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How does allele dominance work in polyploid organisms?
You know how there are tables to demonstrate allele dominance in diploids, such as the table found in this question?
Well, I was wondering how this works with tetraploids, hexaploids, octoploids, etc.
One might assume that you would need a four-dimensional table for tetraploids, a six-dimensional table for hexaploids, and an eight-dimensional table for octoploids.
One might assume that if you have an octoploid with a gene that has one dominant allele and seven recessive ones that the dominant trait would be expressed.
One might conclude that recessive traits would be expressed a lot less often in octoploids than in diploids in a population that commonly has both kinds of alleles.
Are all three of these assumptions correct? If not, what is the truth?

Dominance works in the same way.
However, polyploids have complex inheritance patterns!
1. Punnett square for polyploid inheritance

One might assume that you would need a four-dimensional table for tetraploids, a six-dimensional table for hexaploids, and an eight-dimensional table for octoploids.

The table you mentioned in this case should be the Punnett square. And its two dimensions correspond to two types of gametes that fuses in sexual reproduction. So even if you want to utilize Punnett square to work with tetraploids, hexaploids, or even octoploids, you still use a two-dimensional table because there are only two types of gametes involved. The fundamental difference is that you have to assign combinations of alleles to the first row and first column of the table instead of a single allele as you would do with a monohybrid cross.
However, deciding what combinations are allowed will be really intricate in this case, depending on two different factors: pairing behavior during meiosis and the resulting chromosome segregation. Variations in those aspects make general rules for polyploid inheritance impossible. In extreme cases, we can consider the organism to be either fully autopolyploid or allopolyploid.
An autopolyploid has more than two complete copies of the genome of a single ancestral species, and in the extreme case we consider the chromosomes have multivalent formation during meiosis and undergo unbiased segregation.
An allopolyploid has more than two complete copies of the genome derived more or less complete from different species, and in the extreme case we consider the allopolyploid has strictly bivalent formation between the chromosomes of a common origin.
This is a monohybrid cross, and it seems familiar and boring, right?

The following pictures depict how to use Punnett square with a tetraploid with two different alleles at a certain locus, and they are really captivating...

In this final picture you may find that the cross has "degenerated" into a monohybrid cross. If we try to depict something more complex, like a tetraploid with four different alleles at a single locus, we will obtain resultsvery different from normal crosses for diploids.

2. Dominance in polyploids

One might assume that if you have an octoploid with a gene that has one dominant allele and seven recessive ones that the dominant trait would be expressed.

This is true based on the definition of dominance:

Dominance in genetics is a relationship between alleles of one gene, in which the effect on phenotype of one allele masks the contribution of a second allele at the same locus.

3. Recessive traits in polyploids

One might conclude that recessive traits would be expressed a lot less often in octoploids than in diploids in a population that commonly has both kinds of alleles.

For this one, you cannot simply assume it because as I've said above, the inheritance patterns for polyploids, including octoploids, can be really complex and dependent on the particular species and the multivalent formation at the particular gene locus you wish to investigate. Thus, it's difficult to predict the the portion of individuals with a recessive phenotype in a population. There are so many intermediate patterns between two extremities of autopolyploidy and allopolyploidy that geneticists have to rely on sophisticated computational models to help them explain the data collected from experiments!
Source:

Rieger, R.; Michaelis, A.; Green, M.M. (1968). A glossary of genetics and cytogenetics: Classical and molecular. New York: Springer-Verlag.
Soltis, Pamela & Soltis, Douglas. (2012). Polyploidy and Genome Evolution. 10.1007/978-3-642-31442-1.


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Congenital blindness due to retinitis pigmentosa - does it exist?
Retinitis pigmentosa (RP) patients typically become blind after a period of years in which their eye sight slowly deteriorates due to photoreceptor degeneration. Generally RP patients develop night-blindness first, then tunnel vision, after which finally the central eye sight diminishes leaving them with basically no eye sight, barred some crude residual light perception. The wiki page on RP has more information when needed. Typically, the process from diagnosis of RP to (near) complete loss of eye sight takes years to decades.
However, Chebat et al. (2007) make mention that their study group, consisting of congenitally blind subjects, includes one person with RP (see table 1 in the linked article). Hence, this implicates that this particular subject was blind from birth due to effects of RP.
Is anyone familiar with newborns blinded by the effects of RP?

Reference
Chebat et al. Neuroreport 2007;18:1901-4

Just to be sure I understand the question, you're looking for case studies on a neonate that has already had a near total loss (or total loss) of vision from RP?  I'm not sure it would be diagnosed as RP at that point.

Can you link this article?

@AtlLED - correct, I am searching for evidence of congenitally blind folks due to RP.

@Chris - I linked the full-text article.

Thank you for linking the article.  I think I now understand where this question is coming from.  Was this prompted by Table 1?  Because even if RP is not showing symptoms at an early age, you are still "born with it."  As a genetic disorder, you are almost always going to see onset written as birth.

@AtlLED - yes - it was prompted by table 1! Interesting thought, but no - the authors are specifically including early / congenitally blind folks, i.e., visually deprived from birth

I have only ever heard of one case where RP caused blindness in a newborn. Unfortunately, I am unable to release the name or any details of the patient because of privacy issues and so forth.
Usually blindness from RP comes after a few years of life (as you said), making blindness from birth (or even early infancy) very rare.
I can tell you, however, that the formerly stated patient suffered from type I Usher Syndrome, if I remember correctly. I apologize for my inability to provide you with more specific details on this.
I don't know how much this will help in your search, but I sincerely hope that it does.
CDB

Perhaps I shouldn't ask new questions, but just to verify - is Usher's syndrome characterized by RP (i.e., is RP a symptom of Usher so to speak?) or is Usher's characterized as a syndrome with vision loss due to mechanisms related (but different) from RP? Thanks for your answer.

No problem, I'm happy to help. You are correct, RP is a "symptom" of Usher syndrome. Usher syndrome is a combination of hearing loss (usually due to a defective inner ear) and, of course, vision loss, which is due to RP.

Just to verify - this observation has never been published by any chance? Interesting observations ! :)

I don't believe this case specifically has ever been published. I have been searching for a similar article for a while because your question intrigued me so much (no doubt because of my past experiences with this patient), but so far I have found nothing. I am very sorry I cannot present you with even a name, as it is completely available to me, but, as I said earlier, certain privacy issues stand in my way. I will keep searching for an article that studies these observations.

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Phylogenetics and the Tree of Life
As far as I understand, evolution is nowadays pretty much analyzed through phylogenetic trees, that is cladograms. These are constructed using the available records and taking some key structures and deduce whether species acquired or lost it, thereby generating a node. By  this approach, chronology is of utmost importance, but chronological time is not. Hence, cladograms are not 'Darwinian' evolutionary trees as the latter are based on chronological time.
However, I cannot help myself when analyzing a cladogram and interpreting the accumulation of various nodes along a branch as moving through time. Isn't evolution all about time? At the risk of pitfalling myself into a 'this is a primarily opinion based question':
Isn't it just so that along a certain branch, each successive node has taken time to develop? Would it not be plausible to determine and assign a certain 'standard evolutionary time unit (a SETU if you like) representing the average time it takes for any organism to loose or acquire a certain trait, thereby allowing each node to be interpreted as time? Of course, the SETU would be a gross estimate, but could still potentially re-animate the Darwinian look on modern-day evolution.

Let's start with a short comment. You say [..]evolution is nowadays pretty much analyzed through phylogenetic trees[..]. Many evolutionary biologist make extensive use of phylogenetic methods but a good part of evolutionary biologist (most of them I would say) do not work directly with phylogenetic methods.

I am not sure I understand your question but I hope the following may help you either to understand the issue or to edit your question. Note that I am NOT a phylogeneticist (not sure this word exist).
What is the definition of "Node" in Phylogenetics
I think your definition of a node might be unusual. In phylogeny, a node is the most recent common ancestor shared by two sister lineages.
Time in a phylogenetic tree
Also, when you look at a phylogenetic tree, the axis along which lineages diversify represent the time (real time in years). Now, we use different methods in order to make estimation of this real time such as the rate of neutral substitutions. You may want to read about molecular clock

each successive node has taken time to develop?

I am not sure what you mean by "develop" here. Develop usually means the process by which a given individual/organism change phenotypically through its lifetime. See Developmental Biology.

average time it takes for any organism to loose or acquire a certain trait

Again, I am not sure whether you talk about development or evolution here as you talk about "any organism" and not about "any population". In any case, an average time for a population to acquire a given arbitrary trait is a concept that 1) is valid only for discrete trait, 2) that is very dependent on the kind of trait you want to consider, 3) that will varies a lot from one given trait to another and 4) is extremely dependent on when you consider being the starting point of the evolutionary process toward the creation of the given trait. Therefore, it doesn't makes much sense.
Currently used "standard evolutionary time unit"
However, you can use similar concept for quantitative traits. The Darwin (d) is a unit of evolutionary change (invented by Haldane and named after C. Darwin). It is defined as the e-fold (e≈2.7) in a mean of individual's trait in a population over million of years.
Similarly, the Haldane is a unit of evolutionary change (I don't know who invented it and it is obviously named after JBS Haldane) and correspond to the number of standard deviation (of the distribution of individual trait in the population) change in the mean of individuals trait in a population per generation. The Haldane unit is therefore dependent on the selection pressure, the additive and non-additive genetic variance and environmental variance (therefore the heritability) and the mutational pressures.

...phylogeneticist (not sure this word exist). I'm going to say that it does, and just means someone who practices phylogenetics. A better word might be taxonomist.

Thanks tel for you approval! Chris, let us know whether the answer(s) address your question and answer it.

This is definitely very helpful. And it pretty much answers my question(s) as to how I should/can interpret cladograms, their frequency of use, and the meaning of 'time' in a cladogram. Cladograms are very abstract, but very helpful and this answer clarifies a lot about them. I must say that my perception of a 'node' was likely incorrect and I could re-phrase my question to make it more appropriate, but your answer is great and I leave my question as is, if that is OK with everyone :)

Something like what you describe does exist, and is called a molecular clock. The rate of change in certain genes and non-coding sequences has been correlated to other evidence (fossil record, etc.) in such a way as to allow you to estimate in absolute terms how long a given set of mutations would take to occur naturally.
Keep in mind that only certain genes have the required property of accumulating mutations at a more or less constant rate with respect to time. Most genes accumulate mutations in a more stochastic fashion.

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Why perform imputation?
Genetics datasets contain measurements for millions of single nucleotide polymorphisms (SNPs). Some (usually small) percentage of these values are of low confidence, and are labeled as missing values. It is common to impute these missing values using statistical relationships within the high-confidence samples as well as relationships mined from public datasets. This makes sense, to get an estimate of what that small percentage of missing data likely is in reality.
Sometimes, analyses are performed that impute up to a much larger number of SNPs - for example, a genotyping platform might measure 2.5 million SNPs, but imputation is performed to get a larger sample of 6 million SNPs. My question is, what value do the extra SNPs that were never even measured have from an analysis point of view? When performing feature selection or predictive analysis, it would seem that the imputed SNPs are really just encoding statistical relationships that are present in the dataset to begin with. What does it mean to find a highly associated or predictive SNP in the imputed set?

In GWAS we are interested in understanding which SNP has a causal influence on a specific phenotype. At the moment large scale studies are carried out by genotyping arrays. For each SNP we put on the array, we measure the alleles present in the patient.
The cost of genotyping obviously depends on how many SNPs we would like to measure. So the problem when designing a genotyping array boils down to: What SNPs do we put on such an array so that we get most information out of it.
To answer that question it is important to realize that SNP alleles are not independent. SNPs that lie in the same haploblock are highly correlated. So measuring one of these SNPs is often sufficient to predict the alleles of other SNPs that are in so called linkage disequilibrium. When designing a genotyping array, we probably do not want to measure all of those highly correlated SNPs, because we gain very little information. Instead may want to measure just few of them and then impute (predict) the alleles of the correlated ones from population study data.
So back to the GWAS analysis. From the SNPs on the designed genotyping array we now predict SNPs that are associated with the phenotype. Say after our statistical analysis we found an associated SNP. But from the design of our array we know that there may be highly correlated SNPs that we did not measure. All of them will also be statistically associated. If we do not impute, we may come to the wrong conclusion that we already found the true causal SNP. In fact, there may be many and finding the correct is often very difficult.

To add to the other answer, an additional reason is that there are different genotyping microarray platforms (chips) with non-overlapping and different numbers of SNPs. In order to make sense of data from multiple chips, or to run GWAS on a dataset with multiple chips, you would want to impute. Otherwise, the sets of variants you are looking at are different.

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What is this Sacrificial Reproductive Strategy Called?
The reproductive strategy of salmon is 'suicidal'. Before breeding the males metamorph permanently into a form suited for the breeding season but unsuited for survival. The females devote so much of their biomass to producing eggs that they do not survive long after spawning.
Does such a breeding strategy have a name? Where the parents die shortly after breeding, or indeed during the mating process. I'm sure the latter, more specialised, case could only occur in particularly simple organisms (think polyps, think deep sea). But does there exist an organism which as part of its reproductive strategy, after breeding, devote such a portion of its biomass into the production of eggs that it literally dissolves into  cloud of spawn?

It is called Semelparity.
From wikipedia:

Semelparity and iteroparity refer to the reproductive strategy of an organism. A species is considered semelparous if it is characterized by a single reproductive episode before death, and iteroparous if it is characterized by multiple reproductive cycles over the course of its lifetime.

You see semelparity as suicidal but it is more interesting to generalize survival after reproduction in all kind of species and ask why would an individual survive if it won't reproduce anymore anyway?
Why would an individual survive if it won't reproduce anymore?
From an evolutionary point of view, there is no point to keep living after the reproductive age. You will note a few interesting exceptions to the rule though, including Homo sapiens, where the female keep living relatively long after her reproductive age. Of course, modern medicine is part of the explanation but we tend to think that modern medicine alone is not sufficient. Another explanation is based on kin selection and is called the grandmother hypothesis. In consequence, semelparous species die right after reproduction.
Evolution of semelparity/ieroparity
I don't think this point can be summarized in a few words. In consequence, I will just invite you to have a look at wikipedia for an introduction on the subject.
How common is semelparity?
Iteroparity is more common. However it would be wrong to think semelparity is extremely rare or that it exists only in salmon species (in plural).
In invertebrates, Many insects (butterflies, cicadas, and mayflies) are semelparous as well as some arachnids and moluscs (some squids and octopus). In vertebrates, semelparity is rarer, but there are some frogs (i.e. gladiator frog), fishes (smelt, capelin), lizards (i.e. Labord's chameleon) and marsupials (such as the famous opossum). Finally there are semelparous plants (some agave and some bamboos). In unicellular species (and some multicellular species, such as some trees for example), the concept of semelparity/iteroparity may well not apply easily and depend on a philosophical discussion of the identity of an individual.

Thanks for the answer. I am surprised that I used to know this word. To me semelparity is a suicidal, not merely because the organism dies afterwards, but because the nature of the strategy ensures it CANNOT survive afterwards.


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Topology of protein

The domain structure of protein Z, which is composed of 180 amino
  acids, is shown in the upper part of the figure below. Protein Z is
  palmitoylated at a cysteine residue (the third amino acid) through the
  mechanism shown in the box.

Which of the following diagrams shows the correct topology of protein
  Z in the plasma membrane?

I think the second diagram is correct because cytoplasmic side has reducing environment and so SH will not be allowed to react this way. Am I right ?

I think you're right - disulfide bonds don't usually occur in cytoplasmic proteins either for that reason.

I don't think there's any oxidation or reduction going on in this reaction; certainly there is no net reduction or involvement of NADH cofactor or anything like that. Furthermore, I think that it isn't too hard (esp. since these are enzyme-catalyzed reactions) to imagine that the mechanism is simple: nucleophilic attack of the carbon of the thioester by the cysteine, forming a thioketal intermediate, resulting in ejecting the CoASH as a leaving group. No reduction or oxidation.
Instead of oxidation or reduction, I would think about where exactly are the components of each reaction present. In order for the palmitoylation reaction to occur, you need: the protein Z N terminus, palmitoyl-CoA, and protein acyltransferase. Where are these components more likely to be present, inside or outside of the cell? Especially given that CoASH has several negatively charged phosphate groups.

I would say - inside the cell because of the enzymes and the substrates required. But how is negative charge connected with this ?

This review (http://bio.ijs.si/~krizaj/group/Predavanja%202011/Biochemistry%20Lipids%20Lipoproteins%20and%20Membranes/02.pdf) indicates that thioacylation of the type depicted in the question is indeed a cytoplasmic process.

@biogirllajja, a common strategy for keeping cofactors inside the cell is to give them net charge, particularly negative charge since phosphate is the most common charged species around that can be easily added to molecules. The net charge prevents the diffusion of the cofactor across the plasma membrane. For example, one of the main reasons glucose is rapidly converted to UDP-glucose upon entering the cell is to prevent its passive diffusion out of the cell.


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Root hair formation in Arabidopsis
In arabidopsis, 2 cell types arise in the root epidermis : root hair cells and hairless epidermal cells.
The immature epidermal cells that are in contact with 2 underlying cells of root cortex differentiate into root hair cells whereas the immature epidermal cells having contact with only one cortical cell do not develop root hair.
What is the advantage of this ?


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Are we capable to generate sounds of animals to the point that they mistakenly recognize it as members of their species?
From Animal language (Wikipedia), there are many evidences that we can communicate with animals, at least to baboons and dolphins. There is a case that fish moving away when hearing a record of whale sounds, however no examples mentions about the sound we actually make to communicate with them. We can even dog whistle, but this doesn't mean the dogs thinks that there is another dog. In my opinion, the answer is yes, since once we can capture the sound with spectrograms we can ultimately generate it. Is there any research on this?

Consider the long history of using various calls and audible lures in hunting.

I used to work on a ranch and could imitate calves well enough that their mother's would come running over.

@jamesqf can we make all the sound of the animal?

@Ooker: Who is "we"?  Personally, I can't even make all the sounds that other humans make, like the trilled 'rrr' sound in Finnish, or the click (often represented by '!') in some African languages.  And I certainly can't sing soprano :-)

@jamesqf well, but if you learn phonetics and spend ten years to learn opera, maybe you can? "We" means people.

@Ooker: That's what I was trying to say.  Not all people can make the same range of sounds.  Sometimes it's physical, as with the difference between a baritone and a soprano, or why two people with the same vocal range can be good and bad singers.  Sometimes it's a matter of needing to learn phonemes like 'rrr' or '!' at a particular point of childhood development.  So it's not surprising that some people can duplicate some, but not all, vocalizations of animals.


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What is the "mucin net"?
From Giulia Enders, Gut: The Inside Story of Our Body’s Most Underrated Organ

Mucins are proteins that form the main constituent of mucus. They help provide hours of fascination and fun for young children who have just found out they can blow bubbles with their own spit. A more useful function is their ability to envelop our teeth and gums in a protective mucin net. We shoot them out of our salivary papillae like Spider-Man shoots webs from his wrists. These microscopic nets can catch bacteria before they have a chance to harm us. While the bad bacteria are caught in the net, antibacterial substances in our saliva can kill them off.

What is the mucin net the author refers to? No result is found when googling it.

From Wikipedia (emphasis mine):

Mucins are a family of high molecular weight, heavily glycosylatedproteins (glycoconjugates) produced by epithelial tissues in most animals. Mucins' key characteristic is their ability to form gels; therefore they are a key component in most gel-like secretions, serving functions from lubrication to cell signalling to forming chemical barriers.

The "ability to form gel" is the key here. Also from Wikipedia:

Gels are defined as a substantially dilute cross-linked system, which exhibits no flow when in the steady-state. By weight, gels are mostly liquid, yet they behave like solids due to a three-dimensional cross-linked network within the liquid.

So, a gel (and mucins are no exception) is composed of a liquid trapped in a 3D net, much like a sponge. This is the "mucin net" your book is referring to.


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Daphnis Nerii not moving
Its been quite a while since my Daphnis Nerii has passed its eating phase, now its just a sort of recluse and is curled up in one corner and sleeps the whole day. It's a bit brownish in colour now. Although when I check on it, by lifting the container and moving it about, it starts jumping oddly. Like a jumpstart,  everytime it gets provoked. It maybe is the last phase of its instar period. Is it getting ready to pupate? Or is it not well?

Wikipedia tells us the following about the larva of the oleander hawk-moth (Daphnis Nerii):

Just before it pupates, the oleander hawk-moth larva becomes browner in color. The pupa of this species measures around 5.5 to 7.5 centimeters in length, and is light brown with black spots and a black line down the middle

The stage your critter is in probably resembles Fig. 1. It's probably fine.

Fig. 1. Caterpillar just before pupating. source: wikipedia

But the problem is that its quite inactive. Do caterpillars tend to stay inactive in pre-pupation?

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Can you tell me what species of insect this is?
I live in Verona, Italy.
Today I found this black insect and I don't know what species it is. My mom claims it's a kind of mint but I don't think so.

Hello and welcome to Biology.SE! Take the tour to learn about the site and earn your first badge. Also, what do you mean by "mint"? How's that called in Italian?

This looks like a horsefly (family Tabanidae, in Italian "tafani"), maybe Tabanus bromius but I'm not sure. If it's so, be careful: they bite and their bite is painful. Here you can find some quick suggestions about horseflies and their bite.
However, as you live in a city, don't worry too much: as the female horseflies feed on horse and cattle blood, they are normally present in the countryside, so those that you saw are exceptions more than the norm!

The eyes are a bit far apart to be a horsefly; I'm leaning toward Robber Fly (Asilidae) or Stiletto Fly (Therevidae), but can't be sure from the photo (and given how old the question is, I suspect that the model is no longer available for additional photos).

It's obviously not a horsefly


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What are ECT parameters?
ECT or shock treatment is used to treat psychological disorders. How much voltage,  current and duration is used for this? Wikipedia mentions a treatment of 0.8 Ampere for 5 seconds.

Peterchev et al. (2010) reports

The current amplitude is [... ] held fixed at the device maximum (e.g., 800 mA or 900 mA)...

and that

[constant-voltage devices are] now obsolete

The total stimulus duration as I understand is a pulse train of a few seconds (Peterchev, 2010). The duration of total treatment is about 20 minutes in the treatment room and up to an hour including recovery (source: Hopkins Hospital).
Note that the total stimulus duration depends on the total amount of injected charge. This in turn depends on stimulus frequency, stimulus shape, frequency and so forth (Fig. 1). For an excellent overview see (Peterchev et al., 2010).

Fig. 1. Sample ECT waveforms: (a) sine wave, (b) biphasic pulses with indicated parameter definitions, and (c) monophasic pulses (Peterchev et al., 2010)
Reference
- Peterchev et al., J ECT (2010); 26(3): 159–74


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Breathing under water
Why can fish breathe under water but land mammals can't? How can fish extract oxygen straight from water but humans can't?

It's always helpful to other users if you show what you have found on the matter so far so that any input is a constructive one.

shortly speaking. Because they have gills! You may want to have a look to the wiki article for fish gills. You may also want to google "How do fish gills work?". I think you will easily find all the information by yourself. Note: You say that land mammals can't breath underwater. Neither do the aquatic mammals. All aquatic mammals have lung and therefore need to come back to the surface to breath.

I believe that terrestrial animals tend to consume far more oxygen as well, so that even if a land animal had lots of gills, it could still not survive underwater.

@Superbest - I would imagine that great white sharks consume a lot of oxygen when they're hunting, and last time I saw one it was just slightly larger than I am :)

isn't this just a matter of a small Google search..

I'm taking this question at face value. Yes, fish have gills, but we also have a respiratory surface in our lungs so why couldn't we 'breathe' water and extract the oxygen (since extraction is a simple matter of diffusion from the content of the lungs into the blood).
Apparently we use 550 L of pure O2 per day. This works out as approximately 400 g.
The solubility of O2 in fresh water is around 10 mg L-1. Assuming a hypothetical situation where we could breathe water and extract all of the O2 from each lungful this means that we would need to breathe 28 L of water per minute, compared to the 8 L of air that we breathe.
Now of course water has a much higher density than air so that a lot of energy would be expended in moving this much water in and out of the lungs (which in turn would require us to consume more oxygen). Couple this with the fact that realistically we would only be able to use a fraction of the O2 dissolved in each lungful and you can begin to see why this is a non-starter.
Gills allow this problem to be largely circumvented by having a one way flow of water over the respiratory surface, which in the case of fish is often achieved at least in part by moving through the water.

+1 good answer. Note also that because water is more viscous than air, fish can have thiner structures than terrestrial organisms allowing a greater surface exchange.


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Why digest proteins into peptides for Liquid Chromatography - Mass Spectrometry?
Digesting (trypsin or whatever other proteolytic enzyme) proteins generates multiple peptides  so the degree of complexity of the sample, at the peptide level, increases a lot. In addition there is the problem of infering the original protein from its constituent peptides.
Why is this digestion step needed when you have to go back to protein level ? Is it just technological limitation?

As you rightly put, it is a technological limitation. Mass spectrometry based studies require proteins to be fragmented into smaller peptides for the ease of analysis.

It seems though, that intact proteins (even protein complexes) can also be analysed by MS. I just knew that

See pg no. 33 and 35 of this pdf. It says that Reversed Phase HPLC can be used both for studying protein digests and intact proteins.

Yes, LC works on separating large macromolecules, but my guess is that the limitation is on analyzing them by MS. Why can't you just do high throughput proteomics by LC-MS/MS as you would with digested protein mixture but with intact proteins?

I found the answer to my own question
It was formulated in a Nature publication by Mathias Mann (Title: The ABC's (and XYZ's) of peptide sequencing), a pope in Proteomics:

Why are peptides, and not proteins, sequenced?
After protein purification, the first step is to convert proteins to a
set of peptides using a sequence-specific protease. Even though mass
spectrometers can measure the mass of intact proteins, there are a
number of reasons why peptides, and not proteins, are analysed in
proteomics. Proteins can be difficult to handle and might not all be
soluble under the same conditions (it should be noted here that many
detergents interfere with MS, because they ionize well and are in a
huge excess relative to the proteins). In addition, the sensitivity of
the mass spectrometer for proteins is much lower than for peptides,
and the protein might be processed and modified such that the
combinatorial effect makes determining the masses of the numerous
resulting isoforms impossible. Furthermore, it is not easy to predict
from the sequence what the mass of a mature, correctly modified
protein will be or, conversely, which protein might have given rise to
a measured protein mass. Most importantly, if the purpose is to
identify the protein, sequence information is needed and the mass
spectrometer is most efficient at obtaining sequence information from
peptides that are up to approx20 residues long, rather than from whole
proteins. Nevertheless, with very specialized equipment, it is
becoming possible to derive partial sequence information from intact
proteins, which can then be used for identification purposes or the
analysis of protein modifications in an approach called 'top-down'
protein sequencing

This is going to be a very long answer but to give a short response.
You have to consider that MS for peptide detection works on the bases/principle of mass to charge (m/z) to detect an AA molecule, which is then normalised and analysed etc etc (http://en.wikipedia.org/wiki/Mass_spectrometry). Once you have the amino acids, then you just look at the order in which they get through and then you have your peptide sequence. Please read about the B, A and Y-type ions although this page is slightly technical (http://www.matrixscience.com/help/fragmentation_help.html). If the proteins was not digested then it would be far too big to be analysed since it would be read as one massive blob of m/z, which could be anything! So once you have your spectra from a peptide, you need to compare it to a model spectra, and based on that you predict what the sequence is as fragmentations peaks can be anything. Look at SEQUEST (http://en.wikipedia.org/wiki/List_of_mass_spectrometry_software). Now there are tons of correction algorithms that are applied, which you can look up.
Now RP-LC is carried out before MS to prevent all the sample rushing into the MS machine all at once as the machine can not cope if too much sample is inserted hence the flow rate is controlled. What I think you are thinking in terms of the set machine limit, is the (digested) peptide fragment that enters the machine, before undergoing electrospray. Now the experts that run the MS machines do set a peptide mass upper and lower limit, for what size/mass of fragment to accept and what size/mass to ignore. Look at this theoretical digest example (http://prospector.ucsf.edu/prospector/cgi-bin/msform.cgi?form=msdigest). This happens frequently with trypsin digest as it recognises specific AA before cleavage (http://en.wikipedia.org/wiki/Trypsin). Now a days, MS has advanced so much that we have machines such as Orbitrap (http://en.wikipedia.org/wiki/Orbitrap), which can cope with peptides, digested with elastase, which cleaves non specifically, which means you are less likely to get peptides that are far too big for analysis, hence increasing the protein coverage.
Hope this helps!


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Does a reduction in stem cells mean possible earlier death?
The basis of this question relies on my understanding of these 2 facts:
1) A person has a certain number of stem cells from birth
2) Stem cells are the basis of all cells and are used to repair and replenish

I read an article about stem cells being found in fat removed by lipsuction and that the trials that has been done on using these stem cells for repair elsewhere in the body.
My question is, if stem cells are used for repair in the body and you have a certain amount of them, if you "lose" some via liposuction, does this then mean you have less stem cells and therefore less chance of repair and could then theoretically die sooner?
It's more than likely my lack of knowledge on the subject but I would like to understand why.

yes. problems with stem cell function can lead to many diseases like leukemia which is why we have stem cell transplants.

So if you have liposuction, you have an increased risk of leukemia - is it really that straightforward?

I did not say liposuction can lead to leukemia, I said problems with stem cell function which is a very general observation. Please go through this paper (http://www.nature.com/ncb/journal/v16/n3/full/ncb2928.html). As far as your question about the impact of loss of stem cells through liposuction is concerned, I have to say I am unsure and would have to do some research first before I speculate.

I think the question should be edited to say "does liposuction increase leukemia risk by removing stem cells". This is what you are really asking, and the more general current form is arguably unanswerable.

Stem cells persist because they have the capacity to self-renew.  At birth you will have a finite number of each stem cell type (e.g. hematopoietic stem cells that make blood, gut epithelium stem cells that make gut lining etc).  The general picture is that as tissues require replenishment, a stem cell divides. One daughter cell starts to differentiate (and divide) into mature cells required by the tissue, whereas the other daughter cell retains stem cell function.
So a stem cell is typically defined as a cell with the capacity to: (i) self-renew and  (ii) to give rise to one or more cell types in a tissue. A hematopoietic stem cell can give rise to T-cells, B-cells, neutrophils, red blood cells, platelets etc.  The ability to self-renew means that, in general, stem cells don't 'run out' during a lifetime.
[ Its important to note that to define a cell as a stem cell, scientists use strange hybrid of: in vitro or animal assays + cell surface markers + location in the tissue + measures of 'having the capacity to make continued contribution to new cells'.  So lets just say that stem cells are only ever as well defined as our choice of assays combined with the interpretation of those results. ]
I mention the challenge of defining stem cells because, in recent years as assays and technologies improved, cells such a oocytes (eggs) or adult neurons, which were once thought to be finite, have been shown to have be replaced/renewed, presumably by some 'stem cell like' cell(s).
As noted above, stem cells are usually involved in the replenishment of a particular tissue type.  So liposuction, which will remove fat cells, should not affect the numbers of hematopoietic or neural stem cells and so on.
Any claim of clinical benefit of a 'stem cell treatment' using liposuction should be backed by clear data.
A longer answer would get into:
(i) the concept of 'plasticity' where the classical view - a fixed pathway between a stem cell giving rise to one daughter cell that  gives rise to mature cells and the other returns to a stem cell state - is open for debate, and
(ii) the idea that since stem cell definitions are only as good as our assays, there may be potential plasticity even among stem cells that we cannot 'detect' yet.

Death is caused by a variety of factors, our ability to heal is among them. However, it is possible to die from causes other than a deficiency in healing ability. Most people in the world die from cardiovascular disease and cancer.
The role of stem cells in the heart is an area of intense investigation. Vascular clogging is a more likely cause of cardiovascular failure than a disease of the heart muscle itself. In the case of clogged vessels, no biological mechanism exists to heal clogged arteries. Stem cells are irrelevant here.
Stem cells are most applicable to cancer in the immune system for the recognition of cancer cells. A decrease in actively dividing immune stem cells would correlate with an increased progression of cancer. This is exactly what happens with people undergoing chemotherapy. Chemotherapy kills actively dividing cells, including stem cells in the immune system. This is why they often suffer increased infections. It is rare to die from an infectious disease today. Decreased immune response from chemotherapy is a manageable side effect of treating cancer.
If you recreationally took chemotherapy drugs, this would inhibit the activity of stem cells. Your body would rapidly accumulate genetic mutations and systemic damage resulting in eventual death. This is why people coming in contact with individuals on chemotherapy should be careful not to touch any surface contaminated with the drugs. This especially applies to pregnant woman, where the danger is primarily with the fetus. In development, stem cells are vital in organ formation, not healing.
In different circumstances, to different individuals, during different life stages, destroying or preserving stem cells may be therapeutic, or devastating.

Theoretically, yes. Although, to my knowledge it has not been proven. As far as I'm aware there is no known link between liposuction and leukemia, liposuction would most likely not remove enough stem cells to produce such an effect. I've been doing a lot of research into stem cells lately and from what I have found there have not been many, if any, in depth studies on the impact of stem cell removal as the implantation of stem cells is usually the main focus.

theoretically yes to what?

Theoretically it could inhibit the body's ability to repair itself and cause an earlier death. Although the replication of stem cells to form other stem cells would prevent this from occurring. All stem cells in the region would have to be removed along with a life-threatening condition for stem cell removal to have this effect. Sorry this wasn't clear above.


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Can virus resistance be acquired through generational exposure?
If I have a squash plant that has a mosaic virus of some kind, and I breed its descendants (via seed) for generations, each with exposure to the same virus, will future generations be likely to eventually obtain resistance to the virus, and if so, how long would this typically take?
It seems to me that this might be how the resistant plants would have first developed resistance, but I could be wrong.

Perhaps the answer is in natural selection. Over many generations, if these plants are constantly exposed to the same virus, one of them may obtain a mutation or something similar that allows it to be resistant, thus that plant will have higher survival and growth rate and thus more seeds.
The current plant itself may also adapt to the presence of this virus (perhaps in growth patterns, etc.) over a long period of time.
As for the time for the genetic resistance to take place, it is almost impossible to say as it is almost completely random (and would also depend on what other plants you may pollinate it with as an already resistant plant would, of course, cancel the need for a mutation).
I hope this helps.


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How are DNA segments selected in PCR?
I understand that in PCR we're able to amplify only selected portions of the DNA... however despite reading it from multiple sources, I cannot figure out how this selection actually takes place.
I know that by using proper primers, one each for coding and template strands, we can direct the DNA polymerases to specific sites to start with. I also understand that these primers make the replication proceed in opposite directions, towards each other. Like follows:

However, I wonder what makes the replication terminate when the polymerase reaches the primer at the other end? Because as far as I understand, replication should continue indefinitely until the physical end of the sample strand is reached... such that we may decide the starting points but never the ending points.

Termination of replication on the original template is dependent on the processivity of the enzyme or the length of the DNA, but think about what happens if a newly synthesized strand is used as the template.

Note: In your PCR program you always set extension time.
Case:

Product length = 500bp
PCR extension time = 50sec
Assuming that polymerase adds 1000 nt/min

Cycle 1:

Strand that binds FP: extends ~800nt to the right (as per the polymerization rate): 300 bp ahead of RP complementary site. This product is lets say P1
Strand that binds RP: extends ~800nt to the left: 300bp ahead of FP complementary site. This is P2

Cycle 2:
The products of cycle-1 become templates for next round.
FP binds to P2 -300nt from its 3' end. Similarly RP binds to P1 -300nt from its 3' end.
The resultant products will be 500nt which give rise to a 500bp perfect dsDNA.

Some P1 and P2 will keep forming at a linear rate; since your template is low in amount compared to the amplified cycle1 and cycle-2 products, your expected PCR product will be much higher (which gets produced at an exponential rate).

The long products are amplified linear, while the short product (with the primer sequences on the ends) are amplified exponential.

yep exactly... :)

Wow, beautifully explained.

Only now I understand why there are highly controlled timings and temperature control in PCR.

I think that the DNA produced with overhanging ends (i.e that made of P1 and P2) must grow as exponentially as the one of perfect size... only that it will lag one order of magnitude behind.

I'm not completely clear when you say "what makes the replication terminate when the polymerase reaches the primer at the other end" since when you perform a PCR you go through three phases. The denaturation, whereby the two DNA strands become single stranded, then the annealing, which is when primers attach to their appropriate matching site (but the original DNA template is still single stranded) and extension, which is when DNA polymerase use the primers to extend make the matching strand the primer is attached to (http://en.wikipedia.org/wiki/Polymerase_chain_reaction). DNA polymerase continues to make the strand until it essentially either drops off or until the cycle is over and it is time for the cycle to repeat itself. The way you make sure to terminate a specific DNA replication at an appropriate length is to use the extension time as a control since as pointed in the above answer by @WYSIWYG the extension is largely assumed to be 1000 nt/min so if your product of interest is 500 bp, then you do 30-40 sec of extension in your PCR extension cycle program and if the product of interest is 1000 bp you do 60 sec of extension and so on.
In the training I received, it is usually not recommended to PCR DNA template which is very large such as an entire plasmid such as pUAST. The main issue even with high fidelity/proff-reading DNA polymerases is that you can get errors in replication if the strand is very long. what often happens is that you amplify a section of DNA if you want to check for the presence of something or if you need to use the amplified fragment then you design restriction sites at either end of your fragment by incorporating it in the primers itself then you go ahead with you digestion and fragment purification and then you sequence your fragment to make sure you do not have any errors although PCR has much much more applications.

I see... incorporating restriction sites within primers sounds pretty smart. Thanks for the wider perspective.'

authors: ميثم يحيى عبيس الشمري


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Vegetation Monitoring - Why permanent plots
Why do most vegetation monitoring programs rely on permanent plots?
Take the context of a single ecological restoration site, for example.  Let's say the variable of interest is cover by plant species, and monitoring is conducted throughout several seasons to track the relative/total cover of multiple species.
If plots are randomly sampled within homogeneous vegetation assemblages, why not just establish new plots each sampling period, rather than locating and re-sampling the same plots over and over again?
If the goal of sampling the is to represent characteristics of the population (i.e. the homogeneous area of vegetation), then why do researchers always sample permanent monitoring plots again and again rather than using a new set of randomly selected plots each time?

Are you asking in the context of a single longitudinal study using particular plots, or in the context of multiple separate studies over time?

A single study area.  I will edit my question to be more clear.

The answer boils down to statistics rather than anything particular about this type of experiment.
If you have a sample of plots, and then take repeated measurements in that same sample over time, the variance in the values you record is a function of the variance of the time-dependent process causing changes.
If you take future measurements from a new sample of plots, you have additional variance to account for due to choosing a new sample. That is, even if you would have measured no change at all in the same plots, you expect the second sample will be different from the first just because of sampling. Because of this additional variance, you have less ability to detect smaller changes over time: less statistical power.


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How does acupuncture work?
Can anyone actually tell me how acupuncture works?
There are numerous websites with little actual explanation, but assert that it works. For example the below article:
http://www.health.harvard.edu/blog/acupuncture-is-worth-a-try-for-chronic-pain-201304016042
However I have failed to find any article about how acupuncture works, or the mechanism at play. Can anyone tell me how it works?

Welcome to Biology.SE. Do you have any evidence to support that it actually works? If not, your question is off-topic because "primarily-opinion based". If you are looking for evidence f whether it works or not, then you should go on Skeptics.SE. You will find here on skeptics a lit of questions tagged acunpuncture that will probably already give you some answers.

@Remi.b https://scholar.google.hu/scholar?as_ylo=2011&q=acupuncture+placebo+controlled&hl=hu&as_sdt=0,5 There are many placebo controlled articles, it is better than placebo. (Btw. it is interesting, how you do placebo acupuncture. :D)

Dear questioner, let me help: https://scholar.google.hu/scholar?q=acupuncture+mechnism&btnG=&hl=hu&as_sdt=0%2C5&as_ylo=2011

@inf3rno sham needles!

@TanMath I checked the video, but it wasn't about whether acupuncture works. It was about that doctor - patient relationship has placebo effect which I already knew. http://www.dailymotion.com/video/x1moo91_horizon-2013-2014-8-the-power-of-the-placebo_lifestyle

@inf3rno that wasn't my video.. I was just saying sham needles can be used as control

@TanMath Ohh okay. :-)

@TanMath I checked 4-5 article about placebo controlled experiments by different diseases. None of them was better than placebo. It is a bit early to tell, but maybe it is really just placebo. :-)

What is acupuncture
Acupuncture is a form of alternative medicine by which needles are pierced through the skin and helps to treat diseases.
Science behind acupuncture
So far, the research on acupuncture has shown that acupuncture can help to suppress pain but probably will not treat diseases.
Really, it all has to do with connective tissue. Connective tissue is tissue that connects, supports, binds, or separates other tissues or organs. In the connective tissue, there are cells known fibroblasts. According to an article in The Scientist (http://www.the-scientist.com/?articles.view/articleNo/35301/title/The-Science-of-Stretch/):

the cells that are responsible for synthesizing all the proteins that make up the extracellular matrix. These cells reside within the matrix they create, responding to mechanical stimulation by regulating the amount of collagen and other matrix proteins produced, and by secreting matrix-degrading enzymes in response to chronic changes in tissue forces.

Their research also showed that:

the fibroblasts initiated a specific Rho-dependent cytoskeletal reorganization that was required for the tissue to fully relax. Rho is an intracellular signaling molecule known to play a role in cell motility and the remodeling of cell-surface proteins that connect the fibroblast to its surrounding matrix.

They also mentioned that the fibroblasts secrete ATP, which is converted to adenosine which is an analgesic. This leads me to a second article in in Discover Magazine (http://blogs.discovermagazine.com/notrocketscience/2010/05/30/a-biological-basis-for-acupuncture-or-more-evidence-for-a-placebo-effect/#.VjAmFyPn_qD). In this article, they mention about a paper that described the importance of adenosine.
Criticism
The research showed that the A1 receptor for adenosine is important for acupuncture to work. But they mention in the Discover article that there is nothing special about acupuncture. They say:

o answer that, clinical trials have used sophisticated methods, including “sham needles”, where the needle’s point retracts back into the shaft like the blade of a movie knife. It never breaks the skin, but patients can’t tell the difference from a real, penetrating needle. Last year, one such trial (which was widely misreported) found that acupuncture does help to relieve chronic back pain and outperformed “usual care”. However, it didn’t matter whether the needles actually pierce the skin, because sham needles were just as effective. Nor did it matter where the needles were placed, contrary to what acupuncturists would have us believe.

It is hard to also have a control but it seems the best may be the sham needles. However, much of this research is debatrd.
I hope I have answered your question. Please ask anything more in the comments.

It works via the placebo effect which according to recent research, is not the sort of trivial effect as it was thought to be.

What about the research in the articles described in my answer?

@TanMath What has transpired in recent years is that sham acupuncture and real acupuncture work just as well, the best results are obtained when  patients have long discussions with the doctor about the complaints  before undergoing treatment, whether it is a sham or real treatment.

but there is scientific evidence that it is a physical phenomenon...

@TanMath The relevance of such induced phenomena must be established. E.g. if I treat patients suffering from vertigo by letting them be subject to a roller coaster treatment, then obviously I'm subjecting them to nontrivial physical effects that influence balance. However, if I'm not doing any better than alternative treatments where they are not subject to such influences, then I can't say that the roller coaster had any effect on the vertigo. My theory may well be very plausible, there may exist experimentally confirmed mechanisms that support my theory. But it's then all irrelevant.

@inf3rno says that your video wasn't about whether acupuncture works... Maybe another link about placebo and acupuncture is better?

If you watch the entire video, you'll see sham acupuncture with patients discussing complaints compared to real acupuncture.

Every major, large, blinded, well-controlled study shows that it is no better than placebo.
Here's one article with references:  https://sciencebasedmedicine.org/acupuncture-doesnt-work/


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What kind of spider is this? And is it dangerous? (photo)
I found this spider hanging from a web off the side of my house (in Buffalo, NY). It's probably 3-4in total length. Any thoughts on what kind of spider this is? And if it's dangerous?

I would think this is a European garden spider (or cross spider). See here and here.
It can bite humans but it is not dangerous for them.

Indeed, I recognise it from my European garden. It's not dangerous.

i think its a cross spider because it doesnt have hair around its legs

Looks like a variety of the very common and diverse group of "garden" and/or "orb weaver" group(s).  They really pop up everywhere during the spring/summer but die off w cold weather (in southeastern US).  Like mentioned, they'll bite but not poisonous...  They're the guys whose webs you're constantly being freaked out by when u hit it face-first---but then never see the spider, or at least aren't bitten normally.
The ones you gotta watch for around here don't make webs that you'll typically see, and either leave their webs often and/or remain in cracks/crevices (e.g.) brown recluse or black widow...).

If you're in NY- I'm pretty sure you would need be worried only about brown recluse and black widow- if even applicable up there (I'm in GA, so warmer here...).


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What (if any) is the shortest evolutionary process observed by humans?
So when I think of evolutionary processes, I think of it taking millions of years to happen. Like how humans evolved from monkeys or birds evolved from dinosaurs (I know that is super-duper simplified). Or how humans have parts that we don't need or use (the appendix, for example), but we don't have any records of a time when it was. But I wonder if there have been any evolutionary processes that happened on a human timescale or if we have evidence of something evolving in, say, thousands of years instead of millions? I think this would be interesting to learn about.

All species are evolving with every generation. Check out Remi.b's favorite site https://evolution.berkeley.edu/evolibrary/home.php for some basics on evolution.

@BryanKrause Remi.b's favorite site $\ddot \smile$. I often refer to this site following Corvus advice here

Haha that's nice, I hadn't seen that Q&A before. I'm more familiar with your use of the advice you got there than the original advice itself I suppose. :)

Definition of evolution
The whole problem boils down to the definition of the term "evolution". Typically, evolution is defined as a change in allele frequency over time. See wikipedia > allele if needed.
Answer with definition "evolution = change in allele frequency over time"
Using this definition, any event of death or birth is an evolutionary event. As such, in the human species, there are about 6 evolutionary events per second! This number will vary a lot among species / lineage of course.
Do you want to consider another definition?
If you are willing to use another definition, I am happy to investigate how common are events matching this definition. Please make sure to clearly define the term so as to leave out possibility for subjective appreciation. If you need inspiration for definitions, you might want to have a look at this post.
Sidenote: Evolutionary experiments
You might be interest in evolutionary experiments. An evolutionary experiment consists at putting individuals in a lab, let them breed under some circumstances and let them evolve. Of course, doing such experiment with elephants would be pointless as the generation time is so long. Common species that we use for such experiments include E.coli, S. cervisae (yeast) and D. melanogaster (fruit fly). Some of these experiments can be as short as a few days while others have been running for decades.
Somewhat related posts

How come most animals never seem to evolve over millenia?
Evolutionary chronology - if any, which species have evolved in the last 100 years
Why don't we keep evolving until we are super-human?

For a very introductive source of information in evolutionary biology, you can have a look at the website that @BryanKrause recommended: evo101

How are you defining "evolutionary event"?  You can do a lab experiment to generate antibiotic-resistant bacteria from antibiotic-sensitive parents strains in a few days or weeks, I think.
Humans drive the dodo to extinction over the course of a few centuries.
In Lake Victoria:  https://www.nytimes.com/1996/08/27/science/lake-victoria-s-lightning-fast-origin-of-species.html

Now an international team of researchers, using remote sensing to
  probe the sediments at the lake's bottom, have found evidence that
  what is now Lake Victoria was a dry, grassy plain just 12,000 years
  ago. For evolutionary biologists, the implications are enormous. The
  discovery means that the 300 unique fish species that have been
  documented in the lake must have evolved in the unthinkably short
  interval since the current lake began to form, a geological instant
  ago.

Another example:https://payseur.genetics.wisc.edu/IslandEvolution.htm

Gough Island, located in the South Atlantic about 3000 km southwest of
  South Africa, is home to the largest wild house mice in the world.
  These animals are about twice the mass of wild mice in the United
  Kingdom. Body size evolution has been rapid: mice were recently
  introduced to the island (in the 19th century) and a major size
  increase was observed over just a 40-year period. The drastic size
  change of Gough Island mice has been attributed to low temperature,
  extended longevity, reduced predation, and carnivorous eating habits.
  In a highly unusual behavior, these mice cooperatively feed on live
  and dead chicks of severely endangered albatrosses.


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Does the human eye see things at twice the distance in a mirror?
If I'm standing 3ft away from a mirror and looking at something in it that is behind me but 5ft away from the mirror, do my eyes see that object as 3ft? Or 8?

8 feet. You can do ray tracing for a plane mirror and see that the image will "appear" at an equivalent distance behind the mirror. The light hits your eyes at the same angle as if the object really were that far away.

As a side note, this is why nearsighted people will have trouble seeing distant objects in mirrors, even if they put their eyes close to the mirror.

@user137 don't answer questions in the comments. With the link attached and a little more elaboation on the answer it's a good answer imo

I'm voting to close this question as off-topic because it appears to be primarily about optics rather than biology.


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Why sleep? No, actually, why wake?
I was just reading the sleep threads, and I wondered, why is the body so constructed so that sleep is necessary? (Is it just a design error?) But then, how do things come to be awake at all? How did this happen? Yes, I can see the advantages, but how did it happen? What is "awake"? Are single-cell animals awake?
The question I want to ask is, how did things progress from just sitting around ingesting and growing, like plants, to being something more? Is it more? What do "wakers" have that the rest don't?
Sorry, I'm not a biologist, this may be a foolish question, or in the wrong place.

Hi and welcome to the Biology part of SE! I think you're tying in a few different concepts here, and they're really more philosophical than biological. I don't think it makes for a good SE question, but feel free to join me in Chat and I can talk you through some of the basics that I'm aware of.

We should be fine using this: http://chat.stackexchange.com/rooms/1997/biology

That chat room won't let me in. Never mind. But if you want to copy my question I could follow other people chatting about it...

these are fundamental questions in sleep research done by neuro/sleep biologists... probably a field which is poorly represented in the stackexchange community. Its a common question about sleep, but also regarded well enough for it to be funded by the NIH for research...

Based on various comments, I've expanded this answer. Though long, I cannot cover the depth of the topic of sleep but I tried to address the issues asked in the original question while broadly highlighting various aspects about sleep research. I welcome any suggestions for improvement.
What is sleep?
To know what it means to be awake, you must know what it means to be in a state of sleep. These are two alternative states for animals that sleep.
Finding a concise scientific definition of sleep is difficult, probably because sleep is a very complex process. For example, Diekelmann and Born (2010) state that,

Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory...

and later

Sleep is characterized by the cyclic occurrence of rapid eye movement (REM) sleep and non-REM sleep, which includes slow wave sleep (SWS, stages 3 and 4) and lighter sleep stages 1 and 2....

Most attempts to explain what sleep is include the four stages of sleep along with REM (rapid eye movement sleep). The stages are nicely explained by this National Institutes of Heath website on Brain Basics: Understanding Sleep. Each stage of sleep can be identified by specific types of brain waves, shown below (image from here).

Notice that the first wave pattern is characteristic of being awake.  The wave patterns change as an individual becomes drowsy and then falls asleep. While asleep, the brain cycles through the different stages, each with its characteristic brain waves.  Associated with these stages are changes in metabolic activity and physical capabilities. For example, the Brain Basics site notes that we become less responsive to external stimuli and metabolic activity slows. During REM, breathing becomes rapid and we can't move the muscles in our arms or legs. Similar states are found in other invertebrate and vertebrate organisms, which suggests that these are common indicators of sleep or a sleep-like state. Some examples of these states are given in the citations and links below.
Defining "awake" seems just as difficult as defining "asleep" but once again neural activity seems to be key indicator. As shown in the figure above, being awake has characteristic wave patterns in the brain that are distinct from the wave patterns associated with sleep. In addition, none of the physiological/physical states associated with sleep stages are present when you are awake.
In both cases, asleep and awake, the indicators seem to be based on characteristic neurological activities in the brain or, in the case of some invertebrtes, the organized nervous system.  This interpretation is important when considering whether organisms without any type of nervous system is capable of sleep or the alternate state: awake.  More on this at the end.
Why sleep?
Science magazine, in the 125th anniversary issue, made a list of 125 big questions that remain to be answered by scientists. One of those questions was "Why do we sleep?" The role of sleep remains elusive but many ideas have been put forth about the role of and the evolution of sleep. The leading idea seems to be memory consolidation. This article by Kavanau (1997) reviews ideas about the function of sleep and why it evolved.  He suggests that sleep and memory evolved as as ways to improve or maintain effective connections among the nerve cells in the brain. Some circuits are used frequently, such as those used to process sensory information like vision. Other circuits are used less frequency, such as circuits that can be used to store memories. Sleep may allow those infrequently used circuits to be activated and used without causing conflict with the circuits used during "restful waking." In other words, sleep may allow the lesser used circuits to be exercised, which can help to consolidate memories. So, at least one function of sleep may be to help maintain efficiency in how information is moved around the brain by maintaining the brain circuitry.  See also this review by Siegel (2005) and the previously mentioned article by Diekelmann and Born (2010).
This Scitable article has a nice overview of the importance of sleep for humans, as does the Brain Basics site.
What organisms sleep or have sleep-like activity?
Sleep has been well-studied in vertebrates, from fishes (Marshall 1972) to mammals (Pace-Schott and Hobson 2002). However, not all vertebrates necessarily sleep (Kavanau 1998). For example, continuously swimming fishes like some sharks and blind cave fishes may not sleep. These are just three references of many about sleep in vertebrates.
Sleep and sleep-like activity has not been as well studied in inertebrates. As noted in this thread, there is evidence for sleep in at least some insects. Cephalopods like octopuses show signs of sleep (Mather 2008). Caenorhabditis elegans, a nematode worm and model biological system, shows sleep-like states tht are similar to mammals and fruit flies (Raizen et al. 2008). The most basal organism that shows evidence of sleep-like patterns is a jellyfish called Chironex fleckeri (Kavanau 2006). Cnidarians like jellyfishes are the basal (most "simple") group of organisms with an organized nervous system. Interestingly, C. fleckeri process a lot of visual information obtained through their 24 eyes. Twelve of the eyes are simple, light-receiving structures but 8 of the eyes are camera-like, meaning they have a lens.  Kavanau (2006) argued that sleep (up to 15 hours) in this jellyfish allows time for its simple nervous system to process the visual information obtained while it is awake. The presence of sleep-like activity in jellyfish and nematode worms suggest that sleep is an evolutionarily ancient phenomenon.
This Wikipedia page on sleep in non-humans overviews evidence for sleep in vertebrates and invertebrates. It's not clear whether androids sleep or what they dream about if they do sleep.$^1$
Do single-celled organisms sleep?
This is (to me) a tricky question. Sleep is associated with specific types of neural activity in the brain or nervous system. In addition, sleep-like neural activity has been found in diversity of organisms with some type of nervous system, and seems evolutionarily old. I therefore think that any organism that has some form of organized neural center (brain, brain-like organ or centralized nervous system) has the potential to show some type of sleep-like patterns.
In contrast, organisms lacking any type organized nervous system would not be capable of sleep, at least as currently defined. If they do not sleep, then they also cannot be awake because being "awake" seems to be recognized as neural activity not typical of sleep.  Therefore, it seems to me that single celled organisms like bacteria and paramecium are neither sleeping nor awake.  Plants are neither sleeping nor awake. They are metabolically active but they are neither asleep nor awake because they do not have any type of neural activity.
I'm not a sleep researcher (but sometimes I am a sleepy one) nor am I a neurophysiologist. I just walked through my train of thought. I welcome contrary views along with the supporting science.
Literature Cited
Diekelmann, S. and J. Born. 2006. The memory function of sleep. Nature Reviews Neuroscience 11: 114-126.
Kavanau, J.L. 1997. Origin and evolution of sleep: Roles of vision and endothermy. Brain Research Bulletin 42: 245-264.
Kavanau, J.L. 1998. Vertebrates that never sleep: Implications for sleep's basic function.
Kavanau, J.L. 2006. Is sleep's 'supreme mystery' unraveling? An evolutionary analysis of sleep encounters no mystery; nr does life's earliest sleep, recently discovered in jellyfish. Medical Hypotheses 66: 3-9.
Marshall, N.B. 1972. Sleep in fishes. Proceedings of the Royal Society of Medicine (abstract).
Mather, J.A. 2008. Cephalopod consciousness: Behavioral evidence. Consciousness and cognition 17: 37-48.
Pace-Schott, E.F. and J.A. Hobson. 2002. The neurobiology of sleep: Genetics, cellular physiology and subcortical networks. Nature Reviews Neuroscience 3: 591-605.
Raizen, D.M. et al. 2008. Lethargus is a Caenorhabditis elegans sleep-like state. Nature 451: 561-572.
Siegel, J.M. 2005. Clues to the functions of mammalian sleep. Nature 437: 1264-1271.
Footnote

I could not resist.

I think your answer can be considered totally complete to this broad question if you could add a bit more about the standard definitions of "sleep" and "awake" in science and precise for which species the concept of sleep applies.

@Remi.b Thanks for the suggestion. I'll try to carve out time later today after my classes.

That article is really interesting. I think you have answered my question, and in doing so, have made it seem more reasonable than it was. I look forward to the changes Remi.b suggests.

So sleep is the brain defragmenting itself. OK. If you don't have any software running you don't need to sleep. OK. And the reason we do it is that evolution threw it at us and it seemed a good idea. OK. I would give you +10 if I could.

@RedSonja Yes, sleeps helps to consolidate memories. Having memories, even very simple ones, may provide an evolutionary advantage (remembering where food resources are, what food is safe to eat, which organisms are dangerous, etc.). You accepted the answer (thanks!) but you can also click on the upward arrow to say "Good answer" if you wish.

All organisms (except viruses?) need some kind of nutrition to survive and reproductive activities for the species to survive. As humans don't do these while asleep in a first approximation I would consider those life phases as sleep when these do not happen. In this sense clostridium bacteria could be considered asleep when in their endospore states, a sunflower seed could also be considered asleep as it is inactive.

So we could say sunflower seeds wake up at some point?

@RedSonja Yes, along the above I would consider the seed awake as soon as it starts using up its stored food.

I don't think I can see any phase of a plant's life as being awake. No. But then I don't really know what "awake" means.

Sleep is associated with neural activity. Bacteria and sunflowers do not have a nervous system so could not have any form of sleep. Endospores and seeds can be dormant but not asleep.

@MikeTaylor Is the “neural activity” criterion widely accepted in the definition of sleep?

If “neural activity” is a necessary condition to call a state of an organism “sleep”, then the original question “Are single-cell animals awake?” makes little sense to me.

Sleep includes changes in neural activity patterns of the brain see here. These changes in neural activity do cause changes in metabolic activity, such as rapid eye movement and suspension of voluntary muscle activity. I agree than awake doesn't make sense for organisms that don't have sleep-like patterns but I did not address the philosophical implications of that part of the question.

btw, it always sounds a bit weird to say "for the species to survive". It seems like you suggest an evolutionary goal to allow the species to survive.

@MikeTaylor It's not a philosophical implication introduced by the answer, rather one of the original questions you have ignored: “Are single-cell animals awake?”. If you think that question does not make sense then please criticise the question, not the reply that takes it seriously and attempts to give a logical answer.


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Can turkeys run around when their head is cut off like chickens do?
Chickens may run around after their head is cut off if the head is severed near the base of the skull leaving the brain stem intact and missing the jugular vein.  This usually only lasts for a few minutes, however there is the case of Miracle Mike that survived for 18 months after his head was cut off.  Do turkeys also exhibit this same behavior and if not, what makes this possible in a chicken but not a turkey?

The brain does not control all bodily movements. Some movements are to a great extent controlled by neural networks in the spinal cord. The spine contains a network which is pre-programmed to control the muscles in frequently-used movements such as running or swimming in chickens. This is why a chicken can run away after you chop its head off. Likewise, turtles swim using their a spinal neural network. As long as a signal is received somewhere in this network, the network will activate the swimming movements. Such a system is coined an ‘attractor network’ (source: Science Nordic). A similar system has been shown to occur in a sea slug. I couldn't find similar information in the turkey though. Happy Thanksgiving :)
Note that walking and running in higher animals (mammals) is controlled by the motor cortex higher up in the brain, involving a more complex system including the pyramidal system. Reflexes, however are controlled by quick, short spinal relay circuits in higher animals as well.

Wow, attractor networks are fascinating.  I thought for sure turkeys would display the same behavior but could not find any supporting evidence either.  Happy Thanksgiving indeed.


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Factors That Would Promote Eusocial Development In Mammals?
What would cause mammals to evolve to be more eusocial, like the naked mole rat did? What advantages does eusociality give in such scenarios?

Welcome to Biology SE! Your question as it stands is more appropriate for Worldbuilding SE. Perhaps if you could rephrase it to ask about a biological question that can be answered with evidence it would be better received here. For example, are you interested in the ecological conditions with which eusociality is correlated? Even so, some prior research from your part is typically required in our site.

What?
Eusociality in mammals can be defined by the following criteria:

reproductive altruism (which involves reproductive division of labor and cooperative alloparental brood care);
overlap of adult generations;
and permanent (lifelong) philopatry (stays (or returns) at (to) breeding ground).

Why?
Burdo et al. (2000) state that eusociality in mammals is a special case of monogamy, involving prolonged pair bonding for more than one breeding period. They argue that eusociality in mole-rats evolved from a monogamous mating system where cooperative brood care was already established. A tendency for group living is considered to be an ancestral trait in some genera of mole rats. The solitary lifestyle seen in some other genera is assumed to be a derived trait.
The aridity food-distribution hypothesis (AFDH) suggests a causal relationship between cooperative foraging for patchily distributed resources and the origin of eusociality. This theory states that limited nest sites or patchy resources leads to benefits of staying within the natal group, including reduced dispersal risk, and the possibility of inheriting the natal nest (Plowes, 2010).
How?
In proximate terms, in eusocial mole-rats either puberty is assumed to be developmentally delayed so that under natural conditions most animals die before dispersal is triggered. If genetic relatedness among siblings is high, then philopatry would not invoke an appreciable loss of fitness, especially if the cost of dispersing is higher than staying within the natal group. High genetic relatedness is more likely in a monogamous mating system or a highly inbred population (Burdo et al., 2000).
References
- Burda et al., Behav Ecol Sociobiol (2000); 47(5): 293–303
- Plowes, Nature Education Knowledge (1010); 3(10): 7


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Identification of a plant (in a pot)
I have in my flat a plant which sometime make strange flowers. When the start it looks like plastic stars:

Then the flowers are opening after few days and looks like this:

The smell is a bit strange (I cannot say bad but definitively not good as other flowers). In general this plant does not need many watering and even I am in Switzerland, I guess it is living normally somewhere else.
For the size, mine is quite small (30 cm high but many wires) but my mother have a very long one along the wall (few meters).
Many picture with higher resolution are in my flikr gallery.
Anybody can tell me what is the name of this plant and where it lives normally?

http://en.wikipedia.org/wiki/Hoya

It is a Hoya Carnosa Krinkle Kurl flower. It is native to Australia and East Asia. Hoya Carnosa links to wikipedia and Krinkle Kurl links to plant rescue in case you want to read more on it.


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Identification of a larva
Last week-end I was working in my parent's garden and when I dig a bit the ground, I found few larvas I never seen before. My father told me there are there every time when he's doing the garden springtime.
I took some pictures (I just put it on leaves for the picture to see better than on the ground).
One low-res:

And the gallery hi-resolution pictures
The location is in northern of Switzerland (Jura) at around 700 meters above the sea and the larvas were inside the ground in around 3-5 centimeters (1-2 inches) deep.

What you are seeing is a cocoon for a moth pupa.

Here is a link to a YouTube video of one hatching that is normal found in the soil.

Interesting, do you know how it look after?

@ruffp watch video link

Ok mine are a bit smaller (1-2 cm) but the video is impressive. But I don't know if there are still alive because it's not moving at all.


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Mitochondrial D-Loop
I know that the D-loop is  a DNA complex in which the strands of double helix DNA molecule are separated for a stretch and held apart by a third strand of DNA. Usually, this third strand has a base sequence, which is complementary to one of the main strands and pairs in accordance with it. The third strand then sub sequentially displaces the complementary main strand in the region. Im also aware that D-loops occur in many DNA systems, such as in DNA repair, telomere activity, and in mitochondrial circular DNA molecules.  However, my question is why does the D loop only provide information about maternal DNA ancestry?

because roughly speaking, sperm mitochrodrias do not enter the ovule, just the sperm DNA

All the mitochondria of an individual are originating from the mother. This means that if the mother is afflicted by a mitochondrial disease, the offspring will also be affected. This is why the three parent model is being considered in some cases (1).
(1) Pritchard, C. (2014, September 1). The girl with three biological parents. BBC News. From http://www.bbc.com/news/magazine-28986843


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How Behind is the Human Mind (Latency of the Senses)
I would like to know if there is any research into the latency of human perception.  Particulary:

What is the minimum time for various inputs (vision, touch, sound) to be recognized by the conscious mind?
How different are these times?  (Loud sound vs sense of touch in your toe)
Given the above, is there a number we can put on how many milliseconds behind reality the human mind is?

are you the same person from the youtube channel that makes the picture videos or are you just using his name?

I'm the guy from YouTube.

awesome to know.. i am subscribed to ur channel.. fan of ur work..  this probably is ur next project.. will try and answer ur question if i get good references..

There is a huge amount research into this subject. It is vast and nebulous as such I cannot give you an overall picture of this. I can however illustrate some of the complexities to this.
Firstly I would say that what you mean by human perception is extremely complex, there are different modalities of perception. For example in terms of a visual stimulus, we may simply perceive its basic shape, outline, colour, whether or not it is moving. We then may also perceive higher levels of information such as the function of the object. Similarly there are different aspects to other stimuli.
These different components of perception are transmitted by different neurons leading to the brain and then processed by different areas of the brain suited to specific tasks and then are integrated together to give us a conscious idea of what the object is.
Therefore when measuring the latency of human perception you would first have to decide what exactly you mean by this?
The other aspect is that a lot of study has occurred in this area as we are aware that perception can be altered by states of illness (for example audio evoked responses in schizophrenia, or visual evoke responses in multiple sclerosis). The perception of pain is yet another huge area of study.
Again this is such a vast area of research that I wouldn't really know where to point you to. However for a entertaining read on how perception can change in neurology I would recommend reading the books of Oliver Sacks, in particularly "The Man Mistook His Wife for a Hat" and an "Anthropologist on Mars".
I am sorry I haven't provided you with more detail but good luck in reading around this subject. If you are more specific about what perceptions, (e.g. perception of faces, perception of danger etc..) then maybe you will receive more specific answers.

If I had to pin it down, my question is really 'how far behind the current moment is the conscious mind?'

Again that is very difficult, first of all there is no real understanding of what consciousness is, and we also know that we become consciously aware of different things at different rates. This conscious awareness is highly variable. Take the conscious awareness of pain, this is highly dependant on type of pain, where it happens, what your underlying state of mind is. How would we ever measure such a thing? What we do know are things like reaction times, how long it takes for various stimuli to reach the brain, how we process input on different levels, etc.


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How can cells produce antibodies despite error-checking mechanisms in their genomes?
How can immune cells produce so many different kinds of antibodies with different variable regions if there are so many mechanisms inside the cells that try to keep the DNA sequence as constant as possible (i.e. prevent mutations, which are actually necessary to create the different kinds of antibodies)?

This process is called somatic hypermutation. I just looked it up in my Alberts and it seems the exact mechanism is not known (though the book is a bit older now, this might have changed).

B- and T- cell receptors are the only place where the DNA sequence is edited, changed, mutated and altered in the body on purpose. Have a look at somatic hypermutation in the Wikipedia.


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Does sodium lower the harmful effect of potassium on kidneys?
As far as I have read so far, it seems that potassium and sodium are trying to expel each other from the human body. A lot of documents on the web say too much sodium pressures the kidneys could cause a kidney failure. The same is also said for potassium.
If a person eats a lot of potassium-rich foods, does increasing sodium intake cancel out the harmful effect of potassium on the kidneys, or just double the harmful effect (he/she gets the harmful effect from both potassium AND sodium)?

Chemically speaking, sodium and potassium are very, very similar, and also pretty common, and our body needs both.
Due to their similar electrical properties in particular, they are used as kinds of 'counters' in some processes in the human body, as they can be distinguished to some extent by other processes, and the balance of the two is important.
What it is important to note, however, is that more potassium than sodium is needed, so an overly-high-potassium diet is rarely considered a health risk, even if only due to it being infrequent. People tend to be potassium-deficient rather than sodium-deficient.
Generally speaking, unless you are consuming way too much of both, having a potassium surplus is less problematic than a sodium surplus, and harmful effects certainly don't "stack", at least not trivially. Rather, extra potassium will tend to offset extra sodium, ameliorating rather than aggravating health effects.
Even so: All of this can vary wildly with general diet and other factors, so the prudent thing to do regarding ones sodium/potassium balance is to see one's doctor and have blood work done.


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Confirmation for a picidea
I am sorting some pictures and found this one taken from Swiss Jura Mountains (North part, alt ~700m) in March 2013.

The day before I saw a Dendrocopos major (Great spotted woodpecker) and without looking thoroughly before I though it would be a young one.
Now when I examine in more details the picture it seems to be a Dendrocopos medius (Middle spotted woodpecker).
Am I right? Can someone confirm this?

You are right, this must be a Middle spotted woodpecker Dendrocopos medius. It has clear stripes on its belly, and the black stripe on its cheek does not reach the beak. The beak is also  smaller, but size is always hard to judge.


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Identification of a probable sylviidae
One summer (August) I was in Bulgaria (Dobrich province) and in the middle of the city I take picture of this bird:

He was making a sound like "Tchek-tchek" like the sound of a Eastern Olivaceous Warbler (lat. Iduna Pallida) but the greenish color make me think it is more a Icterine Warbler (lat. Hippolais icterina).
I found a song similar to the bird I saw on this page (second record).
It could also be a Common Chiffchaff (lat. Phylloscopus collybita) or a Willow Warbler (lat. Phylloscopus trochilus) as they are very common but the length of the tail make me feel it more one of the above (or another one) and the sound does not seem to fit.
Anyone can help on identification of this bird?

Are you sure it is always the same bird? The one in the first pictures seems very different: white edges on the wing, legs of a different color, less prominent supercilium.

I thought first it was the same, but after your remarks I noticed the pictures are done on the same tree but two different days. What confused me is the sound of the bird, but I can admit I did not see them singing in front of me.

Warbler can be difficult at the beginning that's why now they are my favorite to identify, I provided the correct answer below, if you have any question feel free to ask.

The first picture is an Icterine warbler. Because of the yellowish plumage (never in the eastern olivaceous) and the with fringes of tertiary characteristic of the species and never present in the genus Phylloscopus. Also the color of the leg, greish-bluish is quite specific of the Icterine.

The second and third picture are of a Willow warbler (Phylloscopus trochilus). The legs are pale compared to a chiffchaff and the primary projection (the length of the primaries that pass the tertiary) is extremely long and very typical of the willow warbler. You can see the difference in the image below.
 Here a useful webpage

please provide reputable citations to back up your claims. Thanks

There is no citation involved in identifying birds. In Europe this is the best guide https://www.amazon.com/Collins-Bird-Guide-Lars-Svensson/dp/0007268149          But a guide is not enough to identify birds, the field experience is essential (I have been birdwatching for 20 years).


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Identification for a bird in the middle of the tree
In the central city of Dobrich Bulgaria, I was following a Great spotted woodpecker in a tree and suddenly I found this other bird on the same tree.

The context of the picture is:

Country: Bulgaria
City: Dobrich, Center urban area
Period: mid August (2016)

I think this is a specimen of Silvia Curruca, can anybody confirm this?

Yes, Lesser whitethroat indeed. Grey head with contrasting white throat and brown body, small bill (the similar Orphean warbler has a much bigger bill).

Please add additional detail/evidence and reputable citations supporting your claims. The point of answers is to be helpful to others searching for similar questions in the future, which is made possible by evidence/citations. Unsupported responses to [tag:species-identification] questions should be added as comments and not as answers. Thanks.

There is no citation involved in identifying birds. In Europe this is the best guide amazon.com/Collins-Bird-Guide-Lars-Svensson/dp/0007268149 But a guide is not enough to identify birds, the field experience is essential (I have been birdwatching for 20 years).


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What is this red mushroom with the "inverted" cap?
Picture taken on 29 March 2020, Czech Republic (Middle Europe). The cap is red, and its shape is "inverted". It is quite tough, first I thought it was a piece of plastic, but apparently it is growing from the ground.
What is the mushroom - if it is a mushroom :) ?

Looks like Sarcoscypha Austriaca (scarlet elfcup). It's actually used in many textbooks as a representative species for the Ascomycetes.
Details from Wikipedia and Messiah.edu both confirm that this species is found in Europe and that it is typically found either as solitary or clustered fruiting bodies (2-5 cm wide) growing among rotting wood matter in damp wooded floors in the spring.
Photos below:

 Source: Wikimedia

 Credit: William Roody; Source: Messiah.edu
Read more at MushroomExpert.com.


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Does the sun light have to have *direct access* to fruits to make them sweet?
I understand that sun light is needed for fruits to ripen. In the years with less sun light, the fruits are usually not so sweet. So the sun light is needed to make the fruits sweet.
Where and how does the sweetening process occur? Does the sugar in the fruits come from the photosynthesis occurring in the green parts of the plant (leaves) and is then conducted to the fruits, or is the sugar produced in the fruits themselves? Does it matter whether the sun shines directly to the fruits, or is it enough if just the leaves have enough sun light and the fruits become equally sweet even if they are hidden under the leaves?

It would depend if the fruit has the ability to sense or capture light. This depends on chlorophyll mostly, found in cellular organelles called chloroplasts. If the fruit is incapable of capturing light, the light can still have an indirect impact by being captures on leaves, since plants circulate nutrients - this is why roots can grow without having access to sunlight.
Here's a few excerpts from the following paper (https://www.ncbi.nlm.nih.gov/pubmed/11337414):
"To date, molecular regulation of the role of light in fruit ripening has been studied most thoroughly in tomato, and available evidence suggests that light has its greatest impact on pigmentation, with apparently little effect on additional ripening phenomena."
"The green to red color transition typical of ripening tomato fruit is largely due to the developmental transition of chloroplasts to chromoplasts; as photosynthetic membranes are degraded, chlorophyll is metabolized, and carotenoids, including β-carotene and lycopene, accumulate."
In plain English, the pigment that captures and absorbs sunlight for metabolic reasons (photosynthesis) gets transformed into a pigment which absorbs sunlight for other reasons, such as 'looking tasty' or protection from ionizing radiation. Essentially the same thing happens to leaves in autumn - the green chlorophyll pigment, which absorbs the energy of the sun for the plant to grow, becomes the orange carotene, and the leaf slowly dies off.
Interesting sidenote: biological pigments are very important molecules in ecology and in cell biology. Take a closer look: https://en.wikipedia.org/wiki/Biological_pigment
As for your question about how ripening occurs... Google would do a better job than most.

"tomato... light has its greatest impact on pigmentation, with apparently little effect on additional ripening phenomena."
Does this mean that if you shaded the tomato fruits agains the sunlight, but left the leaves uncovered, the fruits would become sweet, but remain green?

Yes. That would be the experiment!


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What causes the pain when a bone fracture is healing?
Why does a fracture still hurts when it is healing? I understand the pain at the beginning - the bone is not in its place, there is a pressure against the nerves, also the swelling pushes the nerves etc. But why does it still hurt after several weeks, when the swelling is gone, the bone is more or less fixed? Is the cause of the pain mechanical, or chemical?

At the initial phases of the healing the broken ends are mobile (and this is time when it can be set and put into a cast).
At later stages soft callus than hard callus forms and now any movement will pull on the broken ends and stimulate the nerve endings: it hurts.
This also has the effect that the nearby muscles will spasm in an attempt to immobilize the bone. Another source of the pain can be that these muscles become tired and start to hurt as well.
The pain will continue until the two broken ends are completely welded together so there is no longer any movement that would stimulate those nerves.

Well, but aren't the two broken ends more or less welded together after 3-4 weeks? Why does it hurt longer?

@HonzaZidek It's not fully welded together until the cast is removed, which takes 6-8 weeks usually. Even after that there is a remodeling phase which can cause disconfort as your body restores the bone's original shape. Also the changes in posture during the 2-3 months injury needs to be corrected, unused muscles need to regain their strength, overused ones need rest, which can cause pain (even elsewhere).