text:
Growing crops on the Moon
The short version of my question is this:

It's some time in the future. I go into my back garden and focus my telescope on the Moon. The surface is virtually covered with giant greenhouses, growing food to support the cities that have sprung up there. The question is: what plants are they growing in those greenhouses?

Factors such as temperature, water, soil quality etc. can be controlled easily enough if you already have the ability to build sealed greenhouses in a vacuum. There are also a number of experiments on growing food in closed systems where air and water are recycled (the Biosphere 2 project being the best known). The low gravity can't be controlled, but there have been a number of experiments on plant growth in microgravity conducted on the international space station, so growing plants in Lunar gravity should be possible. There have also been some interesting results from growing plants in an Earth-based approximation to Lunar soil.
However, another important issue is the length of the Lunar day, which is 28 Earth days long, meaning that the Sun shines continuously for two Earth weeks, followed by two weeks of total darkness. I'm interested in what's known about how plants could adapt to this, but I haven't been able to find any research papers on the subject. Of course it would be possible to simulate an Earth day using artificial lighting, but the energy costs of doing this on a large scale would be rather high, so for economic reasons future Lunar farmers would likely want to keep it to a minimum.
So my first question is, has any research been done on the effect of extreme changes in day length on plant growth?
Secondly, is there any type of food plant that would be particularly likely to cope with such an environment (perhaps with some suitable genetic modifications)? For example, would normal crop plants such as cereals be able to build up enough sugar reserves in two weeks to survive the next two weeks in total darkness? If not, is there another type of plant that's more likely to be able to adapt to this? Or as an alternative strategy, is there any crop that grows fast enough that its shoots could be harvested after only two weeks of continuous sunlight? (Some individuals would have to be grown to maturity under artificial light in order to produce seeds, of course.)
Finally, I'd be grateful for pointers towards research on any other issues that I might have missed that are relevant to the problem of large-scale Lunar agriculture.

this question is quite long, perhaps you could make it clearer what you are trying to ask

@GriffinEvo are long questions considered bad here? If so that makes me sad. I think I've set out quite clearly what I'm asking in the final three paragraphs - could you please be more specific about what you found unclear?

There is no limit on length, I just feel that the key points you are trying to get to get a little lost and could be made to be more obvious, questions that are long or difficult to get to key point of are less likely to get good answers. So don't be sad :)

I suggest you rephrase your question to remove the reference to the moon. The obvious answer is that artificial light can be used and controlled so there is no reason why growing crops on the moon would be affected by its day/night cycle. Consider that if we have bases on the moon, we will already have lighting and the expense will be negligible compared to everything else necessary to make that possible. The question you are asking is how plants can/could adapt to different day/night cycles and it is a very interesting question but mentioning the moon distracts from it and confuses the issue.

@terdon I'm not talking about bases, I'm talking about large-scale agriculture. From basic thermodynamic considerations, providing a square kilometre of crops with full strength artificial daylight would require at least a square kilometre of solar panels, thus reducing the overall yield by 50%. Lunar agriculture might use some artificial light, but you'd really want to keep it to a minimum. I'll consider your suggestion, but I really am interested in the specific issues imposed by the Moon.

I agree with @terdon and think that the Q should be rephrased. Both "how plants cope with extreme day/night cycles" and "what plants that might be suitable for lunar greenhouses" are interesting questions, but at the moment your question is a bit unclear.

@Nathaniel the specific issues imposed by the moon also include the details of lunar soil (different pH, lack of bacterial species and nutrients etc, see here), the lack of atmosphere both as a source of necessary gasses and as a filter for UV. Since you seem to be exclusively interested in the effects of a different day/night question, I suggest you restrict your question to that.

@terdon I explained in the question that I'm aware of the relevant research pertaining to those issues (with the exception of the UV filtering, but that's trivially solved by coating the glass). However, there may be other issues that I haven't thought of. The question is about growing crops on the Moon, and these "I like your question but you should change it to a completely different question" comments are starting to bug me. I agree that a more generic question about adaptation to day length would also be interesting - please feel free to ask it yourself.

@Nathaniel I don't mean to bug you and you are, of course, welcome to leave the question as is. I am just pointing out that you are not making your point clear and that is reflected by the answer you have received and by the fact that you have already collected 3 close votes one each for unclear, too broad and primarily opinion based. Your call.

@fileunderwater if you can be specific about what you found unclear, I will gladly attempt to clarify it.

@terdon I expected better from this community, but if they choose to close it it's their loss. I'm an expert from another field with what I believe is a perfectly specific and well-defined (if somewhat speculative) question about biology, and if that's not welcome here then I guess this just isn't the site for me.

@Nathaniel don't take it personally! You may well believe that your question is clear but if people do not understand what you are asking, then it is obvious that others do not agree. Various people have already suggested ways of clarifying and there is clearly an interest in your question which I, personally, hope will stay here and get a good answer. You know how the SE sites work,this kind of back and forth is normal. You are also combining many questions in one which is bad form on all SE sites.

@terdon there is only one question. It is stated in a quotation block  at the top. The rest is clarification and background material - something which on most other stack exchange sites would be appreciated. I'm very happy to try and make it clearer, but if people keep just saying "it's unclear" without being specific about what they're having trouble with then there really isn't much I can do. Closing it would be perfectly reasonable if the question was against site policy, but it patently isn't, and the fact that the close votes are all for different reasons reflects this.

The question in the quote block is what plants are they growing in those greenhouses? which cannot be answered, there are too many ways of dealing with the various problems that lunar cultivation raises. You could have GM crops, airtight greenhouses, a terraformed moon, artificial gravity, unicellular chemosynthesizing algae, solar mirrors, artificial light, soil transferred from Earth, modified lunar soil, unmodified lunar soil with modified plants, the list goes on. What seems clear to someone outside the field can be very complex to experts who know more of the underlying complexity.

@terdon yes, the quoted part can't be answered on its own. That's why the following section on background and clarification is necessary - but then people complained it was too long, so I can't win.

@terdon again, most of the things you mentioned are already covered in the question. People keep bringing them up even though I already covered them, and I don't understand why. But Basically all the options you mention are possibilities, with the exception of artificial gravity, which is physically impossible (trust me, I'm an expert and know more of the underlying complexity) and artificial lighting unless it's kept to a minimum, for reasons already discussed. The question is aimed at someone with the knowledge and imagination to weigh those options up and arrive at a solution.

I think I can re-write it to be clearer, but it will have to wait until I'm at my computer, either tomorrow or next week.

@Nathaniel One can be concise whilst being being clear. Your question has too many unknowns to give a specific answer and you seem to be looking for an overcomplicated answer. The basic answer is simple, humans would have to adapt (by modifying conditions on the moon to resemble those found on earth) the plants would likely have to do very little adaptation.

@GriffinEvo the question I have asked is difficult and requires a considerable amount if expertise to answer. That is quite a different thing from being too broad, and I didn't think it was against the rules. It must definitely does have a specific answer. I completely disagree that it can be asked any more concisely than its current form, and when I edit it for clarity it will necessarily get longer. I have explained many times why modifying the day length won't work, and if you ignore that then you are simply not addressing the question.

@Nathaniel you think that getting to the moon, providing sufficient water (a resource not found on the moon [in any large amounts at least so far]), building farms and filling them with artificial atmospheres (from gases not found on the moon), providing a nutrient rich soil substrate (again I believe this is not already on the moon), dealing with low gravity, and starting human colonies large enough to maintain and require these farms across the entire moon surface (not currently on the moon) are all feasible... but we can't manage to produce a light source?

@GriffinEvo those things are all one-off costs. Lighting requires a continuous supply of energy. Maybe there are other options (fission, fusion) but the most obvious source for that energy is solar panels, and as I've discussed at length, the issue then becomes one of land area. The idea of agriculture is to maximise yield from a given area of land, and if half that land is occupied by solar panels then only half can have crops growing on it, which seems quite inefficient.

@GriffinEvo that's not to say there can't be any light. The sunlight that reaches a shady spot on a cloudy day on Earth is probably less than 1% (maybe much less) of the total energy provided by the Sun, and supplying that level of artificial light becomes much more feasible. But you still have to use plants that can cope with a 28-day dusk-daylight cycle.

About availability of energy needed to artificially light the plants during lunar night, I wouldn't worry much: it's probably a lot smaller than the energy needed to keep greenhouses warm during that night.

Plants are adapted to the conditions we have here on earth, therefore, for them to grow on the moon we would have to recreate the conditions found on earth (or at least find conditions that we can create and they can grow in). To do this we would need to replicate climate (temperature, air pressure, humidty etc.), provide (sun)light at the necessary intervals and intensity, provide water, air, and nutrients of the right composition, intervals and intensity. That is a simplified version...
In reality there is great variation in how plants require these things. Some cope with long dark periods better than others, some cope with drought better than others, some cope with chemical variation in the soil better than others so answering this question is hard. But generally growing plants on the moon will require the ability to recreate (to some degree depending on the sensitivity of the plant) the conditions a plant has evolved under on earth.
Thus to answer your questions:
Length of day can have strong effects on growth patterns, two weeks of darkness is likely to be a major upset for plants! Just transplanting plants of the same species from different latitudes can affect the growth patterns because of changes in length of day. Try putting some plants in darkness for two weeks and see what happens.
Plants all vary in their ability to meet the requirements of space growth. There will only be a short list of plants that could with "small" modifications to the moon's environment, the more we adapt (adding artificial light, watering, adding nutrients etc) the longer that list would become - the limitation is in our ability to adapt the moon.
See above for reasons why plants might struggle. Oh and we would need to consider the effects of reduced gravity too...
Here's a little something from nasa about how plants are used in space vehicles. And another on light and gravity.

Thanks, but I did mention in the question that I'm aware of research on most of these issues. I'm asking if there is any research specifically on the day length issue, and also about which specific types of plant are most likely to be able to adapt.

@Nathaniel I think if we get to the point where we can realistically inhabit the moon and modify it to grow some plants, then we should be able to get it to the point where most can grow. Whether it's wheat, corn, or oak trees, there will have to be some significant modifications made by us to the moon before we can grow any. Once we can grow one then small tweaks to the system will be needed to grow the others. Feels like its more how we could adapt the moon than how the plants can adapt. It's likely small simple things would be easiest for us to grow but crop plants would be most necessary

Sure - my thinking is that factors like water, soil quality, atmosphere etc. are easy enough to control if you already have the technology to build sealed greenhouses in a vacuum. Gravity can't be controlled at all, but if we can grow plants on the ISS then it should work on the Moon. That leaves the day length, which can only be changed using artificial lighting, which will need an expensive source of energy. So my guess is that the choice of which crop to grow would be mostly determined by its ability to cope with weeks of darkness.

@Nathaniel I can't find any research testing such long periods of light deprevation but my gut feeling is telling me not much would do well. These shade tolerant plants still need a few hours of sunlight per day http://www.motherearthnews.com/organic-gardening/shade-tolerant-vegetables-zm0z11zsto.aspx#axzz2jr6hxNjP

something like this might work... http://www.nytimes.com/1993/01/12/science/russians-to-test-space-mirror-as-giant-night-light-for-earth.html?pagewanted=all&src=pm


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Are there known examples where an evolved mechanism "echoes" one originally provided by the environment?
Short summary
I am a researcher in origins of life, a field that deals with hypotheses about evolutionary processes that took place before LUCA (the last universal common ancestor), and with the chemical processes that gave rise to life and evolution in the first place. This is very hard to study empirically, and as a consequence there are many competing hypotheses. However, I've noticed that many of them have a common form, which I will describe below. My question is about whether hypotheses of this particular form exist (and have been investigated, for example using phylogenetic methods) in post-LUCA evolutionary biology.
My reason for asking is that my colleagues and I were not able to think of a good example. If no example is known in post-LUCA evolutionary biology then it casts doubt on the plausibility of this type of hypothesis in pre-LUCA evolution. I suspect this is the case, and therefore my ideal answer would provide me with bibliographic material to support a claim that there just aren't any good examples of this in evolutionary biology. However, I would also be happy to be proven wrong with a really good example.
Longer explanation
Hypotheses regarding the origins of life are difficult to test empirically, because phylogenetic methods can give us little direct evidence about anything before LUCA, and because there are no fossils dating from that time. (The entirety of Earth's surface has since been replaced by plate tectonics.) Consequently there are a number of competing hypotheses that differ from one another in almost every way. However, I've noticed that many of them have a common form: they say that

one or more of the features of a modern (i.e. post-LUCA) cell were originally provided by an external mechanism, in the form of abiotic chemical processes that took place in some very specific microenvironment, and
evolution eventually provided a solution that very closely echoed the one that had originally been provided by the environment.

Point (1) seems relatively easy to satisfy in an evolutionary scenario; it's point (2) that I'm specifically interested in. The two most popular hypotheses in the field both have this form:

Some forms of the The RNA-World hypothesis hold that originally, RNA nucleotides were produced by purely chemical processes in the environment, and that life evolved from self-replicating RNA molecules made up from these abiotically-produced monomers. Later, life evolved a cellular metabolism by which it could construct its own RNA monomers. This satisfies point (2) because it says that the environment provided RNA rather than some other heteropolymer with catalytic properties; the evolutionary solution echoes the environmental one in that it uses the same complex molecule.
Wächterschäuser's Iron-Sulphur World theory, and many of its descendants, including Russel's alkaline vent theory, hold that the reductive tricarbolic acid cycle (rTCA cycle, aka reverse citric acid cycle) was originally catalysed by mineral surfaces. This enabled the formation of the first cells, which eventually evolved enzymes that could be used to catalyse the rTCA cycle without the mineral catalysts. This satisfies point (2) because it says that the first evolved solution used essentially the same chemical pathway as the one provided by the environment, just with different catalysts.

(Not all hypotheses in origins of life have this form. Some versions of the RNA World theory hold that RNA-based life was preceded by life based on some other heteropolymer, for example. But the hypotheses described above are very popular.)
From an evolutionary biology point of view, point (2) seems rather an odd feature for a hypothesis to have. Evolution is great at producing novel solutions to problems, but to my knowledge it isn't good at copying old ones. (Mimicry doesn't provide a counterexample to this, since it's about appearance rather than mechanism, and often the mimic produces the same visual effect through a very different mechanism. For example, although the treehopper Cyphonia clavata mimics the outward appearance of an ant, it does so not by being anatomically similar to an ant but by having a face on its butt.)
Consequently I'm looking for known examples from evolutionary biology that satisfy both point (1) and point (2). That is, I'm looking for examples where a species originally relied on some relatively complex process in its environment, and became less dependent on its environment by evolving a mechanism that closely echoes the one originally provided by the environment.
An example that might fit the bill would be a species that was originally unable to produce a key metabolite (e.g. an amino acid), but then later evolved the ability to produce the metabolite for itself. Evidence for this might be constituted by finding a species that produces the metabolite using a novel set of proteins, indicating that the capability to produce the metabolite was lost and then re-evolved. It would make an even better example if the novel proteins catalyse substantially the same chemical pathway that other species use to produce the same metabolite.
It may be that no good examples of this exist, which is actually better for me than if they do. More than any particular example, the main thing I want to know is whether ideas along these lines have been discussed in evolutionary biology at all (perhaps outside the context of the origins of life), and if so where I can find the literature on it.

If cold blooded animals get their heat from the environment, then warm blooded animals might be described as evolving to provide their own heat.

You should narrow this question down to a specific topic. It seems too broad to me.

I don't think the question is too broad, however after reading @user137's comment I would tend to think that maybe, the question is not very well defined. What do you think Nathaniel? Would endothermic (see here to understand this terminology) animals be an answer to your question?

Note the interesting but controversial examples of genetic assimilation

@WYSIWYG I can only imagine I've phrased the question poorly, as in asking for example of something very specific. If you can point me to particular parts of the text that can be interpreted as asking for something broad, I'll do my best to fix them.

@Remi.b I can't deny that endothermic animals are an example. However, they are a poor example for my purpose, because generating heat is quite an easy thing to do chemically, whereas the hypotheses for the origins of life require things as complicated as the TCA cycle to evolve this way. When I'm at a non mobile device I'll edit the question to put an emphasis on that.

@Nathaniel I don't think it is badly phrased. I just think that to list all possibilities would be a little difficult. You can narrow down to some specific environmental factors (like temperature; as discussed in previous comments)

@Remi.b genetic assimilation can't be used to draw a good analogy with the origins of life, because there was nowhere to assimilate genetic material from, so I'm telly looking for examples where the feature was evolved independently. (I'll also edit that in.)

@Remi.b On a different note. Is endothermic for warm-blooded a correct term? In the sense of reaction it means one that absorbs heat. Isn't homeotherms (and poikilotherms for ectothermic) a more appropriate term

@user137 your example is useful and appreciated. See my comment to Remi.b above.

@WYSIWYG I've done my best to narrow it down to something much more specific. (Re-reading it, it indeed seemed to be asking for something much more general that what I'd intended.) I've also made the edits referred to in my comments above.

@WYSIWYG endothermic is standard terminology. Endo means 'within', so I guess in biology it means something that makes heat within itself, whereas in chemistry it means something that needs heat within itself in order to happen. I agree it's annoying that it means the opposite thing in the two fields.

@Nathaniel Would a potential example be something like essential amino acids that an organism cannot make on its own, so it has to get them from the environment or food? So if that species somehow developed a method to produce that amino acid, then it wouldn't need to obtain it from the environment anymore. I'm not aware of any examples, just trying to figure out what you're looking for.

@user137 yes, if there's a known example of that it would make a very good example. (Of course I know that there are many known examples where a species has lost the ability to make an amino acid, but this is the point I eventually want to make - if the environment provides a species with something, there's no pressure for the species to evolve that thing for itself, and so it doesn't tend to happen.)

Interesting question, but I would imagine that it could be difficult to obtain evidence for this (even when it has occurred), since I would imagine that these kinds of features are rarely seen in fossils (especially along with knowledge that the feature was originally provided by the environment). And the time period we have been able to observe these kinds of processes directly is not very long from an evolutionary perspective.

It was getting long for a comment:

A species that was originally parasitic, but then evolved to survive     independently of its host by independently evolving the
  same       metabolic functions
A predator that originally relied on its prey to synthesise some vital metabolite, but later evolved the ability to produce the
  missing metabolite for itself through a similar pathway

A parasite is generally evolved from a free living form. It has a reduced genome and cannot synthesize many vital nutrients. It is unlikely that it would acquire a gene that would enable it to live freely. A parasite, in general does not require to synthesize nutrients; so it is not under any pressure to acquire that function as long as its host is surplus.
Same is in the case of predators.
Basically, in higher organisms it is difficult to conjure a new gene; it is a slow process and happens via gene modification. However, in lower (basically unicellular) organisms lateral gene transfers are much easier and it is possible that they can acquire new metabolic pathways from other organisms. Have a look at this article.
In lower eukaryotes endosymbiosis, is another way by which new metabolic pathways can be acquired relatively fast. A diatom called Rhopalodia gibba, which already had a red alga derived secondary plastid, acquired another cyanobacteria derived green plastid for nitrogen fixation. You can have a look at this post too.
For your question on independent acquisition of traits; almost all metabolic pathways are evolved like that only. Enzymes isoforms that can bind to a slightly different substrate gave rise to another step in the pathway.
It is also possible to engineer a new trait:
Nucleotide analogs have been created to make a 6-letter nucleotide system which can be replicated by PCR[1, 2]. Earlier this year this was demonstrated in-vivo[3]. It has been shown that these new nucleotides can also be transcribed (see cross references in [3]).

I'm very sorry for not making my question clear enough. I'm not just asking for examples of the evolution of metabolic pathways. I'm asking for examples (if they exist, which they may well not) of metabolic functions which at one time were provided by the environment but which are now performed by the organism using a similar molecular mechanism. It's not a particularly easy thing to make clear, but I will have a think about how to do it better.

@Nathaniel well, by pathway I meant that a newly acquired function plugs itself in the network an expands the pathways. But by endosymbiosis new networks can also be incorporated (thats what I meant there). But for your question I guess the answer is - almost every gene. Recent examples would include genes for drug metabolism.

You're answering a different question from the one I'm asking. As I said, this is my fault for not being clear enough, and I will have to think more about how to improve the question.

The E. coli long term evolution experiment showed that E. coli had evolved a function (the metabolism of citrate) which was not required in the ancestral environment, but which evolved naturally and was selected for in this new artificial environment. AFAIK, this is the only example of a function that has been observed naturally evolving under controlled conditions.
The reason we are unlikely to see any metazoans evolving new metabolic pathways is due to the fact that they have long lifespans and therefore reproduction times. However, as WYSIWYG has already mentioned, almost all metabolic pathways evolved that way, it is just hard to observe due to the long time spans involved.

I'm very sorry that I wasn't able to make my question clear. I'm not just asking for examples of the evolution of metabolic pathways. I'm asking for examples (if they exist, which they may well not) of metabolic functions which at one time were provided by the environment but which are now performed by the organism using a similar molecular mechanism. Examples would likely come from phylogenetics, rather than direct experimental observation.

See this more as a comment than an answer, since it became too long for a comment. However, I think some of the examples should be relevant to refine your question.

One thing that I find vague in this question is what exactly constitutes a "process"/"function"? To me, this can be almost anything. You seem to be focusing on molecular biology and biological pathways, but I think it is just as reasonable to think in terms of large scale processes. If so, there are lots of processes that seem valid in my mind, relating to e.g. reproduction and dispersal.
For instance, in primitive plants (and other taxa) fertilization is external and dependent on environmental moisture to transport gametes. Organisms with internal fertilization has bypassed this by providing their own mechanism for fertilization, which does not depend on environmental processes (to the same extent). The evolutionary forces behind this was maybe/probably that it was more efficient and allowed colonization of new environments.
Another similar example is seed dispersal in plants, where some are wind dispersed ("primitive" state) and others use active measures to eject seeds (ballochory). By doing this they have bypassed the dependence of wind to disperse their seeds. The same kinds of mechanisms can also be found in groups of mosses.
In both these cases a function that was previously external and environmentally mediated is now provided by the organisms themselves, and they involve quite complicated morphological and anatomical adaptations. Do you find them valid for your question? These are just two examples, but there are lots of similar cases.
More in the line of comments to your question, I think you should provide one or two references to the hypothesis you are referring to (i.e. where it has been used/discussed), which would make it easier to understand exactly what you are after (and also provide an entry into the literature). This could maybe also help explain why the "...evolved solution 'echoes' the one provided by the environment". At the moment I don't understand at all why this should be the case in general. Adaptive evolution happen because of selection that acts on differences in fitness, and it is indifferent to whether the mechanism echoes a previous solution to a similar problem (except for the fact that evolution is constrained by the evolutionary history of organisms).

Thank you for the answer. The examples are indeed relevant. I do intend to make the requested improvements to the question, including references, its just a little hard to find the time and enthusiasm at the moment. I also don't understand why evolved solutions should echo those provided by the environment, yet hypotheses of this form are common in the origins of life, hence the question. (I hope my future edits will make it clearer what I mean by that.)

(Though I guess your examples are somewhat lacking in the "echoing the environment" property, because the 'complicated anatomical mechanisms' they use don't resemble the original environmental mechanism. I do need to clarify what I mean by that, and I hope to find the time today or this week.)

I've re-written the question, and I hope it's clearer now.

@Nathaniel I think the questions was greatly improved by the rewrite. The "echoing" aspects are also more clear, since the examples you've provided indicates the reason why this might occur. In both your examples, it is plausible that the primitive "organisms" have evolved other pathways/features that depend entirely on the function in question (RNA & rTCA). Therefore, the original solution had to be mimicked to be successful.

After considering this question some more, I think a key feature for this hypothesis to work is that the original function must be so integrated and vital for the biology of the organism that it must be mimicked/echoed to some extent. In terms of your RNA-example, it was not enought to evolve the ability to synthesize any complex molecule that could function as an enzyme and information carrier, but had to be RNA since this was already used in the biological pathways of the primitive organism.
With this in mind I think that you should look closely at vitamins (or other essential nutrients) for evidence of similar processes. The key think about vitamins is that they are often large complex molecules that are vital nutrients and the ability to synthesize vitamins differs widely between taxa. In a sense, the nucleotides were essential nutrients for the organisms in the proposed RNA-world, so vitamins/essential nutrients should be a relevant analog to look for similar evolutionary processes. However, keep in mind that molecular biology is not at all my field, and I might be mistaken on some aspects.
Take the example of Vitamin C. This cannot be synthezised by humans, but by most other mammals (vitamin C synthesis is considered ancestral in mammals). It can also be synthesized by plants, yeast and many other animals. However, vitamin C is used in different ways in different organisms. Plants use it e.g. for photosynthesis, photoprotection, cell wall growth and in the synthesis of plant hormones, while humans and other mammals use it as enzyme cofactors and for immune responses. Another key aspect is that plants, yeast and animals all use different pathways to synthezise vitamin C (Drouin et al, 2011), which indicates that the synthesis of vitamin C is not ancestral to all these taxa (i.e. not an ancestral feature of all eukaryotic life). In mammals, the synthesis of vitamin C has also switched between organs multiple times, which also indicates novel adaptations that results in the same molecule.
To me, it seems very likely that vitamin C was initially obtained by animals from plants (which have very high concentrations of vitamin C) as part of their diet (i.e. environmentally provided) and became an essential component in many biological pathways. If this is the case, animals later gained the ability to synthesize vitamin C themselves, using a different biological pathway than plants. This feature has later been secondarily lost (e.g. humans and teleost fish) and regained multiple times in different taxa. However, this is speculation on my part, and I don't know this literature well enought to say if there are studies on the origin of vitamin C synthesis in animals, or if the pathways of vitamin C synthesis in plants and animals are fundamentally related. A review by Smirnoff et al (2001) indicates that there are some similarities between the enzymes involved in the final stages of vitamin C synthesis:

The gene and/or cDNAs encoding GalLDH, GulLO, and AraLO have been isolated and described from several organisms including cauliflower, sweet potato (GalLDH, 54, 121), rat (GulLO, 70), and Saccharomyces cerevisiae (53). In addition, complete nucleotide coding sequences of the A. thaliana and Nicotiana tabacum GalLDH genes (Accession No. AB042279.1, AB024527.1), and the Candida albicans AraLO gene (Accession No. AF031228) have been submitted directly to GenBank and associated databases. The predicted amino acid sequences of these related proteins share substantial amounts of identity. The mature cauliflower GalLDH amino acid sequence shares 28% overall identity with the rat GulLO and 26% identity with the Candida albicans AraLO (using the J Hein method with PAM250 residue weight table).

However, this doesn't necessarily mean that the synthesis of vitamin C is ancestral to both plants and animals. I haven't been able to find any papers on the origin of vitamin C synthesis, and if there is evidence that it is ancestral to all modern life.
In either case, I think it could be useful for you to look closely at vitamins in animals or other organisms for possible examples of the type of processes you are looking for, since they are (by definition) essential nutrients that some animals can and others cannot synthesize. They should therefore be good potential targets to find similar processes as your RNA-example. Vitamin B12 is an extreme to the other end, since it is essential for most animals but can only be synthesized by bacteria (so the main source is through bacterial symbiosis).
It is also possible that I'm mistaken, and that synthesis of all vitamins is ancestral to modern life, and that there has only been subsequent loss of the ability to synthesize certain vitamins/nutrients. Helliwell et al (2013) mentions this as a possibility in relation to the RNA-world, but also points out that the pathways for biosynthesis often differs between taxa, which would suggest that there has indeed been secondary acquisition:

The fundamental nature of vitamins is illustrated by the close structural relation of many vitamins to nucleotides (Figure 1), reflecting the likelihood that they were present in the ancient RNA world. Yet, their biosynthetic pathways appear to have arisen via the patchwork model of pathway evolution [31], resulting in the recruitment of unrelated proteins in any one pathway. Indeed, many vitamins are synthesized by different routes in different organisms [20]. For example, alternative pathways are found for thiamine biosynthesis in prokaryotes and among different eukaryotes (Figure 2) [20]. Despite this diversity in biosynthetic pathways, there appear to be common trends in the causes and mechanisms underlying pathway loss.

I apologize if it is unsuitable to post this as a separate answer, instead of adding it to my previous answer/comment as an edit. However, I felt that they expressed very different ideas, and it felt more logical to keep them separate.

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text:
What fraction of O in dry biomass comes from air vs water?
The net reaction of photosynthesis is, to some degree of approximation,
$$
\ce{6CO2 + 6H2O \to C6H12O6 + 6O2}.
$$
My understanding is that the $\ce{O2}$ comes from water rather than the $\ce{CO2}$, so that the equation breaks down like this
$$
\ce{6 C\color{red}{O2} + 6 H2\color{blue}{O} \to C6H12\color{red}{O6} + 3\color{red}{O2} + 3\color{blue}{O2}}.
$$
(See the answers to Why does the oxygen produced in the photosynthesis come from water and not carbon dioxide?) This suggests the $\ce{O}$ in plant biomass initially all comes from air ($\ce{CO2}$) and not from water ($\ce{H2O}$).
However, there are plenty of other processes in the cell that involve water besides photosynthesis, and I'm wondering whether any of them result in $\ce{O}$ from water being incorporated into biomass to any significant degree.
In other words, if we tagged the $\ce{H2O}$ in an ecosystem with an isotope of oxygen, how much of the isotope would end up incorporated into biomolecules in the long run, versus being expelled as $\ce{O2}$?
For the sake of keeping the question focused I'm only asking about a phototrophic ecosystem. If the answer is interesting I'll ask a separate one about chemoautotrophs.

An issue with this is that it's continually being recycled and mixed up. You seem to be after a snapshot, a picture of proportion in time? Tough to know how to measure that at any specific part of the day/night cycle, seasons and lifecycle. It's also quite unfocused asking about various different subjects. Can you narrow it? (that's assuming it even can be answered, I'm not enough of a chemist to understand how carbon dioxide and water interact to swap oxygen - or not)

@JiminyCricket it's a straightforward question: are there biological processes that replace O2 in cells (which originally came from air) with O2 from water? It might even be that the isotope experiment has been done and we know the answer. You can't really get more narrow and focused than that.

Well, perhaps start with autotrophs and binding of oxygen, then make  separate questions in their own threads (linking to this if you like)  regarding the rest of the food chain.

@JiminyCricket just to keep you happy I've removed the last paragraph, although I really don't think that should be necessary. I'm not going to split the question up by trophic level because that doesn't make sense. It's a question about ecology and you can't learn about ecosystems by studying each species separately.

Fair enough. I just thought it more likely you'd get a narrower estimate range if you narrowed the question, and it would be less likely to be closed as too broad.

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text:
Are there any organisms that lack ATP synthase?
ATP synthase is used by cells to synthesise ATP from ADP using energy from a proton gradient. Depending on which sites I look at, this is either a universal feature of living cells, or it's "almost universal", used by the vast majority of organisms.
As Superbeast points out in a comment, ATP can also be synthesised on the substrate level via the Krebs cycle. However, I would like to know if there are any organisms that only synthesise ATP this way. In other words, are there any known organisms that entirely lack the ability to produce ATP synthase, and produce ATP entirely through the Krebs cycle, or through some other mechanism not related to ATP synthase?
If there are, I would like some information about them. Are there many such species or just a few? Are they all prokaryotes or all eucaryotes, or some of each? What kind of environments do they live in?

https://en.wikipedia.org/wiki/Substrate-level_phosphorylation

Right, Krebs cycle, that was kind of obvious I guess. Thanks! But are there organisms that only produce ATP that way?

As Superbest mentioned, substrate level phosphorylation (SLP) is alternative pathway by which ADP is phosphorylated to ATP. In SLP, phosphorylation is coupled with a highly exergonic chemical reaction. Fermentative organisms (both fully and temporally fermentative) organisms depend on SLP for ATP.
Note: fermentative $\neq$  anaerobic
Fermentation can either be a temporary situation, depending on the growth substrate (for e.g. yeast) or the only option as in the case of amitochondriate organisms like Entamoeba. You can refer this book if it is available to you. See this article too.
You can also see the wikipedia page on fermentation; it mentions the SLP steps.

If you can add a convincing citation (for the lack of ATP synthase in fermentative organisms) or a link to more information, I will accept this answer.

i added some info. see if it is fine

The linked article appears to be referring to organelles within eucaryotic cells, rather than to the cell as a whole. I'm specifically interested in whether there are any cells that entirely lack ATP synthase, not just in the organelles, but in the outer membrane as well.

Eukaryotic cells don't have ATP synthase on their membrane.. It is always expressed in an organelle. There are reasons to have an organelle. I have given some explanation for this on this post. It is energetically unfavorable for a eukaryotic cell to behave like a huge mitochondria.

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text:
Reference request for Sydney Brenner's "it might come in handy in the cretaceous" quote
In {1}, Richard Dawkins attributes a quote to Sydney Brenner without giving a citation. I'm preparing a publication on the same topic and if possible I would like to track down the original reference for the quote. Does anyone know the work (if it exists) in which Brenner made the argument Dawkins refers to?
Here is the text from Dawkins' paper where it is mentioned:

It is all too easy for this kind of argument to be used loosely and unrespectably. Sydney Brenner justly ridiculed the idea of foresight in evolution, specifically in the notion that a molecule, useless to a lineage of organisms in its own geological era, might nevertheless be retained in the gene pool because of its possible usefulness in some future era: "It might come in handy in the Cretaceous!" I hope I shall not be taken as saying anything like that.

Edit: it looks quite likely that this is referring to something Dawkins heard Brenner say, rather than anything that can be cited. There is a footnote in {2} that reads:

...Brenner... has a sardonic wit to match his scientific brilliance. I once heard him lampoon the 'evolutionary foresight' fallacy by imagining a species in the Cambrian that retained in its gene pool an otherwise useless protein, because 'It might come in handy in the Cretaceous.'

So it seems likely that there is no citable source for the quote besides Dawkins' paper, but in any case it would be useful to know if there is a pre-1988 publication in which Brenner made a similar argument.
{1} Richard Dawkins (1988) The Evolution of Evolvability. In C. Langton (Ed.) Artificial Life, SFI Studies in the Science of Complexity. Addison-Wesley Publishing Company.
{2} Richard Dawkins (2009) The Greatest Show on Earth: The Evidence for Evolution. Random House.


text:
The origin of molecular machines
DNA holds genetic information and holds the key to the evolution of living organisms. Transcription and translation mechanisms enable living cells to process information encoded in DNA. To that end, transcription and translation are fundamental mechanisms needed to enable the evolution of organisms. Molecular machines (enzymes) carry out these mechanisms by reading the information in DNA and using it to construct proteins.
Did the first living cell contain the machinery needed for translation and transcription? or  Did they evolve over time?
EDIT: Edited the question to narrow the scope.

Thank you for your feedback. Please let me know if the question needs further editing.

I was wondering a similar question but I see you have posted it!

The main hypothesis is that all starts from RNA. "The RNA world". There was no DNA and no proteins. Both function was performed by RNA. Now there are no living organism that carrying information in RNA (only viruses...), but there is "enzymes" from RNA - ribozymes.
The evolution to DNA was later, according to this hypothesis.
There is really good article in wiki.
http://en.wikipedia.org/wiki/RNA_world_hypothesis
or if you want something more look here
http://www.ncbi.nlm.nih.gov/books/NBK26876/
Summary

From our knowledge of present-day organisms and the molecules they contain, it seems likely that the development of the directly autocatalytic mechanisms fundamental to living systems began with the evolution of families of molecules that could catalyze their own replication. With time, a family of cooperating RNA catalysts probably developed the ability to direct synthesis of polypeptides. DNA is likely to have been a late addition: as the accumulation of additional protein catalysts allowed more efficient and complex cells to evolve, the DNA double helix replaced RNA as a more stable molecule for storing the increased amounts of genetic information required by such cells.

It's important to note that the RNA world is a hypothesis, not a theory. Nobody knows how life arose.


text:
How do omega-3 fatty acids reduce cholesterol at the molecular level?
I have heard that omega-3 fatty acids found in fish are a good way to prevent/reduce cholesterol problems.
My question is how do omega-3 fatty acids do that: what are they doing on a chemical level to produce this effect? And is there any way to maximize this effect through other substances, that may work in concert with them?

What do you mean when you say "maximize this effect through other substances"?  Are you asking if there are co-factors that have no/little effect on their own, but act synergistically with omega-3 fatty acids to reduce cholesterol problems? Or are you simply asking if there are other substances that reduce cholesterol problems?

The former. Is there anything that works with them.

i dont think they REDUCE cholesterol.. omega-3 fatty acids comprise the essential fatty acids (omega 3 refers to the position of double bond from non carboxyl end).. and BTW cholesterol is also important for the body- it makes up the membranes and also serves as a precursor of vitamin D [sunlight basically converts 7-dehydrocholesterol to vit-d]. excess causes problems

the above answer is going in the right direction - unsaturated fatty acids keep the membrane more pliable and cholesterol, which is an inflexible planar molecule tends to make it more rigid I think.

@shigeta - Re cholesterol"... cholesterol possesses a slick and rigid structure. ...this would naturally result in a stiffer membrane. Yet, for the past 10 or so years, physicists and biologists have assumed that cholesterol had nearly no effect on the stiffness of membranes ...", https://www.sciencedaily.com

@PeterBernhard its funny i heard even in grad school that they made the membrane stiffer.  in any case as they are linked to hypertension I assume we are on the right track here - interesting factlet :)

I found this research paper (pdf) by D. Roger Illingworth, William S. Harris, and William E. Connor (Journal of the American Heart Association, 1984) that offers some help. Its abstract says:

Diets rich in omega-3 fatty acids derived from fish oils lower the plasma concentrations
of low density lipoproteins (LDL) and very low density lipoproteins in humans. The present study was designed to examine the mechanism(s) by which diets enriched in omega-3 fatty acids reduce plasma LDL cholesterol levels in normal subjects.

In the Dicussion part, you will find your answer:

Reductions in the plasma concentrations of LDL in human subjects consuming diets rich in long-chain omega-3 fatty acids from fish oils or omega-6 fatty acids from vegetable oils may be due to a reduction in LDL synthesis, an increased fractional rate of catabolism of LDL, or a combination of both... The present study indicates that the hypocholesterolemic effects of long-chain omega-3 fatty acids present in fish oils results from a reduction in the rate of LDL apoprotein B synthesis and that such oils do not stimulate the fractional rate of catabolism of LDL. These observations imply that the incorporation of omega-3 fatty acids into cellular or lipoprotein lipids does not enhance the rate of receptor-mediated catabolism of LDL as has been observed with omega-6 fatty acids in vitro.

I could not find a paper on its exact mechanism, so I'd rather say that the process is still not clear. Yet, as the paper suggests, the main effects of omega-3 fatty acids are reducing LDL synthesis and/or increasing fractional rate of catabolism (FRC) of LDL.
A similar article can be found here:

Omega-3 fatty acids have been shown to lower triglycerides, which are a type of fat in the bloodstream. Experts aren't sure of the exact mechanism. Omega-3 fatty acids may also slow down the growth of plaques in the arteries and reduce inflammation throughout the body.
A number of studies going back years have shown the benefits of fatty fish. In an important review of studies, researchers found that getting daily omega-3 fatty acids from fish oil could lower triglyceride levels by 25%-30%. The results were published in The American Journal of Clinical Nutrition in 1997.

BUT, I would also like to point out that the question itself "omega-3 fatty acids found in fish are a good way to prevent/reduce cholesterol problems" seems to be a matter of debate because of articles like this:

New data presented this week provide clues as to why eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)--both components of omega-3 fatty acids--have differential effects on LDL cholesterol.
Presenting the results of the laboratory study here at the National Lipid Association (NLA) 2011 Scientific Sessions, senior investigator Dr Preston Mason (Brigham and Women's Hospital, Boston, MA) said that EPA is an inhibitor of lipid oxidation at normal and elevated cholesterol levels in the presence and absence of DHA, while DHA seems to have no real effect on lipid peroxidation. This trial was one of a number of studies that attempted to address the clinical question as to why LDL-cholesterol levels increase in patients treated with the triglyceride-lowering omega-3 fatty acids. In his trial, Mason et al compared the effects of EPA and DHA--alone or in combination with statins--on lipid peroxidation in polyunsaturated fatty-acid– and cholesterol-enriched vesicles.

Re "may be due to a reduction in LDL synthesis,"
Do you have any more reference on mechanism which you state as not established yet?
Are there any "shunts" in liver, i.e. liver packing its "self-made", i.e. unsaturated fatty acids made from glucose,   into LDL,  in contrast to unsaturated fatty acids that it does not produce? Would you be interested in some other answer elaborating on that point?

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text:
Would non-human carnivores be able to survive on farmed foods?
Certain creatures that are considered carnivores are non-obligate carnivores and are technically omnivores (such as wolves/dogs).  How different is the potential digestive ability of these species compared to humans?  If they theoretically developed sapience and the intelligence for agriculture, would they be able to survive on the same wide variety of plant foods that we do (i.e. could wolves survive on wheat, rice, etc)

The foods people in the developed world typically feed their carnivorous pets (including dogs and cats) are not made primarily from meat.  Instead, they are made from plants, specifically grains, such as corn, rice and wheat.
In order to get our pets to eat foods that are so different from the meat-rich diets of their ancestors, we add flavors to the food.
Check out this episode on the making of pet foods from the television series "How Its Made", http://www.youtube.com/watch?v=220PSFJWHao.
So, to answer your question directly-- yes, in places like the USA, domestic dogs and cats are already living on a diet that is almost entirely plant-based.


text:
Are there human genes that make a cell die when they undergo copy-number alterations?
I am trying to understand if there are known genes in the human genome where copy-number should be stable at a diploid level for the carrier cell to live.
I.e., are there lethal deletions or duplications of specific genes in the human genome? I would imagine "house-keeping" genes might be needed for the regular processes within a cell, but I could not find any reference online on specific studies on the matter. House-keeping genes defined as in this article.
E.g., when looking for "lethal heterozygous deletion genes human allele copy number", I mostly found articles regarding tumor-suppressor genes, so I'm not sure I am using the right keywords.
The genes I am looking for should be exclusively from the human genome.

Why "exclusively from the human genome"?

To make the question more specific. I am currently working on the human genome and, even if genes conserved across different organisms might be interesting, this would be out of scope for this specific question, I think.

Would you consider a translocation/insertion event as a candidate? Say a specific gene (geneA) is reverse transcribed and inserted into a different location of the genome, disrupting an essential gene (geneB). This would result in geneA having a copy number of +1 and it would be deleterious since it disrupts geneB, but it wouldn't strictly be a case where the fact of a change in copy number in and of itself is deadly, it's only because of the specific place where the copy was inserted. For deletions, the answer is trivially yes, house keeping genes being a prime example.

@terdon, thanks. Regarding the translocation/insertion event, I believe this is interesting but not exactly what I'm looking for, since I'm looking for genes where disruption in their copy number is deleterious. Regarding house-keeping genes, is there a validated set of genes that can be used in this case? For example, where the disruption of a gene copy number is verified by different methodologies?

I don't know, but I would guess you should be able to find things at least from mouse knockout studies and you could then translate to human. For obvious ethical reasons that sort of experiment is frowned upon on human subjects and you'll never find actual cases in the wild since any embryo carrying this wouldn't have been born in the first place.

The issue with mouse orthologs seems that "Comparing documented phenotypes of null mutations in humans and mice, we find that >20% of human essential genes have nonessential mouse orthologs. These changes of gene essentiality appear to be associated with adaptive evolution at the protein-sequence, but not gene-expression, level" from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2383943/ . Additional information on "essential genes" can be found at http://origin.tubic.org/deg/public/index.php/index

This also looks interesting: https://www.science.org/doi/10.1126/science.aac7041

There is some evidence that even in a heterozygous null state some essential human genes are haploinsufficient, e.g. it is lethal when fewer than two functional copies is present.
For example, this paper pooled cells after introducing knockout edits in a variety of genes, and measured relative growth in the pool, identifying a number of genes that are quite intolerant of loss of one copy (~600 according to one expansive estimate).
Additionally, this paper abstract notes that there are some 3,000 haploinsufficient genes, which is somewhat more expansive than the previous estimate. I don't have access to the paper so I am not sure where that number comes from. This paper screened mice and humans for various flavors of essentiality, coming up with various estimates for haploinsufficiency, mostly on the order of a few hundred genes.
I would expect that some of this extends to the full loss of one gene copy, but I don't have direct evidence for a "copy number" type genomic alteration yielding essentiality-haploinsufficiency. This paper does comment somewhat on haploinsufficiency in CNVs, but does not appear to consider essentiality.
This paper also considers haploinsufficient and "triploinsufficient" genes with notable phenotypes in humans, though again I think that they are more interested in disease phenotypes than in essentiality.

A gene is defined as "essential" if its complete loss of function results in a complete loss of fitness (Hart et al., 2014). In practice, a prenatal lethal phenotype is typically the criterion for essentiality.
Homozygous deletion ($CN = 0$) is one of the copy number states that can lead to complete loss of function for a gene, therefore, in theory, if a cell undergoes homozygous deletion on one or more "essential" genes, this CN state might be lethal for the cell.
Some useful resources for "essential" genes are at:

https://www.science.org/doi/10.1126/science.aad7925
https://www.embopress.org/doi/full/10.15252/msb.20145216
https://www.science.org/doi/10.1126/science.aac7041
https://www.science.org/doi/10.1126/science.aac7557
http://origin.tubic.org/deg/public/index.php/index
https://en.wikipedia.org/wiki/Essential_gene

I am not sure how different CN states can be assessed for cell lethality.

Why the downvote?

Personally, I don't see how this answers your original question. You ask for genes that are lethal to cells if they suffer copy number alterations (-2, -1, +1, +2 etc), whereas your answer talks about essential genes who are only lethal when completely lost by the cell.

Completely lost means homozygous deletion, which is copy number alteration. This was the only case that I found described in the literature - probably because is more easy to assess with currently available orthogonal assays. I agree that the answer is not complete, but it is the best that I could find in the literature, so I still don't understand the downvote (which implies that the answer is not useful - or out of scope - which in my opinion is not in this case). I am open to choose another, more complete, answer - if that exists. I removed the acceptance to the answer if it helps.

I get your point and agree. Removed my downvote. Sorry for that!

No worries, I totally understand your point-of-view. Just I know that questions with downvotes are usually ignored by the reader even if they are reasonable, and I wanted to share and learn about this topic :)

Btw, I don't have an answer to your question, but you might want to read about gene dosage. The Wikipedia article is short, but seems to have some relevant references that could be a good start. Not sure how much you will find for human genes though...

Thank you, I am somewhat familiar with the concept, but I never reviewed it in depth - and forgot to use this keyword in this case. I will look into the references.


text:
Variant Allele Frequency (VAF) peaks for clonal CNAs
I am reading an overview of the CNAqc package, which defines how the algorithm computes "Variant Allele Frequency (VAF) peaks for clonal CNAs."

mutations present in a percentage $0<c<1$ of tumour cells, sitting on a segment $nA:nB$;
tumour purity $\pi$;
a healthy diploid normal;

Since the proportion of all reads from the tumour is $\pi(n_A+n_B)$, and from the normal is $2(1-\pi)$. Then, mutations present in $m$ copies of the tumour genome should peak at VAF value
$$v_m(c)=\frac{m \pi c}{2(1−\pi)+\pi(n_A+n_B)}.$$

However, I don't understand exactly the definition $n_A:n_B$ in this context.
Are $n_A:n_B$ the number of reads coming from alleles $A$ and allele $B$ in the tumor? But then, why the normal has only $n = 2$?

Migrated to Biology at the request of the question author

On a further inspection on the associated paper, $n_A$ and $n_B$ are the allele-specific copy numbers.
And it definitely makes sense that we have 2 (diploid) for the normal component.


text:
Which data format for mRNA expression matrix is necessary to run pathway analysis with Paradigm?
I am running Paradigm on a matrix of mRNA expression. I read

Vaske, Charles J., et al. "Inference of patient-specific pathway activities from multi-dimensional cancer genomics data using PARADIGM." Bioinformatics 26.12 (2010): i237-i245.

and also the help section in the web application. However it is not defined which format is best-suited for mRNA expression. Using log$_2$-ratios instead of log$_2$ data format gave me different results.
Thanks


text:
How to check if a fastq file has single or paired end reads
I am trying to check if a fastq file has single or paired end reads. How can I achieve this with an error-proof method?
I checked wikipedia and MAQ but I want to know if is there a reliable document that describes all possible variants in sequence ID to check for single/paired end reads.
I am searching also for a library, better in Python, to achieve this.
Thanks

You might be better off asking this question on http://www.biostars.org/

See for example this question: http://www.biostars.org/p/45961/

Thanks @jarlemag. I did some research earlier and I noticed that answer. However there are two problems: first I am not fluent in Perl and it is hard to me to deciphers the content of the accepted answer (not to mention that not being able to check the code could lead to run into bugs that you cannot predict). Second, I read the answer and wikipedia page for FASTQ format but I am searching for the real reference. So I decided to ask a new question not to have a script (related but not main question) but the idea behind that, that could possibly cover all possible variants in this scenario.

I see. I found some info on the read identifiers, but held off from answering since it seemed you wanted a complete script. Have you checked out the SeqIO interface in BioPython?

Not yet, sorry.. I am quite a noob in BioPython.. now I'll try it. Thanks

By now I got some interesting answers in this question on Biostars
Basically what I did is the following:

First of all, I checked if Sequence Id contains paired end notation. As described in this wikipedia page, for Illumina reads there are two possible notation for single/paired end reads:
@HWUSI-EAS100R:6:73:941:1973#0/1
If the last number is /2 in some reads then the reads are paired end; otherwise they can be single end.
The second notation is:
@EAS139:136:FC706VJ:2:2104:15343:197393 1:Y:18:ATCACG
If the first number in the second group is 2 in some reads then the reads are paired end; otherwise they can be single end;
Then I checked for multiple files. If a sample has two fastq files it is likely that the reads are paired end. It is to note however that with a single file it is not possible to exclude that paired end reads can be interleaved in one single file, even if it is not common (in my opinion);
The most general method is to cross check each single reads with the whole set of reads. If the first part of the sequence ID (in this case the field starting from @ and ending before the # - in the first notation - or the whitespace - in the second notation) is unique among all the reads (for each read) it is likely that the reads are single reads, otherwise - if can be found a duplicate for each reads - the reads are paired end.
In this case, on *nix systems it can be achieved with the following command (thanks to the biostars answers):
grep --no-filename @HWUSI-EAS100R:6:73:941:1973 *.fastq | cut -d' ' -f1 | sort | uniq -c | sort -rgk 1,1 | head
If the result shows in the first lines a result like this:
1        read1_ID
1        read2_ID
...
It is likely it is single end. Otherwise:
2        read1_ID
2        read2_ID
...
it is paired end.

I skim read BioPython API documentation but I cannot find something useful to do it.
Suggestions and corrections are welcomed.
Thanks

This is complementary answer to what @gc5 provided.

For cases that are using "the second notation" which looks like:
@EAS139:136:FC706VJ:2:2104:15343:197393 1:Y:18:ATCACG`
                                        ^
                                        |________________what we are
                                                         trying to extract

The following code will go through all the files iteratively and produce one output per file:
grep -P "^@" *.fastq | grep -oP "\s\d+" | sort | uniq -c

or if you have .fastq.gz files:
zgrep -e "^@" *.fastq.gz | grep -oP "\s\d+" | sort | uniq -c

if you have single-end you will only see ones and if you have paired-end you will see ones and twos. Also as sanity check, you can see how many of each you have:
zgrep --max-count=10000 -e "^@" *.fastq.gz | grep -oP "\s\d+" | sort | uniq -c

6333652  1
6333652  2

Note that I added --max-count=10000 to the last one. This is particularly useful if you have paired-ends in separate files as you will get all ones form one and all twos from the other. This will only go through the first 10'000 lines which makes this one-liner much  much faster.


text:
Deciding a reasonable threshold for copy number variation in a CNV (SNP array) TCGA dataset
Is there a methodology to select a reasonable threshold for copy number variation in a CNV (SNP array) TCGA dataset, to define when there is a significative alteration?
Can I download CNV data for normal samples and take the 95th percentile of distribution? Are there better methods?
Update
This is the percentiles plot of the two distribution (Tumor vs Normal) of values, for the same technology (SNP array) and the same genome (hg19).
The tumor distribution has slightly more extreme values, though it is not enough in my opinion. For this reason I think I should not use a percentile score (the 5th and the 95th percentile of the normal samples distribution, for instance) to define the thresholds to call CNV alterations in the tumor samples.

Your suggested approach of comparing to the baseline distribution on a point-by-point basis isn't bad, although it's going to be susceptible to small false positives from noise. You'd probably want to only use events that span a certain minimum number of consecutive observations.
You might also want to look into circular binary segmentation, as described here: http://www.ncbi.nlm.nih.gov/pubmed/15475419.

I have updated my question, could you please give a look at it and let me know what do you think?

Hmm, okay, I think I see. No, you don't want to compare the intensity of the tumor at any one position against the 5-95% distribution of the normal across the whole array. You want to compare the intensity of the tumor at one position against the normal at that position. This will normalize for sequence-specific binding differences.

There are many methods for the analysis of CNV. If you are an R user I would recommend you to take a look at the Bioconductor package list, in particular the section for copy number variation. Currently it contains 50 packages!


text:
Where do I find microsatellite instability annotation for TCGA data
I have searched through the TCGA data portal but I was unable to find MSI annotation for TCGA Colon Adenocarcinoma (COAD) and Rectum Adenocarcinoma (READ) datasets.
I am searching for the annotation on samples, i.e. if a specific sample is annotated as MSI (microsatellite unstable) or MSS (microsatellite stable). In particular, I found this page, and followed the path:

Data Matrix & Bulk Download: Select 'Fragment Analysis Results' for Data Type

but with no results.

I'm voting to close this question as off-topic because this is about the computational aspect of Bioinformatics. While questions on interdisciplinary subjects like bioinformatics are welcome, they must focus on the biological part of the subject.

@AMR No we have clearly agreed that any question on analysis or understanding of bioinformatics data is on-topic. Frubudu, can you please provide a link to these databases. Your question, as it is, is unclear.

I tried to provide links and to specify better what I am searching for. I am searching for a link to these databases, but if I can provide more information tell me.

And it really isn't hard to find out why the OP cannot get access to this information. It is controlled-access data and that requires special authorization to access as it has information that is unique to an individual. https://wiki.nci.nih.gov/display/TCGA/Open+Access+and+Controlled+Access+Data

Thanks. So I need authorization to access them. May you put it as an answer?


text:
Definition of the different DNA regions
Reading from Oshima et al. (2016):

We identified 3,868 noncoding mutations including 394 located <5 Kb downstream, 1,762 intergenic, 1,621 intronic, 81 <5 Kb upstream, 7 UTR 3′, 2 UTR 5′, and 1 intragenic variants.

How upstream, downstream and intragenic variants are defined? Shouldn't intragenic variants be classified within intronic variants, and upstream/downstream within intergenic variants?
Edit: By adding the different numbers it seems they are mutual exclusive. While upstream/downstream variants can be defined as intergenic variants that lie close to genes, I haven't found a definition to tell the intragenic variants from the intronic ones.
Edit 2: The only explanation I could think of for intragenic variant is that it is located in a coding region which is not transcribed due to alternative splicing. Can it be possible?

Oshima, Koichi, et al. "Mutational landscape, clonal evolution patterns, and role of RAS mutations in relapsed acute lymphoblastic leukemia." Proceedings of the National Academy of Sciences (2016): 201608420.

You could try sending them a quick email.

We can take a look at the following picture (from wikipedia):

The regions are then:

intergenic: everything outside of the shown gene region
<5 Kb downstream: outside of the transcribed region, but possibly part of the promoter or an enhancer (yellow boxes before coding region).
UTR 5′: in the transcribed region, but not part of the coding region, as shown in the picture (blue box before coding region).
intronic: In the Introns, as shown in the picture (grey boxes)
intragenic: These have to be mutations inside the coding region (red boxes), which is confusing since the authors specifically describe them as 'non-coding' mutations. If you read that as 'mutations that don't change the protein sequence', these could be silent mutations
UTR 3′: in the transcribed region, but not part of the coding region, as shown in the picture (blue box after coding region)
<5 Kb upstream: outside of the transcribed region, but possibly part of an enhancer (yellow boxes after coding region)

Intragenic is not coding (as it's CDS and introns). Intragenic is region from TSS to TTS.

@SEwontLetMeDeleteProfile can you elaborate more on that? Also, what is a TTS?

The Sequence Ontology project defines an intragenic variant as "A variant that occurs within a gene but falls outside of all transcript features. This occurs when alternate transcripts of a gene do not share overlapping sequence." source
Intragenic means the variant is located within the same gene, which only implies that the sequence analysis assigned a certain variant to a gene. So, there is incomplete data regarding the gene product (such as different splice forms).

You can look up the mutation locations here:  http://grch37.ensembl.org/index.html


text:
Importance of germline and somatic genomic mutations to the purpose of treatment in cancer
Is there a hierarchy in the sets of genomic mutations (somatic and germline) to the purpose of treatment in cancer?
Can they be considered at the same level in the context of targeted therapy or are there reasons to prioritise one set vs the other?

A) There isn't really a fixed hierarchy that is applicable across the board - alterations are often binned into actionable targets and non-actionable ones. In terms of customised cancer vaccine for immunotherapy (Eg - www.sciencemag.org/news/2017/04/personalized-tumor-vaccines-keep-cancer-check ) , more antigenic mutations tend to be prioritised.
B) Sometimes there are reasons to prioritise mutations over others even for small molecule targeted therapies. For example, one would want to target mutations that are clonal rather than subclonal where possible, so that the bulk of the tumour, rather than a small fraction of the cells in it, are targeted. Alternatively where one has, for example, a resistance mutation arising from prior therapy (You see this with EGFR T970M mutations) it is an indication for next generation EGFR inhibitors that specifically hit the resistant mutation.


text:
Why is SF3B3 gene annotation missing in chm13_v2 gff3 file, and is it temporary?
In the annotation gff3 provided for CHM13 v2, I noticed that for the SF3B3 gene there's no entry with type "gene" (third column).
However, transcripts and other annotations are still available. I checked on UCSC genome browser and transcripts still appear annotated:

I was not able to find if this is associated with other aliases. I am trying to understand:

why the "gene" annotation is missing in the gff3
if this is temporary, i.e., the "gene" annotation will be updated later

Note that all of your transcripts for SF3B3 have a source_gene=ENSG00000189091.13 tag in the GFF3 file. A gene with that annotation does exist in the gff3 (see the grepped output below), though for some reason it has the identifier MSTRG.2232. That gene almost but not quite overlaps with the transcript SF3B3-201 and perfectly overlaps with the transcript CHM13_T0084548 represented in your browser shot.
# gene annotation
chr16   CAT     gene    76334966        76388859        .       +       .       source_gene_common_name=MSTRG.2232;source_gene=ENSG00000189091.13;gene_biotype=protein_coding;gene_id=CHM13_G0022147;gene_name=MSTRG.2232;transcript_modes=transMap,exRef;ID=CHM13_G0022147;Name=MSTRG.2232;source_transcript=N/A;alternative_source_transcripts=N/A;collapsed_gene_ids=N/A;collapsed_gene_names=N/A;paralogy=N/A;unfiltered_paralogy=N/A;alignment_id=N/A;frameshift=N/A;exon_anotation_support=N/A;intron_annotation_support=N/A;transcript_class=N/A;valid_start=N/A;valid_stop=N/A;proper_orf=N/A;extra_paralog=False
# transcript annotation
chr16   CAT transcript  76334997    76388857    10000   +   .   source_transcript=ENST00000302516.10;source_transcript_name=SF3B3-201;source_gene=ENSG00000189091.13;transcript_modes=transMap;gene_biotype=protein_coding;transcript_biotype=protein_coding;alignment_id=ENST00000302516.10-0;frameshift=nan;exon_annotation_support=1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1;intron_annotation_support=1,1,1,1,1,1,2,2,2,2,1,2,2,2,1,2,2,2,2,2,1,1,1,2,2;transcript_class=ortholog;valid_start=True;valid_stop=True;adj_start=76337842;adj_stop=76383007;proper_orf=True;level=2;protein_id=ENSP00000305790.5;transcript_support_level=1;hgnc_id=HGNC:10770;tag=basic,MANE_Select,appris_principal_1,CCDS;ccdsid=CCDS10894.1;havana_gene=OTTHUMG00000137582.8;havana_transcript=OTTHUMT00000268972.3;paralogy=nan;unfiltered_paralogy=nan;source_gene_common_name=SF3B3;transcript_id=CHM13_T0084551;gene_id=CHM13_G0022147;Parent=CHM13_G0022147;transcript_name=SF3B3-201;ID=CHM13_T0084551;Name=SF3B3;gene_name=SF3B3;alternative_source_transcripts=N/A;collapsed_gene_ids=N/A;collapsed_gene_names=N/A;extra_paralog=False
# transcript annotation
chr16   CAT     transcript      76334966        76388858        .       +       .       source_gene=ENSG00000189091.13;transcript_class=putative_novel_isoform;novel_5p_cap=True;novel_poly_a=True;transcript_biotype=protein_coding;gene_biotype=protein_coding;intron_rna_support=1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1;exon_rna_support=0,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,0;transcript_modes=exRef;exon_annotation_support=0,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,0,0;intron_annotation_support=1,1,1,1,1,1,2,2,2,2,1,2,2,2,1,2,2,2,2,2,1,1,1,2,2,0;alignment_id=exRef-MSTRG.2232.2;source_gene_common_name=MSTRG.2232;transcript_id=CHM13_T0084548;gene_id=CHM13_G0022147;Parent=CHM13_G0022147;transcript_name=CHM13_T0084548;ID=CHM13_T0084548;Name=MSTRG.2232;gene_name=MSTRG.2232;source_transcript=N/A;alternative_source_transcripts=N/A;collapsed_gene_ids=N/A;collapsed_gene_names=N/A;paralogy=N/A;unfiltered_paralogy=N/A;frameshift=N/A;valid_start=N/A;valid_stop=N/A;proper_orf=N/A;extra_paralog=False

I'm not sure why those genes aren't tagged with the common name, and I'm not sure why it's not in your browser shot (whereas the alternate systematic gene NM_012426 is represented there; a quick grep suggests the NM_012426 IDs are not in the GFF3, and are interpolated by UCSC). But in general it's a good idea to always use the systematic identifier, because the common gene symbol/name won't always be trustworthy. If you use the systematic identifier, you should find the right gene.
Most likely explanation is a clash of competing methods, and a failure of the annotation method to hook the actual gene to the common name that you are looking for. It looks like some of the transcripts are longer than the gene, so maybe that's the reason. Possibly those transcripts derive from RNA-seq, and the gene annotator didn't find a good overlapping gene so it didn't get all the way linked. But I'm not enough of an annotation method expert to say for sure.
It looks like the annotation was done using CAT, so you could look there for more info. You could contact the author or post on the github if you want to learn more.

Thank you! Yes, the issue was reported on github. Your explanation is reasonable, should the Ensembl gene ID solve the issue, too?
I tried to lift the coordinates from hg38 to chm13. After that I noticed that the sequence for SF3B3 (ENSG00000189091.13) is ~93% identical (through blast) between hg38 and chm13, so I believe that 7% difference might also have affected the annotation?

@gc5 Yeah, I would guess that something went weird with liftOff based on the difference, I would be curious to know if that 7% difference is due to real difference or different slices of highly similar sequence. But regardless I think the Ensembl gene ID should fix it.


text:
How can I download histological slide from Cancer Digital Slide Archive
Could you tell me if it possible and how to download images data from http://cancer.digitalslidearchive.net ?
Thank you.


text:
How much does the distance between a transcription factor binding site and a promoter influence transcription?
Assume we have a synthetic construct with a minimal (inducible) promoter that requires activation for significant transcription to occur. Realistically, how important is the distance between an activator binding site and a promoter - would placing the binding site closer to the promoter lead to significantly stronger activation, or more robust system behavior?
In some genomics-related models I saw authors assigned weights to binding sites based on position (orientation and distance from the promoter); the general idea was that binding sites farther away could have a weaker influence on transcription. This can be modeled e.g. by decreasing the binding affinity. But that was genomics, and I'm unsure how much of that has any relevance in smaller scale plasmid constructs.
For example, suppose we have a highly specific binding site (e.g. a TALE binding site) upstream of the promoter:

In Fig.1, the binding site A is only e.g. 40 bp away from the promoter. In Fig.2, it is e.g. 5000-7000 bp away. Should I expect this to make a noticeable difference? Would the same apply if it would be a constitutive promoter, with a repressor instead of an activator? What about more complex networks, could the answer change?

it depends of course :( in eukaryotes the same factor can be found bound thousands of bases down stream.  In prokaryotes the distance can vary by on the order of a score of bases, and also many sites may exist and but not have additive effect.

also depends on the type of site and the factor that binds to it. not that straightforward.

To be more specific, I'm interested in TALE-based transcription factors in HEK cells.

That really depends on your system. At least for yeast the difference influences the strength of the activation ("Analysis of Transcriptional Activation at a Distance in Saccharomyces cerevisiae").
For bacteria such long distance regulations have recently been identified. Before that it was thought that this does happen only in eukaryotes. See the paper: "Long distance relationships: enhancer-promoter communication and dynamic gene transcription."
I eukariotic cells the regulatory sequences (transcription factor binding sites and enhancers as well as silencers) can be really far away. An example for this would be the rs12913832 in intron 86 of HERC2, which influences the expression of the OCA2 gene, which is about 21 kB away. Both genes are not related in their functions. Normally three transcription factors interact here in the regulation of OCA2, HLTF, LEF1 and MITF, which leads to the formation of a DNA loop between the enhancer in HERC2 and the promoter in OCA2. The polymorphism reduces the binding of HLTF to the enhancer and hinders the formation of the loop which results in reduced expression of OCA2 (the whole story can be found here: "HERC2 rs12913832 modulates human pigmentation by attenuating chromatin-loop formation between a long-range enhancer and the OCA2 promoter.")
This paper ("Essential role of microphthalmia transcription factor for DNA replication, mitosis and genomic stability in melanoma.")analyzed (among other things) the binding sites for the microphthalmia-associated transcription factor (MITF) and their distance from the transcription start site. Figure 1 a/b of the paper is shown below. Interestingly a lot of the binding sites where pretty distant.

To go deeper into the topic, the following reviews are interesting to read:

Long distance relationships: enhancer-promoter communication and
dynamic gene transcription.
Enhancer and promoter interactions-long distance calls.


text:
What is the relation between plasmid concentration and mRNA levels?
Suppose a simple synthetic construct, consisting of a constitutive promoter and a single gene:

One of the simplest ways to model GFP transcription is to use an ODE:
$\frac{d [GFP_{mRNA}]}{dt} = a - b{\cdot}[GFP_{mRNA}]$
where $a$ is GFP transcription rate and $b$ is GFP mRNA degradation rate (both constants). Normally, we assume $a>>b$.
Suppose we wish to account for plasmid concentration with the value of transcription rate $a$ - e.g. with higher plasmid concentration, the ratio $a/b$ should increase as the mRNA saturation levels are expected to be reached faster. In other words, suppose we transfect 2 individual constructs depicted above, 10 ng of one and 30 ng of the other - how should this difference in concentration impact the rate constants values, assuming the constructs are otherwise identical?
Assuming this, approximately how does gene transcription rate $a$ change as a function of the amount of transfected plasmid containing the above construct? Ideally, I'd be interested in knowing this for HEK 293 cells, but any other decent estimation is acceptable. One simple option is to simply assume linear relation, but I think that's too simplistic: e.g. if we say $a=1$ at 10 ng plasmid concentration, then $a=3$ at 30 ng plasmid concentration. Note that I'm not necessarily limiting myself to ODE models, just looking for some kind of relation.
I have so far not been able to find anything useful in papers I've examined, so any help would be appreciated.

The amount of transfected plasmid does not correlate at all with the protein expression level. After transfction, usually each cell is going to get and keep only one copy of the plasmid. Once the plasmid is in the cell, it will be replicated and the cell will contain X copies of it, depending on the plasmid copy number. In general, plasmids with low copy numbers correlate with lower protein expression compared to plasmids with high copy number. But there are also exceptions:

Expression of genes under control of EF1α promoter appears to correlate with plasmid copy number.  In contrast, expression driven by the more traditional CMV immediate early promoter appears less plasmid copy number dose-responsive (ref).

Well.. the copy number does matter in case of CMV also. I had observed normalized luciferase activity in HEK cells at different amounts of transfected plasmid- it shows difference. Also, the effect on an miRNA on the luciferase is better as the concentrations decrease. It is not strictly linear, though.


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Does the Jungian notion of collective unconsciousness have any legitimacy in the light of modern neurobiology and epigenetics?
Carl Jung has long ago proposed a rather controversial notion of collective unconsciousness [1, 2, 3],

a form of the unconscious (that part of the mind containing memories
  and impulses of which the individual is not aware) common to mankind
  as a whole and originating in the inherited structure of the brain. It
  is distinct from the personal unconscious, which arises from the
  experience of the individual.

While the complete original formulation of the idea may be interpreted as unfalsifiable and hence unscientific, suppose that we try to redefine it to some more modest idea, e.g. a set of inheritable subconscious memories, impulses and reactions present in populations/groups, with some expected degree of variation.
Now, it has been shown that memories reside in specific brain cells [4]. What is also known is the direct impact of environment (which - as far as I understand it - also includes our thoughts, feelings and expectations) on gene expression and epigenetic inheritance. In the light of these insights, could the notion of collective unconsciousness be revitalized and interpreted in some non-trivial way that could be used to better understand the way we dream, feel, identify with characters in stories etc.?
In other words, do new discoveries in neurobiology, evolutionary biology and epigenetics shed any new light on Jung's writings (e.g. timescale for such structures to adapt between generations etc.) and perhaps confirm some of his ideas? If not, could experiments be performed that would provide some new insights? Or is the idea so trivial at its core that basic evolution is enough to explain it in its entirety?

Perhaps this question is more suited for Cognitive Science.

@Superbest I would agree to an extent, but I think that the epigenetic/evolutionary aspect is better handled here.

Peripherally related: http://cogsci.stackexchange.com/questions/1116/what-form-might-jungian-archetypes-take-in-the-brain

Jung's premise is rather plausible: consciousness evolved rather than appeared suddenly, and therefore carries "pre-conscious" elements common to humans as a species. However, Jung goes very far in his interpretation of what may be hidden in subconscious, bordering on open mysticism - predicting accidents, wars, etc. I doubt there may be any evidence for that.
Among the more plausible of Jung's arguments are his comparative studies of the similarities between fairy-tales, legends and other folcloric features between cultures. This however does not necessarily prove that these existed in subconscious - they could evolve as a part of different human cultures encountering similar problems, e.g., dealing with incest (Edip), reaching sexual maturity (Beauty and the beast), etc. - which was already Freud's view. Essentially, Jung attributes to collective subconscious many of the things that Freud attributes to superego, that is to the cultural influences.
Less far reaching claims are made by modern theoretical linguistics, since all the existing languages are shown to obey similar generative grammar, see my post about the subject. While I am not aware of any conclusive results for this view from neuroscience, the evidence collected by linguists is rather strong.
References

K. Jung, Man and his symbols
S. Freud Totem and taboo
S. Freud The psychopathology of everyday life
S. Freud New introductory lectures on psychoanalysis
D. Isac and Ch. Reiss, I-Language: An Introduction to Linguistics as Cognitive Science

I believe it does. From looking at collective unconscious as a whole it states to say it’s “inherited beliefs and behaviors of ancient ancestors. As it’s been proven the collective unconscious is related to the subconscious. When you think about epigenetics it’s connected to the junk dna, which is 90% of gene regulation they thought to be unuseful, years down the have been proven wrong. Junk dna can be the subconscious of genes so now to put these understandings together, you have inherited (genes) beliefs and behaviors (subconscious mind) collective (genes) unconscious (mind)
A perfect example of this manifestation: imagine an individual in a ancient culture that experience pagan sexual rituals then down the ancestral line in our disposition you have certain events like pride or even home events like house parties this experience causes certain genes to be turn on and off leading to mental activity similar-to those involved in a archaic world.

Most of this answer reads as nonsense opinion to me that's unrelated to the question asked, but at least it shares that with Jung and Freud. In any event, we expect answers here to be cited and referenced when going beyond basic textbook knowledge. What can you cite to support what you write here?

@BryanKrause I think the swipe at Jung and Freud is totally unnecessary.

@RogerVadim I disagree and I think they remain a bit of an embarrassment to psychology, whatever influence on therapy they've had.

@BryanKrause First, let us not confuse psychology with neuroscience. Secondly, apart from their most controversial claims (controversial mainly to laymen) Freud, Jung and their followers are pretty much the basis of modern psychology, to the extent that their most revolutionary claims are considered so obvious, tha they are not even credited to them.

@RogerVadim Guessing we'll have to agree to disagree then. I think Freud and Jung belong with Aristotle and Plato - we can respect their insight and historical role while recognizing that their approaches are extremely flawed. The difference is that Freud and Jung came far far later, once scientific philosophy had advanced quite a bit further, and that their flawed ideas are so embedded in the way the lay audience talks about psychology that it's hard to convince students and the lay public to think another way.

@BryanKrause again, I see no problem witj Aristotle, Plato or other ancient Greeks, who are at the source of modern philosophy, math and scientific method. Neither do I see problem with Darwin, whose theories were mere conjectures and are no less different from modern views than the psychology from Freudian views. Important thing to keep in mind is the limitations and applicability of the scientific method.

@RogerVadim The difference is that when people reference Aristotle and Plato they use them as historical references.

@BryanKrause the point is that psychology, macroeconomics, and many other domains are not sciences - because their subject is not amenable to the scientific events - they are interested in what is unique about their objects of interest, rather than what is in common between them.

Let us continue this discussion in chat.


text:
Near point and far point of myopic eye
Suppose a person wears the specs of power -6D, the far point for that person is 16cm.
But the near point of normal eye is 25cm.
So, is the near point of a  person with myopia (having far point less than the near point of normal person) also changed ?

Let us say this myopic patient has amplitude of accommodation of 8D.  The patient accommodates 8D beyond far point, thus his near point is 1/6+8=0.07m (7.1cm).
If we compare the case with emmetropic eye with accommodation amplitude of 8D, the near point is 1/8=0.12m (12cm).
So, yes, near point of myopic person is different from an emmetropic one. But, you are wrong thinking that near point of "normal" eye is 25cm. The near point is age-and-lens dependent, thus near point is individual one and should be calculated considering amplitude of accommodation.
Look at this picture of age-related accommodation changes -

Look at the scheme of far/near points (near point here is just an example)

Hi!Thank u for answering.I could not understand the first calculation. Why did u take 1/14 instead of 1/8 ? Also - would the near point of myopic eye change after correction of far point ?

That is very simple: in nonaccommodative state the eye in example has 6D and to this power the adds its accommodation power of 8D for nearest point,  thus the near point is at 1/6D+8D...

I forget to answer about correction. By correction we convert a myopic eye to "emmetropic", thus with correction the near point is different (more far from the eye).


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Recombination frequency, linked genes, and independent assortment
Gene R is genetically linked to gene T with a recombination frequency of 0.3. Gene T and gene X assort independently from each other. Your colleague tells you that gene T and gene X reside on the same chromosome. How is this possible?
So I know that R and T are on the same chromosome. T and X assort independently, so they should be on different chromosome. And then due to recombination, X gene crosses over so that it's also on the same chromosome as T and R? Can someone please help me?

remember that chromosomes can be quite large - especially if T and X are on opposite sides of the centromere, if they are far enough apart from each other they will appear to assort completely independently from one another.

I don't understand. If two loci segregate independently, it means that the recombination frequency equals 0.5, isn't it? In which condition they might or not be on the sea chromosome. But as soon as the recombination frequency is lower than 0.5, then the don't segregate independently and therefore, they are necessarily on the same chromosome (except if there is a segregation distorter). Let me know if I'm wrong

homework? If so, use the tag.

The comments pretty much answer the main concern here. But just to sum up:-

"....T and X assort independently, so they should be on different
  chromosome...."

Not necessarily. They can be on the same chromosome at such a distance that there is usually atleast one chiasma formation between them, and will undergo independent assortment, i.e.  segregation of one gene among the gametes will be independent of the other. They will pretty much act and segregate like mendelian factors. Specifically, if the recombination frequency is 0.5 (50cM or map units' distance on the chromosome), they will assort independently.

"....And then due to recombination, X gene crosses over so that it's also
  on the same chromosome as T and R...."

This part is a little bit unclear. I assume (correct me if I am wrong) is that you are assuming X,T,R to be alleles, which can be present on only one chromatid and hence recombination might change their distribution and positions relative to one another. But as the question states, they are genes (or specifically gene loci) which are present on both chromatids and their relative position is fixed. The recombination frequencies refer to the recombination of different alleles at this locus.