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How long can I store extracted RNA?
If I extract RNA from a (leaf tissue) sample using a one-step phenol:chloroform extraction, how long can those samples be stored at -80°C? And how many times can I defrost and refreeze them before they will become degraded?

I'd guess that this will depend heavily on the purification of the sample, pure RNA (no Mg2+ e.g) can be stored for a very long time at lower temperatures. Pure RNA in water can be stable for months at 4°C. Freezing and thawing RNA can affect the folding (for RNA with important tertiary structure) as I have observed.

If you're worried about freeze/thaw cycling, aliquot them into multiple tubes -- that way you only thaw what you need to use.

I've found that extracted RNA using commercial kits has stayed stable for many years at -80 C. I would certainly aliquot it before freezing however as RNA is particularly sensitive to freeze-thaw cleavage.

We've actually checked the degradation of viral RNA extracts, and they will for the most part hold up for more than a year at -80.  We did see more stability variation correlating to sequence than we expected, however.

This is interesting - how did you measure the degradation? I imagine degradation that might have a significant effect on, for example, RNASeq, would not show on a gel.

We can keep extracted RNA in -80°C for a few weeks, but before the start of any experiments, it needs to be validated by gel electrophoresis.

I keep my RNA in 1mM sodium citrate pH 6.4. Citrate is a chelator, and helps trap the divalent metals many RNAses need to work. The lower pH also helps inhibit RNAse activity. EDTA could work as a chelator, but it only chelates well at pH's where RNAse activity is worse. Citrate gives both chelation and low pH.
Of course I also keep my RNA at -80.

Do you need to do anything special to remove the citrate when it comes time to use the RNA, for example to make cDNA?

I've never noticed any problems, but I've never really checked. Only been working with RNA for a couple months now, and my lab is in an old building with a lot of dust, so RNAse contamination has been a bigger issue than enzyme activity. An isopropanol precipitation should be enough to clean up the RNA before any reactions if citrate proves to be a problem.

We're also in an old dusty building, and RNase is a problem for us too. Thanks for the tip - I'll check whether it works for RNAseq purposes.


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Are homozygous carriers of the CCR5-Δ32 allele fully immune to all known strains of HIV?
Or is there documented evidence of even one homozygous carrier contracting HIV and staying infected?

I would say no.
Some HIV strains are X4-tropic and not R5 tropic. That means that the virus uses the CXCR4 coreceptor and not the CCR5 coreceptor for entry into the CD4-positive cell.

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What hydrolyses aspirin within the digestive tract and blood stream?
I have had some further thoughts after my previous question regarding the buccal delivery of medication.  The active compound in aspirin (acetylsalicylic acid or systematically 2-Acetoxybenzoic acid)  is salicylic acid (2-hydroxybenzoic acid).
I understand that the hydrolysis reaction occurs as follows within the stomach - therefore in the body it is an acid hydrolysis:

N.B. The H2O is not shown in the diagram.
However having done this experimentally I know that in the lab to ensure a decent yield of salicylic acid I had to reflux the solution for several hours.  Yet the onset of action of aspirin tablets is much faster than this.  To me this suggests some enzymatic activity, but I have no idea which enzyme this is likely to be.
To follow on directly from my previous question, if the aspirin is absorbed directly into the bloodstream bypassing the stomach then what causes the hydrolysis in the blood stream and is it the same factor that increases the rate of hydrolysis in the stomach if the medication were to be taken orally?

As a side question, how are you doing all this lab work as an A-level student? V. impressive!

@RichardSmith I'm lucky enough to be on a really obscure chemistry exam board - OCR Salters.  It's the most practically based since Nuffield bit the dust. We have to do an extended lab project over a few months, which is a great opportunity for us!

Acetylsalicylate deacetylase is the enzyme responsible for this reaction.

Precisely, the present investigation reveals that the hydrolysis of aspirin in liver, kidney and probably other tissues of
  rats is catalyzed by two highly substrate specific microsomal
  esterases, ASA esterase I and II active at acidic and slightly
  alkaline pH, respectively. The findings that ASA esterases have
  distinct organ distribution pattern and display responses to
  various inhibitors/activators that are different in many respects
  from those exhibited by cholinesterase and nonspecific carboxylesterase suggest that the latter esterases probably do not play
  a significant role in the hydrolysis of aspirin.
From:
  Ali B, Kaur S (1983) Mammalian tissue acetylsalicylic acid esterase(s): identification, distribution and discrimination from other esterases. J Pharmacol Exp Ther,226,589-594

That's an interesting one - according to the handbook of enzymes notably page 357, the enzyme doesn't seem adapted for use in the human stomach.  This suggests that it is active elsewhere - a website suggested the liver. Does anyone know if this is the case (as it would prove an answer to how the hydrolysis happens in the bloodstream)?

@RoryM See my update with a quote from the article.  Much of the drug metabolism that the body does happens in the liver anyway, after all these are just safe dosages of "toxins" that we take for our health!

However in Alexander's Answer to the linked question he states one advantage of buccal delivery as the bypassing of the liver.  As this method supposedly gives faster delivery of the medication there must be another factor at play somewhere =)

See http://en.wikipedia.org/wiki/First_pass_effect.  First pass effect is just that, the reduction in the amount of absorption when the drug is first metabolized.  One's blood volume makes many more subsequent passes through your liver.  The article also notes the kidney as a location of the enzyme, which is just as likely to revisit the same blood volume.

Perhaps I'm misinterpreting, but the 1st pass effect is one that reduces the potency of drugs.  The enzyme you mentioned above that hydrolyses aspirin into salicylic acid would be increasing potency as salicylic acid is the active ingredient, therefore the first-pass effect does not apply?

I don't want to go too far out on a limb here, because I don't know for sure, but there are probably non-specific enzymes that metabolize the ASA directly in first-pass, either by oxidation (e.g., the p450s) or conjugation (the various transferases) which render it inert.  The liver is a complicated machine, and I regret that I don't remember more about first pass metabolism.

You may want to see if Alexander wants to take a peek at this question, too.

@TomD I think you misunderstood, Rory was not referring to the pharmacodynamics of aspirin itself, but the pharmacokinetics of the removal of aspirin from the system.

@RoryM See the answer to my latest question I think it finally clears this one up.  The sublingual drugs will in fact be carried to the liver via the hepatic artery, just not initially.

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What are differences between formation of embryonic disc in chick and mammal embryo?
Exam question which got lowest average points in my university: 1/5 average.
No markscheme available so my attempt below.
I assume that embryonic disk prefers to germ disk such that Formation prefers to only to the 3rd developmental week because of the Wikipedia fact.
I also went through the points during 2nd week of development and did not notice major differences. So let's consider only the 3rd week:

Formation of the primitive streak
Genesis of the germ layers
Genesis of the notochord
Location of the epiblast cell target and the development of the primitive streak
The bilaminar membranes
Evolution of the mesoblast
The intraembryonic coelom
Induction of the neural plate – neurulation

The following differences are based mostly on Gilbert's Developmental Biology 9e -book.
Other Differences which seems to at least start at the 3rd week of development

Chick meroblastic cleavage, human holoblastic. TODO do not know how that causes differences yet during the 3rd week.
Chick has yolk, human not so human placenta development and implantation. Chick dependent on yolk nutrients, human not.
Human embryo gets mother nutrients through placenta.
Chorion formation and finally from it the fetal portion of the placenta.
Chorion also includes the uterine cells to form the maternal of the placenta, the decidua.
The decidua will come rich in the blood vessels that will provide oxygen & nutrients to the embryo.
Human oviduct expansion to the uterus.
Chick embryo externally developing from the mother, human not. Chick egg is telocithal with a small disc of cytoplasm: blastodisc - sitting atop a large yolk. The yolk, eggs of birds undergo discoidal meroblastic cleavage. Cleavage occurs only in the blastodisc which is about 2-3 mm in diameters & is located at the animal pole of the egg. The first cleavage furrow appears centrally in the blastodisc; other cleavages follow to create a single-layered blastoderm.
The cleavages do not extend into the yolk, cytoplasm, so the early-cleavage cells are continuous with one another & with the yolk at their bases.
One chick hypoblast streak, human multiple. Chick must have some control mechanism.

What are the differences between formation of embryonic disc in chick and mammal embryo?

Embryonic disc forms on top of yolk during cleavage on chicken embryo, while between amniotic sac and yolk sac inside blastocyst after implantation on human embryo.

Some further processes take place on and in the embryonic disc: specifically these here during the week 3.
Embryonic disc formation includes still during the 3rd week of development:

Formation of the primitive streak
Genesis of the germ layers
Genesis of the notochord

Formation of the primitive streak: The process of primary neurulation appears to be similar in chick and mammalian. The embryonic disc becomes oval and then pear-shaped, the wider end being directed forward. Near the narrow, posterior end, the primitive streak makes its appearance and extends along the middle of the disc for about one-half of its length from migrated ectoderm cells.

Genesis of the notochord: “The notochord extends beneath the neural tube from the base of the head into the tail.” - As the mesoderm develops between the ectoderm and endoderm it is separated into lateral halves by the neural tube and notochord.
Figure 2: Neurulation. NB the use of neural groove is correct. Notochord is below neural groove. - Genesis of germ layers here: from a flat thing to a developed one.

Figure 3: Genesis of notochord and primitive streak. Yolk-sac surrounds notochord and primitive streak.


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Have there been any positive public health effects due to UV lights?
Occasionally, in hospitals and in eating establishments in the US, they have industrial grade UV lights in sconces attached to the wall (though they seem to be less prominent as the years go by).  I understand the anti-microbial properties of UV light, but are these devices anything more than show pieces?
Have there been any lasting, significant public health gains that have been correlated with the use of UV light in public places?

Regarding UV lights attached to walls going out of fashion - I'm seeing them more and more over washbasins used on wards, particularly on specialist units.

There have been some studies regarding the use of intensive UV light installations in surgical wards or other settings as a anti-microbial tool. Generally speaking, these are part of a general interest in non-cleaning based anti-microbials in hospitals, such as UV light, O3-based machines, and copper/silver coated surfaces.
The answer to your question will depend on what you consider "lasting" and "significant". They're a relatively new technology, and haven't had a huge penetration into the market yet, so the only evidence you're likely to find is hospital-sized non-randomized trials.
So basically, the answer to your question, as I read it, is "No, but..."
There hasn't been an opportunity for these technologies to show any sort of lasting, significant reduction in hospital acquired infections. But there is some promise that these types of technologies, and those like them, may help reduce the burden of infections when they're used appropriately. The current state of research is figuring out just how workable they are, how to best use them, and what they can and cannot be expected to do. That kind of evaluation is actually what I'm doing as part of my dissertation work, though my focus is on the general concept, rather than a specific device.


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Are human chromosomes connected or separate molecules?
Do the 46 human chromosomes form a single unbroken DNA helix?  Or is it rather that a human's genome consists of 46 disconnected helices?
If it is the former, does the common numbering scheme for the chromosomes have any correlation to their actual ordering in the one large strand?
If is the latter, is there a convention on how the chromosomes are ordered in genomic datasets?  Also, is there a clear understanding of how sister chromosomes "find" each other in Meiosis I?
Generally, during periods when Mitosis/Meiosis are not occurring,  what's a good physical picture for how the chromosomes are physically arranged (e.g. a bowl of 46 spaghetti noodles, or maybe the sister chromosomes always stay close together, etc)
thanks!

Each chromosome is a pair of distinct, separate DNA molecules.  A chromosome of an eukaryotic cell nucleus is a (long) helix of two linear molecules and so has two ends, which are called telomeres.  DNA naturally forms a double helix with its complementary DNA molecule, and the double helix can further curl in what are called supercoils.
In humans, the chromosomes occur in 23 pairs (totaling 46). Except for the sex chromosome pair, each member of the pair is identical in appearance in a karyotype (picture) and each such pair has a number assigned from 1 to 22; the numbering generally follows the size of the chromosome, with chromosome 1 being the longest.  In mammals, the sex chromosomes in a male are quite different in size and are labelled X and Y; a female has two identical X chromosomes.

Technically each chromosome consists of two DNA molecules.

@canadianer Well... it depends on whether you consider hydrogen bonding being strong enough to consider the whole thing as a single molecule.

@Remi.b I don't ;) Not that it means anything, but I've also never heard anyone use hydrogen bonding in the definition of a molecule. Is a glass of water a single molecule?

@canadianer My chemistry teacher in high school used to say that $H_20$ should rather be called $H_{12}0_6$ or something like that. :) And the two DNA strands literally stick to each other and are really not moving independently. But I agree with you. I'd rather consider one chromosome as being made of two molecules.

@canadianer, Remi.b,: edited to reflect what you pointed out.


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Is there are evolutionary explanation for why humans and primates are ticklish? How might it have evolved?
Tickling is a rather interesting phenomenon: When humans or apes are touched in certain areas like the armpits or sides, we respond with laughter AND frantic attempts to stop the assault. Obviously our ticklish areas tend to be very vulnerable, so it makes sense that we would want to protect ourselves, but why do we respond with laughter? How might both of these reactions to tickling have evolved? Do they have the same evolutionary purpose or different ones?

I have heard that rats are also ticklish, so apparently it is not limited to primates.

Tickling probably evolved from a defense mechanism but then gradually changed into a more social action, as explained in Provine, 2005 (PDF):

The neurological mechanism of tickling probably evolved from a reﬂex defense mechanism that protects our body’s surface from external, moving stimuli, probably predators or parasites. Our response to tickle is more varied and complex than the typical reﬂex, but it has some stereotypic, reﬂex-like properties (i.e., we laugh when tickled, struggle to escape the tickler, huddle, fend off the tickling hand). Although you can be tickled to laughter by a machine (Harris, 1999) (PDF), most everyday tickle is yet another social context for laughter and a form of communication.

Actually I find the phenomenon of laughing itself a bit intriguing. Does anyone know how laughing evolved? I think we need to understand that before trying to find an explanation for how why tickling needs to laughter.

@VinayakPathak - This answer talks about that.


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Do humans have Coelom?
Kimball Biology 5e says

Coelom is the main body cavity of many animals. It is lined with an epithelium derived from mesoderm.

Gilbert Embryonal Biology 9e says

Coelom is the space between the somatic mesoderm and splanchnic mesoderm that becomes the body cavity. In mammals, the coelom becomes subdivided into the pleural, pericardial, and peritoneal cavities, enveloping the thorax, heart, and abdomen, respectively.

Then my lecture materials and the research site say

Coelom is the secondary body cavity.

Finnish Wikipedia says that Coelom is only with invertebrates.
Again the Wikipedia page about peritoneum suggests that human has abdominal cavity and no coelom, and other mammalians coelom.
Does human have Coelom?
The confusing thing is the use of the word "OR", since I am not sure whether people are using it in different pages like "XOR" or like "AND" in normal speaking.

Wikipedia actually covers this:

Most bilateral animals, including all the vertebrates, are coelomates.

Now, some coelomates have subsequently lost their coelom but primates (actually, I believe, all vertebrates) are not among them. In humans, the coelom forms, amongst others, the pleural cavity.
So, yes: humans do have a coelom that partitions into different, unconnected body cavities during development.

So the coelom is not any specific cavity of human adult. It just a cavity in the embryonal stage which divides to other cavities. - So if you see the preparat of human adult, you cannot show that the thing here is coelom.

I read the following definition somewhere: "Coelom is the fluid-filled body cavity that separates the digestive tract and the outer body wall and is completely lined with mesoderm." - The clause may be wrong, at least for adult human, since it suggests me that you can see such a cavity in adult human. - It may be the case for other vertebrates where you can see in the adult species. - Thinking better definition. So probably it is better to say "Cavity that separates the digestive tract and the outer body wall at some point of development of vertebrates." - What do you think? Is it better?

@Masi Well, where is the mesoderm in an adult human? Or any other adult animal? As far as I know, all of these definitions apply to (some stage of) embryo development. Not only for humans and not only for vertebrates but in general.

I need to find a general definition for humans. - Is the following any better? "Coelom is the lateral cavity between parietal and visceral mesodermal layers. Coelom forms at the time of primary neurulation (formation of neural groove etc)."

I think so that you cannot really see mesoderm in an adult human. - It is a developmental layer between ectoderm and endoderm. You can see it after gastrulation, probably during gastrulation too its development. It forms finally for instance muscles and bones during organogenesis.


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When does Coelom form exactly?
Related to my other question.
I know that the coelom is derived from mesoderm.
Coelom seems to form during organogenesis within 3rd and 8th week of embryogenesis.
However, that answer is not either enough exact or it is wrong.
I am reading the thing in Kimball 5e and Gilbert 9e, but cannot find an exact mention about the thing. I know for sure that the coelom develops within gastrulation and organogenesis, since it is forming from mesoderm.
When does coelom form exactly?

What species you have in mind?

@MartaCz-C It is not specified in the question given to me. Probably chick and human. I am not sure whether human's abdomic cavity can be classified as coelom so unsure about human

In humans, the coelom forms by the splitting of the lateral plate mesoderm, which occurs during weeks 4-5 (Sweeney, 1998).
Sweeney, LJ. 1998. Basic Concepts in Embryology. McGraw-Hill.


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Are there any motile plants?
There are numerous examples of sessile animals (sponges, barnacles etc.) but are there any examples of motile plants? If not, why not? Surely mobility would have conferred an evolutionary advantage to some plant species. I am specifically thinking of locomotion here.

How are you defining motility?  Many plants "climb" or otherwise send out shoots, but I think most plants are dependent on a steady root system.

I was thinking specifically of examples of plant locomotion. Will edit question.

I can think of brunsvigia, which pollenates, and then dries out and dies. The dried husk then detaches from the stem and the wind sends it cartwheeling across the desert, dispersing it's seeds as it goes. Here is a video. It is locomotive like a sailing boat. Other examples given are actually just photo/geotropism and are directed growth rather than locomotion.

As to "why not", it's mainly because directed locomotion is energy-intensive, and plants don't have much energy available. Animals make use of energy that's been pre-concentrated, either by plants or by other animals; but plants just have a slow trickle of energy from the sun and need to be very sparing in its use.

It depends how you define locomotion.
If you take it to mean moving from one place to another, then yes, almost all plants do this at some stage during their life cycle. Primarily seeds and pollen move around, and generally they do so by harnessing either natural forces like wind and rain, or by manipulating animals to do the leg-work, e.g.:

by recruiting pollinating insects
by having barbs which snag the fur of passing mammals
by producing tasty fruit so monkeys eat them, seeds included, and deposit them with a dollop of fertiliser somewhere else

If you take it to mean moving around under ones own propulsion, then yes, some plants do this. The example that springs to mind is the gametophyte generation of ferns:

The prothallus (i.e. the gametophyte) has rhizoids on the underside and uses them to slide around and find some space in which to start the next generation. I have seen this happen when fern spores are germinated on agar - when they reach the tiny prothallus stage, they start sliding around to avoid overlapping with one another. I can't find any references for this, but I'll keep looking.
Another example of self-directed locomotion in plants is the motile sperm of bryophytes. The male sex cells have flagella, which they use to propel themselves through water to the female sex cells (reviewed by Renzaglia & Garbary 2001).

Renzaglia, K.S. & Garbary, D.J. (2001) Motile Gametes of Land Plants: Diversity, Development, and Evolution. Critical Reviews in Plant Sciences. [Online] 20 (2), 107–213.

Many plants crawl by sending out ground vines and replant themselves in neighboring positions. But that's not what you are asking I think.
I don't know if there are any land dwelling leaf bearing plant forms that move.
In the water most chlorophyll bearing algae have flagellae and can migrate through the water.
Reference:
http://science.jrank.org/pages/205/Algae.html

Plant movement can be measured by a crescograph. This mov is not only due to plant growth but also as response to stimuli.
Talking of growth itself  roots frequently go around a rock while the grow, and plants lean towards a light source when kept in shade.
Creepers and climbers do display a kind of locomotion  of the part if not the whole, Partial motility is available to leaves of certain plants(They clasp shut in night)and flowers (Sunflower).The few carnivores we know add to the example.
Free floating aquatic plants have movement though it may not be called locomotion


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Why do people look different after a long sleep?
What happens during a long sleep that makes people look odd when they have just woken up?  Why doesn't the same phenomenon occur in the case of a person who lies down for an extended period of time, but stays awake?  I've noticed that some nights seem to make a bigger difference than others in the appearance of the sleeper, but haven't noticed a pattern.

Can you elaborate on what the characteristics of "looking odd" are?  I think everyone has some sense of (or experience with!) what you're talking about, but in order to address things scientifically the specific characteristics (e.g., dark circles under the eyes) would be helpful.

Not dark circles (that sounds more like long term lack of sleep); I'm referring to the sort of "puffiness" around the eyes and mouth.  It's hard to describe without a picture.

Puffy eyes are caused by fluid build up in tear ducts from extended periods of lying down. Gravity from sitting or standing slowly drains them during the day. The crusty 'sleep' that accumulates in the corner of your eyes is the residue from basal tear liquid that has seeped out of the eye and evaporated during the night.


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How did the huge dinosaurs cope with gravity and loads on bones, etc.?
It's very costly to be a huge animal. Your mass grows in cube when you scale up, but you still only have two/four legs to support the same weight. This increases the pressure that your body needs to cope with.(this is easy to see if you compare an ant with an elephant. The elephants legs are much thicker and strudier in comparison to it's body)
Looking at a T-rex for example, speciemns have been found that are believed to weight more than 9 tonnes, compared to an elephants 10 tonnes. T-rex has ofcorse has only two legs. The heaviest dionsaur is believed to have weight 80 tonnes. That is the weight of about 20 cars on each of their feet.
How could they support such massive weights?

I've heard that the greater amount of oxygen in the atmosphere was a factor, at least in the large size of the dinosaurs.

@shigeta Actually atmospheric oxygen was lower then present day throughout the time of the dinosaurs.

Assuming that gravity was essentially the same (other answers to this question notwithstanding), very large dinosaurs were dealing with the same forces that they would today. There are two clades of dinosaurs in which gigantism evolved, Sauropoda (quadrupdeal sauropods) and Theropoda (including T. rex). Each "solved" the problem of large size in different (but also somewhat similar) ways.
The main reason why large size was not a problem was that, if posture changed to align the forces between the animal and the ground, the bones are compressed. Bone is very strong in compression.
Theropoda
Theropod essential operate as a see-saw, with a large muscular tail balancing a large head. As such, they did not likely use much active muscular force to balance. The analogy is a human standing. Just standing, you don't need much muscle force to balance.
Hutchinson and Garcia (2002) showed that, because of a lack of plausibly large leg musculature, T. rex could not run. For a range of postures, they estimated how much muscle would be required to balance the animal and found that running behavior was unlikely.
Hutchinson, J.R. and M. Garcia. 2002. Tyrannosaurus was not a fast runner. Nature 415:1018-1021.
Sauropoda
Sauropods show many similar adaptations as elephants, the largest extant land mammals. Their limbs were held upright (erect), which requires less energy for balance. Some sauropods had air-filled bones, which would also lighten the skeleton. Wilson and Carrano (1999) document the evolution of posture through sauropod evolution from a biomechanical perspective.
Wilson, J.A. and M.T. Carrano. 1999. Titanosaurs and the origin of “wide-gauge” trackways: a biomechanical and systematic perspective on sauropod locomotion. Paleobiology 25:252–267.

I love your answer! I have been pondering this for year! Do you have any knowledge regarding their ability to survive a fall (I'm mostly thinking of the two-legged giants)

I think this paper (http://www.jstor.org/pss/4523665) deals with falling T. rex.

This is the best day of my life!

Ornithopods got just as large as Theropods, right?

If so why do elephants have trouble with tiny jumps?

@user2617804 mammals are really poorly adapted for being large. Things like having a lumbar spine and having lost a large number of bones( chevrons, gastralia, lumbar ribs, cervical ribs, ect), mammals just lack a lot of support structures dinosaurs have. Pillar style posture also makes for really poor shock absorption, esspecially from falling any distance.


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What is the distinction between F' plasmid and R plasmid?
Is there a difference between an F' plasmid that has taken up a chromosomal gene that conveys antibiotic resistance, and an R plasmid? Is a bacterium containing an R plasmid and yet lacking an F+ plasmid capable of horizontal gene transfer by conjugation?

Can’t help myself …relevant (but here the better word would be “explanation”). Ed Yong thinks to, too.

Explanation isn't really the word I'm looking for, as I do know what the terms mean individually, but not in relation to each other. I'll edit it to read "distinction".

If I understand the nomenclature correctly, an R plasmid is just any plasmid containing an antibiotic (R)esistance gene (eg. Amp, Kan, Cm, etc.). It's a bit of an outdated name from when people didn't know how exactly the plasmids conferred such resistance.
An F-plasmid is any plasmid that contains the genes necessary for (F)ertility, eg:horizontal gene transfer via the tra operon.
The two do not have to appear together -- eg: Many F plamids will contain resistance genes (along with other random chunks from the genome), but resistance doesn't always have to be part of the payload. Likewise, it is common in labs to build pure resistance vectors that lack any horizontal transfer capability in order to select for particular clones.


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Can protein structure be determined by X-Ray Diffraction in a single image?
I'm reading about the use of x-ray crystallography to determine protein structure. According to my book, data is collected at 30-360 angles (dependent on the symmetry of the protein). An illustration is given with concentric rings labelled with distances - the further out the points are, the higher the resolution.
Is the image a composite (where the angle of the point point from the centre is equivalent to the angle of the reading) or is a separate image taken at each angle? Are there any other reasons why more images would be required?
Thanks.

I can't answer on the details, but as far as I understand it they take multiple images while changing the angle.

That's right. I was wondering if the images could be superimposed somehow, since that was not very clear to me.

It is not clear from what you write whether you are familiar with the process of analysis of X-ray diffraction. Is it clear to you that the diffraction pattern has to be mathematically analysed to get the final "3D picture" of the crystal?

I have to agree with the answers below, it's best to collect light diffraction from the crystal at multiple exposures within the 0 - 180 degree range.

You cannot solve a structure with a single frame, even with perfect diffraction.
The reason you need images over a large swath of angles is because the diffraction pattern is also in three dimensions, in the so-called "reciprocal space".  At minimum, a 180° rotation of the crystal is needed to sweep the entire reciprocal space sphere with the plane of detection, though symmetry in the crystal structure can reduce this further (some of my proteins only required 90°, I think hexagonal unit cells with 6-fold symmetry can live with 30°).  Because crystals are real things (read: non-ideal, doubly so for protein crystals), the sweep is extended to gain some redundancy.

Not by analysing a single protein.  There is work with x-ray lasers.
You have to take a simultaneous image of millions of proteins and use that to get a structure.  It's not quite prime time.  People are also doing this with electron beams in electron microscopes.
These methods will reconstruct 3D models of the molecules, sometimes in states which cannot be obtained from crystallography.  Examples being the structure of the many megadalton nuclear pore complex, and the f-actin fiber.   The classic study is  3d model of bacteriorhodopsin, the first membrane protein structure which was at molecular resolution (this was a crystalline sample though).
While in principle, it sounds much simpler - get a pure sample of your protein, or complex and freeze it down and zap it with an Xray or Electron beam, its a lot more work to reconstruct the image and can take as long or longer than getting an x-ray structure.  The resolution is also usually poor as the crystal will reinforce coherence, that is all the proteins are aligned in the same way and have close to the same 3d shape in a crystal.

Thanks for your answer. I didn't mention it in my question, but my book does say that a vast number of crystalised proteins are required, and that simultaneous diffraction amplifies the signal. What I was trying to ask is if a type of crystalised protein conformation can be determined from a single image or if many different images would need to be produced for each angle of rotation. From your answer it sounds as if all the information required is stored on one image - is this correct?

I'm confused by your answer, what do you mean by "it's not quite prime time"? Electron microscopic images also don't provide nearly the resolution you can achieve with X-ray crystallography.

@MadScientist I think the implication is that superimposed images are also used in EM to reconstruct the structure. The case is somewhat different of course since EM in general doesn’t use crystallised structures so that the proteins in the image don’t all have the same orientation, which is crucial.

CryoEM also doesn't use any X-ray beams either.

I think that while they are working very hard, the X-ray laser and cryo EM reconstruction doesn't yield as consistant a set of results as crystallography.  when the proteins just lay on a surface, they can be shape distorted, and so recombining the images makes can be difficult to interpret.

@Mad Scientist comment started running long, edited answer..

Likely not. While one can get excellent diffraction data from a high quality crystal, it would be extremely difficult to solve the phase problem. The extra angles will help constraint the solutions.

Can protein structure be determined by X-Ray Diffraction in a single image?

Yes. Using a technique called Laue diffraction, it is possible to obtain sufficient data from a single image to solve a protein crystal structure. One example is the time-resolved study of carbonmonoxymyoglobin dissociating by photolysis (DOI: 10.1107/S090904959501661X). This is not the standard single-wavelength technique that is usually used, but uses "white" X-rays with a range of wavelengths available only at synchrotron beams. For example, the BioCARS user facility provides infrastructure for time-resolved crystallography. It is also used in "diffraction before destruction" when working with free electron lasers, see for example Nature Methods 8, page 283 (2011).
The remainder of the answer is about conventional single-wavelength crystallography.

Is the image a composite (where the angle of the point point from the centre is equivalent to the angle of the reading) or is a separate image taken at each angle

The desired structural information (3D electron density in real space) is a Fourier transform of the diffraction data (3D reciprocal space). The word "image" is jargon for a single diffraction image, i.e. the diffraction spots you observe when you point an X-ray beam at a crystal in a certain orientation. Using a different orientation, you get more data (and also measure some spots multiple times).

Are there any other reasons why more images would be required?

The more diffraction images are collected, the higher the completeness and redundancy of the data. Completeness refers to having measured every diffraction spot at least once. Redundancy refers to how often on average a spot was measured, and increasing redundancy increases the quality of the measurement through averaging.

I accept this answers the specific question "Is it possible?", but this was rather a proof of concept. Do you know whether this has been adopted to any extent — found use in circumstances where it was not possible to obtain more images? Also, could you cite the original reference. Researchgate is not a journal.

This is used routinely in time-resolved crystallography and in "diffraction before destruction" when working with free electron lasers XFEL, Nature Methods 8, page 283 (2011)

Thanks. You should add this to your answer and I will upvote it. Unfortunately this list is dominated by what I call “furry animal” biologists. Nothing wrong with that, I suppose, but the effort put into factual hard scientific answers is seldom rewarded in Brownie points.

@David Yes, I was visiting from StackExchange Chemistry. There are question in Biochemistry that could go either way, just as there are questions that fit in physics or chemistry, but will get a different type of answer (or none). Not that there is anything wrong with organismal biology.

As long as a sufficient amount of the reciprocal space has been collected, then it is of course possible. How the phase problem is handled when doing Laue diffraction I simply don't know, but I would assume Molecular replacement or Experimental phases can be used?

@JeppeNielsen Often, the structure is solved by Fourier difference, i.e. most of the unit cell is identical to a known structure, except for changes in the ligand binding site. With free electron lasers, one could in principle build a phase-sensitive detector and measure the phases directly.

@KarstenTheis, what you call fourier difference is equivalent to Molecular replacement phasing. I don't know how one would create a phase sensitive detector for an X-ray Free Electron Laser (XFEL) when one cannot do so for synchrotron based X-rays. The major difference between the two light sources is the peak photon flux and pulse duration. Are you aware that the electrons are separated from the x-rays prior to the diffraction experiment, thus you have to determine both phase and intensity of the diffracted x-rays, not the charged electrons.

@JeppeNielsen Molecular replacement requires a rotation and translation search, often with Patterson methods. Once the orientation of molecules in the unknown structure is known, Fourier difference methods are used to adjust the model.

@JeppeNielsen The difference between XFEL and synchrotron radiation is, as far as I understand, that XFEL is coherent (all the same phase) and synchrotron radiation is not (multiple electrons adding up to create the X-rays, not coherent).

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
What factors affect the rate of transpiration in plant leaves?
I'm trying to get my head around factors which affect transpiration in leaves.
For example, how would applying petroleum jelly to the surface of plant leaves affect their rate of transpiration?
I get that it's basically going to decrease the trasnpiration rate because the stomata will be covered, but I'm not sure about these parts:

How would it affect the rate of transpiration if only the top surface was covered?
How would it affect the rate of transpiration if only the bottom surface was covered?

Also, I think I'm right in saying that increasing wind / applying a fan to plant leaves will increase the transpiration rate, but why?

In addition to the above answer : Carbon dioxide : Increase in CO2 level in the atmosphere over 0.03 % causes stomatal closure and results in decrease of transpiration.

The rate of transpiration is very closely linked with the rate of evaporation from the leaf surface.  Increased air movement across the surface of the leaf (e.g. from a fan) increases the rate of evaporation of water from the leaf surface. This happens because water saturated air is moved away; making the osmotic gradient more pronounced.
As for the relative changes from adding an impermeable substance like petroleum jelly to the top and bottom surfaces of leaves, it's a question of plant-anatomy.  In the majority of plants, stomata are only located on the bottom surface of the leaf.  This is to prevent them getting 'clogged' during rainfall and to keep them out of the sun to minimise water loss (again more sunlight on the stomata would increase the rate of evaporation).  Therefore a plant with the underside covered would have a much slower rate of transpiration than one with the top surface of the leaf covered.
Other factors that would affect the rate of transpiration:

Temperature (Positive Correlation)
Humidity (Negative Correlation)
Light Availability Excluding CAM photosynthesis pathway plants (Positive Correlation - the stomata are in the main only open when photosynthesis is occurring, so transpiration is less at night or on a cloudy day in addition to light  heating the leaf surface)
Water content of soil (Positive Correlation)

amount of salt in soil (negative correlation)


text:
Why does cyanide inhibit CuZnSOD, but not MnSOD or FeSOD?
Different types of superoxide dismutase (SOD) contain different metal ions (Zn, Cu, Mn, Ni, or Fe), all of which allow them to catalyze one reaction, dismutation of superoxide anion, O2−. Cyanide can block this reaction, but only in CuZnSOD.
What is the (bio)chemical mechanism behind cyanide inhibition of CuZnSOD and why doesn't it occur in FeSOD or MnSOD?

It would be nice if you could add some references to your question.

I'm just taking a stab, because my inorganic chemistry is rusty.
cyanate (CN-) is well known to bind to iron (it inhibits hemoglobin and causes anoxia), and it also forms a pretty strong complex with Zinc:
http://en.wikipedia.org/wiki/Zinc_cyanide
I would guess that in the case of the SOD that the other liganding amino acids and the pocket of the enzyme are such that the affinity for cyanide is lowered to the point that oxygen can displace it.
In the case of hemoglobin, CN will coordinate to the heme iron in much the same fashion that O2 does, but it doesn't come off.   In the case of SOD, the enzyme will be looking to coordinate to superoxide O2(2-) which would be at a roughly tetrahedral angle to the metal.   This is not a favored geometry for CN coordination, which prefers to linearly coordinate to things.
In the case CuZnSOD it seems likely that this enzyme has enough room and its Zn and Cu binding envirionments don't forbid CN binding. it would be an evolutionary accident really as to why one is sensitive and another is not.
some structures at rcsb:
SODs:
http://www.rcsb.org/pdb/results/results.do?qrid=C0740111&tabtoshow=Current
thiocyanate bound. the pocket is pretty open between the two ions.  no CN bound structure.
http://www.rcsb.org/pdb/explore/jmol.do?structureId=1SXS&bionumber=1

One can argue that only the "eukaryotic" types of SOD are sensitive to cyanide treatment:

FeSOD is designated as "prokaryotic" type of SOD which is uncommon (but possible) for eukaryotes (reference).
CuZnSOD is a cytosolic SOD, whereas MnSOD is located within mitochondria (reference). Taking into account the endosymbiotic theory we might also suggest that MnSOD is also a sort of "prokaryotic" SOD.

This answer is not yet a biochemical mechanism.


text:
Why are Birds and Reptiles with abundant yolk sac polyspermic?
I was given an explanation that birds and reptiles are polyspermic because they have an abundant yolk sac. But how does it explain the thing?
Chicken as an adult is not using in my opinion yolk as an energy source.
Yolk is used during embryogenesis as the primary energy source with blastula and gastrula -stages and during organogenesis, since the embryo needs proteins and energy somewhere.
How does abundant yolk sac make birds and reptiles polyspermic?

My professor says that

The yolk sac is not connected to the mechanism of polyspermy or
  monospermy. [Amount of yolk inside the oocyte is then again.]  The
  oocytes of reptiles and birds are yolk rich  - polylecithal  for instance.

where
lecithal = yolk containing and some pieces of information about here.


text:
Which organisms have the neuroanatomy Roger Penrose supposes play a role in consciousness?
In The Road to Reality, Roger Penrose suggests that certain brain structures might play a role in consciousness

Most particularly, lattice neuronal microtubules, as originally
  suggested by Stuart Hameroff but perhaps also other structures, like
  synaptic clathrins, whose structure closely resembles the c60
  molecules.

He supposes this would have to do with some sort of quantum coherence:

...the scheme would require some kind of large scale quantum coherence,
  acting broadly across considerable regions of the brain having
  features in common with high temperature superconductivity.

In general, which organisms have these structures? Are they common?

note that Penrose's theory for 'quantum coherence' playing a significant role in the brain is largely discredited.

i believe the structures mentioned here are just about in every neuron, fyi.  Artem is right though.

@ArtemKaznatcheev It's important to mention that Max Tegmark who rote paper on Penrose's work used his own model not the one proposed by Penrose and Hameroff.
Currently(2020) 6 predictions of the theory of 20 appeared to be true, other 14 are have not been discredited.

Microtubules are a structure in the cytoskeleton, they are rope like polymers that grow to a length of about 25 micrometers (25000 nm), and have an outer-diameter of around 25 nm. For comparison, the mean spacing between atoms is on the order of 0.1  to 0.2 nm; so the micro tubule really is micro: about 200 atoms across. In terms of quantum effects though, this is pretty big but not unreasonable. Researchers commonly use quantum dots to play with quantum effects, and these are typically spheres on the order of 10 to 50 atoms in diameter. Note, that we don't know how to couple 5000 quantum dots in one coherent chain (how many you would need to get the length of a microtubule).
So microtubules are small, but they are common! Microtubules are found in all dividing eukaryotic cells and in most differentiated cell types. In other words, that mosquito you just smacked and that philosophers always give as an example of something non-conscious is full of microtubules. This should raise some red flags, but we don't need to go into more detail of microtubules to discredit Penrose and Hammeroff. However, if you love cell biology, take a look at Desai & Mitchison (1997).
So microtubules are probably a bad basis, but why did Penrose want quantum effects in the brain? In The Emperor's New Mind, Penrose suggests consciousness is non-algorithmic and suggests that a magical quantum computer could do these non-algorithmic tasks. The reason I use 'magical' is because a real quantum computer is Turing-complete, if a classical computer cannon solve a problem then neither can a quantum one (of course, if a classical computer can solve a problem, then quantum one can as well and might be able to do it qualitatively faster). For a nice computer science debunking of this part of Penrose's argument take a look a Scott Aaronson's lecture notes.
Why did Hammeroff want quantum-ness? To avoid dualism in explaining consciousness. However, he has gone so far down the reductionist rabbit-hole that he popped out on the other side. He arrived at the same 'magic' we feared in dualism except now he called it 'quantum mechanics'.
The biggest irony of this approach is that Penrose was inspired in many ways by Schrodinger's beautiful take on life. Although Schrödinger does bring in quantum mechanics (both as a useful reduction and as an analogy) he uses completely different parts of it (he uses the discritization of energy levels, and specially avoids issues of the uncertainty principle and superposition of states that made him famous).  Schrödinger would completely disagree with Penrose and Hameroff::

[I]f we were organisms so sensitive that a single atom, or even a few atoms, could make a perceptible impression on our senses -- Heaves, what would life be like! To stress one point: an organism of that kind would most certainly not be capable of developing the kind of orderly thought which, after passing through a long sequence of earlier stages, ultimately results in forming, among many other ideas, the idea of an atom.

This response can be made precise through quantum decoherence (Tegmark, 2000) and there is little regard for the physical importance of quantum mechanics in the brain (Litt et al., 2006) although Hammeroff (2007) still defends it.

Nice summary but Schrödinger is wrong. Single, small molecules (few atoms) do make perceptible impressions on our senses, notably in smell and vision (where a single photon can trigger a perception).

@KonradRudolph I didn't want to imply that Schrodinger was right, just that he would disagree with Penrose. If the quote is misleading, the we can replace it by one from later on in What is Life?: "To the physicist I wish to emphasize that in my opinion, and contrary to the opinion upheld is some quarters, quantum indeterminacy plays no biologically relevant role" (emphasis from original text)

Fair enough, in particular since I happen to believe that Penrose is off his rockers here. That said (and unrelated to my first comment), I’m pretty sure that quantum indeterminacy does play a biologically relevant role. Otherwise catalytic effects of certain enzymes are hard to explain (e.g. electron transfer chain). From my limited understanding of quantum physics, these mechanisms rely on borrowing quantum particles, which works thanks to indeterminacy.

"mechanisms rely on borrowing quantum particles" made me shudder, but you are correct in spirit @KonradRudolph that quantum effects are important in chemistry. I will try to think of a way to remove the Shrodinger quote since it seems to make people uncomfortable (I just really like that quote :D).


text:
Where does meiosis II of oogenesis end exactly in tuba uterina - uterus?
I know that metaphase II ends at ampulla tuba uterina, but I am not completely sure where the telophase II ends. Is it in the triangular section of cervix uterii?
I just have an intuition that the thing is not ending at the ampulla, since there is some time to get to the uterus. The thing must happen before implantation to the uterus, since the egg is blastocyst at the stage.
2. When does meiosis II of oogenesis end exactly?

The location is exactly tuba uterina infundibulum, source, since the processes results in the following things before LH peak:

The correct placement of the uterine tube infundibulum upon the
  ovarian surface
The rupture of the follicle wall and the flow of the
  follicle fluid with the oocyte into the infundibulum
The inhibition of
  the maturation of further follicles


text:
Mitosis in human body
I've heard that stomach lining has the fastest reproducing cells and the brain has the slowest.
Where in the human body does mitosis occur and at what rates do these cell reproduce? Is there a chart for the whole body available?

It's not that they have different rates. The stomach epithelium just has a lot of stem cells that can divide non-stop, the brain has very few. Usually, the specialized cells in the body don't divide themselves; a small reservoir of undifferentiated stem cells (maintained for just this purpose) divides and some of the new stem cells differentiate to make more specialized cells. Specialized cells can de-differentiate and revert to stem cells sometimes, too.

In many cases cell division depends on the stage of development an organism is in. The rate of cell division is obviously much faster in a developing organism and from what I understand fully differentiated cells such as neuron and those in skeletal muscles don't divide (correct me if I'm wrong here).
In early development totipotent cells (stem cells that can become anything) begin to differentiate dependent on environmental factors, turning into multipotent (partially differentiated) cells that can only lead to certain cell types. For example: mesodermal precursors can differentiate to myoblasts, which can go on to differentiate into myotubes, later forming muscles.
Epithelial and and blood cells are the two of the main types of cells that need to be constantly replaced in developed organisms. As far as I know cells lining the gut epithelium are fastest to divide. They are created from stem cells in 'crypts' (pockets) in the lining and are pushed outwards, where they are later broken down (by what I would assume would be abrasion and intestinal juices). My book gives them a lifespan of 3-5 days. External skin cells are much slower to divide (though I'n not sure by exactly how much).
Red blood cells have have a lifespan of approximately 120 days. They are replenished by stem cells in the marrow of certain bones (e.g. a femur). Neutrophils are the next most common blood cell, with a circulating life of 8 hours (but lifespan may be a few days). Per day, roughly equal numbers of RBCs and neutrophils are created and are most numerous new cells created per day. Lymphocytes, another white blood cell, are responsible for immune 'memory' can persist for years. The fastest recorded mitotic cycle for a mammalian cell (in culture) is ~8-10hrs.

But from how I understand it, blood cells are not really cells in the sense that they are just bags of haemoglobin without the standard internal organelles found in cells.

That's right, but they do develop from precursor cells that contain a nucleus. To be honest, I don't know of many other cells that continue dividing at a steady rate. As far as I know cells such as fibroblasts and macrophages are mainly produced in response to stimulus. There are probably other types that I am missing however...

Nice answer.   Can you expand the abbrvtn IIRC (not everyone would know). Red blood cells have a lifespan of approx 120days. Neutrophils are the next most common blood cell, with a circulating life of 8 hours (but lifespan may be a few days).  Per day, roughly equal numbers of RBCs and neutrophils are created and are most numerous new cells created per day. Lymphocytes, another white blood cell, are responsible for immune 'memory' can persist for years.  The fastest recorded mitotic cycle for a mammalian cell (in culture) is ~8-10hrs. Feel free add this in, if helpful.

Yeah sure, done :)

Question is two years old, and the answer is approx 20 yo, but I believe both are still pertinent: According to Jared Diamond on pg 12 of his Harper paper version (1993 -- but reissued in 2006) of The Third Chimpanzee, we replace intestinal lining epithelium every few days, urinary bladder lining every two months, and replace every red blood cell about every four months. So though blood cells are fast (and probably more numerous) they are slow compared to the intestinal cells!
It seems amazing that the telomeres of the intestinal walls' cells don't wear out and begin cancerous changes much earlier than they do...if the statements above are all accurate. I do find Diamond an incredibly insightful writer and think you can trust him.

Can you add a link (or a proper citation, First author, Journal, Volume, Issue, and page number) to the answer? It makes finding the reference much easier.


text:
Which organism has the sharpest vision?
Which organism has the sharpest vision in terms of distance and spectrum. Please propose any other useful measure.

You might also want to consider field of vision and acuity.

you may want to pick a metric, humans have decent acuity but see a much smaller portion of the spectrum than non-mammals. Almost any bird see's more of the spectrum than almost any mammal.

A good measure for "sharpest vision" is known as acuity of vision. Visual acuity denotes the ability to perceive detail and resolve temporal motion. This metric informs how sharp or blurred an organism perceives its surroundings. There is software which helps quantitate this metric with visual examples.
The following example shows how a comparison of different organism's perception may look like, visually:

When we broadly compare the various vision systems of organisms based on acuity, a plot below may give one a better perspective:

From the above, it is noted that eagles have specially evolved eyes with high visual acuity. Of note, the Australian wedge-tailed eagle can see 8 times more detail than humans can. Interestingly, their eyeball have the ability to squeeze and elongate similar to a zoom lens on a camera.
Reference:

Wedge-tailed Eagle Factsheet

Visual Acuity and the Evolution of Signals

AcuityView Software

So I guess without glasses, my vision is as good as that of a butterlfy.

This paper suggests that bats have a comparatively high depth of focus.
It's believed that butterflies (depending on species) have the widest visual spectrum.

Don't hawks have exceptional range?

Birds of prey - hawks, falcons, eagles, vultures - along with some owls all have exceptional vision.

I thought bats were blind.

How about the Mantis Shrimp?

T-rex
As an archosaur it sees a wider portion of the spectrum than mammals and it has the largest eyes known in terrestrial vertebrates, and eye size correlates well visual acuity, so the largest eye should be close the the highest acuity.
So yes Jurassic park could not be more wrong about T-rex vision, T-rex would see better than the humans trying to hide.
https://www.karger.com/Article/Fulltext/357830#:~:text=Thus%2C%20as%20eye%20size%20increases,eye%20length%20(table%201).
https://www.academia.edu/13386081/Evolution_Beyond_the_rainbow


text:
Why do mammalian red blood cells lack a nucleus?
How did the red blood cell in humans get to lose its nucleus (and other organelles)? Does the bone marrow just not put the nucleus in, or is it stripped out at some stage in the construction of the cell?

all mammals rbc's lack nucleus at maturity....but camel is an exception to this fact as it posses nucleus in its rbc's even at maturity coz. it makes use of its reserved fats with the help of rbc's.rbc's oxidises its reserved fats which is later utilised by it.

Red blood cells are initially produced in the bone marrow with a nucleus. They then undergo a process known as enucleation in which their nucleus is removed. Enucleation occurs roughly when the cell has reached maturity. According to one research (Ji, et al., 2008), the way this occurs in mice is that a ring of actin filaments surrounds the cell, and then contracts. This cuts off a segment of the cell containing the nucleus, which is then swallowed by a macrophage. Enucleation in humans most likely follows a very similar mechanism.
The absence of a nucleus is an adaptation of the red blood cell for its role. It allows the red blood cell to contain more hemoglobin and, therefore, carry more oxygen molecules. It also allows the cell to have its distinctive bi-concave shape which aids diffusion. This shape would not be possible if the cell had a nucleus in the way. Because of the advantages it gives, it is easy to see why evolution would cause this to occur. However, since little is known about the genes the control enucleation, it is still not a fully understood process.

Are there references for the second paragraph?

I can't find any references to journal articles, but the facts mentioned are often stated in text books or lecture notes. For example: http://faculty.ucc.edu/biology-atsma/misc/blood.htm

It's too bad they don't have citations. It would be nice to get away from just so stories and have a real evolutionary answer.

I don't have access to the full text, but this article proposes resistance to oxidative stress as a reason for enucleation: Red blood cell extrudes nucleus and mitochondria against oxidative stress

It's a matter of geometry and physics. The nucleus is a huge volume of the red blood cell. Without the nucleus, its tissue-specific cytoskeleton arrangement allows it to form a bi-concave disc morphology. This disc shape also maximizes its surface area to volume ratio for maximized gas exchange, as well as affording the immense flexibility when squeezing and pinching through capillaries.

So how do birds manage, with a lumpy nucleus in the red blood cell?

I'm guessing there is no real reference. Its hard to prove that the nucleus is a problem for rbcs - the control experiment - comparing to rbcs with nuclei - is technically difficult.   It makes sense to say it so, its passed on.

Shown to be in mice & rats (and sick humans), the cell-cell interaction between a macrophage (this is a big engulfing cell required for immunity) and young red blood cells (RBC), is known as the erythroblastic island (commonly known as EBI). If you googled it, there is a scientific review in 2008 that describes this structure.
At the embryonic stage (in humans), we still retain our RBC nuclei. But as we developed into fetus and adult, we no longer have RBC nuclei. This is thought to be related to the EBI present (in the fetal liver and adult bone marrow respectively). Currently, there is a lack of information of the EBI in other mammals. The only proven ones are mice, rats and sick humans. It is widely assumed (not proven) that mammals have EBIs. Besides mammals, some other animals (e.g. birds) have enucleated RBC, and some don't. It is unclear why is it so. Our lab thinks that it might be related to the formation of the EBI.
In addition to engulfing the RBC nuclei, it is believed that the macrophage acts as a "nurse" cell as proposed in the 50s. In other words, possibly providing iron, and possibly providing some proteins required for young RBC to mature. In early 2013, for the first time, it was showed that these macrophages are important in animal models (published by 2 research groups in nature medicine journal).
As for enucleation (the removal of erythroid nuclei), the exact mechanisms are unknown. But cytoskeleton proteins are important players in enucleation. However, there isn't enough information, as these proteins are essential for other important cellular activities as well. For example, bringing in nutrients, development and cellular migration. Most animal models that lack these proteins are unavailable for studies, and these animals usually die at the embryonic stage.
The research mentioned by EdoDodo is a proposed model on how enucleation takes place, and is a widely accepted model. Currently, our lab are working on another model that could partially explain how enucleation is being triggered.
Advantages of enucleation
In addition to better oxygen diffusion across the membranes, some older scientific papers mentioned that it lightened the cardiac workload. Each extruded RBC nuclei is approximately 40 picograms. A normal healthy adult individual would produce about 2 million RBC per second. That would be 0.08 milligrams of weight per second are required to be removed. However, I couldn't trace the scientific evidence for this claim, but this have been cited by some scientific papers.
The other advantage would be to reduce risk of hemolysis when transversing through the microvasculature. In other words, mature RBC can move along tiny blood capillaries by changing their biconcave shape (to bell-shaped I think), so that they will not rupture (and die).
Also, not all RBCs have similar shapes and sizes. You might want to google it for more information. I think camels have slightly different RBC morphology.

I checked for the publications you mentioned here. I did not find any publication for macrophages and EBI in Nature Medicine, but I found two reviews from 2008 about EBIs: The Erythroblastic Island and Erythroblastic islands: niches for erythropoiesis. In case somebody wants to read them: they are freely available. It would be nice if you could add the other two papers, too. Thank you!

The only function of the red blood cell is to transport oxygen, and nothing else. Its concave shape is to increase its surface area, so more oxygen can be transported per cell. The absence of a nucleus means it can be significantly more concave than an other cell of analogous size, meaning it can carry more oxygen.
Other answers are more detailed, but this is the main reason that there is an absence of a nucleus.

The relationship between carrying more oxygen per cell and surface area does not follow logically to me. Enucleation will lead to increased surface area per unit volume, which will relatively increase the area for transport across the membrane. But aside from increasing Hb content or concentration, that won't lead to more oxygen carrying capacity.


text:
What's the advantage of autocrine signalling?
In the antibody-mediated immune response, when the helper T cell gets activated by the costimulus (IL-2 and TNF-α secreted by the APC) which in turn produces IL-2, IL-2 acts in an autocrine manner. I'm just wondering why does IL-2 have to be secreted? Why doesn't it just exert an affect while it's already inside the helper T cell? What's the point of autocrine signalling?
I hope the answer isn't going to be, "Well, that's just the way it is..." because paracrine and endocrine make sense and have advantages, but autocrine just seems a bit extra.

Why doesn't it just exert an affect while it's already inside the helper T cell?

Because it interacts with membrane-bound receptors. Those are outside so there is no way IL-2 (or any autocrine factor) could signal while inside the cell. It has to exit.
Now, the next question is why the receptor is membrane-bound and outside. As far as I understand there are two parts to this answer:

Receptors are evolutionarily related so they follow similar synthesis pathways.
Membrane-bound receptors are (all?) transcribed while being secreted into the endoplasmic reticulum. This causes their agent-binding portion to reside inside the ER. From there, vesicles bud off, are transported towards the cell membrane, merge with it, and hence the formerly inside portion of the protein ends up on the outside.

paracrine and endocrine make sense and have advantages, but autocrine
  just seems a bit extra.

Autocrine also have advantages compared to internal signaling. Even if when you study mechanisms you think at single cells, cells are never alone in the body. If the message (IL-2) would be internal, each cell will individually respond according to its internal signaling levels. With the 'extra' to secrete the message, and having it sensed at the exterior (the receptor is membrane-bound), all the cells in the nearby are going to contribute to the average signal and will respond with average magnitude. It's a form of communication between a single cell population that does not affect other cells populations (the ones that does not express the IL-2 receptor).

That's a very interesting answer !! It means that fluctuations in the signalization are balanced by this phenomenon. Would there be articles about that kind of phenomenon ?


text:
How does a plant grow before photosynthesis is possible?
During photosynthesis, a plant translates CO2, water and light into O2. I assume the carbon C is further used for the growing process. I wonder how the plant grows before the time where photosynthesis is possible, i.e. before there are even leaves, in which photosynthesis occurs.

To what extent does the plant grow from the seed/the minerals in the ground?
How much carbon are relevant for which parts of the plant and at what times of the evolution of the plant?

I don't know if there are only these life periods of the plant, i.e. if there are other major biochemist-of-growing changes, than in the comparison before and after the plant got leaves. So are there other relevant aspects to this? If there are leaves present, is the rigid structure of the plant only coming from the CO2 in the air and not from the ground anymore?
The answer will probably depend on the plant. So here is another formulation of the question:

What are typical characteristics of different plants in this regard? I.e., how do common species of plants manage their C consumption before (and after) the development of leaves?

Photosynthesis fixes carbon dioxide into organic molecules - the water is broken up during the process and the oxygen from it released and light also doesn't really belong in the equation.  I think the important bits you are looking for are about carbon fixation specifically but I didn't want to edit your original meaning out - could you clarify? =)

@RoryM: Okay, done.

There are quite a few questions and thoughts in there, I'll try to cover them all:
First, to correct your initial word equation: During photosynthesis, a plant translates CO2 and water into O2 and carbon compounds using energy from light (photons).
You are correct to assume the C is further used for the growing process; it is used to make sugars which store energy in their bonds. That energy is then released when required to power other reactions, which is how a plant lives and grows. C is also incorporated into all the organic molecules in the plant.
Plants require several things to live: CO2, light, water and minerals. If any of those things is missing for a sustained period, growth will suffer. Most molecules in a plant require some carbon, which comes originally from CO2, and also an assortment of other elements which come from the mineral nutrients in the soil. So the plant is completely reliant on minerals.
Most plants, before a leaf is established or roots develop, grow using energy and nutrients stored in the endosperm and cotyledons of the seed. I whipped up a rough diagram below. Cotyledons are primitive leaves inside the seed. The endosperm is a starchy tissue used only for storage of nutrients and energy. The radicle is the juvenile root. The embryo is the baby plant.

When the seed germinates the embryo elongates, the endosperm depletes, the testa ruptures, and the cotyledons emerge from the seed. The cotyledons are green, and like leaves can photosynthesise, so as soon as they are in the light the plant is able to make carbon compounds. The radicle elongates at the same time, and becomes the root, so the plant is very quickly able to obtain fresh nutrients from the soil (or whatever it's growing in).
At all stages of a plant's life it is using both energy stored in carbon compounds (from CO2) and nutrients which it took up via its roots. At no point does the plant start to depend solely on the CO2 in the air for its growth.
You are right that the way in which plants acquire energy and nutrients prior to leaves and roots being established varies between plants. Above I outlined the way most plants use. But there are lots of variations. For example, orchids have very tiny seeds, some barely visible to the naked eye, like specks of dust. They have no endosperm or storage tissue, so they have to rely on a symbiotic mycorrhizal fungus to get carbon and nutrients. The fungus grows through the coat of the orchid seed, then provides everything the growing plant needs until it has its own leaves. Then the orchid repays the fungus by providing sugars.
There are lots of other examples, but we could go on all day!

Sweet diagram. :)

Thanks! I always find things easier to explain with pictures.

Simply put. Plant growing from sugar (both energy and material). So if they could store sugar (or even find sugar from anywhere). They could grow even there are no sunlight
And photosynthesis never make plant grow immediately. It just make sugar. And plant store it. Actually many plants grow at night while eating sugar it stored on daytime
Some plant store sugar so much in their root (all root vegetables), so they could survive on dark winter or even all the leaves was eaten. There are one plant even evolve into a parasite without any chlorophyll and live by growing from another plant's root
Another trick plant was used is, it grow by decreasing density, make it bigger with a little more weight compared to the seed. By consume water it spring out larger and ready to catch sunlight. It like you pack your travel bag tightly and it explode when you open it again


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Is there any reason for the variation in mitochondrial DNA size?
As my textbook An Introduction to Genetic Analysis points out, yeast mitochondrial DNA has approximately 78 kb of genetic data, while the human mitochondrial DNA contains 17 kb. Is there any evolution reason for this drastic change in size? Also, are there any particularities about mitochondrial function that have been compromised with this reduction in size?

References

Griffiths, Anthony J. F. An Introduction to Genetic Analysis. New York: W.H. Freeman, 2000.

I know yeast is supposed to have very little non-coding DNA, but could it be possible that mitochondria in yeast have more intron regions?

There is a diagram showing the decrease in intron regions for humans. Nonetheless, could the sole evolutionary reason for the decrease be that it's simply more efficient in replication, or the efficiency of use of nucleic acids?

I think that to look at the evolutionary aspect of this question fairly, one needs to consider many other organisms in addition to human and brewer's yeast. An alignment of the genomes, or perhaps a simple list of the encoded genes will address the question of compromising of function with changes in genome size.

One of the contributing factors the size of the yeast mitochondrial genome are 'selfish' mobile genetic elements termed homing endonucleases genes (HEGs).  These genes are typically found in introns that encode site-specific DNA endonucleases.  These endnoclueases cleave the HEG- alleles during yeast mating leading to DNA recombination using the HEG+ allele as template.  I suspect over time as organisms became more complex and HEGs become unable to mobilize they would become fixed in the organisms genome.  Upon being fixed there is no selection pressure to maintain the open reading frame of the HEG or the intron its encoded within (ref).  This causes the eventual loss of the HEG and intron since they provide no real benefit to the organisms genome.
I don't know how much of the yeast mitochondrial genome is taken up by these introns.  I believe that there are 4 of them in yeast some of the introns also require reverse transcriptase for splicing and mobility.  Other fungal species can have many more introns and sometimes weird things like introns embedded within introns.

Shorter DNA would allows easier synthesis, but more introns could  allow for more different transcription factors to influence gene expression.
Human mitochondria probably does not need to be as adaptable as mitochondria in yeast, since the a human cell's environment tends to be more stable. This could provide a viable reason as to why human mitochondria does not need as many introns, but this is only how I imagine things. I have no proof or experience to validate any of this - its just a possiblility.

Multicellular have mt-DNA that contain 14 - 20 kb  but planta have mt-DNA that contain 200 -2500 kb.
Yeast mt-DNA ís in between.
It seems that the role of the mitochondria determines its size rather than its evolution.lífið

Hi and welcome to biology.sx. It would be great if you could add some references so that interested readers can follow this up.


text:
Can two humans with 44 chromosomes produce viable offspring?
It is known that there are very few individuals having 44 chromosomes, not the usual 46 chromosomes.
One example is a male in China: the first article, the second article.
The other is a female in Turkey, unfortunately the article is in Turkish.
It is claimed in the links that they might reproduce and make healthy children if they mate. So I wonder if this already happened and such a couple is living, or if it would be theoretically possible?
Edit: As requested, here is the Karyotype of Turkish female, which the professor in the video call her HomoNeoSapiens, with Robertsonian translocation between 13 and 14 chromosomes. So, this translocation is different from Chinese Man's translocation, which is between 14 and 15 chromosomes. So in this case they can't breed a healthy children? Gosh, I was about to create a new species :((

I migrated the question to Biology and also rewrote it to include the question if it is at all possible, not only if it already happened, please correct it if I did misinterpret something.

"both his chromosome 14s are stuck to his chromosome 15s" - means both his mom and his dad had a Robertsonian Translocation which doesn't really result in the loss of any genetic material.

The article says "both his chromosome 14s are stuck to his chromosome 15s" - meaning both his mom and his dad (46,XX,rob(14,15) and 46,XY,rob(14,15) had a Robertsonian Translocation which doesn't really result in the loss of any genetic material. The very small chance occurred which one sperm carrying the translocation chromosome fused with an oocyte carrying the other translocation chromosome.
So the genotype of the dude is 44,XY,rob(14,15)(14,15), meaning he's normal because he technically has all the genomic information of a normal human.
If he mates with a normal woman (46,XX), then the resulting progeny will have an extra copy of chromosome 15, resulting in trisomy 15, which is non-viable.
If one such 44 chromosome individual mates with another person of the same chromosomal arrangement, then probably a viable fetus would be produced if a translocation chromosome ends up with the same translocation chromosome from the mother. I wouldn't call it a new species per se because it still contains the genetic material from a human. For example, there are many humans with chromosomal abnormalities (I.e trisomy 21, XXY, etc...). Also the background rate of translocations and chromosomal aberrations in somatic cells is notable, so I wouldn't use this as a new species definition.

same Robertsonian Translocation is claimed to have happened for us the human. and This translocation might have created a few new genes that separated us from Chimpanzee. I mean, although that 44 chromozomed guy have the same genetic codes, he might have additional genes as well which lead him to be a different species, right? http://www.thetech.org/genetics/news.php?id=124

I don't see where additional genes may come from. Also, speciation is a very gradual process that takes tens of thousands of years so I doubt the appearance of this 44 chromosome man is the defining point of a new organism.

If he did have 22 chromosome children sounds like they could start a new species!  exciting if you like science fiction.

Interesting question. You refer to aneuploidy.
I don't have idea, but I loved to make some calculations. Feel free to edit because there are some very approximative assumptions.
Aneuploidy, the loss or gain of a chromosome, is estimated to occur in 13-25% of oocytes, 1-4% of sperm, 20% conceptuses and 0.3% of newborns. (reference)
The 46 chromosomes are made of 23 pairs, if the chromosome loss is evenly distributed, we have 0.3% / 23 newborns with the same chromosome loss (0.013 %).
Now, consider that the lost chromosome is likely not really lost, but just translocated on another of the 22 chromosomes. For instance, the individual you refer was having two chromosomes (the 14 and the 15) fused together.
So individuals with the same chromosome loss (0.013%) should have also the same translocation on one of the remaining 22 chromosomes (0.013% / 22 = 0.00059%).**
Chances are now that two of the 0.00059% newborns with exactly the same chromosome loss, will mate together.
Assuming random mating between humans, we have 0.00059% x 0.00059% = 0.0000003 % of possibilities, which is 1 possibility every 333,333,333 human beings.
We are now 7 billions on the Earth, so assume 3.5 billion couples all fertile despite of the age. If we assume also no spatial constraints, so that everyone could mate with every else one on the Earth, there could be no more than 10 couples with the same aneuploid mutation.
Provided the mutation does not affect genes important for reproduction, for instance genes between the two chromosome junctions that get interrupted, this couple could reproduce I guess.
To find that child, chances are now that he/she will have a kariotype done. Quite difficult to find isn'it?

There could be more than 10 couples with the same mutation. Probability does not mean actuality. 10 is only the expected result.

I want to carry answers from soon-to-be-deleted forum to here (I also asked this in Coursera's Introduction to Evolution And Genetics), since I find them valuable. All of them belong to Andrew Wilmoth :
1st Answer:

The man has a Robertsonian whole-arm translocation which fuses
  chromosome 14 & chromosome 15. Essentially all of the genetic material
  is there, just packaged differently. He could have children whole are
  phenotypically normal regardless of whether his partner has a normal
  chromosome complement or a similar translocation.
My Turkish is inadequate to understand the karotype of the woman in
  the other link.
Persons with translaocations are well known. It is rare but hardly
  unique. The odds of two such persons randomly meeting each other and
  mating are probably pretty low. Depending upon each partner's exact
  karotype there may be no difficulty producing healthy offspring with
  unusual chromosome complements.
"If they will have make a new species, let's breed them!! Why doesn't
  science try that? :))"
Because they are people and they might not want to have a child
  together? Experiments on humans require informed consent. I cannot
  imagine conducting any such experiment to satisfy scientific
  curiosity.

2nd answer:

A child born of such a voluntary mating would not by itself be enough
  to be considered a new species. There are a wide variety of
  chromosomal rearrangements that are known and there is no serious
  speculation that persons with such karotypes are members of a
  different species.
It is quite possible that one of the many evolutionary changes that
  separate humans from chimpanzees evolutionarily is a translocation
  that fused chimpanzee ancestral chromosomes 2a and 2b to form human
  chromosome 2. There is strong genetic evidence for such a fusion.

3rd Answer:

As you surmised, every possible combination of gametes with those two
  karotypes will result in an aneuploidy... unless there is a mutation
  which "fixes" the problem.
But the gametes produced by these two individuals would not inherently
  be expected to result in a problem in an offspring. The F1 offspring
  would have only 44 chromosomes but likely be normal phenotypically.
  Any F2 generation produced by crossing two individuals from the F1
  would have a problem with possible trisomy 14 which would be expected
  to be fatal.

The man in China had both chromosomes 15 split and attached onto both chromosomes 14. If a male with 44 chromosomes wants to have children with a female with 46 chromosomes, this will not work. He won't be able to have viable offspring. During mitoses, he will have 22 chromatids and she will have 23. They will not match up and therefore no viable offspring. He'd have to meet someone who was his match and most likely that match is in his family, such as a sister or female cousin, who would have the same chromosomal arrangement as he has. In China, this man is from a family where a lot of miscarriages happened and other family members have variations on these fused chromosomes. They are very inbred for this to have happened. Only a close relative who matches identically to his arrangement would be able to have chromatids that could line up with his. His parents had chromosome abnormalities for this to have happened, so this is an inbred family. This family could go on to produce another species of humans with 44 chromosomes if they kept trying and future generations were stable with no odd arrangements that don't line up.
http://www.asiahealthcareblog.com/2011/07/03/chinas-44-chromosome-man-may-be-missing-link-between-us-and-the-chimp/

PS... I meant meiosis and not mitosis. Sorry for the confusion on that one.


text:
What causes fingerprints to form and why is the pattern formed unique?
I've found research that suggests that the reason we develop fingerprints is because they aid us with feeling surfaces (Scheibert, et al. 2008) and not to increase friction  and help with the gripping of smooth objects (Warman and Ennos 2009).
One thing I am still curious about is at what stage of growth the pattern is formed and why a unique pattern is created in the fingerprint of each person (including identical twins). I assume it has something to do with the mechanism by which the patterns form, but I couldn't find any detailed research into this. Any insight would be very welcome.

We can expect this uniqueness in foot[toe] prints as well. I suppose, all derivatives of germ layers should have their identity and heritability. Many forensic literature have explored these areas for personal identification.

I would say genetic diversity is the primary reason which results in other reasons that you are looking for. At the lowest level, random crossing over at prophase I, random separation of homologous chromosomes at anaphase I, random separation of sister chromatids at anaphase II, and random fertilization: one sperm fertilizes one egg randomly.
The skin is developed from ectoderm so need to look at the formation of embryonic disc and specifically to the genesis of germ layers: ectoderm.
However, I would stick to the primary reasons, since it is extremely difficult to visualize the given formation - actually we do not have resources for it at the moment.

Very good question the last part. I have an intuition that skin develops randomly because of the above reasons. You would also need a lot of memory to make identical skins for twins! It has not been useful to have identical fingerprints between two people so evolution has not resulted into it.
Feeling surfaces and gripping are movements - not much space taken things, in contrast to the memory needed in storing the exact surfaces of skin from one generation to another. - Learning is a way to save resources here and it is a lot more efficient and than storing static information to species from one generation to another.

Answer
Fingerprint pattern formation has two components to it: developmental and genetic.
Firstly, this article's abstract describes how fingerprints are physically formed in the womb.

[...] fingerprint patterns are created as the result of a buckling instability in the basal cell layer of the fetal epidermis. Analysis of the well-known von Karman equations informs us that the buckling direction is perpendicular to the direction of greatest stress in the basal layer. We propose that this stress is induced by resistance of furrows and creases to the differential growth of the basal layer and regression of the volar pads during the time of ridge formation.

Also, this OMIM entry describes a study which suggests the function of genes directly related to fingerprint formation.

An assumption is that the basic pattern is all ulnar loops and that a variety of genes cause deviations from the basic pattern. These include (1) a semidominant gene for whorls on the thumbs (one homozygote has whorls on both thumbs, the other homozygote has ulnar loops on both thumbs, and the heterozygote has two ulnar loops or one ulnar loop and one whorl); (2) a semidominant gene for whorls on the ring fingers that acts like the gene for whorls on the thumbs; (3) a dominant gene for arches on the thumbs and often on other fingers; (4) one or more dominant genes for arches on the fingers; (5) a dominant gene for whorls on all fingers except for an ulnar loop on the middle finger; (6) a dominant gene for radial loops on the index fingers, frequently associated with an arch on the middle fingers; and (7) a recessive gene for radial loops on the ring and little fingers. They suggested that these genes may act independently or epistatically.

The first source explains why everyone has different fingerprints, but the second explains why family members and identical twins have increasingly similar patterns.

References

Kücken, M, and A. C Newell. “A Model for Fingerprint Formation.” Europhysics Letters (EPL) 68, no. 1 (October 2004): 141–146.
Slatis, H M, M B Katznelson, and B Bonné-Tamir. “The Inheritance of Fingerprint Patterns.” American Journal of Human Genetics 28, no. 3 (May 1976): 280–289.


text:
What is the main general difference between Mitosis and Meiosis?
I found such a clause:

The general principle is that mitosis creates somatic cells and
  meiosis creates germ cells.

However, I cannot agree. Each gametogonium needs to go through mitosis before it can enter meiosis I. So in that case mitosis is happening with germ cells so the clause is false.
I would rephrase the sentence to be

The general principle is that meiosis creates only germ cells with the possibility of a decrease in chromosome number, while mitosis can create both somatic and germ cells while the ploidy stays constant.

Ok, not perfect.
How would you say the main general difference between mitosis and meiosis?

In plants germ cells are created by mitosis and meiosis creates haploid cells that divide many times before producing gamets so both statements are not generally true.

@MartaCz-C Please, propose your own below. Can be many sentences. Can be in the form like: for this y and for that y. It helps me to think probably other way the problem.

@MartaCz-C Is my sentente, the second one, right for other species if we exclude plants from it? - Is it right for human?

If the question is about the one and only most important difference between mitosis and meiosis, then the answer "meiosis reduces ploidy" is probably correct. But if the list of important differences is open, it would be critical to add that mitosis generates identical cells (identical to each other and any ancestral cells, barring rare new mutations), while meiosis generates genetic diversity by creating cells, which are all different from each other and from any ancestral cells. It does so by independent segregation of homologs and by crossingover within chromosomes.

According to all I've learned and heard, the only thing consistent about meiosis is that it  reduces ploidy because homologous chromosomes are separated. (Not necessarily diploid to haploid - it can be polyploid as well, although odd ploidies usually seem to mess it up.)
Mitosis on the other hand mainly serves to separate two copies of a genome into different cells.

Meiosis is the specialized cell division that generates gametes. In
  contrast to mitosis, molecular mechanisms and regulation of meiosis
  are much less understood. Meiosis shares mechanisms and regulation
  with mitosis in many aspects, but also has critical differences from
  mitosis. This review highlights these differences between meiosis and
  mitosis. Recent studies using various model systems revealed
  differences in a surprisingly wide range of aspects, including
  cell-cycle regulation, recombination, postrecombination events,
  spindle assembly, chromosome–spindle interaction, and chromosome
  segregation. Although a great degree of diversity can be found among
  organisms, meiosis-specific processes, and regulation are generally
  conserved.

Meiosis: An Overview of Key Differences from Mitosis Published by Cold Spring Harbor Laboratory Press


text:
What is the structure and function of chromosomes during interphase?
Ok, it seems to be easy but I have probably ignored something by accident.
Interphase is the phase where things are growing and the preparation for cell division happens. Its stages G1, S and G2. DNA replication in S stage. So the DNA in some chromosomes must have the pieces of information about how to do the DNA replication. - I am not sure  about thing.
I would say to the part: structure that chromosomes are diploid at the given stage. - It does not feel right anyway.
What would you answer to the main question?

So the DNA in some chromosomes must have the pieces of information about how to do the DNA replication. - I am not sure about thing.

Genomes contain what is called the "origin of replication" - specific sequences in the DNA that tell DNA polymerase where to bind and to initiate replication.
As for your main question, I'm a little confused as to what you're asking. In a general sense, chromosomes function as carriers of genetic information. In eukaryotes, nuclear DNA is organized in the nucleus on linear chromosomes which carry most of the genetic information an organism needs to survive. In bacteria, the chromosome is a circular piece of DNA. In eukaryotes, the chromosome is also bound by histone proteins, which serves to regulate expression of certain genes and to help anchor the chromosomes to the inner nuclear membrane.


text:
When do most mammals mate?
Is one part of the day more prevalent then other when it comes to mammal animals mating? Is there an aggregating study that has been done to see if these living beings in nature mate mostly during day or night?

I think this is too vague as written. I think we need a more specific group than "animals."

^ Agree with above. Also, perhaps consider editing the title to read "At what time of day does (inset species name) mate?"

Thanks guys. I am mostly interested in mammals since we can, I guess, consider them most advanced. I've fixed the question title and content to be more specific.

I don't know the answer, but I can help you to restrict your research. With the exception of humans and bonobos that have sex for recreational purposes, all the mammals mate during the estrus. In particular, the female will only allow the male to mate during a restricted time coinciding with ovulation. So if some aggregating study has been done regarding the ovulation, you have your answer.

@96well - ovulations is most likely a few days phenomenon, and I am inquiring especially whether the daylight is accompanying the mating. I suspect that mammals mate only under the day light, but I need someone to confirm it.

Some mammals, including mice, are nocturnal (see a wikipedia list). I know for sure that mice mostly mate during the night (I work with them).

Yes, I have suspected it (about mice), although didn't even bother to check. Thank you again. Now we have one question to answer - are most mammals - daily creatures (non-nocturnal). Most likely yes, right?

I can't vouch for it's accuracy (and can't answer the question), but I found this.
http://answers.yahoo.com/question/index?qid=20090831052348AAOIRCM

Don't have the reference at hand, but I am pretty sure there is a circadian component to it (aside from estral/menstrual cycle obviously)

How are you counting here.  Each mating counts once? Each individual counts once? Each species count once? Each genus counts once?  etc.

Why would it evolve?
No research (that I can find) is consistent with specific time of day mating across many species. I can't think of any reason why even just a few quite different mammals (e.g. mice, bats, lions, whales, and humans) would all find a fitness benefit of mating at the same specific time of day and therefore it is highly unlikely to evolve. I would suggest that if there are consistent patterns they are no reason other than coincidence (correlation over causality).
For example, dawn and dusk peaks in activity...
I have no references to back this idea up but lets see how this goes. The majority of mammals will be awake around dawn and dusk because there is likely an over lap between nocturnal and diurnal species at these times. Given that mating (normally) requires the participants to be awake then this would be a time when more animals are awake it is therefore a more likely time for mating to occur. But, as I already mentioned it would purely be because of the increased numbers awake.
Simple statistical illustration of the dawn & dusk idea...
Imagine a raffle with 2000 winning tickets. You buy 1000 and put 500 hundred of these in a box called nocturnal and the other 500 go in a box called diurnal. The raffle is drawn 24 times (perhaps every hour). The first 14 times it is drawn you can win if the ticket is from the nocturnal box, the latter 14 times you can instead check the diurnal box. This means during the first 10 draws you have a 25% chance of winning, and likewise in the latter 10 hours, but in the middle 4 hours there is a 50% chance every draw.
This comes down to a simple statistical phenomenon, if you don't buy a ticket you can't win the raffle.

Thank you. My idea was to check if there is a corelation between the phases of a Sun (the intensity of light around during different times of the day) and mamal mating activity.

It could be done but choosing which mammals to test would be difficult, they vary substantially in their habitat & behaviour. To get a representative sample of the thousands of different species you would have to sample many of species (from different Orders & Families (biological classification)). It is an infeasible study to do first hand. You could compile data that exists which has been done on single species and conduct a meta-analysis. Again you would have to make sure you capture as much of the behavioural variation as possible. If this answers your question please could you accept it.

also if it does not answer your question then please explain why and maybe I can still answer it