text:
RT-qPCR for RNA quantification
I'm really new to RT-qPCR and probably I've just a minor problem than I think.
So, what's my problem about.
I want to quantify a virus by a specific area within a gene on its genome. I've specific primer which are working fine with the extracted virus rna from my samples. But now I need a template for a dilution series to quantify this virus. And there's my little problem. And maybe you can help me.
So I know that the genome of my virus is a negative sense single stranded RNA, so -ssRNA, and moreover I know the virus strain and the gene, which RNA I want to synthesize for the quantification. So I looked it up on ncib and I found the sequence of the gene, but it is listed as the complete cds of the gene and not the RNA sequence. And as I'm right the cds is the same sequence as the positive sense RNA, with Us instead of the Ts?!? So is it right for synthesizing, that I have to translate the cds first in +ssRNA and then in -ssRNA and this -ssRNA sequence I have to synthesize to get a standard?
If the cds would be: ATG , the +ssRNA would be: AUG and therefore the -ssRNA would be: UAC and this UAC , I would have to synthesize? Sorry for this stupid question but I am a lil bit confused at the moment with the difference of - and + ssRNA regardind the RT-qPCR. Another question would be, whether the Reverse transcriptase with Random hexamer primer is specific for -ssRNA or +ssRNA. It isn't ? So my quantification would also work with the AUG as a template for a standard curve?
Thanks a lot!
dan

To start off with your last question, strandedness is something the reverse transcriptase does not care about. If you use random hexamers it will simply translate your -ssRNA into a + single stranded cDNA. Perhaps this diagram from Wikipedia makes things more clear, it is for an mRNA but the principle is the same:

This cDNA will then serve as a template for your primers in the qPCR which will turn it into a double stranded DNA molecule. In other words, after one round of amplication in a PCR reaction the DNA products of the + and the - RNA strand would be indistinguishable!
It therefore does not matter which strand you synthesise as DNA to make your standard curve. It will be double stranded so you just need to compensate for the other strand being a template in the PCR as well.

First thanks for your answer. I thought that the RT would not care about strandedness, but I wasn't sure. Now, I am.
Okay, for my example above you would say it doesn't matter whether I would synthesise the RNA as AUG or UAC? But what I didn't get is:
What do you mean with 'I just meed to compensate for the other strand being a template in the PCR as well' ? Can't I use the synthetic +RNA dilution series as a standard curve for my unknown sample with -RNA?
Sorry for my questions.

I was not aware you were going to make synthetic RNA as the template. It is certainly the most accurate but it also a lot more expensive to synthesise. Usually people use things like DNA gBLOCKs from IDT but I have no experience with ssRNA viruses and what the acceptable standard is there.
If you do go for dsDNA then you need to keep in mind that there are two strands that can be bound by primers and you will underestimate the amount of ssRNA in your sample if you do not divide by two.


text:
Why is urea not converted to ammonia in the body?
After the liver processes metabolites to produce urea and other by-products, these travel in the blood to the heart, then they are oxygenated, and some travel through the renal artery to the kidneys.
Urea in water can decompose into ammonia which is toxic, as mentioned in a textbook page no 170 (6), under production of ammonia.
Reactant and product are at equilibrium. Also a gaseous product, CO2, is present which could potentially escape during oxygenation of blood. Hence, according to Le Chatelier's principle, an equilibrium shift towards  the product is possible
NH2CONH2 + 2H2O → (NH4)2CO3 ⇌ 2NH3 + H2O + CO2
The chance of urea decomposing into ammonia is high while travelling in the blood (i.e taking long route) and in the bladder, but it still does not happen. Why not?

best to ask 2 different questions. Just ask this: Why does urea not decompose into ammonia inside the bladder? 1 phrase, simple, easy to read. urine degradation is also decomposition.

I tried to rewrite it very concisely. It's an interesting question. Apparently uric acid is responsible for half of the blood's anti-oxidant potential, despite the blood having a pH of 7.35. At that pH and temperature, ammonia can become gaseous and toxic. Urine has a pH of 6, so it has excess H+, so the ammonia would mostly become ammonium NH4, which is 100 times less toxic than ammonia. The nitrogen cycle in aquariums and in plants is something that helps to understand ponds, tap water, plants, aquariums, so i am always interested in the nitrogen cycle.

it's worth noting that the white substance from bird and lizard poop is uric acid. Fish produce a lot of ammonia, and they also have bacterial symbiosis in their gills to absorb it, and water based animals can produce ammonia directly because there is an excess of water, whereas most land animals have had to adapt to nitrogen waste with limited water.

Another info is here, from reading about fish, that secrete 90% of nitrogen as ammonia/ammonium. it sais: most of the ammonia in fish blood is ammonium ion. side note: pK of NH3 = 9-10; fish blood = pH 7.4) i can't explain that though.

@com.prehensible Can you write your comments into an answer?

I don't know the real answer, perhaps it's from the acid dissociation constant, the blood plasma, the time of urea conversion? and I don't know the real reason, I don't know biochemistry. Apparently NH3 ammonia can go through cell walls and NH4 can't.

The answer to this question is quite simply this:

The activation energy for the uncatalysed reaction is such that the
  amount of decomposition of urea in aqueous solution at blood temperature and
  pH is negligible in the time taken for the transfer of urea to the
  kidney.

The literature supporting this is very old, so I shall first cite a relatively recent (2004) and (I think) freely available paper by Robert P. Hausinger on urease in which he writes:

The substrate [i.e. urea]  is highly resonance stabilized (30 to 40 kcal/mol), thus
  decreasing the reactivity of its carbonyl carbon so that spontaneous
  hydrolysis of urea has never been observed. Rather, urea decomposes
  in solution (with an estimated half-life of 3.6 years at 38°C) by
  the slow elimination of ammonia to form cyanic acid (17)

Reference [17] is a paper by Zerner in Bio-organic Chemistry from 1991 which requires a library subscription. In effect it quotes the same half-life:

The urea molecule is very stable. Between pH 2 and pH 12, the
  nonenzymatic decomposition of urea in aqueous media is independent of
  pH and has a half-life of 3.6 years at 38°C (36-38).

References 36 is a book written in 1923, and references 37 and 38 date from 1942 and 1955, respectively. I have not checked the latter, but can if anyone demands it.
All of which is not surprising, as the purpose of the urea cycle in mammals (etc.) is to eliminate toxic ammonia, and, as @Fizz points out, the enzyme urease is needed by bacteria that utilize the compound.

[Partial answer]

[OP claim:] Urea in water can decompose into ammonia which is toxic.

Probably not as easily as you think. If Wikipedia is correct:

Urea alone is very stable due to the resonance forms it can adopt.

Some bacteria use urease to catalyze the reaction by 14 orders of magnitude (says Wikipedia).
There are some primary sources from the 1930s on the resonance forms of urea; I've not read them just yet.
From experimental data in solutions (not blood), urea would be close to its maximum stability in blood, pH-wise at least:

The stability analysis shows that urea is more stable at the pH range of 4-8 and the stability of urea decreases by increase in temperature for all pH values. Within the experimental range of temperature and initial urea concentration values, the lowest urea degradation was found with lactate buffer pH 6.0. The urea decomposition rate in solution and pharmaceutical preparations shows the dependence of the initial urea concentrations. At higher initial urea concentrations, the rate of degradation is a decreasing function with time. This suggests that the reverse reaction is a factor in the degradation of concentrated urea solution.

As for the reaction speed in terms that even I can understand:

The urea molecule is very stable. Between pH 2 and pH 12, the nonenzymatic decomposition of urea in aqueous media is independent of pH and has a half-life of 3.6 years at 38°C.

(This review cites data from older papers, so presumably they had less sensitive methods, so they concluded a wider pH range where it's most stable.)
For the chemistry experts, there exists a lot more information on the kinetics of the reaction.

In effect you are saying the question is based on a false premise, a point of view I imagine is correct, in which case I would vote to close. However neither you or the poster have given any figures for the rate of the uncatalysed reaction. Could you find some so we can resolve this definitatively please.

@David: I'm trying. The best I found is not in blood, but in solution. https://www.ncbi.nlm.nih.gov/pubmed/25043489 I'll have to access the full paper for the details...

@David: I found more urea chemistry than I can handle right now: https://hal.archives-ouvertes.fr/hal-01449373/document

Blood is likely to be irrelevant. Water will do. I’ll have a look later if you can’t find the info yourself. However the poster should be made to justify his claims or withdraw.

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text:
Are longer and shorter DNA similarly charged?
A longer DNA molecule would have more phosphate groups, so it should have a greater negative charge, right? It was taught in my class that only terminal ends of DNA are charged and all the phosphates in the middle are not charged.
My teacher said that this is the reason that Electrophoresis separates the fragments. All DNA have same charge and so same force on all of them. Then difference in masses would give different acceleration and thus separation of fragments according to size. But isn’t Gel Electrophoresis more like a sieve where longer molecules move slowly and shorter pass through easily?

Each phosphate group has a single negative charge. Not just the terminals. The reason gel electrophoresis works so well with DNA is that charge is linearly proportional to size. The longer the fragment, the slower it moves. A double stranded DNA molecule with 100 nucleotides has a charge of -200. If it were twice as long, it would have twice as many, just as if it were 3.4 times longer, it would have 3.4 times as many negative charges. This way, charge is essentially ignored, so DNA migrates through the gel at a rate inversely proportional to its size.

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text:
What is linkage?
If two genes are on the same chromosome, are they always “linked”? What if they are more than 50 cM apart? Then they would follow Mendalian pattern of inheritence. So are they still linked?

The centimorgan is not a measure of the physical distance between gene loci, but a measure of the linkage between loci.
Suppose that you have two genes located adjacent to each other, at the tip of a chromosome. The likelihood of their recombination is almost zero, since it is very unlikely that the two genes will be segregated in a crossover event during meiosis.
In contrast, if you have two genes as far apart from each other, but still on the same chromosome (i.e. they are on opposite tips), their likelihood of recombination is as close to 100%---this means a 1:1 ratio of parental type to recombinant type gamates.
So, if a 0% likelihood of recombination implies that the genes are right next to each other, and a 100% likelihood of recombination implies that they are as far away from each other, we will be able to approximate how far away a gene is from another gene by their likelihood of recombination.
Now, the likelihood of recombination is measured through the calculation of a recombination frequency. Genes that are unlinked give you a 1:1 parental to recombinant type in the offspring, which is a recombinant frequency of 50%. Genes that are 'perfectly linked', i.e. always segregated together, gives offspring of the parental type all the time, so they have a recombinant frequency of 0%.
Having said all that, we are able to associate,
$$\text{0% likelihood of recombination} \implies \text{0% recombinant frequency}\\
\text{100% likelihood of recombination} \implies \text{50% recombinant frequency}$$
And relating that to the loci of two genes on a chromosome,
$$\text{Adjacent genes} \implies \text{0% recombinant frequency}\\
\text{Perfectly Distant Genes} \implies \text{50% recombinant frequency}$$
And if we represent the length of a chromosome as 50 centimorgans, then
$$1\text{ centimorgan} \approx 1\%\text{ recombinant frequency} \approx 1\%\text{ likelihood of recombination}$$
That is to say, the theoretical maximum distance between two genes on a chromosome is the length of the chromosome itself, which is 50 centimorgans.

Note that there are many implicit assumptions in the explanations above. The first is that there are no random fluctuations in calculating the recombinant frequency. The second is that exactly one crossover event takes place during meiosis, and the loci that it acts on is uniformly random. When I say 'likelihood of recombination', I refer to the possibility of a single crossover event between two homologous chromosomes, resulting in a 1:1 parental to recombinant type gamete.

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text:
Why is pith of Cucurbits hollow when mature?
What is the evolutionary significance of pith in cucurbits? Does it serve a function by being hollow? Or is it an evolutionary vestige? What function would it have had in its ancestors?

Pith autolysis is a phenomenon due to which in some dicotyledonous plants like cucurbits, the pith gets hollowed.
Background: We all know that plants get their Carbon from atmosphere in the form of Carbon-dioxide, and fixes it by photosynthesis. During rapid growth Carbon requirement may not be in pace with rate of carbon fixed by photosynthesis alone, So some plants adopted pith autolysis.
This is useful for a  plant when it is in scarcity of carbon, Scarcity here implies that the plant is not able to get enough carbon for its growth with just photosyntgesis. So the plant autolyses it's pith to get required carbon to maintain its growth.Thereafter this carbon resulting from autolysis ,is transported to growing regions of plant.
Source:https://doi.org/10.1006/anbo.1995.1063

Could you explain this a bit further in your answer? As it is,  your answer is a bit vague. Thanks

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text:
What happens when lightning strikes us? How is it fatal?
How does a person die due to lightning? Is the cause of death similar to that due to electric shock? Why do minor shocks don't show similar effects in small magnitude (like paralysis in that part)?

Minor shocks definitely can paralyze a part!  Get on youtube and watch videos of people who cant let go of electrical wires or who are hit by tasers.
Paralyzing a part does not kill you.  Lightning can kill in two ways.

Arrhythmia.  Having arrhythmia or asystole is what kills most people hit by lighting.  As regards lesser shocks - the handymen who are hanging on to a live wire and can't let go (because their hands clamp down) can stay that way for a while.  Eventually the current produces an arrhythmia in the heart and that is what causes death.  If someone goes down this way from lighting or a lesser shock, you might be able to get them back with CPR.

When you see a whole herd of animals killed by a single strike, that is why. The heart is sensitive.  I do not understand why people's hearts do not similarly stop when they are hit with tasers.  I think sometimes they do.

Resistive heating.  Lightning can burn you.  Mostly the electricity goes over your skin and concentrated at conductors, like your phone.  That hurts but won't kill you.  Lightning going thru you can burn you on the inside which can damage your organs.  That is rare.

https://www.cdc.gov/mmwr/preview/mmwrhtml/00052833.htm
https://en.wikipedia.org/wiki/Lightning_strike


text:
Why does colchicine not affect the source plant itself?
Colchicine, being a mitotic poison that blocks spindle fibre formation, should affect its source plant. It should also stop its cells from dividing. So how do they grow?
I think that there might be some cells that synthesise it seperated (by many layers of cells) from other cells. So the rest cells are not affected.

Colchicine is an alkaloid and a secondary metabolite of the plant- a crocus, primarily functioning to protect the plant (like, from consumption by herbivores).
WHY COLCHICINE DOES NOT AFFECT THE PLANT:

It is transported far away from its site of production to the tissue storing it so does not come in contact with normal metabolically active plant cell machinery.
In the storage tissues colchicine is compatmentalised in vacuoles specific for colchicine storage.

The vacuoles are bounded by tonoplast which contains special proteins that facilitate active uptake of colchicine from the cytoplasm into the vacuole protoplast but do not conduct the movement of colchicine from the vacuole to the cytoplasm.
The scientific studies are detailed here.


text:
Clatherin Mediated endocytosis is pinocytosis or phagocytosis?
This was a question in a test. Clatherin mediated endocytosis is which of the two: pinocytosis or phagocytosis?
Precisely what is the difference between the two and CME?

My answer would be pinocytosis
Eukaryotic cells are also able to take up macromolecules and particles from the surrounding medium by a distinct process called endocytosis. In endocytosis, the material to be internalized is surrounded by an area of the plasma membrane, which then buds off inside the cell to form a vesicle containing the ingested material. The term “endocytosis” was coined by Christian de Duve in 1963 to include both the ingestion of large particles (such as bacteria) and the uptake of fluids or macromolecules in small vesicles. The former of these activities is known as phagocytosis (cell eating) and the latter as pinocytosis (cell drinking).
During phagocytosis, cells engulf large particles such as bacteria, cell debris, or even intact cells.In contrast to phagocytosis, which plays only specialized roles, pinocytosis is common among eukaryotic cells. The best-characterized form of this process is receptor-mediated endocytosis, which provides a mechanism for the selective uptake of specific macromolecules.The macromolecules to be internalized the first bind to specific cell surface receptors. These receptors are concentrated in specialized regions of the plasma membrane, called clathrin-coated pits. These pits bud from the membrane to form small clathrin-coated vesicles containing the receptors and their bound macromolecules (ligands). The clathrin-coated vesicles then fuse with early endosomes, in which their contents are sorted for transport to lysosomes or recycling to the plasma membrane.
For more information please see this link https://www.ncbi.nlm.nih.gov/books/NBK9831/
Hope this helps!


text:
Role of ATP and AMP in functioning of Phosphofructokinase
I know that when ATP is more then it inhibits PFK and hence regulate the number of ATP. But how does PFK reactivates itself? Is it due to removal of ATP from allosteric site that just reconfigures the enzyme back to normal functional state, or does binding of AMP (after ATP removal) does that?
To clear the meaning,
PFK+ATP= (inactive PFK+ATP)
So is it (1) or (2)?
(1) (inactive PFK+ATP) => (Active PFK)+ATP
(2) (inactive PFK+ATP) => (Inactive PFK)+ATP removed => (Inactive PFK)+ attached AMP => (Active PFK) + removed AMP

This is clearly explained on the Wikipedia page for glycolysis under the heading Phosphofrucokinase. AMP is an allosteric activator of the enzyme and ATP competes for binding at the same site but is not an activator.
You should think of the interaction between the two regulators in terms of reversible binding of both: since they compete for binding at the same site the proportion of the enzyme with bound AMP will go down if [ATP] goes up, for example.
Neither of your proposed schemes is   correct: the enzyme is more active with AMP bound and less active with ATP bound. The idea that AMP binds, activates, then wanders off is wrong.


text:
When was the first exception to Mendelian genetics discovered?
In addition to the question in the title, I'd like to know, how scientists reacted to the exceptions?

Before Mendel? e.g. Galton. When Mendel was rediscovered by de Vries et al. they immediately found that Mendel's phenotypes weren't quite Mendelian.

The first exception to Mendelian genetics was probably discovered by Mendel.  As a followup to his pea experiments, Mendel used hawkweed, in which his rules do not seem to apply due to some unusual aspects of hawkweed development; see Apomixis in hawkweed: Mendel's experimental nemesis for details.
Mendel eventually abandoned his biological experiments, and though the main reason was probably his increasing other responsibilities, his thousands of apparently-unsuccessful experiments with hawkweed may have contributed.

I would say that first exception might be White gene in Drosophila Melanogaster, described in 1910 by Thomas Hunt Morgan and Lilian Vaughan Morgan. At least, is the first exception we study in genetics since sex linkage its so fundamental. These experiments established the chromosomal theory of inheritance.

Thomas Hunt Morgan, an embryologist who had turned to research in heredity, in 1907 began to extensively breed the common fruit fly, Drosophila melanogaster. He hoped to discover large-scale mutations that would represent the emergence of new species. As it turned out, Morgan confirmed Mendelian laws of inheritance and the hypothesis that genes are located on chromosomes. He thereby inaugurated classical experimental genetics.
After breeding millions of Drosophila in his laboratory at Columbia University, in 1910 Morgan noticed one fruit fly with a distinctive characteristic: white eyes instead of red. He isolated this specimen and mated it to an ordinary red-eyed fly. Although the first generation of 1,237 offspring was all red-eyed but for three, white-eyed flies appeared in larger numbers in the second generation. Surprisingly, all white-eyed flies were male.
These results were suggestive for hypotheses of which Morgan himself was skeptical. He was at the time critical of the Mendelian theory of inheritance, mistrusted aspects of chromosomal theory, and did not believe that Darwin's concept of natural selection could account for the emergence of new species. But Morgan's discoveries with white- and red-eyed flies led him to reconsider each of these hypotheses.
In particular, Morgan began to entertain the possibility that association of eye color and sex in fruit flies had a physical and mechanistic basis in the chromosomes. The shape of one of Drosophila's four chromosome pairs was thought to be distinctive for sex determination. Males invariably possess the XY chromosome pair (Morgan used a more cumbersome notation) while flies with the XX chromosome are female. If the factor for eye color was located exclusively on the X chromosome, Morgan realized, Mendelian rules for inheritance of dominant and recessive traits could apply.
In brief, Morgan had discovered that eye color in Drosophila expressed a sex-linked trait. All first-generation offspring of a mutant white-eyed male and a normal red-eyed female would have red eyes because every chromosome pair would contain at least one copy of the X chromosome with the dominant trait. But half the females from this union would now possess a copy of the white-eyed male's recessive X chromosome. This chromosome would be transmitted, on average, to one-half of second-generation offspring—one-half of which would be male. Thus, second-generation offspring would include one-quarter with white eyes—and all of these would be male.
Intensive work led Morgan to discover more mutant traits—some two dozen between 1911 and 1914. With evidence drawn from cytology he was able to refine Mendelian laws and combine them with the theory—first suggested by Theodor Boveri and Walter Sutton—that the chromosomes carry hereditary information. In 1915, Morgan and his colleagues published The Mechanism of Mendelian Heredity. Its major tenets:
• Discrete pairs of factors located on chromosomes like beads on a string bear hereditary information. These factors—Morgan would soon call them genes—segregate in germ cells and combine during reproduction, essentially as predicted by Mendelian laws. However:
• Certain characteristics are sex-linked—that is, occur together because they arise on the same chromosome that determines gender. More generally:
• Other characteristics are also sometimes associated because, as paired chromosomes separate during germ cell development, genes proximate to one another tend to remain together. But sometimes, as a mechanistic consequence of reproduction, this linkage between genes is broken, allowing for new combinations of traits.
Morgan's experimental and theoretical work inaugurated research in genetics and promoted a revolution in biology. Evidence he adduced from embryology and cell theory pointed the way toward a synthesis of genetics with evolutionary theory. Morgan himself explored aspects of these developments in later work, including Evolution and Genetics published in 1925, and The Theory of the Gene in 1926. He received the Nobel Prize in Physiology or Medicine in 1933.

quoted from: http://www.genomenewsnetwork.org/resources/timeline/1910_Morgan.php
see more: http://www.esp.org/foundations/genetics/classical/thm-10a.pdf


text:
When should you use a stringent plasmid?
I was wondering if anyone had good examples of when you would want to use a stringent plasmid vs. a relaxed plasmid in a research setting.

The three general advantages are:

Lower expression. If your plasmid is expressing something toxic to cells at high levels, reducing the amount of DNA can reduce expression.
Lower plasmid burden. If you are concerned about the stress imposed by maintaining many copies of the plasmid, low-copy plasmids are helpful.
Population homogeneity. Relaxed plasmids tend to replicate such that there will be a wide distribution of # plasmid copies/cell. Meanwhile, stringent plasmid replication is tightly coupled to the cell cycle itself, so the number varies less. In certain cases it may be desirable to control the number of plasmids per cell.

Stringent plasmids are also good for doing mutant screens, I assume.


text:
What is the role of lactic acid bacteria (such as L. acidophilus and L. bulgaricus) in glycolysis during yogurt fermentation?
I am trying to prove that an increase in monosaccharides (glucose, fructose, galactose) that have been added to milk during fermentation will result in a decreased pH. My current argument is:
"The increase in the concentration of Phoenix Dactylifera is representative of an increase in the disaccharide, sucrose, and the monosaccharides, glucose and fructose — the primary sugars in date palm. This source of sugars adds to the natural sugar content already found in low-fat milk, which are lactose molecules composed of glucose and galactose. As such, more energy from these carbohydrates are available in the process of glycolysis, where LAB facilitate the conversion of six-carbon sugars like glucose, fructose, and galactose into pyruvate. This creates a greater frequency of glycolysis reactions, resulting in a greater overall yield of pyruvate molecules which can be converted into lactic acid. Hence, the increase in overall production of lactic acid increases acidity in the yoghurt and, thus, the pH."
What can I fix with my answer?


text:
Did cats evolve from monkeys ? or vice versa?
Did cats evolve from monkeys? or vice versa?
How similar are the genes of cats and monkeys?
What is the proof that they are related or that they are not related?
Most monkeys climb in trees and there are other similarities but I could not find any evidence on the internet.
Do cats and monkeys have a common ancestor?

Cats and monkeys have a common ancestor, both are placental mammals, so at the very least they must have both evolved from the first placental mammal. Cats are members of the Laurasiatheria group and primates are members of Euarchontoglires. These groups of mammals probably split off from each other about 100 millionish years ago. For more information about mammalian phylogeny, look here.

"Evolving from another species" versus "Most Recent Common Ancestor (MRCA)"
One cannot say about two extant species that one evolved from the other. It just doesn't make any sense. It is not only true for cats and chimpanzees (just to pick one species of monkey) but it is true for any pair of extant species. One extant species has never evolved from another extant species.
However, one can say from any pair of species (Eventual exception with viruses but don't pay attention to them now) that they have a common ancestor. Again, it is not only true for cats and chimpanzees but also for yeasts and ants or for chestnut trees and reticulated pythons. The interesting question is always, "when did the MRCA live?" or if you prefer "when was the time when the lineage that will one day yield to cat and chimpanzee was living?"
Do cats and monkeys have a common ancestor?
Yes! All life on earth shares a common ancestor. The question of interest is when did the Most Recent Common Ancestor lived between cats and monkeys lived?
Please consider having a quick look to this post for an introduction to phylogenetics.
Chimpanzee and cats evolutionary relationships
This question has been answered by @user137. Cats and chimpanzee are both mammals. Their most recent common ancestor was therefore also a mammal and this most recent common ancestor lived about 100 million years ago. This is the kind of information you can get with DNA comparison.
How do we know that?
@user137 already linked to an article that shows when the most common ancestor of cats and chimpanzee has lived. If you want, you can learn more about how such inferences can be made. As you like mathematics (I read from your profile), you might be not too scared (although it will take some time) of statistics and algorithmic to have a look at those Wikipedia articles:

Phylogenetics - generality about phylogenetics (=the study of the evolutionary relationship between organisms)
Computational phylogenetics - How to build a phylogenetic tree
Molecular clock - One method to estimate the length of the branches in a phylogenetic tree.

To understand the stats, you may need first to follow a stats course, such as this one from Khan Academy but again it will take some time. Of course, aside from the multitude of tools that one can use to infer time to MRCA from genetic data, one can also make an inference from phenotypic comparison although this method is generally much less accurate.

'One extant species has never evolved from another extant species.' Are you sure about that? What about Homo erectus and other hominin species a few tens of thousand of years ago? H. erectus is both basal in the tree to H. sapiens and co-existed.

@AlexDeLarge Yes, I am sure of that! The examples you are given are those of sister species, not cases where one is the ancestor of another one.  This whole concept can be blurred by how inaccurate is the concept of species (see [here](How could humans have interbred with Neanderthals if we're a different species?)) but it is by large very much considered as if a species give rise to more than one species, then we ought to use two different species names for the descendents and therefore an "ancestor species" cannot live in the same time as a "offspring species"

I'm not convinced. If species A gives rise to two founder populations that, according to whatever species concept, maybe even quickly evolve into species B and C then B and C evolved from A. There is no necessity for A to get extinct or evolve into something like species A* in that reasoning.

A does not become extinct, it becomes either B or C if you want. The whole issue is an issue of how you decide to group lineages into species but pretty much everyone does the same. When there is a speciation event, the two extant species are both considered different from the ancestor species. This is mainly to avoid confusion and avoid to fail to recognize that all extant species have evolved for the same amount of time. Calling one an ancestor make it feel like some extant species would have less time to evolve.

It might be confusing, but the way you put it in your answer is not correct. In the example I give, A, B and C are all extant but the ancestors of B and C are members of A and this is by no means impossible.


text:
How many photons are used to make one glucose?
This was a question in a test. The options were
(1) 8
(2) 16
(3) 24
(4) 48
My answer is 30 which was not in options.  Given answer was 48.
12 NADPH
18 ATP for one glucose
12 NADPH and ATP from z scheme where 24 photons are used.
6 ATP more from cyclic where 6 photons are used.
Net 30.
Can someone point out an argument against this?
One explanation for 48 is:
2 electron each hydrogen atom
4 electrons per water molecule
2 water molecules for one oxygen molecule
8 electrons=8 photons for each oxygen,
each glucose 6 oxygen so 8×6 = 48
But what is the mistake in argument for 30?


text:
Why do humans grow taller than their ancestors?
I'm taking the Introduction to Genetics And Evolution course and in the first lecture it was said that:

Evolution in a biological sense is simply a change through time. And very importantly, that is change through time over generations. So for example, the human species, hundreds or thousands of years ago was much shorter than it is today. Over the course of those generations, the human species has grown taller. That change is an evolutionary change.

I'm wondering why we become taller than our ancestors? Now we almost don't fight with other species and can live doing something that doesn't require physical strength. It's more logical to me if we would become shorter.

Humans compete with each other. The competitor doesn't need to be a different species - it can be a different population, different individuals in the same population, or even just environmental conditions (e.g. moving to colder or warmer climate). Indeed, competition within the species has a huge benefit - it can cause runaway improvement since you're always competing with the best of the given generation. This is one of the explanations for why human intelligence seems to be so far ahead of anything our "species-relatives" have, by the way.

@Luaan conspecific competition can have the effect of reducing competitive abilities with other species. Also, technically, there is no need for competition for selection to happen (even if completely isolated, some genotypes may still be associated to higher fitness than others).

The human species has grown taller since the last 150 years, especially after 1950. During the world wars the humans (at least in Europe) declined in height. In some poor African countries the people are now shorter than they were 40 years ago. It is a lot about nature and nurture.

Yes, worth noting that some of the increase in height (especially recently) is phenotypic (environment) rather than genotypic (evolutionary) (I would hope the course material points this out!)

Related: https://biology.stackexchange.com/questions/457/height-and-natural-selection-in-humans/ and https://biology.stackexchange.com/questions/19101/are-asian-people-genetically-predisposed-to-be-shorter-than-europeans

A likely misunderstanding of yours

Now we almost don't fight with other species

Misunderstanding about selection
As you will go through this course, you will understand why this sentence makes little sense. A change in allele frequency via natural selection is caused by a fitness differential among genotypes within a population. The existence of a competitor species would eventually affect this fitness differential but there is no need for a competitor for having a selection pressure.
I think you are having the view that selection is a process that allows a species to be better at coping with a competitor but this is wrong. Selection will increase the frequency of individuals having high fitness in the population. The resulting population may well not be a better competitor.
False opinion that we are not competing with other species
Also, about nearly 50,000 people are dying every day from infectious disease (UN press release). So, we are definitely still "fighting" with other species. Adaptation to malaria in humans is a famous case study (see this answer and its links).
Also, according to reuters (who fail to link to their source), the worldwide cost of pests in agriculture is estimated to about 540 billions USD per year! So yep... competition there is.
What selection pressures are there on human height?
Review paper recommendation
Stulp and Barrett 2016 is a review paper on the evolution of height in humans that you might want to have a look to have a clearer picture than what I will give here. It is easy to read. I highly recommend having a look at it.
They cite a lot of papers. I won't cite them again below but I will just attempt to make a vague summary of the parts which I think will interest you the most.
What selection pressures are there on human height?
The question appears to not be that easy to answer. In humans, height is highly heritable and there is a lot of variance in height among populations. It is likely that different selection pressures may have acted on different populations.
There are a diversity of selection patterns
In short, selection pressures on height include intra and intersexual selection. Taller adults seem to have a reduced mortality rate. Taller women have a lower risk of complications when giving birth. However, in both men and women, the correlation between height and number of offspring varies a lot from study to study (and likely from population to population). In the USA for example, men having the highest number of offspring are of intermediate height (balancing selection).
It appears that epigenetic variation also have an important impact on height Simeone and Alberti 2014 and there might have a sex-driven intra-locus conflict on height (Gilks et al. 2014; Stulp and Barrett 2016)
There is evidence of current selection on height
We have a fair number of evidence that height was and is still under selection in humans but we think that the exact pattern of selection pressures acting on it is quite complex. Note that there is evidence that height is still under selection today.

Stulp and Barrett 2016 link has limited access.

It's a pleasure to read your answer. I tried to give an answer, but as a non-native English speaker couldn't summarise it so nice. Especially I like the terms you use, lke selection pressure.

@cezar Thank you. Selection pressure is a very standard term in evolutionary biology.

@Artmal My link was broken. Sorry about that. Can you try again? There might have pay wall though.

@Remi.b I don't doubt that. I, as non-native English speaker, couldn't translate back to it. It's hard to discuss using technical terms you have learned in another language.

In my opinion there is a fallacy in your understanding of evolution. First of all evolution is blind to the future. Also living organisms don't undergo evolutionary changes toward something that might appear more logical.
Imagine there were only few tousands exemplars of Homo species left and the planet Earth would change so much that 90% of its surface is under water. It would be practical to have webbed hands. An exemplar with webbed hands could swimm better, and consequently be better equipped to provide food.
So what's going to happen. Are the humans going to develop webbed hands? Certainly not. It's not how evolution works. Just because something appears to be logical or of use, it's not going to come overnight.
But now imagine because of a certain mutation some exemplars have webbed hands. They are more likely to survive in an environment with large water surfaces. Therefore they are more likely to leave offspring. Exemplars without this mutation wouldn't be able to gather so much food, to escape from predators, etc. Eventually after millions of years they might all die out and only exemplars with webbed hands are existent. Then all humans would have webbed hands. The genes responsible for normal hands as we have, are almost not existent in the population.
After further millions years the water masses have retreated and there is much more land surface. The evolution was blind for this. The humans continue to have webbed hands, although they aren't so practical anymore. Eventually a mutation occurs again, or some exemplars with recessive genes for normal hands have offspring. This offspring now has better chances to survive and in the course of many generations there is a substantial part of the population with normal hands.
The humans are today much taller than earlier, because it must have been of evolutionary advantage for very long time. In order to get shorter as a species, the environment (and also other factors) should favour this.
We have food in abundance, good medical care, and most of the offspring can survive to adult age. This enables most of the people can unfold their full genetic potential and grow taller. The humans (at least in the western world) consume milk after the weaning. It contains growth hormons and stimulates the growth.
In order to get shorter in average as species, the shorter exemplars should be able to live longer and leave considerably more offspring, and there should be evolutionary drawbacks for taller exemplars to leave enough offspring.
Do we have those conditions? No. That is why we don't get shorter.

We have food in abundance, good medical care is this also an opinion of yours? Half of world wide infant death is caused by malnutrition (Walker 2008)

No, it's a fact. In the western world (Western Europe, North America, Australia and New Zealand) there is food in abundance and good medical care. The tallest people live also in these regions, the Dutchmen leading the ranking. The shortest people live in poor countries. There are certainly some outliers, like the Maasai in Tansania. Food isn't only factor favouring the growth, but it is an important one. There are differences in the height within same populations like rural vs. urban India, North Korea vs. South Korea. I'd say they are result of better living conditions.

I did not notice (at least in the western world) at the end of your sentence, sorry. You can't draw a general conclusion based on a cherry picked population though. The review I link clearly indicate that there is selection favouring small people in some populations.

I have yet to read the links you provided, but I don't doubt that there are circumstances that would favour smaller exemplars in certain populations. My point was that availaibility of food during the childhood and the adolescence stimulates the growth. Why should people become smaller when they have the possibilities to unfold their genetic potential. The people in the western world became significantly taller only after the II World War. Until the 18th century the people weren't (much) taller than our ancestors in the stone age.

I'd also like to add that there is a ceiling and once the genetic potential has  been fullfiled, the average size isn't going to increase indefinitely. It's very unlikely that further improvement of the living conditions can lead to humans with height of 2.5 meters (it might be however rather 250 kg).

There is a negative correlation between female height and reproductive success in the USA. Nutritional stress lead to a negative correlation between height and survival as well. These patterns really vary a lot and it is not so easy to summarize them in a few simple sentences.

Sure, strong directional selection may yield heritability to reach 0 but variance is still very high in humans. If this sentence is unclear to you, you'll want to read this post


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Why don't we have hair on palms?
We have hair all over the body except palms.
What is the biological reason behind this?

The main functional reason is we need to be able to grip things with our hands (and feet, which are also hairless), and hair would interfere with that. Physiologically, the epidermis in these parts of the body is very thick and highly keratinized, and when combined with the thick underlaying layer of dermis, this results in skin that does not support the growth and maturation of hair follicles.

A support for that is that other hairy animals also don't have hair on their 'gripping surfaces' - palms of other primates and feet of mammals and birds.


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What is the advantage of not having cytokinesis after karyokinesis?
In nature most of the cells are mononucleated, but in some cases like osteoclasts, umbrella cells of transitional epithelium, tapetal cells of another etc. are multinucleated. Wikipedia article about tapetum says that it is a strategy to increase the production of proteins. Why don't cells just up-regulate their genes for more production? What is the benefit of not having cytokinesis?

The absence of cytokinesis allows the two nuclei to remain in the same cell. If a cell has 2 nuclei instead of 1, it can transcribe DNA to mRNA at double the maximum speed, and so produce the desired proteins at double the rate. It's almost as if the cells become tetraploid, or hexaploid, and so on.
Learn more: http://www.nature.com/scitable/definition/cytokinesis-100
Why is it more desirable to have 1 cell with 2 nuclei than actually do cytokinesis and have 2 cells with 1 nucleus each (still 2 total)?
Because it is unfavorable to create two cells, which needs an extra investment in energy and nutrients to maintain, and is also harder to coordinate, and so it becomes more desirable to just have one single cell with the capacity of producing double the proteins.
Then why don't all cells adopt this strategy? What is the reason for such partiality?
First, because most cells don't need the extra transcription speed, as they don't produce a lot of proteins. Second, because of cell differentiation - to have cells doing different things they have to transcribe their genetic material differently, and so must be separate. Third, a lot of times it is desirable to have extra cells. For example, skin epithelial cells: their main purpose is to serve as a barrier or protection, and so there has to be a lot of them. That's why the basal cells are in constant mitosis.

This can happen after cytokinesis too, then why don't they ?

@JM97 cytokinesis divides the citoplasm, and thus the cell, in two, creating two separate cells, each with one single nucleus. I added an useful link to the answer.

Yes, effectively in both cases the proteins produced are doubled , then why do they undergo cytokinesis in some cases like in gut but not in other cases like osteoclasts?

@JM97 What do you mean in both cases the proteins produced are doubled?  Are you counting with both the daughter cells? Then in that case it is because it is unfavorable to create two cells, which needs an extra investment in energy and nutrients to maintain, and is also harder to coordinate, and so it becomes more desirable to just have one single cell with the capacity of producing double the proteins.

Then why don't all cells adopt this strategy? What is the reason for such partiality?

@JM97 first, because most cells don't need the extra transcription speed, as they don't produce a lot of proteins. Second, because of cell differentiation - to have cells doing different things they have to transcribe their genetic material differently, and so must be separate. Third, a lot of times it is desirable to have extra cells. For example, skin epithelial cells: their main purpose is to serve as a barrier or protection, and so there has to be a lot of them. That's why the basal cells are in constant mitosis.

Let us continue this discussion in chat.


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Randomness in living systems
The point of my question is not to talk about events that are uncontrolled by living organisms. My question is about controlled randomness, or I'd like to say adaptive random process. Process that are random because it was selected in order to be random.
The first thing that pop in my mind when thinking of "adaptive random process" in biology is Fair Meiosis. Do you have other examples of "adaptive random process"? An individual might display a random behaviour in order to avoid that others to predict its future behaviour. Is there any evidence for such things? Do you know any other evidence on what I called "adaptive random process"?

Randomness might arise due to ever changing chemical composition of cells and the environment where the process takes place.

I find your computer example inconsistent with the rest of the question. If you are not interested in randomness at the molecular/sub-mulecular level, then you can say that, as PRNG in computers, also biological processes are deterministic. You make a "random" choice between A and B because (as an extremely simplistic example) your neuron "A" fired more than your neuron "B"...

@nico Thks for the comment. I'm not sure I get your point though. Would you think my question to be improved if I asked what type of PRNG does nature use?

@nico I modified my post shortening the computer example.

@nico After more thinking, I kinda aggree that my question might not make much sense. I'll shorten it to keep only the "Do you have other examples?" part

@Remi.b: don't get me wrong, I find the question very interesting. I think at the end it all comes down to the definition of "randomness" which one wants to use. Is a random event something that is too complex to predict? Or is it something even with infinite computing power we could never predict?

@nico Yes I understood this philosophical issue in your previous comments and I had a hard time to know how to deal with it. So that I decided to shorten my question. I might repost the second part of my question later on. Thanks nico

We use the word "stochastic" often in ecology / community biology. Is this the same as "random"?

In an evolution mutations are often random and lead to differences in phenotype that can be adaptive under certain pressures.  A lot of times mutation is a random process, but here are three cases I can think of off of the top of my head where I would say the organism is 'trying' to do it:
HIV is a retrovirus, which means in its viral form its genome is single stranded RNA, which is then converted into double stranded DNA within the host.  That conversion is carried out by a virally encoded reverse transcriptase.  This enzyme has a much higher error rate when making the RNA into DNA because it cannot proofread like our DNA polymerases.  This means that HIV mutates incredibly fast.  Many of these mutants are not very fit, but since there is so much selective pressure against staying the same due to attack from the immune system, some mutants will be much more fit if they can avoid that attack.  Its a numbers game, and by making lots of random mutants HIV is very good at it.
A related, but different case is found in the diversity generating retroelements of certain bacteriophages.  These are double stranded DNA viruses that infect bacteria.  The bacteria these viruses infect could mutate to escape the viruses by losing a certain receptor that the virus binds to.  It was observed however that the the virus would mutate incredibly quickly to bind to a different receptor, a lot faster than would be expected for a DNA virus.  Also, it was found that these viruses contained reverse transcriptases, which is bizarre, since there is no reverse transcription step in a dsDNA viral life-cycle (so we thought).  To make a long story short, this virus will transcribe the DNA that codes for its binding proteins into RNA, then use its reverse transcriptase to turn that RNA BACK into DNA, but uses a sophisticated targeting strategy so that it only mutates the region that is used for binding to the bacteria.  It will only mutate adenine residues, leaving the C's, T's and G's alone.  This is a much more clever system than HIV, because this virus uses site-specific mutations on its binding feet, and doesn't mutate its core proteins, the mutation of which would probably just lead to viruses that couldnt replicate.  Here a reference for the interested: http://www.nature.com/nature/journal/v431/n7007/abs/nature02833.html
Just so you dont think this is reserved to viruses, we do this as well with our immune system.  In order to recognize antigens in attacking pathogens, our immune cells have two methods for making diverse, random, receptors.  First is V(D)J recombination, where the multiple diverse copies of the V, D and J regions of antibodies and receptors are combined at random to make one set.  Wiki says theres 3x10^11 possible combinations here.  After that, theres also somatic hypermutation during the proliferation of B cells.  In this process, the random mutation rate is hugely increased in the region of the B cell receptor gene, specifically for making slightly different versions of the already 'OK' receptor to make it a great receptor.
General theme: raising your mutation rate, either across the board(HIV) or specifically (DGRE and SHM) is a good way to intentionally add randomness for a beneficial purpose (to the extent that you can attribute 'intent' to a viral particle).

Thks a lot for these examples. The article for which you provide a link seems very interesting btw. You examples are interesting. As you say at the end, all the examples you provided are examples where the mutation rate (which is a non-adaptive random process) is raised (which is a non-random adaptive process). It is interesting though. But I would call an "adaptive random process" a process which adaptative process which is directly random but does not use an underlying already existing process. Does it make sense? Thks

Hmm, sorry, I'm not exactly sure what you mean then.  In Meiosis you get the random segregation of chromosomes, after a random cross-over that makes hybrid chromosomes.  In the DNA mutations you randomly change a basepair to one of the other three, and in V(D)J recombination you randomly splice together one of each of the segments.  Each process seems fairly random, and results in an offspring or cell or virus that is slightly different.  Whether that random difference is a good adaptation is for the environment to decide.

I know of an example in development biology. Here is an example where noise in retinoic acid gradients is required for the boundaries in the developing hindbrain to sharpen. A related result is that the zebrafish hindbrain has a protein to modulate noise, but does not reduce the noise to zero. Together these results show that noise in the retinoic acid gradient is beneficial to hindbrain development. So in some sense the amount of crabp2a (the noise modulator) evolved to control randomness (noise/stochasticity) in the morphogen gradient, but was selected to not eliminate it.


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Probability of Extinction under Genetic Drift
Here is the Wright-Fisher model of genetic drift:
$$\frac{(2N)!}{k!(2N-k)!}p^kq^{2N-k} \Leftrightarrow \binom{2N}{k}p^kq^{2N-k}$$
where $\binom{2N}{k}$ is the binomial coefficient.
This formula gives the probability of obtaining $k$ copies of an allele at generation $t+1$ given that there are $p$ copies of this allele at generation $t$. $N$ is the population size and $2N$ is the number of copies of each gene (this model applies to diploid population only).
From this formula, how can we calculate the probability of extinction of an allele in say 120 generations starting at a given frequency, let's say 0.2?
and
How can we calculate the probability of extinction rather than fixation of an allele present at frequency $p$ if we wait an infinite amount of time?

See answer there.

update
The answer is here!

Original comment/answer
Kimura and Ohta (1969) showed that assuming an initial frequency of $p$, the mean time to fixation $\bar t_1(p)$ is:
$$\bar t_1(p)=-4N\left(\frac{1-p}{p}\right)ln(1-p)$$
similarly they showed that the mean time to loss $\bar t_0(p)$ is
$$\bar t_0(p)=-4N\left(\frac{p}{1-p}\right)ln(p)$$
Combining the two, they found that the mean persistence time of an allele $\bar t(p)$ is given by $\bar t(p) = (1-p)\bar t_0(p) + p\bar t_1(p)$ which equals
$$\bar t(p)=-4N\cdot \left((1-p)\cdot ln(1-p)+p\cdot ln(p)\right)$$
This does not answer any of the two questions!
This answer gives...

the average persistence time

but not...

the probability of fixation rather than extinction if we wait an infinite amount of time

neither...

the probability that the allele get extinct over a period of say 120 generations.

Can someone improve this answer?

I was also thinking about Kimura's papers, but have seen some more recent stuff as well. I will look at it later when I have the time.

The probability of fixation given infinite time is just $p$ (the frequency of the allele at that time) - I just ran a simulation in R with initial frequency of 0.2 (1000 replicates over 5000 generations $N$ =10000 and $p$ =0.2) and the average fixation rate was 0.201 (though simulations with smaller populations are more sensitive to stochasticity thus vary more around $p$ but are still very close, $N$ =10 had a fixation of 0.184) ... I'm sure there must be a way to calculate the probability after a given number of generations...

ps. does that answer your second point in your question? @Remi.b

@GriffinEvo Nice! Thank you. You answer to "what is the probability of fixation rather than extinction if we wait an infinite amount of time" via simulation (rather than mathematical modeling). But that's already a very informative point.

@remi.b mathematically speaking it's just simple probability - if something is randomly sampled it, on average, will be sampled at the same frequency it is found in the population it is being sampled from. (Probability of showing heads when tossing a coin is 0.5 because the frequency of head-sides on coins is 0.5). The simulation I did was just to support this (and because I like playing in R) :)

@GriffinEvo Ha ha. This result is not intuitive to my mind! I take it for true but I don't quite understand why. I guess one might re-express the wright-fisher model somehow and find out this same result. I asked (just 30 seconds ago!) the same question here on mathematics.SE

@Remi.b ah cool! I'll ask our departments neutral theory genius too, she will probably know a way if there is one! If you want the drift simulation to play with it's on my homepage

Here is a simple proof that the probability of fixation given an infinite time is indeed p (in a finite population, otherwise there will be no fixation):
Let's look at all 2N gametes in the population. Eventualy, according to the Wright-Fisher model, only one of them will be represented in the population. The probability for this gamete to be of an allele with initial frequency p is just p. Therefore the probability of fixation is p.
Simple.


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Examples of virus originated from a living system
Do you know some examples of virus or a viroid (or a prion) that originated from a known living organism? How does the virus/viroid/prion lives? Does it paratize the organism from which the virus originated?
UPDATE
Thanks to the first answers I have examples of newly originated prions. Does someone know such an example about viruses?

Retrograde evolution is not an impossible concept, I know examples of unicellular parasites (in a way) evolving from multicellular lifeforms (See Devil Facial Tumor Disease and Canine Transmissible Venereal Tumor). A related question would be: how ancient the viruses are. Retrograde evolution of a eukaryotic cell to a virus would be a huge evolutionary jump.

Prion diseases are still very poorly understood, but one of the dominant theories is that they are misfolded proteins that cause disease by catalyzing the misfolding of more proteins of the same type.  If that is the case, then they arise from the organism that they affect simply by protein misfolding.  In the case of bovine spongiform encephalopathy (mad cow disease) being transmitted to humans and resulting in new variant Creutzfeldt-Jakob disease, it seems like it might be transmissible between species, but it probably needs to infect a closely related species so that the protein has a homolog it can act upon.
Can't say I know of any examples where people have shown the de novo creation of a virus from a living organism.  There are definitely virus protein homologs in the genomes of organisms, but directionality is hard to argue since its common for viruses to pick up host genes, or leave behind viruses genes.

Prion diseases arise spontaneously fairly often.  There are only ~170 total cases of human infection by mad cow disease, but there are ~50 cases/year of Creutzfeldt-Jakob disease, which is a spontaneous strain of prion diseases in humans. There is a strong case that Alzheimer's and Parkinson's diseases (among others) are similar in nature, in which case it's a much more frequent occurrence.
However, they are the consequence of a misfolding and aggregation of a naturally occurring protein produced in our brains.  In this sense, they are nothing like the complexity required to produce a de novo virus. The closest viral analogy would be retroviruses, which could insert their genome into your DNA, die off, and then possibly spontaneously revive at a later date.


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Does anyone know what type of Cocoon this is?

I am really concerned with this since I've never seen a cocoon this color before and can't find it anywhere on the internet. I found it just laying on the ground not attached to anything, but it seems to be alive because when you touch it, it will wiggle abit. Any answers are appreciated.

If you keep it in a box or something, you might have better luck identifying whatever comes out. It probably won't be anything dangerous.

Adding your location could help a big time identifying

I think I may have found your cocoon: it appears to be a Magpie Moth (Abraxas grossulariata) cocoon:

According to UK Moths, it's common in the UK.

I don't usually do this, but if you think this answer is correct, I'd appreciate it if you accepted it. Since it's so old, I don't think you'll get a lot of other answers.


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Why do snakes not have eyelids?
Why is it that snakes do not have eyelids?
Is it due to that fact that they are not as evolved as we humans and other organisms that have eye lids, or is there any other significance behind it if any?

"the fact that they are not as evolved as we humans" - there is no such fact. Evolution is not a scale going from "less" to "more". All organisms are equally evolved. So, it can't be due to that "fact" by definition.

@Aneesh For more discussion on the concept of "more/less evolved", have a look at the post Are we “more evolved” than present-day bacteria?

Snakes have no eyelids. Each eye is covered with a single, transparent scale. These eye scales protect the eyes from mechanical damage, and prevent the eyes from drying out, just as an eye lid would do. In effect, snakes developed another solution to protect their eyes.
As a result, snakes cannot blink and they sleep with their eyes open.
A snake’s eye scales are part of its skin. This means that when a snake sheds its skin, it must also shed its eye scales. When it is time for shedding, the eye scale turns opaque, reducing vision (Fig. 1).

Fig. 1. Opaque snake eye before skin shedding. Figure source: Snakes are long blogspot
Source: Museum of Victoria

Good answer +1. It would be great (although that would probably take some work) to have some mapping of this trait on a phylogenetics tree (or just some information about their snakes and mammals sister species).

@Remi.b - thanks heaps. But the phylogenetics I leave up to you my friend. I'm in sensory systems you see :)


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Why both sexes of the species don't show equal level of Competition?
In most species, it is seen that either males or females have evolved to be aggressive towards approaching members of the same species of the same sex and maintaining strict territorial boundaries. The logical explanation is that such behavior is advantageous in the evolutionary context. If you increase competition, then the chance of genes suited to the environment getting passed on increases. Obviously, if one male wards of another male from his territory then the genes possessed by him are positively selected for.
In such a scenario, why haven't both the sexes developed a similar level of aggressive competition (Wouldn't this also increase the chance of genes that are suited to the environment getting passed on?)

Well if women are competitive, doesn't that mean that they risk dying if this competitive is physical? And if a women dies, she cant pass on her child, and therefore her genes to the next generation right?

There are so many species that contradict what you're trying to ask I'm afraid. If you have a specific species in mind then the question would be more answerable.

But what about maternal gene selection? There must have been some way natural selection got around the problem of aggressive competition right? If they competed in a non-aggressive manner, then it would still be an evolutionary advantage, right?

@ChitinousExoskeleton It sounds like you have an example in mind. What species are you talking about?

Three-Spined Sticklebacks from Tinbergen's Experiment...

@ChitinousExoskeleton After making a nest a male wants a female to lay eggs there for him to fertilise and pass on his genes. Why would a male fight a willing female in that situation? And of course the male doesn't want another male to take his hard made nest from him.

@GoodGravy I'm sorry for the edit saying 'members of the same species of the opposite sex' . I want to know that if males fight each other to promote their genes to be selected, then what is the mechanism for females for the same process. Because, they don't seem to have any...

@ChitinousExoskeleton So you're looking for examples of competitive female bahaviour in the context of mate selection? https://en.wikipedia.org/wiki/Naked_mole-rat#Queen_and_gestation is a pretty brutal example.

@RoSiv That exact same sentence could be used to explain why males would be non-competitive.

Why Can't both be competitive? That's all I'm asking. If the males are competitive and its helping them in a way, and females are also competitive in the same population wouldn't it have an evolutionary advantage? (Or vice versa, if females are competitive, shouldn't males also be competitive?)

@ChitinousExoskeleton This article explains the stereotype that I am trying to explain. It is a popular misconception that males are competetive and females passive. This article furthermore shows female armoury and a few have competitive male counterparts too. All the scenarios you mentioned exist in the natural world, and unfortunately the question remains if not unclear, now broad.

The reason for this discrepancy is mainly a consequence of Bateman's principle. Citing wikipedia:

Bateman's principle suggests that in most species, variability in reproductive success, or "reproductive variance," is greater in males than in females. This is ultimately a consequent of anisogamy. Females, especially mammalian females, almost always invest more energy into producing offspring than males invest. Bateman's principle anticipated and is consistent with Robert Trivers's theory of Parental investment—in most species females are a limiting factor over which males will compete. This competition results in some males being more successful than others, leading to greater reproductive variance among males than females

Variation in competition abilities for access to a mate is called sexual selection. As a consequence of Bateman's principle, sexual selection is more common in males than in females. You can split sexual selection into intra-sexual selection and inter-sexual selection. These terms are poorly chosen IMO. They mean:

Inter-sexual selection: One gender try to look sexy and the other gender chooses the mate. Fighting to impress females is one type of behaviour that can evolve under inter-sexual selection
Intra-sexual selection: Individuals of one gender fight for the access to an individual of the other gender. This individual cannot chose who to mate with.

In both case, fighting can be involved. As a consequence, you will see among-males fighting is more common than among-females fighting.

Thank You, I suppose the question was really unclear, but this is essentially what i wanted to know. Whether its necessary for one of the species to always be less competitive (or as you put it 'to have less reproductive variance) than the other!


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Are there any drugs that target the lipid envelope of viruses?
Many drugs go after the unique viral enzymes but do any target their lipids? Viral membranes are of course similar to the host membrane but might have a different composition and do have a different curvature and protein composition. Is anybody aware of research or even existing drugs that attempt to hit the lipid envelope of viruses to limit them?
There are evolved molecules that target the lipid membrane, for example. A subgroup of those pore-forming toxins are cholesterol-dependent, so they might target a membrane high in cholesterol over one low in it. I'm trying to think out of the box here whether properties of the viral lipid membrane could be exploited in a similar way.

For sarscov2 it would be more about S than E and M proteins. Otherwise there are molecular patterns in the lipid membranes that can serve to distinguish between self and invaders (this is more about bacteria than viruses for which double stranded RNA is a more common recognition target) but the exact recognition process is not understood enough to produce some drugs.

Soapification is the process by which detergents break down the lipid envelope. Are you asking about soapification specific to viruses, or are you thinking more along small molecule targetting of lipis?

Thanks, James. Most detergents would dissolve the virus and host cell membrane equally, don't they. If only we could make them more specific to the virus to also use inside the body?

The lipids in the viral envelope come from chunks of the host cell membrane. Therefore, something targeting those lipids is unlikely to be virus-specific, and not suitable for use in a living animal.
Out in the environment where the virus is found in surfaces and such, sure, one can target the lipid envelope using soaps/detergents and such, but you wouldn't want to take those internally.

Thanks Bryan for weighing in. You think there's no way to make those prefer the viral membrane over host membrane using the lipid composition if different, the higher curvature or the unique membrane protein mix?

@SeanJ It's not really a different lipid composition, it's ripped right from the host - even if there were measurable differences it's not really plausible biologically to sit and count them to start getting suspicious from a slightly different ratio. If you're targeting membrane proteins you're not after the lipids anymore :) - MaxB's answer covers this but you said in a comment there you were thinking of the lipids themselves, so I added this answer.

@BryanKrause "it's ripped right from the host" - that may not be exactly true.  1. It comes from viral factories, which are a kind of modified part of ERGIC; the composition is not the same as that of exterior cell membranes, and 2. leaflet asymmetry!  I haven't seen any references about asymmetry of viral membranes, but given the equilibration times, it is hard to see how there wouldn't be (eg) phosphatidylethanolamine on the outside (which mostly doesn't occur in living cells)

Short answer: no in vivo drugs; yes for disinfectants.  Most detergents and solvents would deactivate the virus at least partly by means of breaking up (emulsifying) the lipid membrane (as well as possibly by denaturing proteins).
Targetting the membrane is hard in vivo since it comes from the host cells; most possible drugs (eg snake venom phospholipases) would affect both equally.  However, the host cell membrane has a strongly assymetric composition ("leaflet asymmetry") due to the action of enzymes that maintain it (flippases), otherwise the inside vs outside lipids would tend to equilibrate over time.  This is used a recognition signal, and there may be some natural compounds that recognize specifically inside-out membranes eg lysenin.  It is likely that the viral membrane is equilibrated, and so may be targetted by compounds like lysenin (although I haven't been able to find any experiments or published results along those lines).
I haven't been able to find much detailed info on the virus lipid membrane, so I asked a somewhat related question here before I found yours:
What is the lipid membrane of SARS-CoV-2 made of?


text:
Why is it beneficial for trees to grow that tall?
Why is it beneficial for trees to grow that tall?
This sounds like a kid's question Mom, Dad... why are trees so tall?
Costs and Benefits
There are some obvious costs:

Need much Carbon and other nutrients
maintenance cost
energy cost (for growing, to bring water (and nutrients) up to the higher leaves, etc...)
Sensitivity to wind
etc...

Potential benefits I can think of:

Competition for sunlight
Better dispersal
protection against predation
Some birds (maybe especially those that are potentially good seed dispersers) prefer to land on high trees (avoiding the cost of regaining altitude). Being high attract these birds which eat the fruits and disperse the seeds.

Are there other potential benefits?
Specific to palm trees
I am currently in Bali, Indonesia looking at palm trees that seem to have a very low competition for sun light (the forest is not dense, the light is intense), there are no tall predators (but being tall might be a protection against climbing predators as well and there are indeed monkeys and other potential climbing predators) and looking at coconuts, papaya and banana I can hardly think that being tall helps to disperse further away (seeds dispersal by barochory). So, why (evolutionary reasons) are palm trees so high?

Are the palm trees in a natural forest? You might be looking at an artificially grown oil palm plantation, since it sounds like your description is referring to that.

It might be that non-dense forest you are observing the palm trees in isn't the environment they evolved in. http://www.meltingasphalt.com/parable-of-the-redwoods/ explains this quite well.

Beside the reasons you've given I would add environmental disturbance (e.g. flooding) as a evolutionary factor that could explain selection for taller individuals. Many palms also inhabit and thrive in disturbed habitats (Frangi & Lugo, 1998; Salm, 2005), which indicates that this could potentially (i.e. speculative) be an important factor for this taxon. Palms also have the combination of tall height and a relatively low "wind profile" (relative to many other groups of trees), which indicates that they are adapted to exposed/disturbed habitats.
This, along with the reasons you've already given, seems to cover the most obvious evolutionary reasons for selection on tree height. However, these will naturally trade-off against negative effects on e.g. fecundity from investing and maintaining biomass.

Thank you, this kind of speculations was exactly what I was looking for!

The height of tree species varies, of course, as each tree fills a given niche, much like animals do; you might as well ask why blue whales grow so big.  The answer, of course, is that they seek out and successfully get the nutrients they require.  It is advantageous for some trees to be huge and get the most sunlight possible and so some trees do.
In the specific case of palm trees, however, they aren't true trees but rather a grass, which means they are a monocot and (I'm a little shaky on plant physiology but...) that the outside isn't living but the inside is.  Monocots grow straight up, in one main shoot, and palm tree follow the same pattern.  Tons of sunlight, nothing to come mow or it down, and nowhere to go but up means they'll be big.  True trees, on the other hand, have what is called heartwood in the center, which is technically dead tissue.
Another thing to think about is that trees aren't moving, so they only way they can improve their condition is by growth.  An animal, on the other hand, can migrate to follow food; growth, particularly for mammals, also has a huge heat cost.

Thanks for your answer. It doesn't provide the answer I was seeking though. I was looking for functional evolutionary reasons for a tree to be tall (like the three examples I provided). I know it is a reaction to natural selection, I know the concept of ecological niche. You're saying that tree can improve their condition by growth but my question is why? Or more specifically why growing tall?

For the case of palm trees, saying that they cannot grow wide but only tall is some kind of answer although it still does not answer to why growing tall rather than not growing (and invest more into reproduction)? Hope my comment makes sense!

@Remi.b I tried to say that in my first paragraph, and again in my last.  It's straightforward, and you guessed it: The taller the tree, the more sunlight it can get.  Other factors like soil and temperature can play a role as well.

The taller the more sunlight. Even if there is no competition? For what reason does being tall helps a tree in regards to temperature and various soil factors?

@Remi.b just because a particular individual (tree) has no competitors does not imply that the species evolved free of competition. I would guess that it always comes down to getting more sunshine. For example, a polar bear born in a zoo in Brazil will still be furry and white even though those characteristics don't help that particular individual.

@terdon Ha ha. Ok. So basically the answer is: there is nothing else than competition for sunlight that drives trees to grow tall? And if I can't see any single palm tree on my island that seems to be under competition for light, it is only because I'm unlucky and I observe these trees in an environment which is different than the one who drives the (meta)population to be tall. Are you sure that there's nothing else than "competition for sunlight" that drives trees (with barochorous seeds dispersal) to grow tall?

@Remi.b no, I am not sure at all. I know very little about plant physiology and evolution, it has never been my field, but the sunlight explanation seems sufficient to me. All I am saying is that you cannot extrapolate from the individual to the species.

@Remi.b Additionally, if you remove the competition it doesn't necessarily follow that the species will shrink immediately.  It can still be quite advantageous.

@Armory yes it can be advantageous...but why? That's all my question. Indeed, the trees I've been looking at were maybe not representative of the whole population (in terms of envirronment). Good point Terdon. But I want to come back to my question rather than talking about very basic stuff of evolutionnary theory. Do you have any hypotheses (other than the 4 in my question) to explain what selection pressure make trees grow tall?

@Remi.b And I (we?) are wondering why that's not enough for you?  Trees require sunlight to survive, and growing taller means more sunlight, so why shouldn't they?  A taller tree would have a fitness advantage that would be selected for.  I'm sure in some scenarios predation could play a role but not as strong as the desire for sunlight.

Are you saying that monocots should be more likely to grow tall? I don't understand your argument in the second paragraph.


text:
Should I help this young Magpie?
I found this young Eurasian Magpie in my garden:

He is just standing there, not doing anything. I believe he fell from a tree and can't fly yet and is just waiting for the feeding from his parents until he can fly, but I wonder if that’s true and if I should do anything to help.
There’s another young one on a branch of a nearby tree, also:

Call the RSPCA or whatever animal rescue service there is in your area. Posting it on SE doesn't help the critter in any way I'm afraid.

@AliceD my question was precisely if there is something I should do, or if this just normal in the bird's growing process

And my answer is precisely call the RSPCA or whatever animal rescue service there is in your area. Posting it on SE doesn't help the critter in any way I'm afraid.

@AliceD actually it does help the critter. The OP didn't know what to do, and didn't want to interfere without knowing if he/she should, so came here to ask someone who knows better, which in my opinion was a good thing to do. And you, presumably someone who knows better, said call RSPCA, which is useful information the OP received he/she didn't have before.

It's best to leave the bird alone. The parents are likely still in the area and tending to the young, including feeding and chasing away would-be predators. You're better off staying away so as to not intimidate or upset the parents. If you have outdoor pets, relocate them indoors or to an enclosed area for a few days.
Failing this, the advice given in comments to call your local animal rescue is best.

I actually saw a pair of adult magpies chasing off a hawk in the sky later, so maybe those are the parents. Thank you for the answer

check the guides "what do I do if I find a young bird on the ground"... if there are no cats it should be ok.


text:
What are some examples of non-homologous sequences having similar functions?
I am trying to find some proteins that are non-homologous but functionally similar. However, I cannot seem to find concrete examples. Can someone please point out any resources or provide examples?

Would something as broad as a gene involved in the development of wings in insects and one involved in the development of wings in birds be a satisfying answer?

Yea, sure, that would work.

By, homologous gene, do you mean gene with independent origin and similar function or independent origin and similar sequence?

I mean examples of sequences that are not similar(i.e. you cannot find them by BLASTing) but their functions are similar.

Serine Protease Catalytic Triad
This is classic example of convergent evolution in catalytic mechanisms. Shown below are chymotrypsin (4CHA, green) and subtilisin (1ST2, blue) aligned on their catalytic triads (Ser/His/Asp, darker colours). There is no obvious sequence or structural similarity.

You can check out the MEROPS database for a list of protease clans ("represents one or more families that show evidence of their evolutionary relationship") and this paper for a discussion on convergent evolution of the catalytic triad:

Although the biophysics of rate acceleration are intricate and sensitive to even minor structural perturbations, evolution has converged on a catalytic triad (or diad) with a reactive Ser, Cys, or Thr nucleophile more than 25 separate times to facilitate central biochemical reactions such as hydrolysis, transacylation, and phosphorylation.

Hoxd12 and Hoxd13 are involved in the development of wings in birds (Vargas and Fallon 2004).
pdm and aptorus are involved in the development of wings in insects (Williams et al. 1993, Averof and Cohen 1997)

Thanks. But, which of them are non-homologous?

Hoxd12 and Hoxd13 are of independent origin than pdm or aptorus but all are involved in the development of wings.


text:
Molecular weight of my 2-D gel
I am a little confuse when I try to figure out the molecular weight of the marker on my gel. I used NuPage Novex 4-12% bis-tris gel and Mark12™ Unstained Standard as a marker. Could please someone help me to figure out the molecular weight of the marker on my gel? I find different images in internet and I am confuse.

It looks you have everything except for insulin A and B chain. https://www.thermofisher.com/order/catalog/product/LC5677

Please don't change your question as it makes the answer incorrect. If you have a new question, post a new question.

This is what I think. Does it help? Let me know if you need more information.


text:
Why do I see so many kinetochores?
I am analysing RPE-1 cells from humans and I do not understand why I see so many kinetochores by immunofluorescence (more than 100 in many cells). They are in prometaphase.

Are you sure that they are RPE-1? Not a cell culture expert but other common cell lines are highly aneuploid (e.g. https://www.researchgate.net/post/How_many_Chromosomes_are_there_in_this_picture), and cell line contamination is very common.


text:
DNA Topology of two circular chromosomes
I'm reading DNA Topology: Fundamentals from where I quote :

Topological aspects of DNA structure arise primarily from the fact that the two DNA strands are repeatedly intertwined. Untangling these two strands, which occurs in all major genetic processes may prove rather difficult. In the simplest case of a linear DNA in solution, untangling is possible due to the free rotation of the ends of the DNA. However, for all natural DNAs, free end rotation is either restricted or forbidden altogether. Consequently, untangling the two DNA strands becomes topologically impossible.

And from Wikipedia:

However, a circular chromosome can provide other challenges for cells. After replication, the two progeny circular chromosomes can sometimes remain interlinked or tangled, and they must be resolved so that each cell inherits one complete copy of the chromosome during cell division.

Is there any evidence that proves the idea represented in the figure?

Yes, there is an abundance of evidence. I think the following electron micrograph is pretty convincing.

This image is from a review:
Gil-Ramirez G, Leigh DA, Stephens AJ. 2015. Catenanes: Fifty Years of Molecular Links. Angew Chem Int Ed 54:6110-6150.
It was adapted from the first paper to observe naturally occurring catenated DNA molecules, which were isolated from HeLa mitochondria:
Hudson B, Vinograd J. 1967. Catenated Circular DNA Molecules in HeLa Cell Mitochondria. Nature 216:647-652.
You can see this answer for an explanation of why catenanes form during replication:
How do catenanes form when DNA replicates?


text:
Smallest unit on which selection can act
Traditionally, the individual was considered to be the smallest unit on which Natural Selection (NS) acts. Today, we usually consider the gene as being the unit of NS. Of course, we should also consider all sequences that affect the fitness even though they are not genes (even though the do not code for polypeptide). And theoretically, any sequence of DNA does have an effect on fitness because it influences the time and energy for DNA replication (although it might be negligible). The decision of considering the gene as the smallest unit of NS seems rather arbitrary to me. We might as well consider a group of genes or a given exon of even a smaller sequence.
Here are my questions:

What factors influence the minimal size of a sequence to be considered as a unit on which NS acts? Mutation rate, generation time, selection differential for this sequence, recombination rate, ...?
Could we consider a nucleotide as a unit of NS? Why?
How does the quasispecies model fit into the question of what is the smallest unit of NS? (for those interested, you will also find a very good explanation of this model in Martin Nowak's book called Evolutionnary Dynamic: exploring the equations of life)
Is it worth talking about that? Is this question biologically relevant? Or is it rather a question based on a choice of definition such as "Is a virus alive?"

As I asked several questions, let me know if I should split my post into several. Otherwise, please do not hesitate to answer only very partially to this post!
UPDATE
Terdon's answer makes sense to me. I should be a bit more accurate in the reas of my question.  I read The extended Phenotype from Richard Dawkins quite a long time ago and if I'm not mistaken, Dawkins says the following things
A unit on which selection acts has to be:

active
germ-line
replicator

A replicator has the 3 following properties:

fecundity
longevity
fidelity while being copied

Therefore for fidelity to be respected a unit of selection has to be a sequence which is not too long, so that it is not too often modified by recombination or mutation. He argues in this sense.
He also argues that nucleotides are not possible unit of selection. Indeed, it is hard to imagine a nucleotide being an active replicator. The word active means that it influences its not probability to be replicated. I don't think a nucleotide can do such a thing.
Unfortunately I don't have the book with me right now and I can't check what I have said, give you a citation nor a more accurate a reference. If anyone has some citations from this book, it will be welcome for the discussion!
Thank you!

Who considers the gene as the smallest unit? I have never come across that idea (at least not in a modern context) . For example, SNPs can be selected for/against. Also, gene does not mean protein-coding sequence. As a simple example, think of tRNA genes (let alone the more complex cases).

Plus a single SNP can destroy a functional gene (nonsense mutation). Frameshifts are also huge changes because of 1-2nt indels. So the minimum possible limit on size is 1nt.

@WYSIWYG heh, your comment came as I was writing my answer, frameshifts are exactly what I had in mind.

perhaps i had a telepathic perception .. lol

Yes, you're absolutely right for the gene definition! Thanks!

The smallest unit that can be selected is, of course, the single nucleotide. The most striking examples of this are Single Nucleotide Polymorphisms (SNPs), many of which confer selective (dis)advantages.
To take a simple example, imagine a SNP that introduces a frameshift mutation, rendering a gene incapable of producing its protein. If that protein is something relatively important like p53, the SNP in question will be lethal and will be selected against. So, to take your questions one by one:

What factors influence the minimal size of a sequence to be considered as a unit on which NS acts? Mutation rate, generation time, selection differential for this sequence, recombination rate, ...?

any sequence unit whose alteration can affect fitness is a candidate for NS.

Could we consider a nucleotide as a unit of NS? Why?

Yes, if it can affect fitness (which it can, see above) it can be selected for or against.

How does the quasispecies model fit into the question of what is the smallest unit of NS?

As far as I can tell, it is irrelevant. NS can act on any self-replicating entity as long as the process of replication can produce variation that can affect fitness. If I understand correctly, the quasispecies model simply posits a group of entities with a very very high mutational rate. However, the rate of mutation does not affect the smallest unit that NS can act on, as I said above, anything that can affect fitness will be subject to NS.

Is it worth talking about that? Is this question biologically relevant? Or is it rather a question based on a choice of definition such as "Is a virus alive?"
Yes, it is worth talking about it if you have the misconception that the smallest unit is a gene :). No, but seriously, it is an interesting concept and a very useful tool. The selfish gene hypothesis for example, helped us see the world of evolution in terms of sequences rather than species or individuals. NS did not change, our conception of it did.

These are all useful conceptual tools that allow us as scientists to understand complex questions. However, NS is not a directed or conscious process so it does not care or know what it acts on.

PS. Please do not confuse protein-coding sequences with genes. As I said in my comment, there are many genes that do not produce proteins (tRNA genes for example) and that was even before the waters were muddied in the past few years. The current definition of gene is something like:

any nucleotide sequence with a job to do

Read the ENCODE papers for a more technical definition or take this one from wikipedia:

A gene is a molecular unit of heredity of a living organism.

UPDATE: First of all, you have to remember that Dawkins wrote The Extended Phenotype more than 30 years ago, in a time when the only complete genomes available were those of a few viruses. The first bacterial genome was sequenced in the mid nineties and the first human genome draft human in 2000. It was a time when selection was seen as acting at the level of the individual, and the importance of genes was underestimated. Dawkins books were instrumental in bringing genes into the spotlight.
However, if he did argue that a nucleotide cannot be selected (I have not read this particular book) he was simply wrong. A nucleotide can indeed affect its chances of being replicated. Think about it, if you have a G at a given position in the genome, and that G is mutated to an A, then the chances of the original G being replicated are obviously very low. Therefore, the nucleotide 'affected' its chances of replication. Alternatively, a mutation of a single nucleotide in the promoter of a gene can also cause the entire gene not to be transcribed and, as I mentioned before, frameshift mutations can wreak havoc as well. All of these are down to single nucleotides.
In any case, our vision of what a gene is has changed enormously since Dawkins wrote his book, we understand the genome much better now, and we have realized that it is far more complex than originally believed. 30-year old literature about genes, even if written by such luminaries as Rihard Dawkins, should be taken with a pinch of salt today.

@terdon Thanks for your answer! I updated my question, you might want to have a look and react to it.

@Remi.b see my updated answer.