deal with the latter in sections on nervous tissue. There is a quantitative treatment of the free energy changes involved in Chapter 18 of Berg et al. online.

Does the electric potential gradient Δψ refer to the potential gradient due to all ions including H+ ?

@trinitrotoluene — Δψ is the potential gradient resulting from the membrane polarization. It has nothing to do with the ions in solution, save for any role their transport across the membrane may have had in producing this. I am not the best person to explain this further — electrophysiology is something I never studied and scares me rather. The ΔpH is easier to understand, which is one of the reasons text books focus on it. I have added a reference to Berg in my answer, where this is considered from a bioenergetics standpoint.

OK thank you, I'll try looking into it myself


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What is this larva/insect?
What is this larva/insect that I saw crawling on one of my books?

It moves by wriggling motion and seems to be able to retract it's head(?) when disturbed. It is about 8mm long.
Location: Chennai, TamilNadu, South India

Does this answer your question? Identify this smooth-cocoon worm from Southern India

@tyersome While the question is the same I'm not satisfied with the answer given. The larva mentioned in the answer has a white body. This one has alternating white and black stripes. Moreover this larva has two small protruding structures that arise from its head while the one in the answer doesn't. I would like to know the exact species of this larva. If they are just different developmental stages of the same larve then please correct me.


text:
Are there real world examples of one way isolation between two populations?
I know that for two populations A and B, there are situations in which there is a two way exchange of individuals between the populations, and there are situations in which there is no exchange of individuals between the populations.  I have thought before of a situation involving one way isolation between two populations, in which it's easy for individuals from population A to immigrate to population B, but impossible for members of population B to immigrate to population A.
I tried searching to see if I could find any examples of one way isolation between populations, and couldn't find any examples, although I don't know if this is from not using the correct keywords to find it, not knowing where to look, or there being no known examples of it.
Are there any real world examples of the one way isolation I mentioned between populations?

pit caves come to mind.

Fishes leaving on both sides of a waterfall too high to climb up. Sunflowers living along rivers and that reproduce clonaly through cutting, where cuts gets transported by the water stream. Plants reproducing with seed flying in the air and living on a windy sea shore. Plancton living in a water stream.

@Remi.b Do you know the names of any of the specific species that would be examples of this?

Are you thinking of modern-day politics e.g. it was easy to go from one side of the iron curtain to the other, but a lot harder for the reverse?

https://www.livescience.com/nuclear-bunker-cannibal-ants.html

You might want to look for asymmetric dispersal.
Asymmetric dispersal has been found in many freshwater fishes (such as bullhead; Junker 2012), freshwater mussel (Terui et al., 2014) and in marine kelp (bull kelp; Collins et al., 2010).
That being said asymmetric dispersal does not mean that dispersal goes exclusively one way. Maybe Blondel et al. (2020) reporting asymmetric isolation caused by waterfalls in guppies can be helpful to you.
I am also thinking of polyploid and invasive lines of sunflowers that often live along rivers and reproduce clonally through cutting, where cuts gets transported by the water stream. I co-authored a paper on the evolution of these invasive sunflower lines (Bock et al., 2018) so I should know the literature well but I don't and I am not able to cite a paper that really describes the dispersal and population structure of these sunflower lines. Such patterns might be found in Mimilus as well.
Planctons follow water streams and can therefore have very asymmetric dispersal too (Pringle and Franks, 2001).
I am also thinking of plants reproducing with seed flying in the air and living on a windy sea shore or in windy wide open plane (e.g. tumbleweed). But I cannot give you a reference.

Thank You!  I liked reading about how in the case of guppies, natural selection would tend to favor traits that would make the guppies less likely to go through the waterfall in guppies living above the waterfall, which makes sense seeing as how a guppy going past the point of no return would be equivalent to dying with respect to the above waterfall population.


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Why do animals yawn? What is the biology behind it?
We yawn whenever we are tired and body needs rest. Why does the mouth open wide and a large volume of oxygen is inhaled?

Does this answer your question? Why do we yawn?

To some extent. Thank you for the link.