text:
Relationship of the DNA of a eukaryotic gene to the 5'-UTR of its mRNA
In eukaryote pre-mRNA I am having a little trouble grasping exactly what the 5 prime untranslated region is defined as.
It seems that it could be defined as the difference in pre-mRNA between the transcription and translation, is that right?
If so, does the transcription begin immediately after the end of the promoter sequence? Immediately after the promoter region on the DNA ends, does the next nucleotide become part of the 5'UTR?

Possible duplicate of http://biology.stackexchange.com/q/38783/3340

Concise Answer
The 5′-UTR region of a eukaryotic mRNA is derived from the RNA transcript of the region of a gene between the transcription start site and the DNA corresponding to the translational initiation codon. It differs from that region of the initial transcript in most cases by having a modified guanosine nucleotide added at the 5′-end in a ‘cap’ structure, and in some cases by lacking an intron present in the former.
The Transcriptional Start Site (TSS) and the Promoter
This answer is in terms of the TSS rather than ‘promoter region’ or ‘promoter sequence’, favoured by the questioner because in eukaryotes, at least, there is no simple and easily definable promoter sequence. A 2012 review of metazoan promoters begins with the definition: “Gene promoters are the loci overlapping transcription start sites (TSSs), at which the total regulatory input of a gene is integrated into the rate of transcriptional initiation. The immediate role of the promoter is to bind and correctly position the transcription initiation complex…”.
A simplified diagram of some components of human promoters (adapted from an earlier review by Hahn) is shown below. The position of ‘Inr’ — the Initiator box which contains the TSS — varies with respect to the TATA box (usually from –25 to –30 in humans),  as does its sequence. Hence, even ignoring the alternative TSSs mentioned by @Luke it is not possible to identify the TSS unequivocally by inspection of the DNA sequence of a gene in the way the questioner would apparently wish.

The Translational Initiation Codon
It should be mentioned that it also not possible to identify the mRNA translational initiation codon unequivocally by inspection of the DNA sequence of a gene. Although 90% or more cases follow Kozak’s rule, so that it corresponds to the first ATG, in some cases it may correspond to the second ATG, and in a small minority — where internal initiation occurs — to some distal ATG. There are also a very few examples of initiation of translation at codons other than AUG.
Introns in 5′-UTR regions of pre-mRNA
A common rationalization of the intron/exon nature of eukaryotic pre-mRNA is in terms of alternative splicing to produce different protein sequences. Perhaps because of this, the presence of introns in the primary transcript containing the 5′- and 3′-UTRs is often ignored (see Bicknell et al. for a review). In fact, approximately 35% of 5′-UTR precursors contain introns, not present in the mature mRNA.
5′-capping of eukaryotic mRNA
The vast majority of eukaryotic mRNAs have a cap at their 5′-end, produced by the addition of a guanosine nucleotide in a 5′-5′ pyrophosphate linkage to the 5′-residue (usually A) of the pre-mRNA. This is subsequently methylated at carbon-7; and 2′-O-methylation of the ribose of the subsequent one or two nucleotides may also occur.

Footnote
Although “DNA makes RNA makes Protein”, I do think it important to describe features of information molecules in terms of their actual composition. Thus, the 5′-UTR has to be defined in terms of mRNA, not promoters or exons. If one makes reference to the information content of DNA or RNA than I think a form of words should be used to make that clear. Muddled forms of words can easily lead to muddled thinking.

Short answer
The 5' UTR on the mRNA includes sequence from the Transcriptional Start Site (TSS) to the first exon. Promoters are usually associated with a corresponding TSS.
Longer answer
In defining a UTR we must consider where transcription begins. Strictly speaking transcription begins at the Transcriptional Start Site (TSS). A useful website for exact definitions for terms such as this is the Sequence Ontology - see here for the TSS definition (link) - although admittedly in this case it does not provide more information than that (i.e. the TSS is where transcription begins... which we might have gathered from the name). TSS will have an associated promoter region, which is where the RNA polymerase (and various regulators and transcription factors bind).
To expand: a gene may have multiple TSS' which may be promoted under different circumstances (e.g. with different factors present). We therefore have the concept of a TSS region "The region of a gene from the 5' most TSS to the 3' TSS" (link). TSS have to be empirically determined, and seem to vary by tissue (a database of all known TSS has been accumulating evidence since 2002: DBTSS). I have just performed a search for gene APOE (chr 19) and this is a small excerpt of the data presented, just to give an idea:

From DBTSS

So the TSS for a gene is context dependent on the when/where the transcript is being produced.
In searching for further information I found a paper that describes the 5' UTR on the mRNA, which is not necessarily an exact copy of the genomic DNA (e.g. by addition of the cap). Here is the corresponding paragraph and diagram, which explains it better than I can paraphrase (highlighting by me):

Transcriptional control is mediated by transcription factors, RNA polymerase and a series of cis-acting elements located in the DNA, such as promoters, enhancers, silencers and locus-control elements, organized in a modular structure and regulates the production of pre-mRNA molecules, which undergo several steps of processing before they become functional mRNAs. Introns are removed, a 7-methyl-guanylate (m7G) cap structure is added at the 5' end of the first exon, and a stretch of 100-250 adenine residues (the poly(A) tail) is added at the 3' end of the last exon, which is itself generated by endonucleolytic cleavage of the primary transcript. Sometimes the sequence of the mRNA is also altered in a process called mRNA editing, and the resulting coding sequence of the mature RNA differs from the corresponding sequence in the genome. The resultant mature mRNA, in eukaryotes, has a tripartite structure consisting of a 5' untranslated region (5' UTR), a coding region made up of triplet codons that each encode an amino acid and a 3' untranslated region (3' UTR). Figure 1 shows these and other features of mRNAs.

Figure 1: The generic structure of a eukaryotic mRNA, illustrating some post-transcriptional regulatory elements that affect gene expression. Abbreviations (from 5' to 3'): UTR, untranslated region; m7G, 7-methyl-guanosine cap; hairpin, hairpin-like secondary structures; uORF, upstream open reading frame; IRES, internal ribosome entry site; CPE, cytoplasmic polyadenylation element; AAUAAA, polyadenylation signal.
Reference: Mignone, F., Gissi, C., Liuni, S., & Pesole, G. (2002). Untranslated regions of mRNAs. Genome Biology, 3(3). http://www.ncbi.nlm.nih.gov/pubmed/11897027

Promoters
To conclude my answer (apologies for its lack of brevity) there are different types of promoter, not all of which directly include a TSS, but the majority of promoters are called "Major promoters" and do include the TSS (in addition to the RNA polymerase binding site, and other transcription factor binding sites).

Eukaryotic Promoter Database
Dreos R, et al. EPD and EPDnew, high-quality promoter resources in the next-generation sequencing era Nucleic Acids Res. 2013 Jan;41. http://www.ncbi.nlm.nih.gov/pubmed/23193273

Well I guess it's just not as simple as I had hoped, but I feel like now I have more questions than I started with. Thank you for such a really thorough answer.

Thanks for accepting it so quickly - I've updated it some more as I realise it was quite long and hadn't quite answered you question. Included more info on the promoter aspect. :)

You state in your summary that "The 5' UTR on the mRNA includes sequence from the Transcriptional Start Site (TSS) to the first exon". But this is surely wrong as exons are those parts of the transcript that appear in the mRNA, so the 5'-UTR will include the first exon (at least). Indeed, that is what appears in bold in the piece you have quoted.

Since there are genes with different transcriptional start sites regulated by different promoters, it would be interesting to see if the resulting differences in 5' UTR are used to regulate expression of the mRNAs. This could allow an extra layer of regulation, such that gene X not only needs promoter Y, but micro RNA Z to function, but when promoter W is used, the 5' UTR is different and RNA Z is no longer needed.

Hi @David - maybe I've also misunderstood something but the exons by definition are the translated regions, therefore would not be part of the UTR (un-translated region). On the diagram you can see there is a long stretch of sequence between the start of the mRNA (the cap) and the "coding sequence" i.e. the exons (bear in mind introns have been removed by this stage so all included exons appear together). -- user137 that would be interesting, and I expect it would affect pre-mRNA processing to some degree.

No. The definition of exon given by Wikepedia (which is consistent with every other you will find in a text) is "An exon is any part of a gene that will become a part of the final mature RNA produced by that gene after introns have been removed by RNA splicing." I shall address the question of introns in the 5'UTR in a replacement for my original answer which should appear later today.

Actually, not every text. I found a definition in terms of coding regions at http://www.nature.com/scitable/definition/exon-exons-270. But that is nonsense. What else would you call the part of a transcript that is not an intron and appears in a final mRNA but an exon? It can include the 3'UTR as well. Exons and introns are to do with splicing of pre-mRNA. One function may be to allow for different coding regions in differential splicing, but they can also allow for different 5'UTRs.

The UTR is the region of the transcript upstream of the starting methionine.  The promotor is not itself transcribed.

Sorry to push the issue, but I don't feel like you answered my question. This is exactly how the book phrases it as well. Is it everything after the promoter but before the methionine?

In other words, does transcription start immediately where the promoter ends?

DPEs can be in the transcribed region. http://biology.stackexchange.com/q/38783/3340

@WYSIWYG It seems like there are no hard and fast rules. Thanks for finding that, it pretty much answers my original question.


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Is it possible for a parasitic wasp to alter the behaviour of its host after emerging from it?
I know that parasitic wasp larvae can live for a long time inside their live host (eg. caterpillar), but I always thought that they kill the host when they eventually get out of it. But I've seen a film, where it's shown that not only can a caterpillar survive the emergence of a wasp larva, but also the parasites infect the host with some kind of virus that changes the behaviour of the caterpillar to protect the wasp’s pupa. Is it possible and common among parasitic wasps? What species of wasps and viruses cause such effect?

Are you asking about parasites (i.e not lethal to host) or parasitoids (i.e. host killing) insects? In the question, the distinction seems to be muddled.

Another example is the wasp species Dinocampus coccinellae, which lays its eggs inside certain species of ladybug/ladybird - most notably the "twelve-spotted lady beetle" (Coleomegilla maculata). It also infects the "seven spot" ladybird.
(I'll stick with "ladybird" instead of "ladybug" for the remainder of this post.)
This is actually very similar to the Glyptapanteles example in the most-upvoted answer so far. (Though I would like to point out that OP's video in fact does not in fact show Glyptapanteles, but the extremely similar Cotesia glomerata.) In this case, though, only one egg is laid inside the host, and the wasp larva is nothing like as small relative to its host as the Cotesia and Glyptapanteles larvae were.
The wasp larva, after emerging from its ladybird host, spins a cocoon underneath the ladybird, between its legs, and pupates. Unlike Cotesia, this wasp larva needs to use its own silk and spin its own cocoon. The hard-shelled ladybird is trapped on top of the wasp pupa, rather like an armoured shelter. While mostly immobile, if potential predators/hyperparasites come close, the ladybird will thrash out at them with its limbs. I'm not sure if this is to attack them directly, or to deter them from coming close, or both.
Since no other larvae are left behind in the host, Dinocampus coccinellae must be using some other means to influence its behaviour after emergence. A virus, the "D. coccinellae paralysis virus", is injected by the adult wasp at the time the egg is oviposited. As well as suppressing the ladybird's immune system, it infects the ladybird's brain and may explain one or both of:

The ladybird's general immobility after the larva emerges
The ladybird's thrashing out at potential predators that may attack the larva.

The virus replicates rapidly but for unknown reasons doesn't spread to the beetle's brain until just before the larva emerges from her belly. At first the virus seems to build up harmlessly in brain cells, but as soon as the larva breaks out, these cells burst open, unleashing destruction all around them.
The researchers suggest that the beetle's own immune system may be responsible for this damage. They discovered that crucial immune genes are suppressed while the larva lives within the ladybug, but then reactivate after the larva emerges. The researchers speculate that the beetle's revived immune system discovers and attacks DCPV-infected cells. The self-inflicted brain damage could temporarily paralyze the beetle just when the newly vulnerable wasp larva needs protection.

Also:

DcPV is stored in the oviduct of parasitoid females, replicates in parasitoid larvae and is transmitted to the host during larval development.

If I understand correctly, this virus is not one of the so-called "polydnaviruses" injected by other species of parasitic wasp.
For some reason, the wasp prefers to parasitize female ladybird hosts, although I think it will still use male hosts in a minority of cases.
Sources:

Dheilly Nolwenn M. et al. (2015). Who is the puppet master? Replication of a parasitic wasp-associated virus correlates with host behaviour manipulation. Proc. R. Soc. B vol 282 issue 1803:
http://doi.org/10.1098/rspb.2014.2773
Maure F et al. (2011). The cost of a bodyguard. Biology Letters volume 7 issue 6: http://doi.org/10.1098/rsbl.2011.0415
Davis D.S., Stewart S.L., Manica A. and Majerus M.E.N. (2006). Adaptive preferential selection of female coccinellid hosts by the parasitoid wasp Dinocampus coccinellae (Hymenoptera: Braconidae). Eur. J. Entomol., 103(1), 41-45. doi: 10.14411/eje.2006.006.

See also:

https://www.naturespot.org.uk/species/dinocampus-coccinellae
https://www.discovermagazine.com/planet-earth/biological-warfare-parasitic-wasp-uses-a-virus-to-control-its-host
https://www.sciencemag.org/news/2015/02/wasp-virus-turns-ladybugs-zombie-babysitters

Great job (+1). (I have the same suggestions for improvement that I made on your other answer and did a little tidying up of the formatting for your sources.)

The species of wasp in the video you link to is Cotesia glomerata. Furthermore, there is at least one other species, Glyptapanteles, which parasitizes other caterpillar species in the same way and induces the same behaviour in its host.
I'm not sure which virus it is.
http://www.newscientist.com/article/dn14053-zombie-caterpillars-controlled-by-voodoo-wasps.html?feedId=online-news_rss20
Is it possible? Of course, you have an example! Though, there is a small caveat. Some of the offspring sacrifice themselves to induce the behavioral change after the rest of the brood has emerged.
Is it common among parasitic wasps? No. While injecting offspring into host species is a common theme for parasitic wasps, and while there are a handful which somehow induce behavioral changes in the host animals - continuing the manipulation after leaving the host animal is extremely rare among parasites in general.

Thanks! It's even more fascinating, because of altruistic motive (unless polyembryony was common among Glyptapanteles so that all larvae in one host will be genetically the same). I ask if such change in behaviour is possible, because I don't completely trust the information in popular science sources. I would accept your answer, but first I'd like to wait, maybe someone will find anything about that mysterious virus.

In the study by Whitfield 1990 (1) I found the information that the parasitic wasp from family Ichneumonidae have interesting symbiotic viruses called polydnaviruses. This virus stay as provirus in the wasps genome and is transmitted vertically between subsequent generations of parasitoid. It does not harm the wasp and it is transmitted to the wasps hosts (usually caterpillar). The virus does not replicate in the caterpillar, but alter it's physiology: supress immune response and metamorphosis and increases the amount of nutrients in caterpillars hemolymph.
Still, I have not found any references about this kind of virus altering the behaviour of the caterpillar after the emergence of wasps larvae.
[1] Whitfield, J. B. (1990). Parasitoids, Polydnaviruses and Endosymbiosis. Parasitology Today, 6(12), 381-384. (free PDF)

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Why use two stop UGA codons instead of one in the spike protein mRNA for the BioNTech/Pfizer SARS-CoV-2 vaccine?
Unlike the SARS-CoV-2 virus, the BioNTech/Pfizer SARS-CoV-2 vaccine has two stop UGA codons  at the end of the Spike protein:
          V   L   K   G   V   K   L   H   Y   T   s
Virus:   GUG CUC AAA GGA GUC AAA UUA CAU UAC ACA UAA
Vaccine: GUG CUG AAG GGC GUG AAA CUG CAC UAC ACA UGA UGA
          V   L   K   G   V   K   L   H   Y   T   s   s
               !   !   !   !     ! !   !          !

What is the motivation behind using two stop UGA codons instead of one in the BioNTech/Pfizer SARS-CoV-2 vaccine?

The two stop codons are obviously to prevent read-through of the termination codon.  Why this should be necessary is not clear to me, but the following may be relevant:

The synthetic mRNA differs from the natural mRNA in a particular respect that is easier to explain with reference to the transcript map of the virus, below.

The two ORFs 1a and 1b are translated directly from the virus RNA as polyproteins, which are subsequently cleaved, but the proteins at the 3′ side of the viral RNA are transcribed into a series of nested mRNAs, each starting from a different 5′ position immediately preceeding the gene that will be translated. These mRNAs also retain RNA corresponding to the remaining genes (coloured grey, and not translated because of the monocistronic translation of eukaryotic mRNA) and the common 3′ polyA tail. The synthetic mRNA for the spike protein (S) lacks the RNA for the non-translated genes, and has the polyA tail near to the stop codon. Hence the secondary structure near the stop codon in the synthetic mRNA may well differ from that in the natural mRNA and possibly influence the likelihood of readthrough.

The stop codons used in this artificial mRNA are not UGA but m1ΨGA, as U is replaced by m1Ψ (N1-Methylpseudouridine)* in the synthetic mRNA to prevent degradation. As the anticodon is recognized by a termination factor — not a tRNA anticodon — the interaction with m1ΨGA may possibly be poorer than for UGA.

Footnote
*The structural relationship between uridine, pseudouridine and N1-methylpseudouridine is shown below. The NH and CO involved in base-pairing are similar in each case.
In displaying the base in RNA sequences — where single characters are normally used to represent nucleotides — N1-methypseudouridine is generally represented as Ψ, rather than m1Ψ. However this is not necessary in other circumstances, and, because of the ambiguity it introduces, is highly discouraged.

As was observed (by others) under related q's here on material from that site, it seems Pfzier/BioNTech has done a global optimization to increase CG contents in the sequence, generally thought to be beneficial to mRNA expression (in addition to all the other things they've done, like U -> m1Ψ global substitution, specific to mRNA therapeutics).
That (global CG target) may also explain why they replaced UAA with UGA, even though the latter is actually a "worse" stop codon, in terms of allowing more read-through. As one paper (preprint) notes:

despite having the lowest efficiency of translation termination among the three, UGA is the most common stop codon in many multicellular eukaryotes. The relative frequencies of the three stop codons are dependent on multiple factors and strongly associated with regional variation in GC content. The frequency of UAA is strongly negatively correlated with GC content, while the use of UAG and particularly of UGA increases with increasing GC content.

Using two UGAs may be a way to compensate for this choice (of using the lowest efficiency stop codon).
Actually, one more complex theory is that the stop thing is actually a tetranucleotide:

In both bacteria and eukaryotes, the base immediately following the STOP codon (position +4, with the first nucleotide of the termination codon marked as +1) exerts the strongest influence on RT (readthrough) efficiency. This has led to the hypothesis that an actual translation termination signal consists of a tetranucleotide sequence, not only the STOP codon itself. Which tetranucleotide is the most efficient in eliciting the RT in eukaryotes remains controversial. [...]  For example, the level of basal UGA-C readthrough in mammalian cells (3–4%) was shown to be 3–6 times higher than for the remaining UGA-N tetranucleotides.

If we go by this, then UGAU is the stop tetranucleotide here, which is perhaps better than just UGA, especially if see that a C follows the 2nd UGA in the actual WHO doc, so that might have tripled (or more) the read-through chance if the UGA were not doubled before it:

ΨGA ΨGA CΨC ...

Aside: The CΨC begins... a "double UTR" (dUTR) as they call it (even though this one is composed of two different UTRs) for which there is a published paper that it is more efficient (in terms of stability etc.) than a single UTR. So, generally speaking, the doubled stop seems part of a strategy to "double everything" in that terminal region if it helps with translation efficiency.

Detailed Dissection and Critical Evaluation of the
Pfizer/BioNTech and Moderna mRNA Vaccines hypothesizes that it is a fail-safe against misreading (but maybe not a very good one (and the premise that m1Ψ leads to misreading may itself be incorrect)):

When nucleotide U in stop codons was replaced by Ψ, the rate of misreading of a stop codon by a near-cognate tRNAs increased [17]. Such readthrough events would not only decrease the number of immunogenic proteins, but also produce a longer protein of unknown fate with potentially deleterious effects.
…
Pfizer/BioNTech’s BNT162b2 mRNA features two consecutive UGA stop codons. Moderna’s mRNA-1273 uses all three different stop codons UGAUAAUAG.
…
One might think that the consecutive stop codons in the two vaccine mRNAs would offer a fail-safe mechanism
…
However, in many cases, misreading UGA stop codons in prokaryotes is associated with a +1 frameshift [81–84].
…
With such a +1 frameshifting, a downstream in-frame stop codon cannot serve as a fail-safe mechanism. UGA is a poor choice of a stop codon, and UGAU in Pfizer/BioNTech and Moderna mRNA vaccines could be even worse.

Thanks for sharing this interesting quote!

From my knowledge of frameshifting, the wider sequence context of the position of the shift seems to be the primary determinant. Hence I am highly dubious regarding this postulate of Xia. One imagines the developers of these vaccines analysed the products of translation of the artificial mRNAs very carefully. To suggest that they achieve the opposite of their presumed purpose seems rather naïve.

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Plant respiration produces carbon dioxide, so why are plants regarded as decreasing its atmospheric concentration?
In the absence of sunlight, plants give out the greenhouse gas, carbon dioxide. So why is it said that plants increase the concentration of atmospheric oxygen? Do they not increase the concentration of carbon dioxide and use the oxygen produced in photosynthesis.

Possible duplicate of Confusion regarding photosynthesis and respiration in plants

@tyersome that answer says "At night there is, of course, no photosynthesis and respiration will dominate and the plant will be a net producer of CO2 and a net consumer of O2." And I want to know if this is not a source of pollution.

possible duplicate of https://biology.stackexchange.com/questions/39253/how-long-can-a-plant-generate-oxygen-from-its-own-carbon-dioxide-produced-durin?rq=1

the plant grows and gains mass too, using $CO_2$.  I could be completely wrong, but perhaps during the growth phase a plant would photosynthesise more than it respires (because it’s gaining mass) which means there is a net loss in atmospheric $CO_2$ per plant.

Think! What are plants’ stems and leaves made of? Where does the carbon for that come from? So what is the net balance?

There are two factors here.  First is that you have to look at the plant's net production over time.  Say for instance (I'm just making up numbers here) that during the day the plant takes in 88 g of CO2 and uses photosynthesis to convert it to 64 g of O2 that's released into the air, and 24 g of C that is incorporated into the plant.  Then during the night it uses 12 g of the stored C for respiration (combining it with 44 g of O2 from the air), leaving a net daily production of 12 g C that goes into plant growth, and 44 g of O2 in the air.
Second problem is perhaps better classed as either linguistic confusion (to be polite) or ignorance.  CO2 is not "pollution": it is a normal part - more accurately, a fundamental part - of the carbon cycle https://earthobservatory.nasa.gov/features/CarbonCycle on which almost all life depends.  The problem is not plants (or animals) releasing CO2: it's humans digging up lots of fossil carbon and burning it, thus increasing atmospheric CO2 concentrations beyond the levels to which the ecosystem has adapted.
Now that you've changed the question, it's even more important to read the basic description of the carbon cycle at the link.  (Honestly, wasn't this covered in your high school biology class?)  Again, the bottom line is that plants produce a net surplus of O2, which animals consume along with the plants, so that the cycle remains balanced.

The tag you used on the question shows you know about photosynthesis, but it seems you don't fully recognize its significance.  Yes, plants use oxygen and release CO2 all the time for energy use, but they absorb much more CO2 (and release much more O2) while storing energy during the daytime than that 24-hour energy usage undoes.
While plants release CO2 as well as absorb it, they do much more of the latter.  By one scientific estimate, of all the the CO2 plants remove for photosynthesis, they release 40% of it back into the atmosphere.  But that means that 60% of that CO2 absorption is never released back into the atmosphere by the plants.  So, overall, the net change is that plants remove CO2 from the atmosphere (unlike animal metabolism and combustion which only add CO2 and remove none).
All those plant stems, branches, and trunks you can see are built out of CO2 that the plant will never release back into the atmosphere.  The only CO2 the plants release is CO2 that they previously absorbed from the atmosphere.

Do they not increase the CO2 proportion?

No, because the CO2 they emit came from the atmosphere to begin with.  And the carbon they don't release as CO2 stays as carbon compounds that make up the plant.
The issue with CO2 is not plants taking CO2 from the air and re-releasing it.  That doesn't cause a steady increase in atmospheric CO2.
Taking CO2 that has been sequestered in the ground for hundreds of millions of years and adding it all to the atmosphere in a geologic eyeblink of time, that's a problem.

Plants start to grow first, from tiny size (from seed in higher plants), and from there, any size in later stages they achieve to have, they achieve it only by first absorbing all the Carbon they need, from air first.
So huge part of plant's later dried weight is actually made from carbon. And all that carbon was incorporated into it's body through continuous photosynthesis - so it was "sucked" from CO2 in the air around the growing plant.
Importantly:
Unlike us, plant can not normally absorb carbohydrates (sugars, fat etc - we eat them, plants don't) in order to use them for metabolism and respiration (ie breathing). For this they can use only carbohydrates they themselves already created first from CO2, through photosynthesis.
Even when they can not use photosynthesis anymore (because of age or in the dark) - they use for respiration only that carbon which they stored in the body before by catching it from air.
And as long as the plant continues to grow and have access to any light it continues to absorb much more CO2 than it releases through respiration. So in balance it keeps absorbing CO2 and releasing oxygen in net balance.
As an mental exercise: It would be different if You would take, let say same house pot plant and place it into a completely dark room for a long time. That plant there is without light, while it already has body which it created previously through photosynthesis, it now can not capture any light and any carbon any more, yet it would still need to be continually breathing. So as this particular plant in the dark, have no source of energy for photosynthesis, and it still is breathing, so in this particular case it would produce CO2.
Practically something resembling such theoretical example happens with significance only, when we store plant body-parts like fruits and vegetables (or potatoes) for a long time. Fruits, vegetables and potatoes (often stored in the dark) breath and not photosynthesize.
The cycles between a day and night are also bringing plants for short time into the dark and as such they have negative balance (net producing CO2) for a short while, but it is insignificant from the whole day perspective (overal they consume much more CO2 than they produce it)
Interestingly, there also exist very rare species of parasitic plants (they are parasites of other plants) which are not having their own photosynthesis - in this case they have no chlorophyll and suck sugars out of other plants - and yes, they only breath and yes, they only produce CO2, so they would be probably the only plants which are net producers of carbon dioxide.

Welcome to Biology.SE! Your answer is helpful, but it is much more likely to receive a favorable response if you edit it to include supporting references (primary literature is best though probably not needed for a question at this level). ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thanks!

Thank You. I saw quite nice answers already, so I just took it easy and and thought about possible weaknesses in them to relay the message and tried reiterating from different point of view, which would help to absorb it. So, I just didn't thing about sources, as You sad, it feels kind of very basic. But I will try next time.


text:
Genetic variance for a behavioural trait among human populations
From this article from The Guardian:

We instinctively assume that differences in behaviour that are in fact due to culture must be linked to – even caused by – characteristics of appearance. That is what the traditional notion of race is all about. But genetics has found no such innate origins of behavioural differences between “races” – and it is highly unlikely, given what we know about genetic variation, that it would. (my emphasis)

Because the term "race" is so poorly defined and because this categorization has been and still is an immensely important source of hate and discrimination, I will use the term "human populations" (despite the term being at least as vague). The fact that the term categorization into "races" does not make in any way a good representation of the partitioning of the genetic variance in human populations (e.g. see this post) is irrelevant to our discussion.
Are there any study who investigate the partitioning of genetic variance for a behavioural trait (e.g. drug dislike, aggressiveness, agreeableness, openness, reading performance, etc...) among "human populations" (defined one way or another)? Did they find a significant correlation? What is their correlation coefficient?

The article I refer to says

We instinctively assume that differences in behaviour that are in fact due to culture must be linked to – even caused by – characteristics of appearance.

In no way, do I expect that the phenotypic variation used to define races could "cause" much of an eventual genetic structure for a behavioural trait. I know it is a politically sensitive topic. Let's raise above it and discuss the evidence.
Estimating partitioning of genetic variance
If need be, see this post for a definition of heritability.
I realize that estimating the partitioning of genetic variance is a difficult endeavour and can easily be confounded with other sources of phenotypic variance such as the ones caused by social and educative systems. Any article that does its best to estimate a correlation coefficient between a behavioural trait and "races" is welcome.
Behaviour
Of course, the term "behaviour" is not perfectly defined. This has never prevented us from massively using this concept in biology and I don't think it should prevent us from using this vague categorization of phenotypes to answer the current question.
What behaviour am I interested in? ... pretty much anything that one might want to call behaviour. I am not particularly interested in behavioural differences that might be directly cause by a difference in the prevalence of a specific disease.
In the book IQ and the Wealth of Nations, Lynn and Vanhanen attempts measures of IQ among countries. These methodology has been highly criticized. I double that IQ could be considered as a behaviour but, while I would welcome anyone to include such work in an answer (along side its criticisms on their methodology; e.g. Witcherts et al., 2010; see also Rindermann 2007), I would rather like to focus on evidence that are not directly focused on IQ. I am fine with evidence that are on behavioural traits that somehow relate to our intuitive notion of intelligence (e.g. reading performance, spatial abilities, ...). This answer in the post Genes and Intelligence is very relevant and lists three articles that looks for loci that explain some variance in IQ.

Obviously, this is a politically risky topic.  It might be safer to approach it from a perspective on dog breeds.   It should be possible to model evolutionary mechanisms that might cause genetic linkages between physical and behavioral phenotypes to emerge.

Is there any evidence that (outside of a few pathologies) there is any genetic component to behavior?

My understanding was that variation within the so called races of humans was much larger than that among the "races". I'm also sure that I've read that there is more genetic diversity among "Africans" than among the rest of the worlds peoples. To me that suggests this question isn't actually scientifically based since it presupposes that the culturally based (i.e "made up") category of race has a genetic basis. See for example this Scientific American article.

@jamesqf Thanks for your comment. I tried to address it by extending the long follow-up to my question. Let me know if you think my question is unclear.

@tyersome Thanks for your comment. To me that suggests this question isn't actually scientifically based since it presupposes that the culturally based (i.e "made up") category of race has a genetic basis. I think we can all agree that there is some genetic structure for skin color and hair straightness among Nigerians and Japanese. I do not want to state that such phenotypic variation have been more important that cultural differences in defining races but the existence of some non-zero (yet eventually very small) genetic structure exists.

@tyersome I do not state either that races are in any way a fair partitioning of the existing genetic structure in humans (I have now added a link to a post that discuss the impressive genetic diversity among modern day Africans compared to the rest of the world). I am asking whether any such structure has been investigated for a behavioural trait. If you still think my question isn't scientifically based, please let me know why and how I can improve it. Thank you

I guess the problem I have with this is that "race" is known to not be a valid categorization. Consequently it seems to me that any question based on "race" is inherently problematic. There are genetic factors that control traits like skin color and hair curliness, but there are also genetic factors that control ear lobe attachment — you could define ear-races based on that, but it also wouldn't be meaningful. It isn't clear to me how to fix this problem — maybe you could substitute "human populations" for "races in humans"?

@tyersome I rewrote the post using the term "human population" instead of "race". It allowed me also to shorten the post as I don't have to clarify that I understand how meaningless the concept of race is in explaining the partitioning of genetic variance among humans. Thanks


text:
We know that the hepatitis C virus can live on surfaces for at least six weeks. Maybe longer. The infectivity study ended after just six weeks; why?
Background
A paper has found that the hepatitis C virus (HCV) can remain infective for at least six weeks on ordinary household surfaces. You can see the free full text, or a summary for busy clinicians.
Elsewhere, Brian Krause has added:
"They tested their samples for (up to) 6 weeks.  At the time of the 6th week they still found infectious virus.  They did not test samples beyond 6 weeks, so they can't say anything about infection past that time."
My question
So, at six weeks, they saw that the virus was still infective. Why might they have ended the study right away instead of continuing it for a few more months?

I removed the postscript as it had nothing to do with the question. If you pose a question it will stand alone and people will answer it or ignore it as and in the way they think fit. If they have the reputation and think the question is subjective in a way that does not fit with SE Biology they will vote to close regardless.  I would vote to close this question as of little general interest, but am happy to leave it to die of neglect.

They ran out of samples
Their test is destructive, they can't test the same sample twice. They planned out a number of samples to test for each time period and tested them. At the end of six weeks, they were done.
It doesn't really matter
The point of the paper is that HCV is infectious long-term on surfaces when not cleaned properly, indicating there is a risk of fomite transmission long after an infected patient leaves the area.
They also show that if surfaces are cleaned, the virus is killed effectively. The authors are not advocating to quarantine a hospital room until any residual HCV dies from air exposure, they are advocating being sure to appropriately clean hospital surfaces to prevent potential disease.
It isn't typical (in fact, it is impossible) for a single scientific study to answer all open questions in one shot. If someone wants to put an upper bound on the duration that HCV remains infectious in the world they can do a new study with longer time points.


text:
During starvation, does the human body do anything to prioritize which organs receive nutrients?
When food is scarce, the body slows its metabolic rate to conserve energy. Are there any other systems or processes that prioritize which organs receive nutrients?

Glucose is prioritized for the brain and erythrocytes over the muscle and adipose tissue, for example, by hormonal control.
The hormones insulin and glucagon respond to strarvation, insulin secretion falling and that of glucagon increasing. The glucose transporter, GLUT4, in muscle and adipose tissue is dependent on insulin, so that in starvation less-essential uptake of glucose to these tissues declines. The glucose transporters of erythrocytes and brain (e.g. GLUT1) do not depend on insulin, so the supply of glucose to these tissues, which absolutely require it, is not cut off.
References

Hormones and Starvation: http://www.ncbi.nlm.nih.gov/books/NBK22414/
Insulin and the GLUT4 Glucose Transporter: https://en.wikipedia.org/wiki/GLUT4
GLUT1, insulin-independent Glucose Transporter: https://en.wikipedia.org/wiki/GLUT1

Could you add some references and good sources for additional further/reading?

Done. Let me know if you think any further clarification is needed.

The switch from glucose to ketone bodies as the principal blood metabolite accompanies starvation. This prioritizes the heart, which preferentially uses ketone bodies as a fuel (update; actually it's fatty acids, but they're metabolically similar.) This de-prioritizes the brain, which preferentially uses glucose.
[edit]
I was asked for a source. This is definitely in Voet, Voet & Pratt's Fundamentals of Biochemistry, but I vouch for Wikipedia's description.

Welcome to Biology SE!  This is a great answer, but perhaps you could include a reference? (I learned this also in undergrad, but citations are always helpful.)

The glycogen in the liver begins providing blood glucose. Muscle glycogen is used as fuel by the muscles, fat cells (adipose tissue) release fatty acids to manufacture ketone bodies in the liver and to be used by the brain as fuel, and body proteins are converted to glucose.
In short, the body's metabolism shifts to catabolic reactions.
If this continues for too long, you begin to see effects of starvation:

Inadequate tear production
Enlarged/tender liver
Muscle atrophy
Rashes, sores, or peeling skin

In short, deficiencies of energy, protein, iron, and zinc can really mess you up in the long term.

Are you sure this is right: "ketone bodies in the liver and to be used by the brain as fuel".  If I recall correctly the human brain uses glucose as fuel.

Could you add some references and good sources for additional further/reading?

@GabrielFair yes, brain is dependent on glucose and requires some amount of it, but it can get some portion of energy from metabolism of ketone bodies as well, you can see: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874681/  or https://en.wikipedia.org/wiki/Ketone_bodies#Uses_in_the_heart.2C_brain_and_muscle_.28but_not_the_liver.29

The brain is the most metabolically active organ and will sacrifice the body for fuel.
starvation is characterised by the catabolism of muscle tissue for gluconeogenesis, and the provision of glucose and amino acids for fuel.
Before this occurs, the liver, when glycogen depleted, will switch from creating glucose, to creating ketone bodies from fatty acids. Ketosis is not starvation.
Ketones are eventually preserved for the brain, heart and lungs, whereas the rest of the body can utilise fatty acids, while certain glucose-dependent organs such as the kidneys will still utilise glucose.
Starvation will only occur when there are no free fatty acids to convert to ketone bodies, and the sacrifice of muscle tissue will begin.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
How do insects know what is edible?
What is the current scientific consensus on how insects innately know what is food and not food? If they are introduced to new food sources do they experiment with eating the new food? Could you teach a preying mantis to eat beef?

I think these are too many questions in one.

Insect feeding behaviour is generally triggered by one or more conditions which may include colour, shape, chemical traces or temperature.
Insects generally locate food based on some combination of olfactory, thermal and visual queues (colour and shape). If their minimum criteria are met to specified tolerance, they will attempt to feed on whatever is nearby using their usual feeding method.
When these conditions appear on the 'wrong' target, it attracts insects and triggers feeding attempts. Insects can be triggered to feed on atypical food sources if the relevant aspects of their environment match those of their normal feeding environments. For example, here is a report from a professor of entomology recollecting his observations of being bitten by pea aphids while handling plants, which he assumes is because of the scent on his hands.
We can exploit this in various ways for research. One is for artificial blood-feeding of insects: most systems, like the Hemotek membrane feeding system, warm blood to the body temperature of the host. They do not normally resemble a target host in any other way. Some blood-feeding insects have very specific requirements for temperature (for example they will only feed on blood if it is heated to the body temperature of birds; the same blood heated to mammalian body temperature will be ignored) but we do not need to make the target look or smell like the natural host. Other species may need olfactory cues, which can be provided by researchers rubbing the membranes on their forearms before placing them on the feeding system, or by breathing on cages as you add the food.
A second way we exploit this is for insect traps. Although not all traps work this way, some work by mimicking the host and attracting insects that are looking for a meal. This can be via olfactory/chemical mimicry (for example carbon dioxide baited traps - try Googling "CO2-baited traps") or visual. Different degrees of visual 'deception' may be needed; for instance to attract tsetse flies, colour is important but shape is not:

[tsetse traps] often use electric blue cloth, since this color attracts the
  flies. Early traps mimicked the form of cattle but this seems
  unnecessary

(https://en.wikipedia.org/wiki/Tsetse_fly#Trapping)
The exact reason why blue is so attractive to tsetse is unclear:

But, why are tsetse flies attracted to blue and black colors? What is
  the evolutionary advantage for them? It has been hypothesized that
  certain areas on humans, where tsetse like to bite, are a darker
  shade. Or, that the dark color simply identifies the object as not
  plants.

(https://www.acsh.org/news/2016/11/28/do-dark-colors-really-attract-tsetse-flies-10471)
If such behaviour increases the fitness of the insects, there is a selective pressure to change the cues used to identify situations where feeding behaviour is appropriate, which may result in consistent feeding shifts. We can infer by comparing insect taxonomy and feeding modes when shifts in diet have occurred. For instance, the moth family Calpinae has evolved piercing mouthparts to feed on fruit, but species in the genus Calyptra ('vampire moths') have adapted to feed on blood (which generally moths cannot access because their mouthparts cannot pierce the skin).

Maybe some interesting reading here:
https://www.ncbi.nlm.nih.gov/pubmed/27210550
"dopaminergic neurons (DANs) play a critical role in reinforcement and motivation"
"Olfactory learning in Drosophila could provide an inroad. Flies assign negative and positive values to odors in aversive and reward based paradigms"
Also
https://www.ncbi.nlm.nih.gov/pubmed/28334410


text:
How can I determine the sex of a tree seedling?
I would like to plant some home grown female mulberry trees in a circle, with a male plant in the center for pollination. How do I determine the gender of a tree seedling? I know it's possible, because I've seen mulberry trees labeled as 'male or 'female' at nurseries. Do I need special equipment?
I've seen the related question: Can you tell the sex of a white willow when it's not flowering?

There is absolutely no way to tell to be honest because mulberry trees have the capability of changing sex (reference). From a paper titled "Diversification of mulberry (Morus indica var. S36), a vegetatively propagated tree species", I quote

The sex expression of plants appears to be a function of hormonal
  control; there seems to be evidence that dioeciously plants (male and
  female reproductive organs on separate plants) are potentially
  bisexual and that a delicate internal hormonal balance results in one
  sex "over-riding" the other. A traumatic incident might, therefore,
  act by temporarily upsetting this balance, which is later restored in
  a way that leads to the opposite sexual character being manifested.
  Another pointer in this direction is the fact that a variety of
  artificially applied chemical substances has been shown to affect the
  sexual expression of a significant number of different plants. It is
  also reported that some chemicals known as the steroid hormones might
  be a major key to the sex expression lock. Thus, it is
  possible that to "create" a new sex in a plant by either a physical
  shock or a controlled chemical process

They could also have male and female flowers (monoecious) on one plant with most of them being self pollinating (references).
So, in effect, nurseries that are advertising these trees by sex are ignorant or quite plainly taking people for a ride. I would suggest that you plant your seeds and don't worry about it too much since they have the ability to self pollinate. If by bad luck, you find them all male/female or are not pollinating to your liking, go for a tree sex change after consulting an expert on the topic. Here is a basic guide to identifying between male and female trees/branches (reference)

White mulberry male flowers (reference)

red mulberry female flowers (reference)

Funny... I ran across both of those photos while researching.

@jmusser well u know I did my research as well then..


text:
Evolution of the energy generating system in mitochondria
Both yeast and humans have mitochondria. Given that yeast have a much shorter time between generation I would expect evolution to have had more time to optimize mitochondria of yeast.
The main function of mitochondria in yeast is essentially similar to that in human cells.
Is their efficiency roughly the same or did the stronger evolutionary pressure allow yeast to evolve much better mitochondria? Is there empirical research about mitochondria that studies the difference between the mitochondria of different species that includes metrics of their efficiency?

Please express your concept of efficiency in precise chemical/thermodynamical terms. Without this your question is unclear and is likely to be removed as such. I would be interested what examples you can cite in support of your apparent assumption that generation time favours yeast evolution over that of man. Enzymes with greater turnover numbers, for example?

@David : I don't believe that it makes sense to specify a specific way to measure efficiency in a question like this. If someone did research into this question they chose their own metric. Formulating this question in a way that rules out particular metrics makes no sense.

@David : The idea that evolution is a process that's faster then time between generation was a basic idea I learned in my bioinformatics classes in university. I don't see why it should have be justified in order to ask a question.

If you don't define your terms we can't discuss your question sensibly. I have suggested a particular form of efficiency, which is not restricted to mitochondria, enzyme turnover number. You could define it as ATP produced per pyruvate molecule and I can answer that. 2. My immediate response is that I don't necessarily buy this "basic idea". I might argue that the time for evolution of mammals has been sufficient to "optimize" their mitochondria. Therefore you need to formulate the idea precisely, citing a reference in support, if possible, in order to rebut this default counter-argument.

If you have numbers about enzyme turnover numbers or about ATP produced per pyruvate molecule to argue that the time for the evolution of mammals has been sufficient to optimize their mitochandria I am happy to hear that argument as an answer to my questions.

Before I provide a sort of answer to this question, could you indicate what you know about mitochondria? Do you know what their prime function is and its biochemistry? Do you know how they are believed to have originated?

Yes, I do have taken a biochemistry courses in my bioinformatics studies.

ANSWER SUMMARY
The criterion of efficiency of mitochondria is taken as the yield of ATP per carbohydrate molecule oxidized using the electron transport chain and oxidative phosphorylation. Experimental values for this are similar for yeast and humans, whereas theoretical values derived from differences in the structures of the ATP synthases actually imply a higher yield for mammalian mitochondria.
It is argued that it is not surprising that the difference in generation times did not produce the result expected by the poster. First, the period after the separation of eukaryotes from prokaryotes is no longer than the period between the origin of eukaryotes and that of the aerobic bacteria from which their mitochondria arose. Second, the stage would have been reached when there were mechanistic limitations on further increases in efficiency of this complex system. If the differences between mammalian and yeast bacterial ATP synthases is real (and an even ‘worse’ yield for bacteria, that have an even shorter generation time), this suggests that the main evolutionary pressure on this system varies between organisms, rather than being simply to maximize the yield of ATP.
ANSWER ELABORATION
Criterion of efficiency
The main function of mitochondria is to use molecular oxygen to oxidize NADH and FADH2 via the electron transport chain and oxidative phosphorylation to produce ATP. A suitable and generally accepted measure of efficiency — reminiscent of that applied to man-made mechanical devices — would be the percentage of the energy of this oxidation that is converted to ATP (rather than being released as heat). Any reader not familiar with the biochemistry of this system is advised to read the footnote* before proceeding further.
Is there any difference?
The traditional way in which the yield of ATP in oxidative phosphorylation has been measured is by the P/O ratio (the ratio of ATP produced to oxygen consumed). Results obtained over the years have varied becauase of technical problems — see review by Hinkle (2005). As summarized more recently (2010) by SJ Ferguson,  the historical controversy was not about differences between species — they were no indications of differences even between bacteria (the precursors of mitochondria, performing oxidative phosphorylation in their intermembrane space) — but merely about the true value of the P/O ratio.
As Ferguson goes on to say, the gradual elucidation of the structure of the ATP synthase and the elucidation of its mechanism led to a believe that deductions from this were a more reliable indication of the stoichiometry than the experimental measurements. Specifically, a 360˚ rotation of the F0 component of the ATP synthase could be seen to result in the synthesis of one molecule of ATP, and that this required on hydrogen ion bound to each of its c subunits (see diagram from Wikipedia article, below).

He describes the results with yeast as follows:

X-ray crystallography of yeast ATP synthase revealed a ring of c subunits attached to F1 even in the absence of other subunits of the F0 sector (9). This work not only suggested that a and b were not interdigitated with c but also revealed the surprising stoichiometry of c10. The C-terminal helix of the hairpin c subunit is at the outside of the ring and contains an essential aspartate or glutamate residue. This residue is believed to pick up an H+ and rotate away from an interaction with the α subunit. Thus, 10 protons should drive a 360° rotation of the c ring, which is structurally connected to γ, giving synthesis of 3 ATPs as γ rotates through 360° within F1; the H+/ATP ratio would be 10/3 = 3.3. The P/O ratio for NADH would be 10/(3.3 + 1) = 10/4.3 ≈ 2.3, thus moving below the range of values directly determined.

It was assumed that ATP synthases other than yeast would also have 10 c subunits, but, surprisingly, although bacterial ATP synthases also have 10 subunits, the bovine (and other vertebrate) one has only 8, suggesting a higher P/O ratio than yeast — greater, not poorer, efficiency.
Mitochondrial evolution in context
Whatever the actual P/O ratios in different aerobes, the more rapidly-dividing species do not show a clear increase in efficiency in this respect. I suggest that in this respect the evolutionary timescale shown below (adapted from The Cell: A Molecular Approach) should be considered.

What is clear is that the time for an improvement in efficiency of energy production to occur between the divergence of yeast and animals (A) is much less than that between the time at which mitochondria were acquired from bacteria by the first aerobic eukaryote (B–A). Note also the long period the system had to evolve in the aerobic bacterium that gave rise to mitochondria (C–B). My argument is that by the time of appearance of mitochondria, the system had time to evolve to the optimum that mechanistic considerations would allow. Otherwise one would have expected those bacteria to further evolve a system much superior to yeast or mammals in the C–B timescale.
Other aspects of the evolution of the mitochondrial energy generating system
It should be noted that there have been changes in the mitochondrial energy generating system over evolutionary time. For example, in the cytochrome oxidase system the same set of core subunits are found in prokaryotes and eukaryotes. However additional subunits have been acquired in primates. Rather than being concerned with the catalytic efficiency of the system, these additional subunits are thought to be concerned with regulation.
Better systems to study the effect of division time on evolution of eukaryotic ‘efficiency’?
Because mitochondria had probably reached optimal mechanistic efficiency in energy generation when they were acquired, they do not appear to be a good choice for studies of the type the poster envisages. Perhaps he might do better with something related to nuclei, which are not present in bacteria. However there are problems of interpretation. For example, if it were found  that some aspect of the DNA replication machinery in yeast allowed this process to proceed faster than that in mammals, could one conclude that this was due to the shorter generation time of yeast? No! One could equally argue (and it would seem to me more likely) that the lower generation time resulted from an evolutionary pressure for faster DNA replication, a pressure that does not exist in the more slowly dividing mammals.
FOOTNOTE *
ATP in mitochondria (and the inner membrane of aerobic bacteria) is synthesized from ADP using the free energy released by the oxidation of the reduced cofactors, NADH and FADH2 (produced from the oxidation of particular carbohydrates), by molecular oxygen. The mechanism of this, rather than involving simple coupled chemical reactions, involves the movement of hydrogen ions across a membrane in which there is a concentration gradient (strictly through a proton motive force, to which membrane charge also contributes) using an ATP synthase, a molecular machine, the structure of which clearly indicates the stoichiometry of input hydrogen ions to ATP synthesized. The hydrogen ion gradient results from three stages in the electron transport chain (complexes I, III and IV) where a hydrogen ion is translocated into the inner mitochondrial intermembrane space. This is described in standard text books of biochemistry such as Berg et al..

How do you know that perfection was reached back then? It's an empiric question and you aren't refering to any empirical work that made any attempts at measuring.

@Christian — OK. I had assumed a little greater knowledge about the ETC. I'll add a footnote in a day or two explaining things in detail. While waiting for the coup de grace you might do something to clarify your question (or your mind). How about an evolutionary diagram with a time scale showing 1. The time between the origin of life and the origin of aerobic bacteria. 2. The time between the origin of aerobic bacteria and the origin of eukaryotes with mitochondria. 3. When  short-generation time eukaryotes, such as yeast diverged from longer-generation ones that gave rise to mammals.

My question is pretty clear. I want actual empirical evidence about the differences between mitochondria of different taxons. Given that this doesn't seems to be clear enough (I'm used for Skeptics.stackexchange, that empiric evidence is a default for a decent answer), I added the desire for empiric evidence explicitly. You haven't provided any empirical evidence but only argued that you don't think that any difference exist based on theoretical arguments.

@Christian — The wait is over. I have completely rewritten my answer following the discovery of the data about the number of c subunits in yeast and bovine. The two-page Ferguson review is a must-read in relation to this.


text:
What distinguishes "coding" from "noncoding" DNA?
I've been reading a bit about "junk DNA" and how much of our genome consists of this "non coding DNA" in comparison to "coding DNA".
I'm just an interested layperson but I thought all combinations of three base pairs encoded one amino acid, with some amino acids being encoded by more than one combination of base pairs.
But if that were true then all of our DNA would encode something.
Or if only a tiny percentage of our DNA is "coding" that would mean that the vast majority of possible combinations of three base pairs don't represent any amino acid.
Or it could mean that there are a small number of "meaningless" combinations of three base pairs, but that those combinations are vastly overrepresented in our genome.
Which is correct? What am I missing?

Would anyone like to add junk-dna and/or noncoding-dna (or should that be non-coding-dna tags? I barely have enough rep here to breathe (-:

Wikipedia has a well-written page on the genetic code with tables and pictures showing all the possible triplets and their meaning!

@Hippietrail To the meta!!!!

You are correct in thinking that any sequence of bases corresponds, via the genetic code, to a sequence of amino acids. However not all stretches of DNA are actually transcribed into mRNA for translation into proteins. For this to happen the stretch of DNA requires (DNA-encoded) elements to promote and regulate the transcription and translation processes, and this, very broadly, is what defines a gene: a segment of DNA which has the required components to direct the synthesis of a protein (or in some cases an RNA that will not be translated into a protein). The segments of DNA that correspond to mRNA for proteins and to other RNA molecules are referred to as coding sequences.
Now, I've omitted lots of details here: some genes encode RNA molecules, such as ribosomal RNAs, which are not translated into proteins; eukaryotic genes include stretches of sequence (called introns) that are spliced out of the transcript before the mRNA>protein step. The original definition (if there ever was a definition) of "junk" DNA included these introns, as well as regions of DNA lying outside the coding sequences. We now know that there is useful information stored in much of this DNA, even though it doesn't code for anything directly via the genetic code.

Hmm @DanielStandage 's answer got more votes but AlanBoyd your answer here answers my actual question. Both answers are full of interesting stuff but this is the one I'm accepting.

What "useful information" it could be?

You bring up a good point. "Coding" is a term that obviously carries some historical baggage that is gradually becoming less and less relevant. "Coding DNA" has typically been used to refer to DNA that encodes one or more functional protein products, which are constructed from an mRNA intermediate. As we've been learning over the last several years (and as was confirmed by the recent release of 30+ coordinated, high-profile publications from the ENCODE project), DNA that is not "coding DNA" is not "junk" or "meaningless"--it simply does not, to our knowledge, encode a protein. There is still a lot to learn about what precisely the function and purpose of this DNA is, but we do know that a lot of it is transcribed into RNA and that a lot of it has been associated with human disease.

Yes I put "junk" in scare quotes precisely because it's not really junk. So while I knew it wasn't junk I wanted to know a bit more deeply what non-coding DNA is. It seems that the terms "coding" etc are ambiguous if my understanding is right.

@hippietrail Agreed. A lot of what is sometimes called "non-coding DNA" indeed encodes something...just not a protein! We're definitely going to have to revisit our terminology as a community, but that is a slooooow process. Case in point: "junk DNA" is still commonly used. :-/

Coding is a term with a clear meaning in relation to DNA. It implies that that DNA encodes a protein (via mRNA). This is not historical "baggage", it is historical usage. Non-coding does not imply non-functional, nor did it historically, when all that was known was the genomes of bacteria. Promoters? Origins of replication? A misleading answer.

DNA regions coding for proteins and RNA's comprise a rather small portion  of total eucaryotic DNA.They are associated with special upstream signal sequences
(promoters,enchancers,"boxes"etc) translation initiation triplets  and translation termination  signals ,which all together establish a reading frame
provide information for  the formation of the translation complex and the regulation of the whole translation process.
Non coding DNA is by no means junk just because  we do not understand it well enough yet.However it is known to play important roles in the formation of chromatin structure and its transformations which are crucial for exposing /hiding  genes and their regulatory sequences to the proteins and cofactors
working on them.They are characterized by large amounts of repetitive sequences and may also contain silenced ancient genes .

It is better to add a citations to further cement your claims in your answer.


text:
How many genes can be knocked down at the same time
In mice, gene knockdown is a useful technique for deactivating individual genes to study their function. In practice what is the maximum number of genes that can be knocked out at the same time?

I think this question needs clarifications / constraints. Assuming we're talking about mouse knockouts, are you interested in the technical limitations of creating knockouts, or are you asking about the biological limitations of KO mice (i.e. a minimal mouse genome)? Must that mouse live a full mouse life? Should that mouse be able to make more mice?

My interpretation was that he is asking about transient reduction of expression (e.g. antisense oligos) rather than genomic knockouts.

My confusion is the discrepancy between the title (knock down) and the text of the question (knock out), though I think my initial comment stands in either case.

Potentially many if you knock down a transcription factor that up-regulates genes. There is a nice database that contains information on the effects of knock downs of transcription factors on gene expression: KnockTFv2

As the OP asked about mice, I am mostly going to talk about organism-level things here.
First of all it is important to distinguish between knock-down and knock-out. Knock-out is where a gene is either removed or made non-functional and as such will never be able to be turned on again. This may in some cases be compensated for by having heterozygous animals, where one allele contains the normal gene and the other allele the non-functional, so that normal expression from the normal allele is enough to produce a normal animal. The heterozygous animals are then mated to produce homozygous (both alleles removed) knock-out progeny.
Knock-down on the other hand is either a transient reduction in expression (mostly done in cells, I don't think there are any methods for this that are viable at the whole mouse sort of level) or a conditional knock-out where expression of the gene is made conditional on a treatment, whereby you remove the treatment and the gene stops expressing. For example you can make a transgenic mouse with a tetracycline dependent promoter for expression (or not) of the transgene (Tet-On/Tet-Off). Knock-down in the strictest sense is only a reduction in the level of expression and may not be complete removal of the expression, which may result in viable cells through residual expression where a knock-out, with complete removal, might not.
However, back to the question at hand:
The answer to this is a rather unsurprising it depends on the genes being knocked down
Knockdown a single gene essential for cellular function such as something in a major metabolic pathway, and cells just won't function, so cells and animals will be non-viable. Knock-out or knock-down of non-essential genes and animals may survive, but also may not. As far as I know at this point in time we have no way of knowing whether knock-down or knock-out of something will result in viable progeny other than experimentation.

Why the downvote? - please let me know how I can improve my answer.


text:
The GUG start codon in E. coli: identity of initiating tRNA and efficiency of translation
Translation in E. coli is usually initiated at an AUG codon, which encodes the amino acid methionine. In some cases, however, the start codon is GUG, which normally encodes valine. If GUG is used as the start codon, is a tRNA charged with methionine used or one charged with valine, and does the use of GUG as a start codon affect the efficiency of translation?

Below I think is the most extensive study so far quantitatively comparing all codons as a possible initiation codon in E. coli for sfGFP and Nano-Ogra-luc ("Nanoluc") proteins (published in 2016): "Measurements of translation initiation from all 64 codons in E. coli"
Ariel Hecht, Jeff Glasgow, Paul R. Jaschke, Lukmaan Bawazer, Matthew S. Munson, Jennifer Cochran, Drew Endy, Marc Salit https://doi.org/10.1101/063800
https://doi.org/10.1093/nar/gkx070

There are two substantially different questions here. As this was posted 7 years ago (before I was involved) there may be little to be done. It would be better if they could be separated, and certainly others should be discouraged from doing likewise.

The NCBI translation table translates all alternative start sites as methionines. To my understanding, all translation is initiated by the fMet-tRNA. I don't know if there are any exceptions to this rule.
Regarding translation efficiency, I only found a 1985 paper in PNAS (Reddy et al, PNAS 82:5656-60), in which they compared the translation efficiency of adenilate cyclase's own UUG start vs GUG or AUG, obtaining a translation ratio 1:2:6 UUG:GUG:AUG, suggesting that AUG is the most efficient one, followed by GUG. Also, Romero and Garcia, FEMS microbiology letters 84:325-330 (1991) compared the efficiency of AUG vs AUC, AUA and AUU, showing a much lower efficiency for those codons, but they did not compare it to GUG.


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Why is hydrofluoric acid so dangerous if it is a weak acid?
I've read that hydrofluoric acid (HF) is extremely dangerous to touch, but what exactly makes it so toxic? It's a weak acid ($K_a = 7.2 \times 10^{–4}$) and dissociates approximately 1/1000 as much as hydrochloric acid does in water, so why is it so much more dangerous? Wouldn't a stronger acid cause more damage? What exactly happens when human skin comes into contact with hydrofluoric acid that causes it to get so badly damaged?

Acidity is not the only dangerous effect a compound can have, fluorine will oxidize almost anything, including oxides. it is highly poisonous to nearly all biological systems.

@John But HF will dissociate into fluoride, not fluorine, surely?

The confusion arises from the term weak, which has only to be interpreted in chemical terms.
Weak acid, as you say, just means that the acid does not readily dissociate, not that its effects are weak! Just to say one, HF corrodes glass, something that not even smoking HCl does.
Wikipedia has a nice summary of HF toxicity (see also the references in the article itself):

Hydrofluoric acid is a highly corrosive liquid and is a contact poison. It should be handled with extreme care, beyond that accorded to other mineral acids. Owing to its low dissociation constant, HF as a neutral lipid-soluble molecule penetrates tissue more rapidly than typical mineral acids. Because of the ability of hydrofluoric acid to penetrate tissue, poisoning can occur readily through exposure of skin or eyes, or when inhaled or swallowed. Symptoms of exposure to hydrofluoric acid may not be immediately evident. HF interferes with nerve function, meaning that burns may not initially be painful. Accidental exposures can go unnoticed, delaying treatment and increasing the extent and seriousness of the injury.
  Once absorbed into blood through the skin, it reacts with blood calcium and may cause cardiac arrest. Burns with areas larger than 25 square inches (160 cm2) have the potential to cause serious systemic toxicity from interference with blood and tissue calcium levels. In the body, hydrofluoric acid reacts with the ubiquitous biologically important ions Ca2+ and Mg2+. Formation of insoluble calcium fluoride is proposed as the etiology for both precipitous fall in serum calcium and the severe pain associated with tissue toxicity.

But how it can penetrates the skin if it is a polar compound? How is it soluble in the tissues?

This suggests transport occurs by non ionic diffusion https://pubmed.ncbi.nlm.nih.gov/6266462/ and as Wikipedia says it is lipid soluble

helpful source, it is about treatment but has a good breakdown of effects. https://www.sciencedirect.com/science/article/abs/pii/S0305417914001508

This question appears to have a revived interest? I would like to clarify this Q&A you don't mind.

HF(aq), like other hydrogen halides, does completely give up its proton to $\ce{H2O}$ but since F is the most eletronegative element on earth, it will pair up with hydronium ion in the aqueous environment, making the proton "less available", at least to a pH electrode. This is one of strongest hydrogen bond known.

$\ce{HF(aq) -> F^-.... H3O+}$

Thus HF(aq) has a depressed pKa in water whilst its "real acidity" can be much higher.

Homo-association of HF only occurs in very high concentration (close to unity). You can estimate the extent of homo-association of anhydrous HF by measuring its conductivity. Anhydrous HF has lower conductivity (<1.6 $\mu$S/cm) than deionized water (~5 $\mu$S/cm) [1] so it's probably not terribly important in driving disassociation of HF, esp in water.
HF causes deep burn, often with a delayed onset because while the skin prevents charged raw hydronium ion from penetrating too deeply, HF or the hydronium-flouride ion pair can be absorbed and releases the hydronium ion (by exchanging with water abundant in tissue) at deeper level. (Thus it's often reported as more painful than other acid burn)
Although fluoride in ppm level is anti-microbial and prevents cavity (by reacting with calcium mineral in tooth), high concentration of fluoride is toxic because, as cited in previous answer, fluoride interferes with calcium metabolism in forming insoluble calcium fluoride. It causes skeletal fluorosis and suppresses some essential metabolic enzymes.
HF is corrosive because of its proton; it's corrosive to bones because of its fluoride. HF corrodes glass and HCl doesn't because silicon tetrafluoride is a more stable complex than the highly reactive silicon tetrachloride. It has little to do with whether the acid is weak or strong.

I am not a chemist and unfortunately I will have to refer to wikipedia, but the ionization constant for HF (10−3.15, according to wikipedia) does not take homo-association into account.
Homo-association is an association between a base and its conjugate acid through a hydrogen bond. This process stabilizes the conjugate base, thereby increasing ionization. Often this behavior increases acidity, especially at high concentrations. In case of HF (double arrows indicate equilibria):
2HF <- -> H2F+ + F− (autoionization of HF)
HF + F− <- -> HF2− (homoassociation)
The formation of the bifluoride anion (HF2−) encourages the ionization of HF by stabilizing and removing F− from solution hence pulling the dissociation equilibrium of HF (HF + H2O <- -> H3O+ + F-) to the right. Thus, the usual ionization constant for hydrofluoric acid (10−3.15) understates the acidity of concentrated solutions of HF.

Although the importance of that would depend on the reaction constants of those three reactions... do you by chance know what they are?

@nico - great comment - but no. I'm just a humble biologist and stumbled upon this info after digging into it. HF is absolutely a strong acid from my perspective and this proves it, albeit just qualitatively. A quantitative answer has not even appeared on chemistry.SE, where a few related questions were posted.


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How is the extraordinary eyesight of some deep-sea creatures explained?
Mantis shrimp is a marine crustacean that is known to have a vision system that is much more complex than the eyes of many animals living on the ground. As explained here, it has 12 types of photoreceptor cells, can detect a wider frequency range than humans (into UV and infrared regions), and even polarization.
These animals live in dark underwater environments where sunlight cannot reach, so that a vision system would not seem to be useful.  Why is this present?
My own thoughts are that even though some types of these creatures live in deep ocean waters, they mostly live in shallow waters where sunlight can reach:

"They occur in coastal waters but are sometimes found as deep as 1,300 meters"

Therefore their vision system is not useless. But what about those species (including but not limited to some types of mantis shrimps) that live in deep dark waters? Is their vision system considered a vestigial feature?

It's an interesting question, but could you [edit] to make the title consistent with the question in the body?

@ARogueAnt. I edited the title to better match the question. Feel free to edit it!

I have edited your question to reduce it to its essentials. This is “what purpose does this serve?”  If you can answer that you know why it evolved. If you can’t, you are in trouble.

Its worth noting that mantis shrimp eyesight is much worse than ours in some way, they are far less sensitive to small differences in color while detecting a much wider range of colors. it is also worth asking if deep water mantis shrimp stay in deep water all the time.

You will find quite a lengthy and nice discussion and review of current hypotheses (all with some support) in Porter et al. 2020,PNAS.
To add even more intrigue, parts of the vision system (e.g.: number of photoreceptor genes) seems more complex than needed for the actual performance of the visual system (e.g.: whether certain visual stimuli are detected).
Suspected:

Parts of "visual system" do not primarily serve "vision" but something else (e.g.: touch as in some insects)
There is an advantage for heterozygous animals
There might be some sort of vision-based advantage to be discovered (e.g.: rather than helping to better discriminate seen things in real time, the complexity might serve to integrate visual cues over time)


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Are mature erythrocytes prokaryotic?
Mature mammalian erythrocytes have all the characteristics of a eukaryotic cell except that they don't have a nucleus, they don't have any cell organelles. Does this mean that erythrocytes are classified as prokaryotic?

I have removed the abbreviation from your title (and also from your content). Titles should not contain other than the most common abbreviations (DNA) so they are immediately comprehensible and index properly. In general you should avoid them, or at least define on first usage.

I don't think any Eukaryotic organism can possibly have prokaryotic cells in their body

@OneFace The ca. 30 trillion cells of your microbiome would like to disagree with you - particularly the 1-2 kg of them in your gut. -- You're right that no eukaryotic organism has genetically identical prokaryotic cells in their body, but that's because the presence/absence of the nucleus is only a diagnostic feature, not a defining feature. Like most taxonomy these days, prokaryotic/eukaryotic is now defined based on cladistics and common decent, rather than a pass/fail checklist of phenotype. If you're descended from eukaryotes, you are a eukaryote, even if you don't have a nucleus.

I meant no eukaryotic organism can possibly have prokaryotic cells as a self tissue. Flora is not considered "you". They are commensals living in you. @R.M.

No.  Nobody considers red blood cells to be prokaryotic, perhaps most importantly because they are part of a eukaryotic organism.  Red blood cells begin life with the full complement of organelles, including a nucleus and mitochondria, but our RBCs shed their organelles during maturation.  In actuality, though, only mammalian RBCs lack nuclei; other animals' RBCs still hold on to their traditional eukaryotic characteristics.
As an analogy, apoptotic or necrotic cells don't have intact organelles, but they are still considered eukaryotic.

How this intellectual deception works
There have been several admirable comprehensive answers to this question, but, having seen it come up again recently, I thought it would be useful to point out why something like this that is clearly wrong can sound plausible. In general there is some sleight of hand involved.

In this case the sleight of hand is the (deliberate?) confusion of
‘cell’ with ‘organism’.

Prokaryotic and eukaryotic are terms that apply to organisms. (see definitions on Wikipedia pages) Prokaryotes are unicellular, so a prokaryotic organism is often loosely referred to as a prokaryotic cell. Some eukaryotes are multicellular, and multicellular eukaryotes such as those containing erythrocytes have a variety of different specialized cells, but these cells are not organisms. The interchangeable terminology for prokaryotes does not apply here, and, as one always knew, it is nonsense to talk about particular cells being prokaryotic or eukaryotic.
The fact that nuclei are a characteristic of eukaryotic organisms does not require every cell of a eukaryotic multicellular organism to have a nucleus (and anyone who tries to define it that way is wrong.)
It should also be emphasized that the term prokaryote has a different meanings from anucleate. Indeed, in anucleate* — “lacking a cell nucleus” — the prefix a- indicates not. In prokaryote — “any of the typically unicellular microorganisms that lack a distinct nucleus and membrane-bound organelles and that are classified as a kingdom — the prefix pro- means before, in a temporal sense. (The karyo portion means kernel or nucleus in Greek.) The idea presumably being that prokaryotes evolved before eukaryotes.
The moral
Don’t look where the conjurer wants you to look.

Note that the reason mature erythrocytes are eukaryotic is the same reason snakes and dolphins are tetrapods. "Eukaryote" and "Tetrapod" are clades, i.e. groups defined by common descent, which leads to pervasive similarities within the group and differences with organisms outside the group which justifies defining that as a group in the first place, even if we didn't know they were descended from a common ancestor.
That is an important fact about life that is obscured with classifications like "mammals are animals that have fur, bear live young and feed them milk". We could imagine a situation where we could list traits ("has fur"/"has feathers"/"has scales", "swims"/"runs"/"flies", "bears live young"/"lays eggs", etc) and we would find creatures with any combination of those traits. If you knew an animal had fur, that wouldn't tell you what any of its other traits were, because the combinations were endless. At that point, "it feeds milk to its young... but it has no fur and swims!" might lead to big questions of "mammals feed milk to their young, but they also have fur, so should we call this a mammal?". But words like "mammal" would also be a lot less useful, because knowing an animal had fur, gave birth to live young it fed with milk wouldn't actually tell you anything more about the animal in question, since its other traits could be anything.
That is NOT how it turns out living things are. Traits are distributed in a very specific way: a nested hierarchy, groups within groups that don't overlap. This was found by Linneaus, the first person to try and classify all of life. He found that when looking at the similarities and differences between animals, they naturally fell into groups within groups; you had mammals and birds and reptiles and fish, and within mammals you had primates and carnivores and whales, and within carnivores you had canines and felines, etc... with no creature that was, say, half like a dog and half like a duck to the point there was a question of whether it fit in "mammals" or "birds".
This classification isn't arbitrary. Linneaus admittedly did have a thing for the nested hierarchy, and tried to classify rocks the same way. That didn't work out; today's biologists have changed Linneaus' classifications a lot, but the nested hierarchy has proved an enduring fact of how the traits in living things are distributed. On the other hand today's geologists classify rocks completely differently, because it turns out the traits of rocks are not distributed according to a nested hierarchy.
Moreover, biologists have since discovered the cause of this nested hierarchy, which is common descent with modification. Organisms reproduce and have offspring that are slightly different from them; over time species differentiate into different groups that are slightly different from the parent species and those groups become species and differentiate in turn. As a result, how similar two organisms are to each other is directly related to how recently they share a common ancestor. Groups emerge within groups because they descend from one another, and don't overlap with far-away groups because there is no mechanism for that to happen (main exception being bacteria, who can swap genes with other bacteria from very different groups, and as a result they don't fall in as clear a nested hierarchy as eurkaryotes do).
This means that there is a difference between modern biology and that of Linneaus's time; Linneaus listed visible traits and classified organisms based on them. It so happened that they fell into a useful nested hierarchy, so "has fur and feeds milk to its young" told you a lot more about the animal, like "has lungs, has a backbone, probably has four legs", etc, but the list of traits was still the main important thing. Nowadays we know of a lot more traits; we know an organism's genes, the structure of its proteins, details of their physiology that biologists of Linneaus's time could only guess at. While in Linneaus' time you might be able to say "dolphins have no fur and swim like fish, but they have lungs like mammals and bear live young; where to classify them? I guess they're kinda more like mammals?", today we know that dolphins are overwhelmingly like mammals down to the molecular level, in literally every way other than "they have no fur and swim". And we also know the reason why: dolphins share a common ancestor with all other mammals dating back to the Triassic or so, while their common ancestor with fish dates back to the Ordovician, hundreds of millions of years earlier.
This means that today's organisms are by and large classified on the basis of common descent. The "Eukaryotes" group certainly is (it's a clade). What makes an Eukaryote an Eukaryote today isn't technically any specific trait, it's whether it descends from the common ancestor of Eukaryotes or not. Red blood cells absolutely meet that criterion. But this isn't just an arbitrary classification choice; it so happens, because of this common descent, that red blood cells are a lot more like other eukaryotes than they are like any prokaryote. "Has/Lacks a nucleus" is one single trait; an important one, important enough to make it the name of the group, but it's not the only one. And in their proteins, ribosomes, metabolic processes,... really everything BUT "does it have a nucleus", red blood cells have more in common with Eukaryotes than with Prokaryotes, so it makes absolute sense that they would be classified that way. Same reason snakes and dolphins are "Tetrapods" even though they don't have four legs; four legs is an important trait, it named the group, but it's still only one trait. "It's almost totally like a lizard, but... it has no legs!" is not actually a riddle or a stumper; "almost totally like a lizard" trumps "number of legs" any day.


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Why do organisms excrete nitrogenous wastes?
Organisms excrete nitrogenous wastes in the form of urea, uric acid or ammonia. But isn’t that a bit of a waste? There is a shortage of biologically available nitrogen in the ecosystem, and plants convert nitrogen in ammonia and nitrates into amino acids. Why do organisms then deaminate these amino acids and then excrete them?
It seems to me that it would make much more sense to store the nitrogen for further use. I understand that ammonia is toxic, but surely it could be stored in some specialized structure.

Some amino acids are essential, that is, they cannot be synthesized.  For all the others, however, you need building blocks.  Nitrogen, and specifically ammonia, is required for non-essential amino acid synthesis, the transfer of which is accomplished through a process called transamination.  Amino acids are also broken down for energy as a metabolic process, producing glutamate (in addition to energy-containing molecules such as pyruvate).  The body has thus produced some amino acids and metabolized others for energy,  but glutamate must be deaminated to remove the nitrogen, which by this point is now in excess.
To evolve a specialized storage unit for highly toxic substances could be useful, I suppose, but it would be unlikely and would pose a huge risk compared to just getting rid of 'em.  I'd rather urinate a few times a day than save a lot of toxic material for later and run the risk of something malfunctioning and killing me; besides, eventually that storage unit would get full.  You could ask the same question for any substance we might eventually want.

Preamble: The problem with questions on evolution
Obviously, evolutionary biology is a reputable discipline, but unfortunately there are two types of questions on evolution that are posted on this site that I believe are often of dubious value and can lead to dangerously unscientific habits of mind.
The first is questions of the type “Why did such and such evolve this way?”. The problem with this type of question is that there is generally no way of proving a hypothesis because it makes no predictions — the end product of the evolution is known. There is sometimes an anatomical or biochemical paper-trail to support arguments, and I have presented one such in an answer to another question. However many answers to this type of question are pie-in-the-sky or circular reasoning.
The second type — typified by this one — asks “Why has such and such not evolved, it would obviously be advantageous?” The posters of such questions tend not to ask themselves why, because if they did they would realize that the answer is likely to be either:

“It would be too difficult, costly or would have disadvantageous
  consequences”

or

“The assumption that it would convey a selective advantage (and
  that is what evolution is about) is incorrect.”

The accepted answer to this question addresses the former explanations. Although this is an old question at the time of my answering it, I am doing so partly because a similar question came up recently, but also because I feel it would be generally useful exercise to consider the second explanation — to emphasize the need to question the assumptions of those who think that they know better than Nature.
A story my mother told me
The story is apocryphal, but it is true my mother related it to me. It concerns two youths who had applied for a general office job. (This was not quite Dickensian, but not so much later.) In order to chose between them they were each given a parcel to unwrap. The first youth carefully untied the string, took off the paper wrapping, neatly folded it, and placed the parcel, the string and the wrapping paper on the table. The second youth ripped off the wrapping and stuffed it into the waste paper basket and placed the parcel on the table. Who do you think got the job? In the era in which the question was posed, most people (including myself) assumed that the youth who had saved the string and paper for reuse would get the job, rather than the youth who wasted them. However (in the story) it was the latter who got the job — the manager was interested in speed and efficiency, not in economy in office stationary. And the moral is that if you make the wrong assumptions (that avoiding waste was paramount) you will come to the wrong conclusion. So it is with “wasting nitrogen”.
Is the assumption in the question valid  for human metabolism?
Although the original question had plants in mind, like @Amory I shall consider it from the perspective of a single species, Homo sapiens. The argument in the question is, in effect:

“There is a shortage of biologically available nitrogen in the
  ecosystem, so why do organisms deaminate amino acids and excrete them
  rather than store the nitrogen for future use.”

The first logical flaw is equating the shortage (limitation?) of nitrogen in the ecosystem with a shortage in any individual species. Let us, however, consider a modified argument:

“Nitrogen is a necessary component of proteins and nucleic acids, the
  synthesis of which is necessary for life. If this were stored in good
  times it could help survival when dietary protein became unavailable.”

This seems more reasonable. But one first needs to ask whether there is actually no storage of nitrogen. In effect there is in the form of structural protein, which is broken down in starvation. This is relevant, as considering this phenomenon allows one to address the real question:

“Would (further) storage of nitrogen in some more dedicated molecular
  form provide a selective advantage by enhancing survival during
  periods of starvation?”

This is the office boy question, but whereas we had no way of knowing what was most important in the office — speed or frugality — here we have information from which to draw a conclusion. In prolonged starvation protein is broken down to amino acids. Why? To utilize the carbon backbone of glucogenic amino acids to provide glucose for the brain when all other substrates for gluconeogenesis have been exhausted. This is key to survival. What happens to the nitrogen? It is partly used as ammonia to buffer the acid produced from some of the ketone bodies produced from ketogenic amino acids and the rest is excreted as urea. It is certainly not used to make protein or nucleic acid, which would entail using precious carbon constituents. Thus, it is clear that energy requirements, and particularly the generation of glucose are the limiting factors in survival during starvation — not nitrogen. The conclusion, therefore, is that there is no point in storing nitrogen in times of plenty: what needs to be stored is carbohydrate/fat.
One might raise the existence of Kwashiorkor, a disease of protein malnutrition. However this is a relatively rate disease, and it affects only children: it is not the normal situation in starvation. Clearly the demands for protein and nucleic acid synthesis are much greater in growth than adulthood.
Coda: Another counter-intuitive evolutionary development in nitrogen metabolism
The fallacy of “wouldn’t it be better to evolve…” is evident if one considers another aspect of nitrogen metabolism — our lack of the apparently useful facility to make all the amino acids, resulting in a dependency of man on certain so-called ‘essential’ amino acids. Here the situation is not one of failing to evolve a facility, but actually loosing it — simpler organisms from which we have evolved had it. The inescapable conclusion is that such a facility can never have been sufficiently advantageous to result in an evolutionary disadvantage for those who had lost it. Presumably we have evolved in a way that allows us (or a sufficient number of us) to survive in our particular ecological niche, not to be supermen.