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If post transcriptional modification happens , how can a gene code for amino acids in a particular order?
Post transcription, introns are removed and exons are rearranged randomly. If that's the case (which it is according to the book EDEXCEL SNAB A2 topic 6) then shouldn't the protein produced be different every time? Shouldn't the order of amino acids be different? And if it is, doesn't that mean that the protein produced is different?
To quote : "When mRNA is produced, its introns are removed by spliceosomes and a different number of exons is put together at different orders which changes the sequence of amino acids in proteins."
Quote from the book:

Genes contain sections that don't code for amino acids.

These sections of DNA are called introns. All the bits that do code for amino acids are called exons.
During transcription both introns and exons are copied into mRNA.
The introns are then removed by a process called splicing -- introns are removed and exons joined forming mRNA strands. This takes
  place in the nucleus.
The exons can be joined together in different orders to form different mRNA strands.

If this process happens,how can a gene code for a specific protein? This process means that exons are arranged differently, and this means that amino acids are arranged differently, and doesn't that mean that different proteins are going to be produced than the one coded for?

Can you provide a quote or something from the book? It's hard to evaluate the statement otherwise, but "exons rearranged randomly" is certainly not the usual way of business, if it happens ever (I can't think of a situation where it would). Maybe somewhere in the immune system which I am not fully familiar with.

See also https://biology.stackexchange.com/questions/5/is-exon-order-always-preserved-in-splicing

@user1136 Differential splicing isn't the same thing as "rearranging exons randomly"

@user1136 But OP doesn't seem to, and that makes your statement misleading and OP might misinterpret it as an answer to their question.

@Lia What's the context of the quote from the Edexcel book? Is it talking about a specific group of proteins? Different arrangements of exons occurs in various proteins such as antibodies but if it occurred in every protein, no receptor or enzyme would be the right shape to allow its biochemical effects. As Bryan says, it's not the usual way of business.

"then shouldn't the protein produced be different every time? Shouldn't the order of amino acids be different? And if it is, doesn't that mean that the protein produced is different?"
It is not different every single time, but it is different depending on what kind of post transcriptional modification takes place. The proteome is larger than the genome thanks to this, genes can code for many different proteins thanks to post transcriptional and post translational modification as well.
So as I understand it, gene segment = same order of nucleotides = same primary mrna
post transcriptional modification to primary mrna = different mature mrna = different order of amino acids = different polypeptide chain (then different protein later on)
Hope this helps


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Question about the threshold potential
I am a student of Physiology, and I have ended up a bit confused after what I've read today regarding events during a threshold potential. So, while cells are in their resting membrane potential, the inward current of sodium is equal and opposite to the outward current of potassium. The same is true about the threshold potential.
When the threshold potential is reached, the inward sodium current is exactly equal and opposite to the outward potassium current. If this is true, why is there a change in the voltage of the membrane, let's say from -70 mV to -55 mV? I mean, both of the currents are equal and opposite and therefore there shouldn't be any change in the resting potential of the membrane.

Welcome Lydia. Obviously, of course threshold is different from resting potential, as the former generates an action potential and the latter does not. This question is really basic. What are your own thoughts about this?

Okay, so I know that in order for depolarization to occur, the influx of sodium must be greater than the efflux of potassium, and therefore the threshold potential is reached. However, I still don't understand how can the inward Na+ current be the same as outward K+ current in a threshold potential. I am sorry if the question is too basic, I just started the course few days ago.

Below is a figure showing the sequence of events during an action potential (AP). While the resting potential is characterized by an equilibrium, during an AP this balance is markedly 'disturbed'. The action potential is characterized by a specific timed series of events, namely the opening of Na+ channels in the initial depolarization phase, followed by an opening of K+ channels in the subsequent repolarization phase. During these phases, the Na+ and K+ currents are anything, but balanced.

Fig. 1. Series of events during an AP. source: Brigham Young University-Idaho

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What photoreceptors are necessary to permit infrared vision?
Humans have red green and blue photoreceptors allowing them to sense colours in the spectrum of about 400-700nm. Certain proteins allow for the extending of wavelength range in the RGB receptors, this however is only perceived as more shades of the colour in question. Additional photoreceptors are necessary to sense a new colour, explicitly separate from RGB.
Organisms such as mantis shrimp can sense infrared light as they have 12-16 cones, allowing them to see into the infrared spectrum.
The issue is that there seems to be no information detailing the the structure of mantis shrimp eyes, specifically regarding the the aspects of which are responsible for vision into the near infrared spectrum (roughly 700-1000nm).
What would the cones of an organism that saw exclusively in infrared look like? (assuming the organism had eyes like a human)
Would they be differently coloured or structurally different to our own?

Are you asking what the photoreceptors of a mantis shrimp look like?

@AliceD Infrared light sensing photoreceptors in general, although mantis shrimp would be a good example.

The photoreceptors of the mantis shrimp (Fig. 1) are quite different from that of the human retina (Fig. 2).
Importantly, when light enters the units in the shrimp's eye, it must first pass through a crystalline cone, which lies over the receptors. These crystalline cones contain frequency-specific light-blocking substances called MAAs (mycosporine-like amino acids). These filters help to filter the spectrum and this means that less different opsins are necessary tod etect different wavelengths. In other words, a mantis shrimp does not feature 16 different opsins. Instead it utilizes the same opsins for various wavelengths by putting a filter on top of the cone (source: National Geographic).

Fig. 1. Mantis shrimp photoreceptors. source: Physiologizing

Fig. 2. Human cone cell. source: Wikipedia

Interesting. Do the Crystalline cones of the mantis shrimp have set colours which they detect such as a humans red, green and blue?

Yes they do; each class is devoted to a specific [range of] wavelength[s]

I know i'm asking a bit much, but would you happen to have any information regarding how they are devoted to different ranges of wavelengths? E.g. different colours or lengths.
Also, could you please define what you mean by 'class'.

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What happens in a nerve cell when a thought is generated?
I know basic nerve physiology of impulse conduction and transmission, but I don't know what actually happens in a nerve cell when a thought is generated. When a external stimulus (like tactile stimulation, injury causing tissue damage) leads to stimulation of respective Na+Channels and action potential is generated. But what is the stimulus in the neurons of the Central Nervous System when we think about something? What exactly is the stimulus that cause the neuron to generate action potential and then following it, it is transmitted to different circuits and then we react accordingly?

This is a recurring question that many people are bothered with. I read an interesting answer on Quora. Basically, the author says that there is always on-going activity in the brain. Each thought is triggered by something, let it be conscious or unconscious. The brain is never silent, even in your deepest sleep with only slow-wave synchronized activity, there is still activity. Even when it seems that a certain thought pops up totally randomly, it is still triggered by certain inputs, let they be sensory or internal. Note that action potentials can be triggered either by signals from the outside world (sensory receptor neurons), or by signals from other cells in the brain and body.
Also note that most, if not all neurons show background activity ('neuronal noise'); they never stop firing even without inputs. When one or more of those background potentials impinge on a postsynaptic neuron, that neuron may be activated an fire an action potential. This may also explain some random events in the nervous system.

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Best colour for a dog to track an object against green background
As dogs have limited colour perception, what colour would appear with most contrast against a green background for a dog? I understand that red and green are very close in a dog's colour perception, so would blue offer better contrast?

Dogs are a dichromatic species, featuring only a long wavelength (L) and a short wavelength (S) cone (source: Smithsonian). As such, they are thought to perceive mainly blues and yellowish hues (Fig. 1). This is unlike trichromatic species like humans, who are able to distinguish red and greens as well (Fig. 2). Whether dogs perceive greens or yellows is hard to say, but either way, they see those longer wavelengths (red, green, yellow) as one hue (say, yellowish).
Hence, in dogs, green hues are basically seen as yellow (or vice versa) and indeed blue (short wavelengths) are best to create a good color contrast.
Of course, brightness contrast will work fine too (white and black).

Fig.1. Dichromatic (dog) color spectrum. source: Dog Vision

Fig. 2. Trichromatic (human) color spectrum. source: Dog Vision


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What is structural RNA?
In genbank (ftp://ftp.ncbi.nlm.nih.gov/genomes/archive/old_refseq/Fungi/Saccharomyces_cerevisiae_uid128/) there are an archive .frn (nucleotide sequences of structural RNAs in fasta format), and  I want to know the differences between structural RNAs and genes.
Are the nucleotide sequences of structural RNAs a coding region?
My goal is separate the coding region from the non coding region of a given complete genome.
I'm physicist so, I apologize if my question is pretty simple.

@David I guess "structural RNA" is not a standard term. I won't even expect biologists to be sure about what it could mean.

@WYSIWYG — Inspection of one file with extension .fm gives names for some of these structural RNAs, such as Pro tRNA, 15S ribosomal RNA. I assume the poster has read this. I would have expected him to try to find out what a tRNA and a ribosomal RNA actually was. If he is not prepared to put the effort into reading about molecular biology he is wasting his (and our) time.

To be very brief: A gene is a sequence of DNA or RNA, which is hereditary and has a biological function. In the Saccharomyces cerevisiae genome you posted, every gene is a DNA sequence. The function of most genes is to be transcribed  to messenger RNA (mRNA), which is then translated to a protein. "Coding" DNA refers to DNA which eventually has its sequence translated into protein
Structural RNAs are encoded by genes but not translated to protein, and thus are not coding regions. They are made up of RNA, but function more like proteins. When they enable reactions, like enzymes, they are called Ribozymes. The most well known ones are the Ribosomes, which are an essential part of protein biosynthesis. Others form special structures which help molecules recognize each other. tRNAs are needed for the ribosome to recognize the right amino acids.
As David said, this is very basic molecular biology and gene regulation/expression in eukaryotes can get quite complex. The wikipedia articles provide a good introduction and the Berg biochemistry book he linked is excellent further reading. If you want to know more about yeast genomes, you can check out https://www.yeastgenome.org/. It provides a whole lot of information regarding the amount of coding/noncoding regions and their function. There is also a graphical genome browser, where you can view each region in detail and compare it with your own findings.

Coding DNA refers specifically to regions that are translated into protein. Non-coding RNA like tRNA or rRNA are by definition not part of coding regions.


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Why do some reflex actions involve interneurons, but some don't?
According to what I know, the reflex arc of knee jerk reflex doesn't involve interneuron, but other reflex action (e.g. removing your hand when touching hot things) do involve interneurons. Why is that the case?

I believe the knee jerk reflex does involve interneurons.

@John my biology textbook specifically say knee jerk reflex doesn't involve interneurones and the teacher also kept telling us to remember that knee jerk reflex is the only reflex in the exam syllabus that doesn't involve interneurone

The "knee jerk" reflex is a stretch reflex, as @John's answer indicates. It is unfortunately named the "knee jerk" for the response observed in the corner case where rapid, short extension of the leg at the knee is elicited by tapping the patellar tendon with a percussion hammer during a physical exam. Despite being named for this specific phenomenon, this reflex contributes to setting resting muscle tone, controlling the response to a load, and coordinating synergist and antagonist actions. You can read about this in some detail in Kandel's Principles of Neural Science, Chapter 36.
The sensory portion of this reflex involves a proprioceptive sensory organ called a muscle spindle that detects the stretch of a skeletal muscle.  All human (and most mammalian) skeletal muscles have these sensory organs, so this is not specific to the quadriceps at the knee. Several are tested in a similar way to the quadriceps as part of a neurological exam (see Brust, Practice of Neural Science, Chapter 6), but, as is the case with most reflexes, they are more complex than is taught in introductory biology. This sensory organ is continuously active, sending information to the cortex, the cerebellum, synergist and antagonist muscles, as well as back to the muscle in which the organ itself is found (again, see Kandel).
Answers about "why" a physiologic system is set up in a particular way are generally speculative, but stretch reflexes in muscle are definitely different from other reflexes. Unlike, for example, the withdrawal reflex, the sensory organ (the muscle spindle) is actually part of the effector (the muscle), and provides continuous feedback to the effector, controlling its primary function (contraction/production of tension). Additionally, the processing and sensitization/desensitization that an interneuron might provide in a different reflex arc are provided by innervation and control of the spindle itself by $\gamma$-motonuerones, among others.

$\gamma$-motoneurone function is essential for controlling the sensitivity of muscle spindle afferents as length detectors

There are additional reflex arcs with the same sensory part that involve processing and inhibition/excitation by interneurons. But in these cases the outflow is to a separate effector (antagonist muscles). See the figure below from Brust, Chapter 6.

I did not realize it but the knee jerk reflex is a stretch reflex and thus only involves two neurons (monosynaptic). Many many more reflexes use 3 or more neurons (polysynaptic) so include interneurons.
monosynaptic are common for muscle stretch limiting reflexes, that is why I knew them by their more common name stretch reflexes and did not make the connection. They don't involve interneurons becasue they would offer little benefit, they are self regulating most of the time and only involve a single source and a single destination and will not see much benefit from modification of the signal.
This slideshare on reflexes can provide some detailed information and a place to keep researching from.


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Can acetylcholine leak away from the synapse and cause spasms?
I am currently studying Pharmacology and a question came to mind. We know that Acetylcholine is used as a neurotransmitter in the neuromuscular junction, both Sympathetic as Parasympathetic, but as I understand, correct me if I am wrong, they don't interfere with each other because of their locations being physically separated. My question is, could somehow occur the incomplete absorption of Acetylcholine in the receptor of the organ, let's say for a Parasympathetic response and it "leaked" to a nearby muscle or even into a Sympathetic receptor and create a involuntary movement for example?

The enzyme responsible for the breakdown of acetylcholine (Ach), i.e., acetylcholinesterase, rapidly degrades, and inactivates Ach in the synaptic cleft after release. This process is particularly fast, as the synapse has to be cleared of neurotransmitter for a next action potential to occur (Čolović et al., 2013). So no, Ach does not leak away under physiologiocal conditions (Fig. 1).
In fact, common cholinesterase inhibitors that lead to Ach buildup by inhibiting its degradation, do not cause involuntary muscle twitches (spasms) as side effect. However, they do evoke muscle cramps, but that is easily explained by the increased retention of Ach in the synaptic cleft, leading to prolonged muscle contraction.

Fig. 1. Cholinesterase is active in the synaptic cleft. source: Health & Fitness.
Reference
- Čolović et al., Curr Neuropharmacol (2013); 11(3): 315–35

"So no, Ach does not leak away under physiologiocal conditions "
I beg to differ. During times of  psychological stress, after a physical injury or infection, these can interfere with mitochondrial biogenesis and acetylcholine  leak from the neuromuscular junction damaging the sarcoplasmic reticulum and creating a feed forward loop.
Even though the pathophysiology of myofascial trigger points is not fully understood, the hypothesis of acetylcholine leakage is mostly accepted. Indeed, leakage of acetylcholine leads to impairment of sarcoplasmic reticulum with following extensive calcium release, as well as secondary sarcomere contraction and cell membrane damage. It results in local vasoconstriction leading to ischemia and hypoxia [3, 4]. That is why acetylcholine leakage at the neuromuscular junction may be significant in the context of thermal imaging.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053472/
Myofascial Trigger Points Therapy Modifies Thermal Map of Gluteal Region
Grzegorz Onik, Teresa Kasprzyk, [...], and Karolina Sieroń
Zhuang X, Tan S, Huang Q. Understanding of myofascial trigger points. Chin Med J 2014;127:4271–7.
Bron C, Dommerholt JD. Etiology of myofascial trigger points. Curr Pain Headache Rep 2012;16:439–44.


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How exactly does sensory substitution work?
Sensory substitution, when one of sensory modality changes into another sensory modality to help someone restore the ability to perceive defective sensory using a working sensory modality. For example, blind people who have improvements in their other senses like auditory system or olfactory system compared to normal people. Or deaf person who have enhanced vision ability than normal people.
Questions :

Does this work the same way as Alternative Sensation ?
Is there any pattern of which senses will probably improve according to which kind of senses someone's lacking ?
Is there actually any method to train which senses someone would like to improve ?

Tot start of with your definition:

Sensory substitution, when one of sensory modality changes into another sensory modality to help someone restore the ability to perceive defective sensory using a working sensory modality.

I personally like to use a more subtle definition of sensory substitution (Stronks et al., 2015):

[T]he process of obtaining information about the world through an alternative intact sensory channel [] that would normally be obtained by the deficient [sensory] system.

In other words, the information is not changed into another modality; it is simply processed by a sense normally not used for that purpose. Your definition seems to imply that the information stream is swapped. Although this is not strictly true, and hence the reason I like the second more subtle definition better, it is nonetheless true that cross-modal plasticity results in the deafferented cortical regions being taken over by other senses; for example in the blind, it has been shown that tactile and auditory information is processed in the visual regions, even down to the V1. The primary visual cortex is normally strictly associated with low-level visual processing, being the first central brain area where visual information enters the brain. Although this view is contested(V1 is also activated by tactile grids for example), in blind folks there are gross rearrangements where the somatosensory and auditory cortices take over the visual system (e.g., Pascual-Leone et al. (2005)).
To your questions

Does this work the same way as Alternative Sensation ?

'Alternative sensation' is unfamiliar to me, it doesn't pop up in a Google search, and its nonexistence is backed up by this answer.

Is there any pattern of which senses will probably improve according
  to which kind of senses someone's lacking

Yes. It depends on which senses are used most extensively to substitute for another sense. Training is an important factor in improving alternative sensory capabilities. In fact, it is the determining factor; the loss of a sensory system in itself does not propagate compensatory mechanisms (Stronks et al., 2015). Compensation being

partial compensation for [the] loss of [a sense] by developing enhanced abilities with [] remaining senses

For example, training with the BrainPort Artificial Vision Device (Fig. 1), which projects electrotactile 'images' onto the tongue using 400 electrodes, gradually improves performance in the blind, all the while the somatosensory information is funneled progressively into the visual system (Stronks et al., 2016).

Is there actually any method to train which senses someone would like
  to improve?

Pick your sensory substitution device of choice and train away; popular ones include, as said, the BrainPort (improves tactile-to-vision substitution), but also visual-to-auditory techniques like the vOICe (Striem-Amit et al., 2012). Also don't forget the guide cane, which funnels tactile information to the brain. especially the visual-to-auditory sensory substitution devices require a lot of training (Stronks et al., 2015). You can try the vOICe out yourself on an Android. However, I have tried the BrainPort myself and it is really difficult!
References
- Pascual-Leone et al. Annu Rev Neurosci (2005); 28: 377–401
- Striem-Amit, et al. PLoSONE (2012); 7(3): e33136
- Stronks et al., Brain Res (2015); 1624: 140–52
- Stronks et al., Exp Rev Med Dev (2016); 13(10): 919–31

Fig. 1. The BrainPort converts camera images into a 'grayscale' 400 pixel electrotactile image on the tongue. It partially restores visual function in the blind. Picture source: Midday Daily

Thank you very much for detailed answer! The references also very helpful, I really appreciate it and will check on them. About the definition, I don't really grasp the difference of "the information is simply processed by a sense normally not used for that purpose" and "the information stream is swapped"? Are they not the same? For example in Aural Antennae,2008, they try to create artificial synesthesia by swapping sensation,"by swapping audio sensation for haptic sensation we illustrate one variety of artificial synesthesia"

@raisa_ my pleasure. The definition used in the answer and 'swapping it' seems to imply that tactile information is processed by the visual system. This may not be true. Ultimately, after years of training it may happen, but it doesn't have to. If you need references, let me know. They may be paywalled. The Stronks guy is actually me.

Actually, can I ask one more thing ? If for the same sensor we change the stimuli for example in skin, to gain respond for someone who has less sensitivity with pain (pinch), we change the stimuli into heat instead. Is it still part of sensory substitution then ? Because the sensor doesn't change, the same sensor will process the information, but another stimulus is replacing the original stimulus as the input information.

@raisa_ I guess it is still SS

I couldn't find if there's any other terms related to the condition I asked previously : if the processing sensor is the same and we just replace the stimuli. I thought SS worked with 2 different sensor, so it also fits the condition for 2 different stimuli for the same sensor.  I'm gonna look for some more information on this. Thanks again !

As another analogy that I find heartwarming every time I see it represented, it's a bit like telegraphing a game like some people do for their deaf and blind friends: https://www.youtube.com/watch?v=Xzvdu9u1eUA They are using hand motions to effectively translate the visuals of the game, letting the subject build an internal representation of what's happening out in the world: that's all our senses can do anyways.


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Why do we make T4 if we only use T3?
So, recently, I learnt that T4 and T3 are both released into circulation but only T3 is the active form. Why then, do we make T4 in the first place? I read that T4 has a higher half-life, which might be the reason. Also, my professor said that it might be because thyroid peroxidase is not specific enough to control if it adds one Iodine or two. So, what is the actual reason?

T4 also has some biological activity, albeit less than T3. Nevertheless, besides the longer half-life, conversion of T4 to T3 can be regulated at tissue-level. So it adds another layer of control.

It sounds like what you read and what your professor mentioned are different types of causation.
T4 is the primary form produced by the thyroid; T3 is metabolized from T4 in other tissues and more strongly activates thyroid hormone receptors. Metabolism from T4 to T3 then allows tissues to have control over how much active thyroid hormone there is - multiple levels of control are very common to hormones, and other signaling pathways as well.


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What causes goose bumps?
What is the actual process and reflexes that cause the goose bumps? Why is it an evolutionary advantage to have goose bumps in the first place?

Even wikipedia has all details you required for mechanism.

We get goose bumps because of the flight or fight response or because of cool temperature. The process is that whenever our body experiences such stimuli, the arrector muscles contract and thus the hair follicles straight out. As per the evolutionary point of view, mammals possessed this feature to portray the enemy our response ( in fight). Given photo will tell you the arrector muscle's position so that u can understand how the follicles straight up.
And the thing about cool temperature, the goose bumps appear so that they can form an insulation sort of thing to prevent us from losing our body heat to the surroundings.

Where is this pic from?

Working kindersley publication- ultimate visual dictionary

Goose bumps are the hair follicles raising up to increase the surfaces area of your skin. This is flight or fight response as it increases ability of the skin to transfer body heat.


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Anesthetics, specifically inhaled anesthetics
I have had a look at previous inhaled anesthetics and many of them appear to be fluorocarbons. What could be the mechanism behind fluorine's anesthetic properties? Is it the specific bonding pattern or the molecules involved?
I realize anesthetics are rather unknown I just wondered what people have as a hypothesis?

Note that Fluorine is not anaesthetic. Inhaling fluorine would give you a permanent anaesthesia. :P

The following is one of the many elegant statements in General Anesthetic Actions on GABAA Receptors:

It is the fervent view of the authors that general anesthesia is no different from any other pharmacological process: exogenously administered drugs interact with key sites on cellular proteins in the body which results directly in the alteration in the function of these proteins, in the present case, neuronal proteins that control how information is conveyed through the nervous system.

Isoflurane, Sevoflurane, and Desflurane, the current inhalation general anesthetics, along with Halothane and the intravenous anesthetics Propofol, Etomidate, Methohexital and Thiopental, enhance the function of GABAA receptors (GABAARs), the most abundant fast inhibitory neurotransmitter receptor in the CNS (ligand-gated chloride ion channels) by increasing the affinity of the receptor for GABA. Since these receptors are abundant in parts of the CNS that process higher-order brain functions, it stands to reason that GABAAR function is central to memory, awareness and consciousness. GABAARs are involved in mediating hypnosis, depression of spinal reflexes, and amnesia, three of the classical components of general anesthesia. Isoflurane, Sevoflurane, and Desflurane enhance the amplitude of responses to low concentrations of GABA and prolong the duration of GABA mediated synaptic inhibition.
A very good starting point for your investigations can be found by clicking on the linked article above.
Agent-selective effects of volatile anesthetics on GABAA receptor-mediated synaptic inhibition in hippocampal interneurons
The sedative component of anesthesia is mediated by GABA(A) receptors in an endogenous sleep pathway

You would find it interesting that Xenon is also an anaesthetic (blocks NMDA receptors) [ref].

@WYSIWYG - Yes, it is very interesting! But, as you pointed out, the receptor is different, and I stuck with GABA(A)Rs (as OP wanted info on the halogenated anesthetics), but it's all very interesting. That was a nice article, thanks! Very informative.


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Why do the major and minor groove exist in DNA?
So I know that the major/minor groove arise from the offset pairing of the two strands in the helix.  All my textbook tells me is that "pitch causes the off-set pairing of DNA and this gives rise to the major and minor grooves."
I'm not too sure what this is saying.  What exactly is pitch and how does it give rise to the grooves?

Have you read the articles on DNA, nucleic acid tertiary structure, and the structure of a nucleic acid double helix? They all talk about DNA structure and should be quite informative.

Possible duplicate of How do the major and minor grooves arise in the DNA helix?

Pitch is not a great word for this, as its meaning is ambiguous. It's hard to find a universal nomenclature for DNA geometry, but see the "Base pair geometry" section of this wikipedia page. The relevant property is what they call "opening".
From the biochemistry textbook by Berg:

To explain in words, if the glycosidic bonds (which attach the nucleic base to the sugar in the backbone) stuck straight out at 90 angles on both sides, then the grooves in double-stranded DNA would be symmetrical. Because the glycosidic bonds are at an angle (relative to the interface between the AT or GC pairs), one of the "faces" of the base pair is larger than the other.
Words and flat pictures, however, will never really give you a good intuitive sense of what's going on with the 3D structure of the grooves. A good modeling kit will be of great help to you.

Would it be correct to claim that this is because the nucleobases they're attached to wouldn't base-pair properly (and would likely experience clashes) if they weren't? For instance, in the image in your answer, if the sugar-phosphate backbones were to be diametrically opposite to one another, then, the atoms on the major groove side would clash (i.e., physically encroach upon one another), while the atoms on the minor groove side would be too far away to establish a hydrogen-bond.


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Why are triacylglycerols broken down before being absorbed?
So when dietary fats are in the small intestine, they are emulsified by bile salts in order for action by lipases to occur.  Lipases degrade the triacylglycerols into monoacylglycerols, diacylglycerols, free fatty acids, and glycerol, and these are taken up by intestinal epithelial cells.  Once taken up, these are reformed into triacylglycerols.
My question: why do these have to be broken down in order to be absorbed, and what is the driving force for reformation of triacylglycerols once absorbed?

Your question does not have a clear answer yet, as stated in Metabolic regulation: a human perspective / Keith N. Frayn. – 3rd ed (2010) on page 39.

There is still debate about how fatty acids cross cell membranes.

On that page they claim that a simple diffusion transport is possible through a 'flip-flop' mechanism, where the fatty acid inserts itself in the membrane and then experiences a reversal movement. The kinetics of the process seem to be in agreement with the observed utilization rates.
Also, it is claimed that there is growing evidence specific fatty acid transporters like FAT and FATP (fatty acid translocase and transport protein) play a key role in the process. They might join forces with the fatty acyl-CoA synthase, consuming ATP. ATP consumption activates them, i. e provides energy, for the acyl-CoA formation (not in order to move against gradient). The activated state would enable them to both move into the cell and regenerate a triacylglycerol.

Why do these (triacylglycerols) have to be broken down in order to be absorbed?
I would say that the hydrolyzed products (fatty acid and glycerol) are more readily internalized because their structure is simpler. Fatty acids can perform the flip flop mechanism, but whole triacylglycerols might not (I am not sure). There is a fatty acid binding protein that may help maintain the fatty acid importation gradient too.
What is the driving force for reformation once absorbed?
It is the secretion of chylomicrons loaded with regenerated triacylglycerols. Since they are secreted, they don't pile up inside the enterocyte (intestine cell) and the equilibrium in the synthesis route (the monoacylglycerol esterification pathway) favors the production of triacylglycerols.
Remarkably, not all fatty acids are reesterified, those of short length (< 14 carbons) are not compatible with the acyl-CoA synthase and enter the plasma in a free state. That happens when digesting dairy products.

So there is a mechanism for efflux of triglycerides, but not for uptake?

I'd like to just add on with some more detail.  According to this, gastric lipase cleaves 15-20% of fatty acids in the stomach.  The rest is completed in the duodenum by lipases secreted by the pancreas.  Bile salts, phospholipids and cholesterol coat these lipid particles to prevent them from coalescing.  The reason is because lipases have adapted to oil-water interfaces.  Therefore breaking down dietary fact into "into an emulsion of fine oil droplets enhances the action of lipases.  The smaller fat globules have an increased surface area and are more easily accessible to active pancreatic enzymes for further breakdown."
As for your question on the driving force of why they are reassembled, "several enzymes reassemble the fatty acids and monoacylglycerides to reconstitute triglycerides.  Subsequently, the enterocytes package the reconstituted triglycerides with proteins and phospholipids into chylomicrons."  These chylomicrons travel into the blood stream through the lymph system where they go to adipose tissue and muscle cells for further breakdown.
Barbara E. Goodman
Advances in Physiology Education Jun 2010, 34 (2) 44-53; DOI: 10.1152/advan.00094.2009

Triglycerides are "huge" molecules relatively speaking compared to carbohydrates like glucose or amino acids like alanine. Within the intestinal lumen they are broken down by lipases and solubilized by bile for absorption, which also enhances the activity of pancreatic lipase. So, to get into the enterocytes of the small intestine they need to be broken down. However, once they are reformed you can't just excrete them into the venous circulation because there are exceedingly hydrophobic and can't circulate in their native form. In fact, they first pass into the intestinal lymphatics before entering the arterial circulation. Before this happens, though, triglyceride particles and other lipids like cholesterol are packaged onto lipoprotein molecules for their transport. These lipoprotein molecules are still large, but they have proteins (i.e. Apo-B48) that act as signals to the peripheral tissues for particle uptake into the muscle, adipocytes, etc.

Thanks for your contribution. References are appreciated at Biology.SE. I think it is a great answer, but without references no one can follow up on your information.

Yes, many answers come from the top of my head too, but everyone can claim to be an expert and start selling nonsense :) Like in your previous answer I simply added a wiki link. Personally I don't like wikis and prefer primary literature instead of open-source stuff, but if you are reluctant adding primary literature, some links to credible sources are an easy alternative

Could the reason that triglycerides being neutral and non-polar, require the aid of additional proteins for their transportation but when broken into glycerol and free fatty acids, the individual components being polar are more easy to transport. Also, in terms of storage, the triglyceride form is better because of its non-polar properties and that it would remain relatively inert in the cytosolic environment.

Some points that you mention have already been covered in other answers. Can you please [edit] your answer to add some more details so that your answer provides additional information?

Welcome. Answers need to be founded on credible sources. Please cite relevant references to allow other users to background read on your material.


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What is the role pyruvate carboxylase in lipogenesis?
I just know that Acetyl-CoA is a positive allosteric modulator for pyruvate carboxylase, but I cannot find anything else.

Okay so pyruvate carboxylase is a ligase-class enzyme, meaning it forms covalent bonds. What we see is that pyruvate is carboxylated into oxaloacetate by pyruvate carboxylase, here's our proposed reaction,

What this does is replenish mitochondrial oxaloacetate levels, because when we switch into lipogenesis, TCA intermediates must be shuttled into the cytoplasm for forming triglycerides, like so,

Also here, page 2, they go into how the production of NADPH is coupled to acetyl group export and how PC must perform the aforementioned function to keep substantial flow maintained. Block quoted them for ease of access,

As shown in Scheme 1, the
  generation of NADPH is coupled to the transport of mitochondrial
  acetyl groups into the cytosol for fatty acid synthesis.
  Acetyl-CoA is generated in the mitochondria by the oxidative
  decarboxylation of pyruvate, and, after condensation with oxaloacetate,
  acetyl groups are transported to the cytoplasm as citrate,
  which undergoes ATP-dependent cleavage to yield acetyl-CoA
  and oxaloacetate. This pathway requires a continuous supply of
  oxaloacetate, which is produced by the activity of PC. AcetylCoA,
  a building block for the synthesis of long-chain fatty acids,
  is then converted into malonyl-CoA by acetyl-CoA carboxylase
  (ACC). Meanwhile, the oxaloacetate generated in the cytosol
  from citrate is reduced with NADH to malate, which in turn is
  oxidatively decarboxylated in a reaction catalysed by NADP+-
  dependent malate dehydrogenase (‘malic enzyme’; EC 1.1.1.40).
  The pyruvate thereby produced is taken up by the mitochondria
  and carboxylated to give oxaloacetate, while the NADPH
  generated is used in the pathway of fatty acid synthesis.


text:
Better understanding the life cycle of lasioderma serricorne (cigarette beetle, cigar beetle, tobacco beetle, drugstore beetle)
Lasioderma serricorne, commonly known as the cigarette beetle, cigar beetle, tobacco beetle, or drugstore beetle:

Live 2–4 weeks.
The female beetle lays as many as 100 eggs loosely on the substrate to be fed upon.
The larval period usually ranges from four to five months, but under very favorable conditions the development from egg to adult may occur in 6 to 8 weeks.
When the larvae are fully-grown, pupation occurs and they remain in this resting stage for 12 to 18 days.
The complete life cycle takes 26 days at 37 °C and 120 days at 20 °C.
In the Northeast (presumably USA, as the primary source is a USA university), there is usually only one generation per year.

Sources:
http://idl.entomology.cornell.edu/wp-content/uploads/Cigarette-and-Drugstore-Beetles.pdf
https://en.wikipedia.org/wiki/Lasioderma_serricorne
So it appears their life history cycle is:
EGG -> LARVA -> PUPATING -> ADULT
       2-5MO    12-18DAY    2-4WK

Given that the total cycle duration is much less a year, why do some regions only experience one generation per year?
Are the eggs just sitting for months on the substrate without hatching into larvae?

What happens when cold? Often eggs or pupae wait until warmer.

@PolypipeWrangler Thanks for your comment.  Would that mean in a climate-controlled environment they will prosper year-round?

With other indoor pests in climate controlled house; they do live and breed constantly year round.

@PolypipeWrangler Thank you for the update.


text:
Relative densitometry from SDS PAGE
I'd like to perform densitometry on a Coomassie stained SDS PAGE gel to compare a recombinant protein's expression levels under two conditions. I'm using BioRad's Image Lab software.
My questions are about what estimates can be made, given that Coomassie staining can be nonlinear has protein-to-protein variability. Unfortunately, I do not have a standard curve, and the lanes contain total lysate.

Can I take the percentage of band volume to lane volume as an estimate of percentage of total cell protein mass? (25% vs 20% total cell protein)
Or would it more appropriate to take the band volume normalized to an arbitrary band in the lysate, and then report the percentage difference between conditions? (6 vs 4.8 normalized band volume, or 20% decrease in expression levels).

I don't think you can get away with either. You have no way of knowing that a specific band represents a single protein. Sounds like you should be doing a western blot.

@canadianer Even western blots have nontrivial levels of background staining (especially for polyclonal antibodies), so one will still need to run a standard curve.

@MarchHo that depends on the antibody...


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Why is oxaloacetate made in the mitochondria?
I'm looking at the gluconeogenic pathway:
Pyruvate is shuttled into the mitochondria from the cytosol, converted to oxaloacetate by pyruvate carboxylase, converted to malate which is then shuttled out of the mitochondria, and then converted back to oxaloacetate in the cytosol.  Why is the mitochondrial step necessary?  Why can't pyruvate just be made into oxaloacetate in the cytosol?

http://www.chembio.uoguelph.ca/educmat/chm452/lecture6.htm

Got it.  The ratio of [NADH]/[NAD+] is about 100000 lower in the cytosol than it is in the mitochondria.  The conversion of malate to OAA reduces a molecule of NAD+ to NADH, and that NADH can be used for the later step in gluconeogenesis: the conversion of 1,3-bisphosphoglycerate to glyceraldehyde 3-phosphate requires a molecule of NADH.

It's a way to transport reduction equivalents across membranes, you are absolutely right.


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What color does the other cone in Tetrachromacy correspond to?
Human with normal vision possesses 3 cones, which correspond to blue (S), green (M) and red (L). What about tetrachromacy, where people have 4 cones in their retinae? What is the fourth cone exactly, and what color does that other cone correspond to?

According to Deeb (2005), there are two relatively common types of causes for tetrachromacy in humans:

The common Ser180Ala polymorphism, which results in two spectrally different red pigments in the retina. This mutation also plays an important role in variation in normal color vision. This polymorphism most likely resulted from gene conversion by the green‐pigment gene.
Another common variation are several red/green pigment chimeras with different spectral properties. The red and green‐pigment genes are arranged in a head‐to‐tail tandem array on the X‐chromosome with one red‐pigment gene followed by one or more green‐pigment genes. The high homology between these genes has predisposed the locus to relatively common recombination events that give rise to red/green hybrids and deletions of green‐pigment genes. Such events constitute the most common cause of red‐green color vision defects. Only the first two pigment genes of the red/green array are expressed in the retina and therefore contribute to the color vision phenotype. The severity of red‐green color vision defects is inversely proportional to the difference between the wavelengths of maximal absorption of the photopigments encoded by the first two genes of the array. Women who are heterozygous for red and green pigment genes that encode three spectrally distinct photopigments have the potential for enhanced color vision.

Reference
Smeeb, Clin Gen (2005); 67:(5): 369-3
Further reading
- Color vision across species


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Visual phototransduction, neurons depolarization when no light: why?
While reading into visual phototransduction I was surprised to learn that photoreceptor cells are actually depolarized when there is NO excitation (no light, i.e. when you see nothing, black) and hyperpolarized when there is light (I expected the opposite).
This got me thinking...
Let the collection of neurons located within the eye be referred-to as IEN (inside-eye neurons) and, similarly, the collection of neurons directly linked to the eye, yet external to it be referred-to as OEN (outside-eye neurons).
Let the collection of neurons directly getting input from the retina be referred-to as RN (retinal neurons). I'm assuming RN < IEN (subset of -
 correct me if I'm meaningfully-wrong).
And finally, let the collection of neurons that directly link to OENs but are part of IEN be referred-to as XN (eXporter-neurons, in the sense that they export visual information from the eye to the "listeners" outside of it).
So the path of visual stimulus would then be RN -> [...] -> XN -> OEN.
Now, if my eyes were to be completely popped-out I'm assuming that relative to OENs that would have the same effect as XNs not passing along any excitatory/inhibitory information at all. Also, since what I'd perceive would be pure black, that seems to imply that XNs also don't get activated at all when we actually see black (e.g. close our eyes in a very dark room).
So, when we perceive black => RNs get depolarized => they release glutamate continuously => XNs don't excite/inhibit OENs at all (seems to also imply that RNs don't intersect XNs). It is this inversion that intrigues me - why is it that for XNs to transmit NO information RNs have to continuously be excited? By that sense, this makes me think of the eye as if it was a big NOT gate.

Short answer
The reason for the depolarized state of photoreceptors in the dark is unknown as far as I know. It probably has its roots deep in the evolution of the eye.
Background
Indeed, photoreceptors are continuously active in the dark. A steady current flows through open channels (mainly Na+ ions). This current is called the dark current and it partially depolarizes the photoreceptor cell. The depolarized photoreceptor releases neurotransmitter (glutamate) to secondary neurons. Upon illumination of the photoreceptors rhodopsin molecules are isomerized to the active form and the photoreceptor cascade (Fig. 1) is initiated. This ultimately closes the cation channels in the photoreceptor's membrane, stopping the dark current.  This leads to cell membrane hyperpolarization and inhibition of glutamate release to the second-order neuron (Fig. 1).
Admittedly, I do not know why phototransduction exactly is organized this way. There is a lot known about the evolutin of phototransduction (e.g., Lamb et al., 2016), but why the dark current exists is unknown as far as I know. I surmise it is probably an evolutionary relic. Evolution eventually has to work with pre-exisiting features to generate new structures, or alter them. Simple photosensitive spots evolved into the complex eyes observed in today's vertebrates. Evolution thereby used what was there and that happened to be an energetically unfavorable 'NOT' gate.

Fig. 1. Phototransduction in photoreceptors. source: Kolb, (2012)
Reference
- Kolb, Webvision. The Organization of the Retina and Visual System (2012)
- Lamb et al., Molec Biol Evol (2016); 33(8): 2064–87

Thank you very much for your detailed answer. As I was reading it, another possible explanation struck me that might make the NOT gate behaviour actually energetically favourable: with a NOT gate it's always one or the other (primary/secondary neurons) consuming energy - the alternative would make both consume energy at the same time when there's light. So maybe a NOT gate makes it possible overall to consume less energy.

And yet another idea: even if the overall energy consumption is slightly larger with the NOT gate behaviour, there might actually be another trick evolution has played - energy consumption is still smaller in the case when there is light - but unlike darkness, light also means substantial visual content to process. In short, it might matter more to consume less energy in light (to "redirect" the rest to the secondary neurons processing the visual content) than consuming none in darkness.


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Have skeletons of "failed" animals been found yet?
I don't know what the correct term for "failed animals" is, but I mean those animals which wheren't able to survive due to their "failed" evolution process. Because evolution, as we see it today, has gone through a lot of "this doesn't work" and "this does work" - so the "good" outcomes of mutation have survived and the others haven't.
This is for some an argument against evolution, but just because they don't know really why nothing has been found or that something has been found.
So I want to ask if skeletons of any of those "failed animals" have been found or not. So is there any evidence of animals who had a "really bad" mutation (not illness, but mutation) and haven't survived in the process of evolution?

Yes I meant those which failed, so not those who really made it or had an impact on creatures today.

You could just say fossil of "organisms that left no descendent today". In fact most, if not all, fossils we find are of individuals that left no descendants today. They might be very closely related to the individuals who left descendants but they are likely not themselves. This is the magic of coalescence. Only very few individuals actually contribute to distant generations.

Here's an example of a "failed animal" - the Atacama desert mummy that some people were claiming as an alien - that's been in recent news: https://www.theguardian.com/science/2018/mar/22/genetic-tests-reveal-tragic-reality-of-atacama-alien-skeleton

Short answer
The dodo and Irish Elk, both going extinct relatively recently, are examples of species that have yielded skeletons and went extinct, at least partly, due to maladaptations.
Background
Extinct animals are an example of an answer to your question, barred those species did not go extinct through a cataclysmic event of course. No species can evolve into a meteor-resistant species. The term you are looking for is, I think, maladaptation.
For example, the Irish elk (Fig. 1) has been proposed to have gone extinct at least partly through a maladaptation. The male Irish elk was grew the biggest antlers ever recorded, (over 10ft (3 m) wide. Irish elk became extinct 10,600 years ago, and the male antlers have been proposed as a possible reason, although this is debated (source: Wikipedia). For example, males might have suffered because they got entangled in thickets. The climate changed at the end of the last Ice Age, causing the woodlands in which elk live to shrink. And food shortage might have resulted in a lack of nutritional support for the hefty antlers. However, extinction of an entire species is always caused by a multitude of cooperative factors, so the antlers alone can't be blamed (source: Love Nature, Wikipedia).
Also the dodo (Fig. 2) can be an example of an answer to your question. While not caused by a natural phenomenon, some animals simply become maladapted due to human influences. The dodo is the classic example. The dodo went extinct in the 1600's. It was adapted to life without ground-dwelling predators, as it nested on the ground and couldn't fly. The plump, slow, flightless birds were unable to escape from the sailors and their dogs, rats and pigs who landed on Mauritius (sources: Smithsonian, Love Nature).

Fig. 1. Skeleton of Irish Elk. source: Love Nature

Fig. 2. Dodo skeleton. source: Physiology
Sources
- Love Nature
- Smithsonian
- Wikipedia page on Irish Elk

The anon downvoter is prolly thinking that dodos were perfectly well adapted till humans ruined their party.

@RoniSaiba - Very true - dodos were adapted to their habitat before they encountered humans, as is mentioned in the answer quite explicitly. Since we are currently experiencing a mass extinction event due to us human actions, it might be categorized a cataclysmic event and given my first lines of my answer, the dodo might have been left out of the answer. Nonetheless, I think it serves as an illustrative example of an answer to the question, as it meets all question criteria (maladapted + skeletal proof)

Well, should have known someone would come along with a more complete and better sourced answer than mine. :)  +1.

Of course, we don't need evidence of that in the fossil record: we have evidence of that on going.  All around us we see mutations which lead to life-impairing or life-removing disease.  However, if the mutation causes early death, it never has the chance to reproduce.
Not the most official source, but Wikipedia does say it well:

Alleles that need only be present in one copy in an organism to be fatal are referred to as dominant lethal alleles. These alleles are not commonly found in populations because they usually result in the death of an organism before it can transmit its lethal allele on to its offspring. An example in humans of a dominant lethal allele is Huntington's disease, a rare neurodegenerative disorder that ultimately results in death. A person exhibits Huntington's disease when they carry a single copy of a repeat-expanded Huntingtin allele on chromosome 4.

(Emphasis mine)
It bears mentioning that Hungtington's is a disease which only shows up later in life, giving a carrier the opportunity to pass it on before it shows up.  This allows it to be passed on to its offspring.

Thanks for the upvote above. I didn't vote on yours as I have difficulty seeing how your answer addresses the question?

@AliceD I was particularly addressing the last paragraph: "... So is there any evidence of animals who had a "really bad" mutation (not illness, but mutation) and haven't survived in the process of evolution?"  My point was to point out that evidence of that is going on all around us; finding it in the fossil record wouldn't be evidence for anything tangible.

Yes
There are lots of them, at one time scientists were far more entered in them than normal critters. So called aberrations or anomalous creatures.  Animals born with two heads, extra limbs, and other deformities, even some congenital defects would count.These of course are most likely to be fond in organisms we have lots and lots of fossils of like invertebrates. Note most of what you find are injuries which makes sense statistically, it is rare to find a modern wild animal that is has no sings of injury.
Below is an example of a skull of a horse with cyclopsia, an entire website is devoted to abnormal trilobites, and here is paper listing known abnormal ammonites.


text:
Can someone identify this male Zygaenidae (subfamily Procridinae)?
Photo taken in 2018, Near Berlinchen, Germany.
The immediate vincinity is Calluna on sands. The area has a an interesting vegetation with heather and broom, species-rich grasslands on poor and sometimes raw soil, and extensive pine forest areas with a lot of lichen. Different Prunus species (including P. mahaleb and, sadly, P. serotina) occur. In a flight range agricultural areas (some with rather rare weeds, possibly organic agriculture), but also lakes, rainage ditches, and marshlands. A bit further paludal forests and remnants of (mostly drained) mooreland exist. Some areas within possible flight range have deciduous forests with Fagus, Quercus, Betula, Carpinus, Populus tremula, and some rarer species (planted, including intrduced species).


text:
Evolutionary chronology - if any, which species have evolved in the last 100 years
I heared somewhere, I cannot remember where, that there has not been an evolution observed in our lifetime. In life science class, right at the start, we was doing the usual MRSGREN (how to tell if something is a living organism), and the tutor said that you can also tell something is a living organism if it evolves. So I asked if there has been an observed evolution in our lifetime. She said that there had been many but could not recite any off the top of her head, so the next week she handed me a piece of paper with 8 or so websites that aparrently corroborated her claim. I have not got the paper anymore but I recall there been on there the peppered moth or something. So I set out to look for a chronological list of evolution but could not find an authoritative one. I could only find something on wikipedia that indicated that species have been dying out for the past thousand years, but nothing saying that any have evolved.

Many, many viruses.

Evolution is a continuous process, there's things that have evolved since you asked this question. I think you are looking for speciation events (what you called an "observed evolution" - this would be a very incorrect term)

Every single species in existence has "evolved" over the past 100 years. Evolution is a constant process. You are asking whether we can observe evolutionary change in a given species over a short time span, not whether evolution is occurring. I know this sounds like pedantry but it is a very important distinction.
That said, yes, of course we've seen evolution in action in short time spans. The classic example is the various bacterial species that have developed resistance to antibiotics. As very nicely illustrated by Garry Trudeau:

If you want more rigorous evidence than a comic strip, have a look at Wikipedia's page on antibiotic resistance or read Demerec, 1948(1).
Another example is described by Yona et al.(2) who show that subjecting yeast to high temperatures (heat stress) for a few generations causes genetic changes that help the cells deal with the stress. This is, clearly, evolution in action. In fact, they even show that the first response is the duplication of an entire chromosome (think of it as a crude, bludgeon-like solution) which is later suppressed by other, more subtle, compensatory mechanisms which arise to replace it.

Demerec, Milisav, "Origin of bacterial resistance to antibiotics." Journal of bacteriology 56(1), 1948
Yona et al., "Chromosomal duplication is a transient evolutionary solution to stress", PNAS, 109(51), 2012.

Of course, these two references are just two random examples among thousands of examples. Would be good to also include a reference of observed changes in gene frequencies observed in nature, eventually among the human population if we can show for example how the sickle-cell/malaria gene evolve in response to pathogen within the past 100 years.

Antibiotic resistance - as antibiotics itself - are evolutionary very old processes. These have not developed in the last 100 years. See for example here.

@Chris well, yes and no. I am not suggesting that all resistance to antibiotics happened over the last 100 years, simply that some have which means they can serve as an answer to the OP. There is a huge wealth of evidence that the widespread use of antibiotics has resulted in the development of resistant strains. Of course some such strains already existed but do you deny that others have arisen recently as a direct result of human medical practices?

As Peteris claimed, we cannot witness the complete evolution of a specie in our life time. Our life, being a frozen moment in the eternal journey of evolution, not always gives us the pleasure to completely understand the process of evolution(also the purposes). But we can witness some minute details, which we can consider as the sub sets of a complete evolution. By evolution, most people think of the complete development from one specie to another, but this kind of evolution to develop a completely different specie will take a millions of years. So we could conclude that those kind of evolutions cannot be witnessed in our life time.
But there are those evolutions which are more dramatic and came into existence within a period of some decades, so considering these minor evolutions(or we can call it variations) we have a couple of cases were some species develop,

Resistance over chemicals(pesticides,insecticides)
Adaptions to withstand predations
Cope with available resources(veg/non veg diets)

1. Resistance over chemicals(pesticides,insecticides)

Reappearence of tougher bedbugs that are harder to kill
Entomologist Dini Miller of Virginia Tech says bedbugs probably developed thicker, denser, waxlike exoskeletons, also called cuticles, that repel chemicals in pesticides. To test the hypothesis, her group is comparing cuticle-coding genes in both insecticide-resistant and susceptible bedbugs, as well as measuring their cuticle thickness and hydrocarbon content, which indicates how much wax is present.
  Reference
Evolution of Microgadus tomcod
  After General Electric dumped polychlorinated biphenyls (PCBs) in the Hudson River from 1947 through 1976, tomcod living in the river were found to have evolved an increased resistance to the compound's toxic effects.1 Scientists identified the genetic mutation that conferred the resistance, and found that the mutated form was present in 99 percent of the tomcods in the river, compared to fewer than 10 percent of the tomcods from other waters.
  Reference

2. Adaptions to withstand predations

Lizards are Evolving to be Dancers
Take the southeast fence lizard, for example. When fire ants were accidentally introduced to the States about 70 years ago, the fence lizard found itself defenseless against them. The ants had no natural enemies, and it only took 12 of them to take a lizard down in about a minute. Seventy years later, the lizards that live closest to the port where the ants were first introduced have evolved an unlikely strategy for dealing with their antagonists. How unlikely? Well, there's a dance involved, which makes these animals the first on record to employ the West Side Story method of self-defense.
While other lizards respond to ant attacks by "sitting still, just hoping the ants would go away," these smooth operators developed an ant-shaking shimmy that they've passed on to their kids. And those kids have longer legs for quicker get-aways. Just so we're clear: Nature, not weird daddy issues, has created leggy lizards that thwart attackers through shaking what their mommas gave them.
  Reference

3. Cope with available resources(veg/non veg diets)

Lizards are Rewiring Their Own Guts, Right Now
  In 1971, scientists introduced 10 Italian wall lizards to an island in Croatia, but right after they dropped them off, the Croatian War for Independence prevented the researchers from following up on their little lizard guinea pigs. In fact, the scientists couldn't get back to the island until 2004. When they did, they found 5,000 lizard descendants who had not only annihilated the entire indigenous lizard population, but also rewired the shape of their own innards to accommodate the local diet.
Before their introduction to the island, the wall lizards were carnivores, so their digestive systems weren't built for leaf-eating. But on an island short on insects and long on plants, a strictly carnivorous stomach would be a one-way ticket to Deadville. So the lizards developed things called cecal valves, which were muscles that slowed down the process of food digestion and gave them more time to break down plant cellulose. But growing new gut muscles wasn't all the lizards had up their sleeves. They also grew bigger heads for stronger bites, and dropped territorial defenses.
  Reference

Evolution is an aggregation of all these combined traits and mostly evolution is accelerated when the species are geographically separated, time is a crucial factor  with evolution. We are unlucky to witness a complete evolution in our neighborhood, but all these accumulating traits which change a specie to adapt with a diverse environment is a powerful evidence towards evolution and its working.

Other examples: nylon-eating bacteria and aerobic citrate usage in E. coli in the long-running experiment by Lenski et al..

Short generation cycles
By definition, we shouldn't expect to observe within our lifetimes the evolution of any species with a generational cycle comparable to our lifetime (mammals and such) since species differentiation requires a multitude of generations.
The directly observed evolution thus is limited to short lived organisms such as bacteria, viruses, plants or insects, with an emphasis on the first two.
It is possible to directly observe evolution in an experimental laboratory setting by taking a strain of bacteria that doesn't possess a certain capability (e.g. resistance to some chemical compound), periodically introducing this compound and accelerating the mutation rate by e.g.  radiation, observing the formation of a new species of bacteria that is able to resist this chemical.

Drastic changes in allele frequency due to differential survivorship can be observed within a single generation. There are examples of important change in allele frequency in human due to disease prevalence (adaptive changes) and bottlenecks (non-adaptive changes).

I think this is opinion based and wrong, as @remi.b notes, I am sure examples of very modern evolution could be found in human

@Remi.b Changes in allele frequency within a population by themselves would not constitute formation of a new species, for that you need to observe creation of a new, different population with traits that didn't exist before. The evolutionary changes that have happened in homo sapiens during the last couple millenia definitely don't constitute evolution of a new species.


text:
Mechanism of Decorticate & Decerebrate Posturing? Also why is only Decorticate Rigidity a misnomer?
I read these two from various books, and got confused. The confusion is -
Reticulospinal tracts control gamma motor neurons. Gamma motor neurons control tone of muscle.
In decerebrate rigidity, the reticulospinal tracts are cut, so the gamma motor neurons start firing excessively, and SPASTICITY develops. I understood this part and why Decerebrate Rigidity is a misnomer as it is actually spasticity.
Question is, in decorticate rigidity, the cerebral cortex is damaged. The basal ganglia are intact. One explanation I found is that the basal ganglia keep the reticulospinal tract activated so gamma motor neuron is under control. But if basal ganglia have no direct communication with brainstem or spinal cord, and their efferents pass through cerebral cortex, then even in decorticate rigidity, the reticulospinal tract should not be working, and thus the gamma motor neurons should fire excessively, in which case the decorticate rigidity also becomes a spasticity.
Am I missing anything? I am keeping red nucleus and vesticular nuclei out of this just to make matter simple. My question is about activity of gamma motor neurons in these two conditions. I hope you got the question. Thank you.

Interesting question, and presented with nice explanation of your difficulty. +1

1)
a. Decorticate posturing means rubrospinal tract is the dominant output to the motor neurons of the body... maybe dominant is the wrong word, I am not all that knowledgable on this subject, but it is certainly altering the standard reticulospinal tract based extensor posturing.
http://en.wikipedia.org/wiki/Rubrospinal_tract
It is responsible for the strange flexion of upper limbs (aka arms). I say strange because when you think coma you think extension, not flexion. The lower limbs (aka legs), as always is extensor. Why the upper limb but not the lower limb? The red nucleus may play an additional role in controlling muscles of the shoulder and upper arm via projections of its magnocellular part.
b. In decerebrate posturing the rubrospinal tract is also cut, since the lesion is below the red nucleus. In this scenario the reticular activating system (aka reticulospinal tract) is the dominant output to the motor neurons of the body. Here you get the classic extensor pose, for both upper and lower limbs...
The point is: Rubrospinal tract was what you were missing. The red nucleus is the specific part of the basal ganglia that is involved...

2)
the difference between spasticity vs rigidity:

spasticity is an increased resistance to the passive movement of a
joint due to abnormally high muscle tone (hypertonus) which varies
with the amplitude and speed of displacement of a joint.
rigidity is an increased resistance to the passive movement of a joint which is
constant throughout the range of joint displacement and not related
to the speed of joint movement.

your supposed to test this out on patients to get a feel for what's the difference.
spaciticity is the case for upper motor neurons lesions (ex. stroke), since the spinal reflexes are not being inhibited from above...
an example of rigidity in neurology is Parkinson's disease, which is the loss of the substantial nigra, which like the red nucleus is also in the midbrain... while the the substantial nigra and basal ganglia loop do influence the motor control of the body... they are not upper motor neurons. Upper motor neuron is specific to the corticospianl tract, it is the neuron going from cortex to anterior horn of spinal cord. Basal ganglia does influence the motor cortex but it isn't part of the corticospinal tract, hence not an upper motor neuron lesion.

3)
Role of muscle spindles in spasticity from upper motor neuron lesions:
I am using this website for this part of my answer:
http://www.d.umn.edu
it's from university of minnisota, which is funny because their acronym is UMN

high resistance to stretch occurs when the spindles are overactive
  (usually due to high rate of gamma motor neuron discharge) -->
  HYPERTONIC (SPASTIC)
removing inhibitory inputs to the gamma motor
  neurons increases their discharge rate, and increases spindle output
this can happen when there is an UPPER MOTOR NEURON lesion

It seems that with an upper motor neuron lesion, the gamma motor neuron is uninhibited, thus the gamma fibers have a constitutively increased discharge rate and muscle spindles are overactive. The machanoreceptors in the spindles then decrease their afferent sign, which should lead to relaxation of a/g-motor neurons, and well, I dunno, I am thoroughly confused on the precise mechanism of UMN lesion causing spasticity. Reflexes are intact so the a/g-motor neurons should relax, since only UMN damaged and not any part of the reflex arc. I seem to be missing something here.
I'm calling for back up, someone please help!

I'm sorry but this doesn't answer my question. My question is why only in Decerebrate rigidity, we see gamma motor neuron overactivity. Red nucleus plays a part in pathogenesis I agree, but the rubrospinal tract ends on alpha motor neurons and not on gamma motor neurons. Another thing which I would like to correct, Red Nucleus is not a part of basal ganglia, but a part of extrapyramidal system. Also basal ganglia have no direct connection to brain stem, they have indirect connection through cortex.

this website has something at the very bottom of the page: http://www.d.umn.edu/~jfitzake/Lectures/DMED/MuscleReceptors/SpindlePhysiology.html It seems that with an upper motor neuron lesion, the gamma motor neuron is uninhibited, thus the gamma fibers have a constitutively increased discharge rate and muscle spindles are overactive. The machanoreceptors in the spindles then decrease their afferent sign, which should lead to relaxation of a/g-motor neurons, and well, I dunno, I am thoroughly confused on the precise mechanism of UMN lesion causing spasticity. Reflexes intact, only UMN damaged.

Since in decorticate posture the lesion is at the level of neurons which originate from cortexand relay in the basal ganglia...but since basal ganglia are still intact they do influence in controlling increased discharge rates of gamma motor neuron. Moreover red nucleus is dominant here since no input from motor cortex flexor posture is present that too in upperlimbs since rubrospinal tract ends in cervical spinal cord.
Decerebrate means no rubro no cortex no basal ganglia...so gamma motor neuron are like "yay, i'm free now" so they keep increasingly discharging causing spastic extensor response...

Overall well-written answer... Please add some reliable references though

Not sure if this helps but its what i know after reading my class notes on reticular formation.This may not help but as I trying to learn also I will share.
Decorticate - The motor part way/Rubrospinal no longer has the influence of the higher centers such as the corticospinal - Flexor Response
Decerebrate - The lesion happens below the red nucleus therefore the rubrospinal spinal tract is not functioning - Extensor Response


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Why don't we see turbulence in the aorta even in normal situations?
I read about the Windkessel effect. Then I read about pulse pressure waves getting reflected from the periphery. If the pulse pressure wave is reflected during diastole and at the same time blood is being pumped forward by the aorta due to the Windkessel effect, then we have two opposite forces acting which should create turbulence even in a normal aorta. Why doesn't this happen?

Why don't we see turbulance in Aorta even in normal situations?

There are different parts of aorta where turbulence is possible and where not.
It is often said that in normal situations, we cannot see turbulence in aorta because aorta is very stiff and its surface is very smooth.
However, this is a simplification and involves an average person (middle aged) which has stiff aortic arch too.
Note that the elasticity of arcus aortae is responsible for 50% of the volume to the peripheral circulation, thus creating a nearly continuous peripheral blood flow as anongoodnurse says, see this publication.
However, not all of this blood travel to the backward direction.
It would be interesting to see how much blood is travelling backward.
This would help to understand what is the likely hood for turbulences.
Those models linked by Anongoodnurse's answer are a few models used to locate places of possible turbulences discretely but they do not seem to consider the amount of blood capable of creating turbulences, just discrete models:

Stalder et al. I do not like the first publication because it is using Reynold's number that is designed originally for laminar flow. Problem with viscosity etc. There are better ways to the same thing and consider explicitly the creation of turbulence. It does much simplifications there. Fitting the equation to the physiological ranges of some set of data is bad procedure.
Fukuda et al. I like the second publication. High velocity and turbulence and nonlinear streamlines in the ascending aorta in normal situation. In other words, high magnitude of the strain rate tensor along aortic curvatures. So we need nonlinear distribution of at least 4D (later 6D) to quantify the amount and degree of nonlinear processes in turbulences.
Lantz et al. Third publication. Linear model for nonlinear situation. I am not convinced by their Mesh selection. Only in Mechanics' journal. Very far from Medical publication or from Mathematical. Not rigorous.

In summary, there are many models and publications to answer the question where are the turbulences. However, they try to answer nonlinear problem by linear models.
I have not seen any models where they do this rigorously.
I think we should narrow this problem even more, like Fukuda et al has done.
They manage to provide some good pieces of information by just considering an intervention with least turbulence in the aorta.
Generally speaking, we can see some turbulence in arcus aortae in the diastole when blood bounces back from the aortic valve.
The walls of arcus aortae can store about 50% of left ventricular volume.
However, I do not know how much of this blood is travelling backward and reflecting back from the atrial valve and causing possibility for turbulences.

[P]ulse pressure wave getting reflected from periphery.

Pulse pressure is systolic minus diastolic pressure.
Pulse wave is those small waves inside respiratory waves:

where vasomotor waves are controlling the big picture.

If the pulse pressure wave is reflected during diastole and at the same time blood is being pumped forward by aorta - -.

Wrong! Blood is pumped by heart. Aorta is just a vessel for transportation.
Generally speaking, Some blood is reflected back from arcus aortae which bounches back from the aortic valve.

[Because] windkessel effect then we have two opposite forces acting which should
  create turbulance even in normal aorta. Why doesn't this happen?

You confuse here different terms and processes.
Generally speaking.
Arcus aortae stretches during systole.
It is coils back in diastole (left atrium relaxing), blood crashing off aortic valve, possibly creating a heart sound and increasing diastolic pressure. Like anongoodnurse says, in this phase, you can see some turbulence in the aorta but little, since the wall of the aorta is very smooth and only small portion of blood is travelling backward from the walls of aorta:

where see the aorta coils part.

I wish I could agree with you here, but I don't. Furthermore, your notes aren't reflecting what you're claiming (mostly they involve the causes of the heart sounds and where they occur in the cycle seen on an EKG. The fourth Heart Sound is pathological and is caused by increased resistance to filling of the left or right ventricle because of a reduction in ventricular wall compliance, and is called the atrial gallop.

Finally, the elasticity of the aorta has a lot to do with the propulsion of blood. See Elastic properties and Windkessel function of the human aorta: "the elastic forces of the aortic wall forward this 50% of the volume to the peripheral circulation, thus creating a nearly continuous peripheral blood flow."

@masi I'm talking about normal individuals who do not have pathological fourth heart sound. I was referring to concept "pulse wave velocity". Now as heart pushes blood in systole, the aorta stretches, and in diastole and aorta recoils, at the same time there is the reflected pulse wave that is coming in opposite direction to that of blood propulsion due to recoil of aorta.

@anongoodnurse How much of this 50% of LV is travelling backward? I have an intuition that not all of it is travelling backward so only a portion is possibly causing a turbulence.

@gautampw Yes, you are right. The heart sound IV is not relevant here. I consider here a situation when some blood bounces off the atrial valve only so possibly creating some heart sound.

As the author states, blood flow is to the periphery, so that is clearly the major direction of the blood. I have little disagreement with your modified answer (except for some nit-picking, like your use of "atrial valve" (do you mean the aortic valve?) which makes for some lack of clarity. Your modified answer basically states what I stated in my original answer: There is some turbulence in the normal aorta.

@anongoodnurse thank you for correction! Please, say specifically where your disagreements. Yes, some turbulence. Yes, to periphery but for creation of turbulence it does not matter how pressure difference is created. Reflections matter here.

There is turbulence in the normal aorta, which is thought to be one mechanism of endothelial injury leading to atherosclerosis and thrombus formation.
Blood Flow in the Healthy Aorta: Turbulent or not?
Flow velocity and turbulence in the transverse aorta of a proximally directed aortic cannula: hydrodynamic study in a transparent model
WALL SHEAR STRESS IN A SUBJECT SPECIFIC HUMAN
AORTA - INFLUENCE OF FLUID-STRUCTURE INTERACTION

I do not like the first publication because it is using Reynold's number that is desigined originally for laminar flow. Problem with viscosity etc. There are better ways to the same thing and consider explicitly the creation of turbulence. It does much simplifications there. Fitting the equation to the physiological ranges of some set of data is bad procedure.

I like the second publication. High velocity and turbulence and nonlinear streamlines in the ascending aorta in normal situation. In other words, high magnitude of the strain rate tensor along aortic curvatures. So we need nonlinear distribution of at least 4D (later 6D) to quantify the amount and degree of nonlinear processes in turbulences.

Third publication. Linear model for nonlinear situation. I am not convinced by their Mesh selection. Only in Mechanics' journal. Very far from Medical publication or from Mathematical. Not rigorous.

@Masi - I agree with your critiques of the papers for the most part. These are three models used to study aortic turbulence. I could have included MRI studies as well, but the catheter studies are most plentiful, and they seem to agree with each other. Most of the most recent studies on turbulence in the aorta involve heart valve studies. But I think it's important to note that there is turbulence in the aorta.

Yes, there is turbulence! Please, include better studies and MRI so I can review them. I am very interested in turbulence in many environments. The catheter study is mosthe beneficial in this research. MRI can describe some fluid dynamics.


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brain and fingers movement theorie
I heard somewhere that when we want to do a repetitive movement of one finger (ex the index) . Our brain (in a very crude way) sends a first message to move all the fingers, and then a second message to hold the fingers that we don't want to move.
The person who said it, was explaining about brain evolution and the fact that the old reptilian part of our brain is the one that send the first message and the higher brain sends the second message.
So is that true ?
If so, do other parts of our brain work like that too? For example more complex behaviors, like sexual mate choice?

The body indeed uses lateral inhibition / surround inhibition. When using a muscle, neighbouring muscles are sometimes activated to. So active muscles are excited while nearby muscles are (partially) inhibited (Beck and Hallet 2011)
This surround inhibition is true for fingers (Sohn and Hallet 2004).

It would be good if you could add a reference stating that indeed each finger is associated with a single 'independent' homonculus.

Thanks for the comment @Remi.b . I went on google and found new information stating that the finger theory might be true. Will update my post..

@tocka This is an entirely different question. You might want to keep it for a different post. Don't forget that you will need to provide reference for the claims on which your question will be based and to make sure to correctly define the behaviours of interest.


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Identify tropical flower
Can anyone identify this tropical flower? It was found on a vine(?) in a garden adjacent to a rainforest in tropical north east Australia, however it may not be indigenous.

It is a passion flower (Passiflora) Here's a similar one: http://www.kew.org/science-conservation/plants-fungi/passiflora-racemosa-red-passion-flower , but if I am not mistaken there are a lot of species.

Some sort of passionflower (genus Passiflora). They have very distinctive flowers.
Could possibly be Passiflora miniata.


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Bird in Taipei knocking on the window glass - juvenile hawk? white throat, white beak(?) striped breast, black head(?) brownish body(?), not small
I received these photos from a friend today - a slightly larger than average size bird tapping on the window glass; maybe a brownish body with a white throat and white beak and black head.
The tail is spread in a fairly wide fan, maybe to scare "the other bird" reflected in the window?
There's a front view and one with its head turned, but it's a little tricky to be sure of the colors since the sun is (roughly) behind the bird. I suppose it's possible that the beak may not be white, but just smooth and shiny and reflecting the sunshine.
Taken on a sunny, hot July afternoon in July in Taipei. Coat hangars for scale suggest it's a bit larger than the typical bird.
It reminds us somewhat of a Chinese Bulbul, but those distinct vertical stripes between its throat and breast are very distinctive.
It looks scary/predatory, could it be a juvenile hawk?
Chinese Bulbul photos (mostly from Hong Kong):

https://nhillgarth.com/2013/10/25/more-birds-in-taiwan/
https://cms.hkbws.org.hk/cms/en/hkbws/work/resarch/hk-bird-atlas-2020-en
http://birdingtaiwan.blogspot.com/p/idiots-guide.html

Light-Vented Bulbul (also Hong Kong)

https://theworldsrarestbirds.com/birds/birds-in-hong-kong/

The light-vented bulbul looks quite promising, but I think this bird looks less song-birdy - the size and the large beak makes me think probably not.
I think the Taiwan scimitar-babbler (Pomatorhinus musicus) is the most promising.
you can check out this gallery: https://media.ebird.org/catalog?taxonCode=taiscb1&sort=rating_rank_desc&mediaType=photo
This bird shares the black stripe over the eyes, the thick and slightly curved beak, the breast feathers, the white stripe of feathers just above the eyes, the black feathers on the top of the head, and I think even the orange shoulder feathers if you look closely in the first image.

This seems inescapably correct, WOW! What a perfect fit. Both ebird's taiscb1 and Wikipedia's Taiwan scimitar babbler say that it's "endemic to Taiwan" and the ebird map shows only sightings all over the main Taiwan island - from coastal to mountains, and the island(s) of Penghu - I'm just curious, is it really never, ever sighted outside of Taiwan?

I mean, I wouldn't say its absolutely NEVER seen outside of Taiwan, but when it comes to its natural range, endemic would mean that, yes, it is only found in there. According to https://avibase.bsc-eoc.org/species.jsp?avibaseid=A37AFA6B7625915F , this species used to be considered a subspecies of a related species found elsewhere in Asia and in fact right next to Taiwan in China, the streak-breasted scimitar babbler.

Interesting! As of August 2005, there are at least 13 recognized subspecies of Pomatorhinus ruficollis.  In Taiwan, the song is lower-pitched with 3–4 upturned notes on the same pitch.  P. r. stridulus. which inhabits hill forests of southeast China (Guandong, Fujian and Jiangxi), is the nearest population to Taiwan.


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Identify these two large, colorful dragonflies in Taiwan?
Here are two dragonflies that I photographed today in Hsinchu county Taiwan. They are both quite large, with a body length of about 5 or 6 cm.
I often see them in the same pond or nearby marshy area. They seem pretty confident and are easy to photograph as long as you don't make a big commotion.
The arrows were drawn for my other question Why do dragonflies have these special little spots on their wings?
Is it possible to identify these two species? I can break them out as separate questions if necessary; I don't want to flood the site with "identify this dragonfly" questions.
The first is jet-black everywhere except for a robins-egg blue powdery coloration along the top side of the first two-thirds of it's abdomen. It's wings, like most but not all dragonflies, are transparent.
The second has some amount of red almost everywhere; its eyes and thorax are dull red and it has bright red patches on each segment of its abdomen. Notably its wings are solid opaque red, except for the furthers 1 cm which is transparent. The tiny "special spots" on the tips of each wing are a particularly bright shade of red!

one more: Identify this dragonfly with orange body and orange wings?

Looks like this species is Orthetrum triangulare commonly known as blue-tailed forest hawk. It is an Asian fresh water dragon fly species.
As you mentioned that the dragonfly had a bluish hue, it became clear.

The other one looks like Neurothemis ramburri, commonly known as red perch Reference

Neurothemis is a genus of dragonflies in the family Libellulidae. Most Neurothemis species are red in color.
Neurothemis ramburii (Brauer, 1866) is distributed from Sundaland to New Guinea. There are records from Peninsular Malaysia, Taiwan, the Andaman Islands, Sumatra, Java, Borneo (Sarawak, Sabah, Brunei and Kalimantan), the lesser Sunda islands, the Philippines, the Bismarck islands and New Guinea. It is a widely distributed and common species that thrives in disturbed habitats.

Wow that was fast, thank you!

@uhoh you may accept the answer if you are satisfied for the future references

indeed, thank you for the reminder. I generally wait a week or more to allow for review by other readers and the posting of additional answers, and a week has now passed.


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Coalescent theory - independence of coalescent times
Let $T_i$ be the time to coalesce from $n(t)=i+1$ to $n(t)=i$, where $n(t)$ is the number of sites that have not coalesced yet. In the below example the maximum $n(0)=6$.

As I understand it, many mathematical developments in coalescent theory depends on the fact that the random variables $T_i$ are independent (but not identically distributed). In other words...
$$f_{T_n, T_{n-1}, …. T_3, T_2}(t_n, t_{n-1},….,t_3, t_2) = \prod_{i=2}^n f_{T_i}(t_i)$$
What are the assumptions for this equation to hold true? Below are some suggestions

No selection
Selection is not varying through time
Stable population size
Random mating
Both sexes have the same genetic background
Both sexes have the same variance in fitness
...

source

[Remi, you always make me read up things with your questions. At least half an hour is gone in this. But it's good :)].. As per wikipedia article on coalescent theory, population is also assumed to be very large for continuous approximation of coalescence time (exponential dist).

@WYSIWYG ha ha I'm glad, I can help you seeking for more knowledge with my questions. I may try to write a longer background for my following questions, so to spare some time to the readers.

@WYSIWYG Remi.b I like the reading for your questions, some have even prompted me to buy new books!

As long as members of a generation "randomly choose" their ancestor in the previous generation the law of independent probability (your equation) will hold.
Any study of coalescent theory begins with the Wright-Fisher model. The assumptions are:

finite diploid population of constant size N,
non-overlapping generations (simultaneous reproduction),
random mating,
no mutation, selection, or migration.

These assumptions are consistent with independent non-identically distributed waiting times. An example of an assumption under which independence no longer holds:
Individual B's random choice in generation 2 of ancestor A in generation 1 reduces the probability that individual C in generation 2 will choose A. In other words, the likelihood that A will give its genes to the next generation falls off with each new recipient. Then the independence no longer holds.
See, e.g., Deonier, Computational Genome Analysis (2005, Springer) at pp. 392 ff.
J. Wakely's paper Coalescent Theory: An Introduction (Systematic Biology, 58:1, Feb. 2009) may be one of the best overviews of this immense topic available. He mentions Kingman's 1982 mathematical proof (which I haven't gone through) of the coalescent process (Stochastic Processes and their Applications 13 (1982)--available as a free download from ScienceDirect).

+1 Good guy @daniel! You're answering to many of my questions. I am actually reading (a bit slowly because I have quite a lot of things to do beside this reading) John Wakeley's book, Coalescent Theory, an Introduction. I was expecting that the only assumptions for the independency of $T_i$ were those of the underlying Wright-Fisher or Moran model. I wasn't sure though. Thank you

@Remi.b: It is good for me to work through some of these questions, which are interesting and thoughtful. I too am busy or I would work on more of them! Thanks.

Your link to the Wakely paper is broke. Could you please write out the full reference so that it can be searched even if the link is broke? Thank you.

@Hans: Thank you I will get to this soon. Appreciate the heads-up.


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Do nucleosomes ever completely unwrap during transcription?
In eukaryotic transcription will the nucleosomes ever completely unwind the DNA and the histone complex disassemble? If an operon is more 160 base pairs it seems it must.

Nucleotide is the wrong term here. I guess you are talking about nucleosomes, right?

Histones can be ejected from the nucleosome, leaving free DNA. DNA can also translocate relative to histones. Both of these processes are catalysed by by chromatin remodelling proteins. It has also been shown that a protein complex called FACT greatly increases the transcription efficiency of chromatinised DNA. It does this by transiently removing an H2A/H2B dimer from the nucleosome. I'm not sure if the exact mechanism behind why this increases efficiency is known, but it does.

Danny Reinberg's group have done a lot of detailed biochemistry to show why FACT aids transcription efficiency. Part of the answer has to do with topological constraints imposed by nucleosomes.

Yes, nucleosomes are completely unwound. Histone chaperones such as FACT (for H2A/H2B) and ASF1, CAF-1, HIRA, Nucleophosmin etc (for H3/H4), associate with RNA Pol II and handle the displaced nucleosomes. As you surmised, the histone octamer complex is disassembled, into the H3/H4 tetramer and two H2A/H2B dimers. Right behind the elongating Pol II, the chaperones reassemble nucleosomes. During the process of reassembly, it has been shown that "new" H2A/H2B dimers (and possibly H3/H4 tetramers too) can get incorporated into an "old" histone octamer. Finally, nucleosome remodelling complexes such as SWI/SNF re-space the nucleosomes.
This is a decent review of the process (by one of the discoverers of the FACT complex, incidentally): "New chaps in the histone chaperone arena". Campos & Reinberg. Genes & Development (2010): 24: 1334-1338
This is a comprehensive review of histone chaperones and nucleosome dynamics during various DNA-dependent processes (such as transcription, replication and repair). There is an entire section on their role in gene transcription, which is the main thrust of this question: "Histone Chaperones: Assisting Histone Traffic and Nucleosome Dynamics". Gurard-Levin, Z.A., Quivy, J., and Almouzni, G. Annual Review of Biochemistry (2014): 83: 487-517
And finally, a good overview on histone dynamics and chromatin structure during transcription: "Histone exchange, chromatin structure and the regulation of transcription". Venkatesh & Workman. Nature Reviews Mol. Cell. Biol. (2015): 16:178–189

I should add that an inability to disassemble nucleosomes (or displace any other factor bound very tightly to DNA) can actually pause an elongating Pol II complex.

It would be nice if you could add some references to this answer.

I've added a couple more references, as requested.

Just to add very recent new information to the first answer: the initial steps of RNA Pol II transcription through a nucleosome have now been revealed at the structural level by cryoEM. See these two articles: - https://doi.org/10.1126/science.aau9904 - https://doi.org/10.1101/437574