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recombination frequency problem

Three loci C, D and E are located on the same chromosome in this
  order. We found that the frequency of recombinants between C and D is
  10% and that between D and E it is 20%. Assuming that crossing over
  occurs randomly on the chromosome, what is the expected frequency of
  recombinants between C and E?

I know that it should be less than 30% (10%+20%) but the answer given is 26%. I don't understand how they figured that out.
Edit :
The frequency of recombination is <30% because of the chance that a crossover happens between C and D & also between D and E. The probability of that to happen is 2% (10/100 X 20/ 100)
So, why is it 26% instead of 28% ?
Another posssibility : Am I totally off the track ?

I got $26$% as the answer.
To get a recombination between C and E, there are two possible mechanisms:-

C and D produce a recombinant, but D and E remain linked, therefore the final genotype will be a recombinant considering C and E(Chiasmata between C and D). Here $P_1=P_{CD}\times P'_{DE}$ where $P$ is the probability of recombination and $P'=1-P$ is the probability of linkage.Hence $P_1=0.08$
C and D remain linked but D and E undergo recombination (Chiasmata between D and E). Here, $P_2=P'_{CD}\times P_{DE}=0.18$

If there is a chiasmata between both C and D, and D and E, the resultant will not have a recombination in C and E locus due to double crossing over. If there is no crossing over, there will be no recombination at either loci.
The net probability of recombination $P_{CE}$ will be the sum of these two, as any of these possibilities can occur to give a recombination between C and E. $P_{CE}=P_1+P_2=0.26$
And Biogirllajja, your calculation (the Edit) was almost correct, but you have to subtract $2$% from both $10$% and $20$%, because, both of them include the probability of crossover at one loci, including the case where the other loci has also crossed over. Hence, you need to subtract it from both, and then add to get $26$%. Tell me if you want me to expand on my explanation or provide some clarifications.
If we simply add the map distances, we get the actual map distance which disregards the possibility of double recombinations. All map units greater than 10cM have significant chances of double crossovers between them, and hence, the observed recombination frequency would be less than the expected 0.1. Hence, for distances greater than 10cM, the observed frequency of recombination will not be the same as (map distance/100).


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Determining sequence of oligoribonucleotide

Oligoribonucleotide X was treated with phosphatase (for removal of 3'
  and 5' - terminal phosphates), then with RNAase T1, which cleaves all
  phosphodiester bonds located in a 3' position of guanosine in a
  5'-specific manner.
As a result, oligonucleotides L, M and N were generated in equal
  amounts. Each of them was further treated with phosphatase and
  subjected to alkaline hydrolysis. Results are listed in the table
  below.

Then experiment was modified: oligoribonucleotide X after treatment
  with phosphatase was hydrolyzed with RNAaseP, which cleaves all
  phosphodiester bonds in a 3'-position of pyrimidines in a 5' -
  specific manner.

This hydrolysis yielded five products in approximately equimolar
  concentrations: uridine monophosphate, cytidine monophosphate and
  oligonucleotides P, Q and R. After resolution of the mixture and
  alkaline hydrolysis of these oligonucleotides data listed in the table
  below were obtained.

My thinking : G can not be at the 5' end otherwise we would get a single Guanosine also in the first experiment. G can also not be at the second last from 3' end as we have not got any singles. We have got A and C in a duplet and so they must have been at the 3' end.
I also have trouble understanding the significance of "mole/mole of oligoribonucleotide".
I am trying to fit  in other results but am unable to do so.
A GOOD HINT WILL BE APPRECIATED MORE THAN A DIRECT ANSWER.
Thanks

@Satwik In the above comment - do you mean UMP and CMP ?

@SatwikPasani And by doublet u don't mean they are 1 after the other because I don't think that is possible.

@biogirl It's not clear from what you have written so far that you realise the significance of getting a cytidine rather than a CMP in one of the products - it means, for example that you can deduce the sequence of M, which in turn allows you to deduce the sequence of Q.

@biogirl Did you solve this? If yes, I wanted to know the answer they(the source of the question) provide, to make sure I had the correct solution.

@SatwikPasani I haven't tried this question again as I was busy in other things. Will ask for your help if I am still not able to do it. The answer to this question has not been given in the source. Thanks.

@satwik pasani Nope! I am not able to solve it .Please tell me the answer (not the solution as I want to "reverse derive"it !)

@biogirl I had forgotten my original derivation but I quickly re-derived it. Please check if I have made any errors in haste. $5'-UACGCCGAC-3'$

@SatwikPasani Thanks a lot : I will "reverse derive it"

@SatwikPasani ok i have done it. It's right. Thanks a ton !

Here are a few hints which might help you:-
1) You get free UMP and CMP (in contrast to UMP + C or CMP + U) in the second experiment before alkaline hydrolysis.
2) There are two CMP in "N" oligoribonucleotide, and a free cytidine (and not CMP) in "M" and "Q".
3)Use the fact that all oligoribonucleotides were treated with phosphatase before being subjected to alkaline hydrolysis.
(Referring to your comment, I dont know why do you think consecutive cytidine is not possible).
These are a few hints that helped me solve this. If you want further clarification or the answer, tell me in the comments.
Answer for reverse derivation:- $5'-UACGCCGAC-3'$

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Histidine - why essential for children?
Why is histidine an essential amino acid for children but not for adults ? What changes in the body occur which lead to the formation of histidine in adults but not in children ? What causes these changes ?
UPDATE : Source : Campbell Biology

Do you have a reference for this fact?

Some sources suggest that histidine is essential for human in all ages.

@Mys_721tx Oh yes. There is controversy regarding this. Some of my textbooks say different things too. Maybe the scientific community hasnt decided on this.

If an amino acid is essential it means that we cannot synthesise it de novo from central metabolites, or from another amino acid. Since histidine isn't related structurally to any other amino acid we can assume that in this case we would require a pathway for de novo biosynthesis.
The biosynthetic pathway enzymes for histidine in yeast (Saccharomyces cerevisiae) are encoded by the genes HIS1 - HIS7. In a BLAST search using yeast His4p against Arabidopsis (plants can make histidine)  there is a significant match to a histidinol dehydrogenase (the penultimate step in the pathway). In a similar search against humans there is no significant hit. Expanding the search to all mammals there is only one significant match, which is to the Tibetan antelope, Pantholops hodgsonii. This puzzled me, but when I searched with the antelope sequence as probe I got lots of perfect matches to bacterial histidinol dehydrogenases, so presumably the antelope sequence is a contaminant.
I also searched for human matches to His1p (encodes ATP phosphoribosyltransferase - the first step in the pathway) and His3p (encodes imidazoleglycerol-phosphate dehydratase - the sixth step in the pathway) and found no significant matches.
I conclude that humans have no capacity for histidine biosynthesis and thus histidine must be essential in the diet.

This has been down-voted today without a comment (17th December 2013). It would be helpful if down-voters would explain why they disagree with a post.

-1 because the lack of a homologous gene does not at all imply histidine biosynthesis is impossible. Just because birds lack homologous wings to insects and insects require wings to fly doesn't mean that birds cannot fly.

There are many articles in health literature debating on the question. Everytime the experimental setup seem to me quite basic and I am affraid that one cannot infer many things from these experimental designs. I guess the ethics is limiting much of the medical experimentation (which is good!). Usually it is just the report of observations of what happen to the global health of a patient when one amino acid is missing in their food. Therefore, these articles does not explain much about the metabolism reasons of these needs (which was your question) but only try to define what are the needs. Moreover statistics seem sometimes a bit fuzzy (or absent) to me.
Anyway here is a review of these results and there is a whole paragraph on the question of histidine. The best is that you read it yourself. To make it short: Histidine doesn't seem to be more important to the children than other amino acid. Moreover there is big storage of histidine in our body suggesting that one that is histidine deprived for a while might use these stored histidines.

The OPs question wasn't about whether or not Histidine was more important than other amino acids, but whether or not Histidine was only essential for children. The article you link indicates that it is essential for both adults and children, even if the experiments are primarily based on macroscopic health effects.

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Blood group probability question

My answer ( after rounding off) is 9% -100( 0.75 X 0.25 X 0.5) but the answer given is 22 %
Am I correct ?

I think the quoted answer is correct.
First, the probability of getting a son( and not a daughter) is $P_s=0.5$.
Next, since both the parents are heterozygous, the probability of genotype $hh$ is $P_h=0.25$. This genotype will not produce any antigen precursor, and hence there will be no antigens on RBC. As blood group O is defined by the absence of antigens, this can be classified as blood group O.For the expression of the antigen (dominant at the $H$ locus), the probability is $P_H=0.75$.
Again owing to the heterozygosity of both the parents at $I$ locus, the probability of getting a blood group with genotype $I^oI^o$ is $P_I=0.25$. This is the probability, that if the antigen precursor is made, $75%$% of the times the expressed blood group will be O. Therefore the probability of blood group O due to homozygous $I$ locus and dominant $H$ locus is $P_I\times P_H=3/16$.
Net probability for blood group O=(probability due to homozygous h+probability due to homozygous I and dominant H)*probability of a son.
$$P_{net}=P_s(P_h+P_HP_I)\approx 0.22$$

The blood group without  hh antigen is also known as Bombay Blood group ! One of the rarest type in the world ! Phenotypically O but when O blood transfusion is done, it will create a severe reaction.

@biogirllajja I knew that but I guessed, it was the phenotype of O whose probability was asked.

I realised my mistake of not considering hh as phenotype O when I saw your working. I just wanted to share the information regarding bombay blood group.


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Why can't cell division happen the other way around?
Mitosis in eukaryotes happen in this order: DNA replicates and then the cell divides. Why doesn't it happen in reverse order (i.e., cell divides and then replicates the DNA)?
I am talking about diploid cells.
Why has evolution favoured the first way?

I was thinking about only  cells having even ploidy levels. I know it sounds stupid if we think about odd ploidy levels.

If you are thinking of a process like meiosis but followed by DNA duplication, the problem is that this would create daughter cells that do not have the same genome as the parent cell.
The diploid genome of a sexually reproducing species' cell has different alleles of the same locus. If the cell replicates itself by passing one chromatid to each daughter cell which then duplicate that to make a diploid genome, the resulting cells will not have the same DNA as the original one since each of the daughter cells will have inherited only one of the available alleles. They will then make an exact copy of the DNA they have inherited and become diploid but with a new genome, one that did not exist in their parent. This is not good since the cells of an organism need to have the same genome in order to function in the same way.

Yes.. it would also lead to  homozygosity.

The biggest problem is this: if you have only one copy of the DNA how is it going to divide it between the two cells so that both have a complete copy?


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Genetics problem-Height of a plant
An inbred strain of plants has a mean height of 24cm. A second strain of the same species also has a mean height of 24cm. When these plants are crossed the F1 are also 24cm in height.However, when the F1 are crossed the F2 plants show a wide range of heights, the greatest number are similar to P1 and F1 but apprx. 4 out of 1000 are only 12cm tall and 4 of 1000 are 40cm tall. What fraction of the F2 plants will be apprx. 28cm in height ?
a)3/4
b)9/16
c)56/256
d)none
The answer given is c).

I know that a and b can not be the answer.

A simple google search will reveal this website where that exact question was asked half a year ago.

Totally unrelated comment: If it is 24 cm high, I doubt it is a tree.

@skymninge done the edit !

From the source that Amory cites :

You know that the number of offspring is shown by Pascal's triangle,
  right?
For two alleles you have 1 : 2 : 1
For three alleles 1 : 3 : 3 : 1
For four 1 : 4 : 6 : 4 : 1 etc.
So, if 4 in 1000 are 12 and 36 cm
  tall, that means that every in 250 plants is tall like that. And on
  which level of Pascal's triangle you have sum of 250? For two alleles:
  1 + 2 + 1 = 4 For threee: 1 + 3 + 3 + 1 = 8 For four: 1 + 4 + 6 + 4 +
  1 = 16 etc. until 1 : 8 : 28 : 56 : 70 : 56 : 28 : 8 : 1 Here you see
  that you have 9 options of height. The difference is 36 cm - 12 cm =
  24 cm. 24 cm /9 = 3 cm, so 1 plant will 12 cm, 8 plants will be 15 cm,
  28 plants will be 18 cm, 56 plants will be 21 cm, 70 plants will be 24
  cm (i.e. "the majority of F2 are like P1 and F1") and 56 plants will
  be 27 cm tall out of 250 plants. Thus C is the closest.


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cellular respiration
What are the effects of addition of these chemicals to actively respiring cells ?
Which of them would lead to INHIBITION of aerobic respiration ? Would cytochromes be actually taken up by cells ?
a.addition of CO
b.addition of CO2
c.addition of cytochromes and flavoprotein

Come on. I know that you know the answers to almost all of them :)

I hope I'm not wrong here: More CO in the cells cause numbness over that region by temporarily inhibiting the functions performed by the cell. (I guess my Biology teacher once told us how some body parts go numb after sitting for hours. Wherein the respiration process is slow with less intake of O2 which causes accumulation of CO in the cells of the parts which is cut out of blood supply).

@WYSIWYG I actually wanted answers to mainly these 3 and I have edited the question. The question given in my homework is  a bit twisted(not exactly the question I am asking) so I think I just got crazy and asked some silly things :)

If you're loving Biology, then you can either try using some sort of Library or Wikipedia, and I am really amazed with that lot much of Questions :) I don't even have answers that much! :P Good girl..

Carbon Monoxide "CO" would definitely inhibit aerobic respiration. This is in fact the mechanism of the toxicity of compounds such as carbon monoxide and cyanide, namely, carbon monoxide binds (coordinates) with an affinity several orders of magnitude greater than oxygen to the heme group of mitochrondrial cytochrome oxidase, thus inhibiting the enzyme. When the respiratory electron chain is no longer drawn by the reduction of molecular oxygen, the hydrogen ion gradient across the mitochrondrial inner membrane is depleted, and ATP production halts.
Carbon dioxide would not effect the electron transport chain directly, but is rather involved in the reactions of the citric acid cycle, although, in all likelihood, the cell would die of acidosis before CO₂ concentrations became great enough to reverse the citric acid cycle. Cytochromes and flavoproteins are complex molecules that if the cell were to endocytize them, it would simply digest them.
I do not know your degree of experience in biochemistry, but if you wish, search on the internet for protein structural images of cytochrome oxidase or hemoglobin bound to oxygen and carbon monoxide. Oxygen binds the iron of the heme group at an angle, while carbon monoxide binds directly perpendicular to the heme ring. This difference in geometry is partially responsible for the differential affinity of the two species for heme.


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Asexual reproduction and Telomeres
Many eukaryotic organisms like yeasts, hydras , planarias, plants etc reproduce asexually.
Replication of End of linear DNA pose a limit to the number of cell divisions.
My question : Do asexually reproducing organisms have telomerase in all their cells ? Is the telomerase activated at specific times at specific places ?
If they don't, how can they reproduce infinitely ?

I'm not sure I can answer generically for all asexual organisms, but would an example of why this isn't an issue in E. Coli and yeast work?

@AtlLED Thanks! but I think I know why it works in Yeast and E.Coli - Isn't it because they have round chromosomes and so there is no telomeres.

E. coli is really a bacterium and has only a circular chromosomes. On the other hand, yeast like S. cerevisiae is an eukaryotic organism and has 16 chromosome pairs if it is diploid. The division in yeast is limited. It is done by budding, where there is a clear difference, which cell is a mother and which one is a daughter. Mother can have only certain number of daughters and stops budding afterwards. I do not know, if this is due to telomeres, or budding scars or both.

@AtlLED Ok, so I was wrong about the yeasts :) You could tell me about them.

Short answer:
No. Eukaryotes have more ways of maintaining telomere length than via telomerase alone and all organisms with circular genomes do not need to worry about telomere length anyway.
Long answer:
Firstly, the telomerase system is not the only observed mechanism in Eukaryotes that elongates telomeres. Other mechanisms such as the transposition of retrotransposons (e.g. Drosophila) or recombination (e.g. Yeast) can also be used in some species. Yeast  has been observed to use several of these mechanisms. So no, telomerase itself is not always necessary for immortality.
Ofcourse prokaryotes do not need to worry about shortening chromosome ends at all since their genome is circular - i.e. it has no ends to shorten with each cell division!

Here is a study of planarian worms, which are immortal in asexual reproduction and mortal in sexual reproduction.
Hydras also become mortal after they reproduce sexually.
Relevant to your question: Cells within planarian worm differ in expression of telomerase active subunit depending on body part. Immortal (asexual) worms have more expression in the area around the pharynx, those cells there are "the proliferative stem cells". There is a nice figure in the article.
I assume it is similar for hydra, that outer body coat has less expression than the cells inside. “Hydra is a bag of stem cells”
(Less relevant (a version of previous version of my answer. But does not answer the "every cell" inquiry well): In planarian worms "We demonstrate that this difference is reflected in the expression and alternate splicing of the protein subunit of the telomerase enzyme." The mentioned telomerase subunit was 1. comparatively more transcribed in immortal (asexual) worm and 2. within the resultant trancripts, there were possibilities of functional and non-functional isoforms due to alternate splicing. Immortal worms had higher ratio of functional isoforms. Summary: immortals have more transcripts and higher proportion of functional versions of them.)

Yeah, I know, I am offering 2 bounties myself. Watch my answer for edits, I might find more clear data when I have time.

I think the worm aspect of my answer is now correct. I must check later, whether really hydra cells have different telomerase expression in the coat versus inside the body. It interests me, but takes time to look at this thoroughly. If you are impatient, try to read the article "Hydra is the bag of stem cells" plus the original un-popularised reference.


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Why are centrioles aligned at 90 degree with each other?
The centrioles are aligned at 90 degree with each other. What is the function of this?

Do you have any preliminary ideas? Also, if your question is a homework question it should be tagged accordingly.

I have some preliminary idea about cell division but I don't understand the use of centrioles being aligned as such.

As far as I know, the function is not truly known, although there are some seriously interesting guesses.  Part of the problem seems, from scanning the literature, to be that it's not easy or obvious to disrupt centriole orientation.  This paper in PLoS Biology presents some really interesting results, in particular two piece of evidence:

Centriole orientation, to some degree, is dictated by the "mother" centriole during centriole division and is thus passed on from cell to (daughter) cell.
Defects in centriole orientation can result in organelle localization defects in the cell (e.g. nuclear orientation), and at least some of these defects are genetic.

So it seems that orientation is, in some part, a product simply of centriole division, but that there are some gene products that do help determine orientation and localization.  This paper puts forth the hypothesis that centriole orientation determines the axis of cell division which can affect embryo orientation, whereas this suggests that external environmental factors could translate into altered centriole, and therefore cellular, orientation.


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Can any one reaction in a cell be at equilibrium?
I know that metabolism as a whole can never be at equilibrium (otherwise the cell is dead !) but I wonder whether a few reactions in the cell could be at chemical equilibrium at a  given point of time.
Is it possible theoretically ? Is there any real example ?

@terdon Your link does help but actually I was thinking about chemical equilibrium i.e. when rate of forward reaction is equal to rate of backward reaction.

Accepted but it would be better if someone could give me a typical chemical reaction. For eg.Conversion of A to B by enzyme C is at equilibrium at some particular conditions.

@terdon Ok. I will search it a bit more. I just felt that it would be uncommon because I thought that there is no point in converting a thing into another thing just to convert it back to the same thing . But after the example you gave I think equilibrium is not that pointless, at least in this case .

let us continue this discussion in chat

@terdon. what you are referring to is perhaps treadmilling and that is a steady state not an equilibrium

@terdon: because polymerization and depolymerization are not the same reactions. New G-actin binds to the barbed end with the ATP whereas depolymerization happens because of degradation of ATP on the other end. This is something like protein formation and degradation. If these rates are equal then the entity is said to be in a steady state, not equlibrium

Polymerization is of course the opposite of depolymerization but they are not the same reactions. An equilibrium is a property of a single reaction.

@WYSIWYG fair enough, I'm deleting my comments since they were just plain wrong and only add confusion. Thanks for clearing that up.

Biogirl, sorry about that, I seem to have forgotten my chemistry :(.

I think there are a few principles that we need to consider before answering your question.
(a) When a reaction is at equilibrium, the rate of any elementary reaction is exactly balanced by that of the reverse process.  This is an important one.
The above principle follows from transition-state theory, which holds that the activated state for the reaction in one direction is that same for that in the reverse direction.  It also follows from the principle of microscopic reversibility at equilibrium or, more correctly, the principle of detailed balance at equilibrium, which states that “in a system at equilibrium each collision has its exact counterpart in the reverse direction, and that the rate of every chemical process is exactly balanced by that of the reverse process” (my emphasis) [Laidler, 1987, p 130]. It is important to realise that these two points of view are equivalent.  To again quote Laidler (p130), if one is working within the framework of TST “the principle of microscopic reversibility presents nothing new”.
To put it bluntly: a system where any elementary reaction, either explicitly or implicitly, is not exactly balanced by the reverse process is not at equilibrium. By this criteria, the actin example alluded to above cannot, even loosely, be considered at equilibrium.
This principle has many important consequences, even when a system is not at equilibrium. One is that the product of the ratios of rate constants along any path on a cycle equals the equilibrium constant between the forms (species) connected, and is equal to one around a full cycle (closed loop) (see Cornish-Bowden, 2004, p 104). [see Addendum for an example of where this consequence was not adhered to].
(b) When a species is in a steady-state, the rate of formation equals the rate of breakdown. The steady-state concentration may differ markedly from the equilibrium concentration.
(c) As @WYSIWYG has pointed out, an enzyme (catalyst) does not change the equilibrium constant for the uncatalyzed reaction.
(d) When we are dealing with equilibria, we are usually interested in Gibbs free energy changes.  For example (Silbey & Alberty, 2001, p 277).
ΔGo' = -RT ln K’
(In the above equation K’ is the apparent equilibrium constant, that is the equilibrium constant at specified pH, and ΔGo' is the standard transformed Gibbs free energy of a biochemical reaction.  More on this distinction, if you are interested, in the Silbey and Alberty reference quoted above).
The important point is that there is a relatively simple relationship between Gibbs free energy and the equilibrium constant. The Gibbs free energy, of course, gives a measure of the spontaneity of a reaction and also its capacity to do work.
When the transformed Gibbs free energy is of a reaction (ΔG') is zero, the reaction (at specified pH) is at equilibrium and cannot perform useful work, and reactions with negative ΔG' may be considered ‘spontaneous’.  It is also important to realize that equilibrium is a dynamic state: chemical bonds are continuously being broken and energy is continuously being redistributed (with no loss of energy). [I am dealing here with the transformed free energy, ΔG', that is the free energy change at specified pH, rather than ΔG (the pH independent value), as this is the most useful when considering a biochemical reaction.  However, similar conclusions apply to ΔG].

Having got those out of the way, I can now attempt to answer your question (slightly rephrased). Can a reaction in a metabolic pathway be at equilibrium?
To be extremely pedantic, if there is a flux through the pathway (net conversion of first substrate to end product) then the answer is no (Newsholme & Start, 1973, p 11). That is, if there is a flux through the pathway, ΔG' cannot be exactly zero for any individual reaction.   However, reactions in a metabolic pathway may be very close to equilibrium (Newsholme & Start, 1973, chapter 1).
Let’s (once again) rephrase your question.  Are there any examples of reactions in metabolic pathways that are close to equilibrium, and how can we determine this?
To again quote Newsholme & Start (1973, p11)  “In a series of reactions that constitute a metabolic pathway, a few may be displaced far from equilibrium, whereas the majority of reactions may be close to equilibrium”.
So how can this be determined? One way would be to measure the ratio of products to substrates (or the ratio of product to substrate pairs) in the cell, and compare this with the equilibrium constant.  Note that it is only the ratio of substrate/product pairs we are interested in, not the absolute concentrations. We might be interested in the NAD+/NADH ratio in the cell, for example.
That is, we measure the mass action ratio and compare this with the equilibrium constant.
Such measurements are fraught with difficulties, but let’s agree that they can be made. We could rapidly freeze the tissue sample to -190°C (using liquid nitrogen), for example, and then measure the ratio of metabolites.  Finally, it should be pointed out that comparison of mass-action ratio with the equilibrium constant is not the only way of deducing that a reaction is near equilibrium, and agreement between alternative methods is highly desirable before any firm conclusions are drawn.
Let’s consider glycolysis as an example.  It is generally agreed that the reactions catalyzed by phosphoglucoisomerase, phosphoglycerate mutase and enolase are all close to equilibrium: the mass action ratios and the equilibrium constants are about the same (see Newsholme & Start, 1973, p 98).
It is also generally agreed that the reactions catalyzed by phosphofructokinase and pyruvate kinase are far from equilibrium (see Newsholme & Start, 1973, p 98).
What is the rationale? In general, it is control reactions catalyzed by regulatory enzymes that are displaced from equilibrium. (A key property of a regulatory enzyme is that the activity is controlled by factors other than substrate concentration).
The enzyme phosphofructokinase is a good example.  This enzyme plays a key role in the regulation of glycolysis. Measurement of the mass-action ratio for this enzyme gives a value of 0.029, where the equilibrium constant for the reaction is about 1000 (see Newsholme & Start, 1973, p31). It is clear that physiologically this enzyme catalyzes a reaction that is far from equilibrium.
In conclusion, many reactions in metabolic pathways may be close to equilibrium, but regulatory enzymes almost always catalyze reactions that are displaced from equilibrium.
Finally, if anyone wishes to provide more recent references or to otherwise improve the answer, feel free to edit.
Addendum
For a well-known controversy in the enzyme kinetics field where the requirement that product of the ratios of rate constants around a closed loop equal the equilibrium constant for the cycle was not adhered to, see Selwyn (1993) and Topham & Brocklehurst (1992).  These authors were critizing the work of Varon et al (1992), who made a bit of a hash of things. If you are interested in this area, you may wish to read up on this controversy, which is very informative. (Selwyn’s paper is a great start). [All the above papers are freely available in PubMed Central].
References
Cornish-Bowden, A. (2004) Fundamentals of Enzyme Kinetics. 3rd Edn. Portland Press.
Laidler, K. J. (1987) Chemical Kinetics 3rd Edn. Harper & Row.
Newsholme, E.A. & Start, C (1973) Regulation in Metabolism. John Wiley & Sons.
Silbey, R. J. & Alberty, R.A (2001) Physical Chemistry. 3rd Edn. John Wiley.

Eric Arthur Newsholme (1935–2011) Obituary

Best answer anyone could give to my question :) Thank you so much !

Are you sure about "the product of the ratios of rate constants around a cycle (closed loop) equal the equilibrium constant for the cycle"? What is the equilibrium constant of a cycle? Shouldn't the product of the ratios of rate constants around a cycle be simply equal to one (Equation 1 in Selwyn (1993))?

Ah, I read the reference: it is not for the full cycle, but for parts of the cycle that connects different forms (e.g.: A $\rightarrow$
B $\rightarrow$ C and A $\rightarrow$ D $\rightarrow$ C in relation to the equilibrium constant for A $\leftrightarrow$ C)

Yes, I think you are right. This follows from the principles of microscopic reversibility and detailed balance, very well discussed by Laidler in Chemical Kinetics. But one needs to be very careful! As Laidler points out, there are many misapplications of these principles.

To quote for Laidler (p 286) "For any mechanism, involving any number of elementary and consecutive steps, the overall equilibrium constant is the product of the equilibrium constants for the individual steps, and is the product of the rate constants for the reactions in the forward direction divided by the product of those for the reverse reactions"

Yes, and this, remarkably, is independent of the specific rate law of each reaction, which often makes people forget that not all reaction rate laws obey the law of mass action.

I am assuming that you know the difference between steady state and equilibria. Your definition of equilibrium is correct; fwd rate = bkwd rate.
In a steady state the levels of a component remain constant over time but that may be because of many reactions.
As terdon indicates many protein-protein binding events are in equilibrium (binding and unbinding reactions; which gives rise to terms like association/dissociation constants). Many metabolic reactions are also in equilibrium. Enzymes don't change the equilibria. They just accelerate both the rates and help attain equilibria faster.
So, if a metabolic pathway has slow rate limiting steps then the faster steps go to  equilibrium.

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text:
Species-area relation graph
When species richness is plotted vs area, the graph follows the equation : log S = log C + Z log A where Z is the slope of the line. Z values are usually in the range of 0.1 to 0.2 but if very large areas like entire continents are analyzed, the slope is much steeper. (0.6-1.2).
Why is it so ?
(Here S = species richness and A= area under consideration)

Interesting question. Can you please add some reference and eventually two graphs that show different slope depending on the range of areas used? Note also that if $C$ designates a constant (which I think it does), then $log C$ is a constant too and could well just be replaced by $K$ (or just write $C$). You should also make clear that $S$ is species richness and $A$ is the area even though it is quite intuitive.

@Remi.b The full log notation is useful to highlight that the basic relationship is a power law: $S = CA^z$

Perhaps because when analyzing large areas, adjacent masses of considerably different climatic conditions are successively bought under analysis, and will hence increase the richness faster than compared to small areas where increasing the analyzed area is still more likely to be confined to the same geo-climatic zone. Just speculations, though. Will get back with a better answer.

Right, @Satwik Pasana. Also consider that evolutionary history becomes increasingly important when you're looking at large areas.

@satwik pasani That makes sense. Actually when I had asked the question I had a wrong notion of what species richness is but now what you say seems logical. Add it as an answer !

@Hav0k Could you elaborate a bit ? Do you mean to say that larger the area, more are the chances that a larger no of species would have evolved in it ?

Well, not exactly. I meant that when you increase area, at some point you will likely add regions that share different evolutionary histories and thus add disproportionally more species, thereby increasing z. Imagine you start with a small area in North America and increase its size until it encompasses all of NA. Now there is no more area in NA to add, so you start adding parts of South America. These species assemblages differ drastically from North American ones and even small increases in area will yield many new species --> your z increases.

@hav0k ok yes. That is a really good explanation too.

What are the data points in the relationship you are thinking about (the "samples")? The number of species vs area for each continent or species richness vs area for subsamples ( or nested samples?) taken at the continent level? Relatively often, slopes of mainland areas or well-connected islands are smaller than slopes for more isolated island groups.

@fileunderwater species richness vs samples of increasing area

Either way, you should add a reference to back up your basic claim (steeper slopes for continent-level samples).

@biogirl Also, what taxa are you considering? To me, it is still also unclear whether you are asking about a species-area relationship where the data points are entire continents, or large-scale species-area relationships within continents (nested or otherwise).

@fileunderwater My question is just a general one. I am asking about large scale species area relations within continents.

Z value is a fitted constant and it ranges between 0.1 to 0.3 regardless  of the region or taxonomic groups.i.e. the slope is almost similar .Among larger areas like continent,the slope tends to be much steeper.becoz, Larger the area larger will be number of species(species richness),for larger areas the Z values tends to be 0.6 to 1.2.(NOTE:if Z is less,lesser area is enough to capture more species).


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Does our eyeball increase in size as we grow?
Does the size of the eye increase as we develop from the stage the complete eye first forms to infancy and then to adulthood ?

First of all, I should quote the sentence from the MOST reliable ophthalmology sourcing in the world - American Academy of Ophthalmology:
Section 11 - "Lens and Cataract"
"The equatorial diameter of the unfixed human lens measures 2 mm at 12 weeks and 6 mm at 35 weeks. Both the growth and the maturation of lenticular fibers continue throughout life." The antero-posterior dimensions of the lens enlarge from 3 mm at infancy to 6 and even more in adult years.
"The lens continues to grow throughout life (page 7 the same source)
Secondly, the growth of the eye continues after birth - at the beginning the growth is fast and later the growth is much slower but still - there is GROWTH of the eye after the birth.

@llan Thanks!  If I assume that growth does continue, then how is new vitreous humor made ? Is the growth of the eye, after birth, so negligible that there is no need to add new vitreous humor ?

@biogirl the vitreous is jelly-like substance with connective tissue as a skeleton. However, it is 99% water, thus to expand vitreous the ciliary body just filtrated more water. Actually with age vitreous becomes even more fluidic which causes specific to this processes, like Posterior Vitreous Detachment.

@llan The ciliary body makes more AQUEOUS humor not vitreous. I have read that NO new vitreous humor is made, it is present in fixed amounts.

@biogirl  check out what is happen after vitrectomy... what replaces the vitreous?

@llan Interesting question ! Though I don't know how that is replenished I can quote two lines from wikipedia which furthers the mystery - It is produced by cells in the non-pigmented portion of the ciliary body deriven from embryonic mesenchyme cells which then degenerate after birth and Unlike the fluid in the frontal parts of the eye (aqueous humour) which is continuously replenished, the gel in the vitreous chamber is stagnant. Therefore, if blood, cells or other byproducts of inflammation get into the vitreous, they will remain there unless removed surgically.

@biogirl You seem to me someone in a way of academic education, thus you should learn that Wikipedia is absolutely unreliable source of any kind of scientific data. Don't use it and don't cite it - search for the information in reliable academic sources.

@llan ok will take care in the future ! Though I should tell you that I have read the same thing in Tortora and Derrickson principles of anatomy and physiology.

So, your homework is to answer the question What replace saline after it (saline) replaced vitreous during vitrectomy. After you answer this question, you will know some essential data needed to answer the primary question...

Ok to settle the debate I asked an ophthalmologist - he says that after vitrectomy the eye ball decreases in size. No replacement happens.

After reading ur comment above I think I will have to search vitrectomy from a reliable source. See from a good textbook maybe.

@biogirl Tell your ophthalmology resident that it probably better to check the source anyway... cause - he told you something he probably cannot support.

Ohk ...lets see what we can find.

No. In fact the lens of the eye, which is nearly optically perfect in humans, does not change or grow after it is fully formed around week 26 of gestation.  Interestingly this is why one of the cues for identifying young children is having small faces with large eyes.  This also the case for puppies and cats and other animals, who are mostly cuter when they are small with large eyes.
The eye lens is composed of dead cells whose remains are almost entirely a single protein called a crystallin.
This doesn't apply to compound eyes though.

Your first link doesn't say anything other than when the eye forms initially.  Your second link has a paragraph that starts out with "The lens continues to grow after birth..."  Neither support your answer.

@shigeta I think you are wrong in saying that eyes don't grow after birth, see the following source : https://www.aao.org/eye-health/ask-ophthalmologist-q/are-eyes-fully-grown-at-birth


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Which fish will have more developed gills?
A fish lives at the depth of 1000-2000m and another at the depth of 200-700m. Which of them would have a more developed gill system ?

Can you expand on what you consider "better"? As long as both can live fine at their respective depths, then I would call both sets of gills "good enough", which is really all that matters.

Moles living in dark don't have well developed eyes. Similarly,which of these fishes would have more developed gills ?

200m is still pretty deep...
However, I'd give my money for the surfacers. Oxygen concentration decreases with the depth, and so abyssal fishes have very low metabolism, mainly focused on anaerobic muscles. This is also true for fishes that live in the bottom (benthic), which probably also applies for those living in a few hundred meters. If not, they will probably be active swimmers and then they will probably need bigger gills in order to maintain aerobic movement. Even if we're talking about abyssal and non-abyssal benthic species, I think the abyssal ones would probably be even more anaerobic.

Does Oxygen concentration decrease with depth? The opposite is true for the first few meters.

Yes, but that is because there's a biotic oxygen consumption (and production) that is higher in the most illuminated area. Once you have descend a bit beyond, the oxygen source is both photsynthesis and diffusion from air, both of wich may be hundreds of meters above. In this dark area, oxygen diffusion is limited, and carbon dioxyde accumulates too.

You make a good point but the solubility of Oxygen increases with depth since it depends on the pressure. I have no idea if this increase will continue or if it reaches a plateau after a few meters. I agree that at great depths, the lack of photosynthesis should mean that the oxygen content is lower, but I wonder how much that is balanced out by the greater solubility. I haven't been able to find a reliable reference citing oxygen levels at greater depths. I would guess the concentration goes up for the first ~10-15 meters and then falls from there.

Solubility may increase due to pressure, but it will remain pretty low no matter what. Without an internal production, and with so many organisms consuming it (below a certain point there is no photosynthesis, but there is still sediments to metabolize and there are animals and bacteria feeding by the leftovers that falls from the surface), the oxygen levels in the bottom of the ocean is minimal.


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What are the statistical tools for distinguishing molecular analogy from homology?
Scientists have developed statistical tools that distinguish "distant" homologies from coincidental molecular homoplasy in extremely divergent sequences.
What are these tools?How are they used ?
I have very less knowledge about statistics.

What do you mean exactly with molecular analogy?

Let's say you sequenced genomes of 2 organisms and found a common sequence - AGATTA in both. Now , you want to determine whether that similarity is because of homology or because of analogy.

analogy is based on function and any experiment that can measure the functional output can compare analogous features.

@WYSIWYG I am not able to understand what you are trying to say.Could you elaborate?

You may be interested in this question. In any case, analogy and homology are not mutually exclusive. Are you thinking of homology versus convergent evolution?

There are lots of statistical algorithms that allow you to evaluate the similarity between two given sequences. For instance, blast allows you a rapid comparison between your sequence and other sequences in a database; while Clustal, with a similar functioning, allows you to compare a set of given sequences between them. They are very simple algorithms, but very fast and useful, and basically they score an alignment by counting how many positions between the two entries are the same. Other algorithms function in a similar fashion, but they use hidden Markov models to compare your sequence with a consensual sequence in order to identify motifs and domains. I'm sure there are even more advanced programs, but I don't know them and don't think it's the point.
Homology usually refers to things that share the same origin, while analogy refers to things that do the same function but their origin isn't shared. While the algorithms I've described you only search for similarity or identity, you must notice a few things:
a) Homology of function doesn't necessarily correlate with high similarity. Two proteins can have the same global structure and their sequences be completely different. The three-dimensional structure is the same, and probably there'll be key amino acids that will remain very similar. This is very obvious in many proteases, which share only the three catalytic amino acids (catalytic triad) between them, and vary enormously even between strains of the same species.
b) Protein domains vary in size from a few dozen to a few hundred amino acids. The odds that exactly the same sequence evolves in two separate moments are very low. Especially in highly conserved domains, which usually carry out key functions.
c) Proteins usually have a modular structure with more than one domain. New proteins often evolve by switching and combining domains by translocation. So, even if the same domain has evolved in two separate times, the association between these two "twin" domains with other domains will probably reveal its unusual origin.
That's why usually the term molecular analogy is not used, and if so, it would refer for example to structurally different domains that catalyze the same reaction or that share the same structure. Note that even if the analogy as you describe isn't impossible by itself, the software won't be able to differentiate them unless the sequence appears associated with others. Furthermore, the origin of many of the current protein families is so far in the past that it's quite impossible to reconstruct it, even more so with the high diversity in prokaryotes.

As Miguel puts it, homology means similarity of origin and therefore of some structural properties. Whereas analogy means similarity of function (like insect wings and bird wings provide the same function of flying).
A homoplastic trait may still be homologous because same set of genes may be involved, whose DNA/protein sequence may be homologous.
Just thought of an example that was illustrated in PhD comics some days back- about dogs and hyenas- they both have snouts and look similar but hyenas are more related to cats.
This is an example of convergent evolution but the genes giving rise to snout- the structural proteins the homeotic genes, growth signaling molecules or whatever is responsible for this trait is present in both animals. This trait has a good deal of structural homology. Now, the rigor with which we say that two traits are similar is another factor. It depends on how many variables you use to define a trait. For e.g. a snout shape can be defined using- snout dimensions, angles, bone morphology, texture etc. The more variables you add the more rigorous it becomes. Sometimes the extra variables don't give any extra info and you may choose to remove these variables (this is precisely what is done in a statistical method called Principal Component Analysis).
If phylogentic study is based on these common convergent characters (snout) then we'll end up predicting that dogs and hyenas are related which is erroneous. Therefore multiple gene families are to be considered while doing phylogenetic analysis.
If we go back to butterfly-bird example; both have wings that are used for flying but they are structurally very different- therefore the genes responsible might also be different.
Since the structure itself is different you wont be able to compare the two traits using structural variables. You need variables that define function. For e.g. Thrust generated, fluttering speed, angle of attack etc. (of course they need to be normalized with respect to body size).
Once you have the set of variables (random variables in statistical terms) you can apply statistical tests to compare them.

I think you have misinterpreted my question.My question in really simple words is - If I give you 2 DNA strands of DNA each from a different organism and you find that they have a particular sequence in common. Now you want to determine whether this similarity is due to convergent evolution or due to homology . Now, using statistics and remaining piece of DNA , can you distinguish between this?

those tools just measure homology. convergent evolution may give rise to homologous genes. you cannot know if it is convergent evlution or not unless you look at other genes in the organism.


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How was Restriction Site of EcoRI sequenced?
The sequence of restriction site of EcoRI - GAATTC was identified in the early 1970s, before Sanger Sequencing was invented.(1977)
How was the restriction site of EcoRI sequenced ?

The first determination of a recognition site for a restriction endonulease was reported in:

Kelly & Smith (1970) A restriction enzyme from Hemophilus influenzae II. Base sequence of the recognition site. J Mol. Biol. 51: 393-409

The enzyme was then called endonuclease R, but is now known as HindII (or HincII).
The method used was to cut DNA with the enzyme and then remove the exposed terminal phosphates with alkaline phosphatase. These ends could then be labelled with 32P using polynucleotide kinase and γ-labelled ATP.
The end-labelled DNA was then treated with nucleases in three different ways to release mononucleotides, dinucleotides, and a mixture enriched for trinucleotides. In each case the labelled products were identified by their behaviour in 2D thin-layer chromatography, and were  further characterised for their total base composition after digestion to mononucleotides where appropriate.
The deduced site was/is
5'----GTY RAC----3'
3'----CAR YTG----5'

Thus the labelled mononucleotides were found to be A and G (purine=R), the dinucleotides were found to be GA and AA and so on.
The EcoRI sequence was determined by essentially the same methodology and was reported by

Hedgpeth et al (1972) DNA nucleotide sequence restricted by the RI endonuclease. Proc. Natl. Acad. Sci USA 69:3448 - 3452

Addendum:
Although Sanger sequencing (the plus-minus method) may have been developed through the 1970s, it really didn't catch on until the early 80s. So for example the first complete plasmid sequence to be determined was pBR322 in 1979:

Sutcliffe (1979) Complete nucleotide sequence of the Escherichia coli plasmid pBR322. CSH Symp. Quant. Biol. 43: 77 - 90
"I have determined the 4362-nucleotide-pair sequence of the plasmid cloning vector pBR322 using the DNA-sequencing technique of Maxam and Gilbert (1977). The DNA structure has several interesting features that lead to testable predictions."

The standard sequencing method in use at that time was chemical sequencing using the Maxam-Gilbert methodology. When I started a postdoc in the USA in 1979 M-G sequencing was the standard method. Sanger sequencing really only took off following the development of the M13 mp vectors (and later the pUC plasmids) by J Messing in the early 80s. And what a relief it was: M-G sequencing was extremely laborious, as anyone who ever did it will testify.


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Competition for mates in sea horses
This source here

...research has shown that it is STILL the males that compete for
  females.

says that male sea horses compete for mates but this source here

Females exhibit a competitive behavior that's normally a male-type
  attribute, and males end up being choosy, which is normally a more
  female-type attribute.

.says that female sea horses compete for mates.
Can anyone provide me a trustable source regarding this ? I would also like to know if there are any recent papers exploring why males get pregnant in sea horses.

Is this question more apt for skeptics.se ?

Are you sure you want to ask about polyandry and polygyny? How do the sources you quote touch on the number of mates per individual?

@terdon The sources I quote seems to answer the question why males get pregnant but if you read carefully there is a mention of polygyny and polyandry. I will quote those parts--

Whether they compete or not is one thing, polyandry and polygyny refer to the number of mates per individual. I think you are asking whether males or females compete for mates and display secondary sexual characteristics. That is not necessarily related to polygamy of either sex. The two sources disagree on whether the males or the females compete for mates, my guess is that both do but I don't really know. Interesting question but not related to polyandry or polygyny.

@terdon Ah I see but in most polygynous socities it is the male that competes for mate. I have never heard that a polygynous society had females competing for mates.

All I am saying is that competition is not related to polygyny or polyandry. Please [edit] your question so you ask what you actually want to know.

That second link even says: "Seahorses, however, are monogamous within a breeding season, and each seahorse only mates with one other seahorse."

@amory edited my question.

Second paper is an article in science Daily and have a pretty decent source from Texas A&M University. It's much better than the first as it is un-sourced post on yahoo answers.
Source:
"Male Seahorses Are Nature's Mr. Mom, Researchers Say." ScienceDaily. ScienceDaily, 2 May 2008.
Why male seahorses gets pregnant?
Genetic answer:
May be because only $MHII\beta$ gene present in the male pouch which carries the babies.
Source and more on this topic:
The impact of sex-role reversal on the diversity of the major histocompatibility complex: Insights from the seahorse (Hippocampus abdominalis)


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How is the mRNA transported out of the endoplasmic reticulum?
In eukaryotes the nuclear envelope is continuous with the ER, so what helps it out of that?

Have you read the pages on Messenger RNA and Nuclear pores?

Yes but I still did not get any information about what exactly guides it through ER.

What exactly are you looking for? The name of the protein channel(s) through which it will pass? The sequence signals that target it for export? It is hard to know at what level to answer your questions, your profile states you are 15 years old so I assume that giving you references to published reviews describing the process in detail is not what you're after since (very reasonably) you won't have the necessary background to absorb that level of detail. However simplifying it while giving more information that what wikipedia does is kinda hard. This is not a simple question.

I'm with @terdon - a few more specifics would be nice.

@terdon  I am actually after what mechanisms guides it through the "maze" of ER.Does it move through lumen? Does it pass straight out,piercing the membrane ?I don't want to know what guides it out of nuclear pores .

Don't hesitate in including any published reviews. If not now,it will be useful in future ! It will also be useful for anyone else having the same question. :)

I'd make a comment if I could, but I don't think mRNA ever enters the ER. When a ribosome is building a protein destined for export or for being inserted into the membrane, it travels to the ER membrane and binds to a protein in that membrane called Sec61, which guides the new peptide sequence through the membrane. However the portion of the ribosome that reads the mRNA is always in the cytoplasm. So the mRNA never enters the ER, it just gets close the cytoplasmic side of the ER membrane.
Have an image from a German website.

I understand that mRNA never enters in the ER for protein synthesis. My question actually is whether it has to pass through the ER when it is exiting the nucleus. Isn't ER membrane continuous with the nuclear envelope ?

The ER is continuous with the nuclear envelope, but the nuclear envelope isn't a solid wall. It is perforated with nuclear pore complexes that form tunnels through the envelope and allow proteins, RNAs, and charged small molecules to pass. Take a look at http://en.wikipedia.org/wiki/Nuclear_pores

The proteins mediating the transport of mRNA out of the nucleus (nucleoplasm/karyoplasm) are called "karyopherins" and belong to the nuclear pore complex family.
Prior the creation of the final form of mRNA, various proteins are attached to the so called pre-mRNA and a mRNA-protein-complex is built (co-transcriptional). Some of these proteins carry factors for splicing and processing, later RNA-binding proteins are added. (RNA binding proteins such as $Npl3p$, $Gbp2p$ and $Hrb1p$ (serine/arginine-rich proteins) accompany mRNA out of the nucleus. )
After mRNA processing mRNA export is initiated by dephosphorylation of $Npl3p$, leading to binding of $Mex67$ (Saccharomyces c.), forming a complex that interacts with the nuclear pore complex.
That is the way mRNA is able to leave the nucleus.

Translation can occur either in the cytoplasm or in the ER. At one point it was believed that all mRNA begin being translated in the cytoplasm. However, if the protein the mRNA codes for happened to be a secretory protein or a membrane protein, it would have a certain sequence near the start of it (N-terminal sequence). This sequence binds to something called the Signal Recognition Particle (SRP). And once the SRP binds to the mRNA/ribosome/partially-synthesized peptide, it would help it locate to the ER.
So to summarize: Many proteins that need to be synthesized at the ER have a certain sequence that binds to SRP. The mRNA begins being translated in the cytoplasm, but once SRP binds it is moved to the ER.
Of course people now are starting to think this is wrong or at least not the whole story. You can read about the SRP and why some people think its wrong in the intro of this paper


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Difference in length of Okazaki fragments
The length of Okazaki fragments in the lagging strand is about 100-200 nucleotides in eukaryotes and about 1000-2000 nucleotides in prokaryotes.

What (molecular mechanism, enzyme type ) determines the length of
  these Okazaki fragments?
Moreover, which, longer or shorter, fragments would be more
  advantageous (energetically and considering accuracy)?

Longer fragments means less use of DNA ligase, DNA polymerase-I (prokaryotes) and other enzymes required to convert the okazaki fragments with dispersed RNA primers into a normal strand, and hence lesser scope of mistakes during replication in the lagging strand. Shorter Okazaki fragments improve telomere longevity, by reducing the capped-off portion after every division. Which of these views is correct?

Do you think it has to do something with our dna molecule being linear ? If there are shorter okazaki fragments there will be shorter telomere. There is no need for short okazaki fragments in prokaryotes as their genomes are circular and thus there are no telomeres.

@biogirl I guess it is the length of the telomere portion that is capped-off at every division, that will be reduced with shorter Okazaki fragments. Anyway, improving telomere longevity possibly could be a reason:)

First off, eukaryotes aren't "more evolved" than prokaryotes, just specialized in different ways. If anything, prokaryotes like E. coli with doubling times of as little as 20 minutes might suggest that they are "more" evolved than slow-growing eukaryotes for the basic aspects of growth, such as DNA replication. So the fact that prokaryotic Okazaki fragments are longer might actually suggest that longer Kkazaki fragments are better for DNA replication efficiency, and that they got shorter in eukaryotes due to some other tradeoff. It's pretty much useless to infer adaptivity in this fashion.

@A.Kennard Corrected in the question.

@SatwikPasani No worries. Sorry to be pedantic; I've worked exclusively with bacteria so far and I can get overly defensive of the little critters ;) Wish I could help actually answer your (interesting) question!

I think you are thinking too much into this. Not everything needs to give an advantage :) There is a famous paper about why one should not assume every part of an organism is meant to give an advantage http://rspb.royalsocietypublishing.org/content/205/1161/581.abstract I would say the length of fragments is more a result of processivity, binding constant of enzyme doing the priming, enzyme concentration etc rather than it being a result of an adaptation to anything in particular.

@vonMises True and probable, but the fact that the difference in replication between prokaryotes and eukaryotes in other factors involved in replication is quite pronounced, definite and attributable in many cases to the improved efficiency in case of eukaryotes.(eg. better repair, regulation owing to multi-factor control of initiation). So, maybe length of okazaki fragments belongs to that class of differences, especially so since the difference in length is of an order of magnitude (about 10 times)!

@SatwikPasani Just wondering ... Could this possibly also be a reason why bacterial replication is a lot faster than eukaryotic ?

Okazaki fragments is based on the interaction between dna primase or dna helicase,in eukaryotes interaction is more so length is short as compared to prokaryotes.

I have found one more possible reason from Bruce Alberts' The Molecular Biology of the Cell: (Ch. 5 page 254)

Nucleosomes are spaced at intervals of about 200 nucleotides pairs along the DNA strand , which may explain why new Okazaki fragments are synthesized on the lagging strand at intervals of 100-200 nucleotides in eukaryotes, instead of 1000-2000 nucleotides as in bacteria.

As already discussed by me and @SatwikPasani in the comments, increasing telomere longevity in eukaryotes by reducing the length of okazaki fragments, and consequently reducing the part of telomere cut-off after every division might be another reason for having shorter fragments in eukaryotes as compared to prokaryotes which do not contain telomeres.
EDIT : Having thought over it again, the relation between Okazaki fragment length and telomeres do not seem logical as only RNA primer length is important when considering telomere length.

Balakrishnan and Bambara (2013) explain the regulation of (and differences between) prokaryotic and eukaryotic Okazaki fragments in detail.

@satwik I was thinking over this question again and I think what I said about telomere length is wrong. Okazaki fragments don't influence telomere length, it is just the RNA primer of the lagging strand which is not replaced and thus leads to shorter telomeres. So, I don't see any relation between shorter Okazaki fragments and  telomeres.  What say ?

@satwik But it would be interesting to find out whether the RNA Primers used in eukaryotes are shorter than those used in prokaryotes.

true. I would certainly be interested in finding a similar trend of lengths for the primers.

@biogirl I was wondering the same thing regarding variation in  the length of Okazaki fragments. Your discussion has been helpful. Thanks.
As you mentioned, did you find any relation between variation in  the length of RNA primer and telomere longevity?

An addition: the lagging strand synthesis involves bending of the ssDNA such that it aligns in the direction of the replication fork. The nucleosomes (and the condensed eukaryotic chromatin) can hinder this bending such that only short stretches of bent ssDNA is available for the lagging strand synthesis.


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Sexual Differentiation in Monoecious plants with unisexual flowers
In monoecious plants having unisexual flowers (eg Zea Mays, Ricinus Communis etc), there must be some mechanism as to produce two sexually distinct flowers from the same genotype. Since both the type of flowers are placed on the same plant, the genetic constitution of the cells of both the type of flowers will be similar. What is the mechanism by which the development of two sexually distinct flowers is carried out in such plants?
Is the mechanism similar to the mechanism for differential gene expression in case of embryonic development (Homeobox genes)? And moreover, is the genetic constitution of the pollen produced by the male flower similar to that of the egg produced by the female flower, with respect to the composition of autosomes and allosomes (if any)?

This article might be helpful. It also provides a lot of other references.

There is a whole book on sex determination in plants - Sex Determination in Plants by CC Ainsworth. You can get it on google books. See chapter 12 for maize flower sex determination. It's pretty interesting.

why not try to make an answer out of it @biogirl?

I will be able to answer only a part of the question.
Sex determination in Zea Mays
Initially, all the flowers in the plant are perfect, ie they have both the male and the female
flowers. This is followed by abortion of stamen or pistil resulting in unisexual flowers.
Which part of the flower undergoes abortion is determined according to the location of the flower. The florets in the tassel undergo the suppression of the pistil primordia resulting in staminate flowers, while the florets in the ear undergo suppression of stamen primordia resulting in female flowers.

The hormone Gibberelic Acid seems to play a role in sex determination.
Source and other useful links :

Sex determination in Plants by CC Ainsworth.
Sex chromsomes in flowering plants
Sex determination in monoecious and dioecious plants
The sex determination process in maize

This review provides genetics of maize sex determination in (a surprisingly!) simple language.

Thank you for the answer. Just for the sake of aesthetic appeal, can you put all the links quoted in the comments at one place?

Dellaporta & Calderon-Urrea. 1994. The sex determination process in maize. Science 266(5190) is also relevant.

@SatwikPasani I haven't answered the second part of your question but I found some related information in Campbell - Interestingly, maize has a homolog of Hox genes calles KNOTTED-1, but unlike its counterpart in the animal world,KNOTTED1 does not affect the proper number or placement of plant organs. ....an unrelated class of transcription factors called MADS-box proteins play that role in plants.

@SatwikPasani I know that MADS-box plays the role of organ identity genes during flower development but I don't know whether they have a role in the process of sex determination.

@SatwikPasani Thought this is relevant -  Plants mostly follow position based mechanisms for cell fate determination (instead of lineage based as in animals) , so cell fate is usually determined late during development and largely depend on signals from other cells


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Telomere shortening during replication
It is widely know that each cell cycle during DNA replication some fraction of the telomeres is lost, and this phenomenon is called the end replication problem. Well this is due to the fact that the DNA polymerase only adds nucleotides in 5´--> 3´ direction, thus the synthesis of one of the two DNA strands will need some RNA primers for its polymerization (and DNA polymerase will replicate DNA in a "jumping" pattern). Then, in the very end of the synthesis of this strand (called lagging strand) one last fraction will not be copied from the template as even if the last primer is set in the very end of the chromosome, once this RNA is degraded a void space is going o remain invisible for DNA polymerase.
Well this is all well known, but my question is whether during each DNA replication it is ONLY the telomere of the chromatid whose origin was in the lagging strand  which will be shortened? (Thus chromosome shortening is happening in a truly asymmetrical and stochastic pattern)

Not only one strand is used as lagging strand. In a replication bubble for half the length from the centre one will be used but for the other half other strand will be used.See the wikipedia article for replication.

you sure?? where do you locate the centre?

and you cannot use the same strand one "side" as lagging and the other as leading as the direction of a strand is the same from beginning to end

See this

Welcome!I love telomeres too! I will post this as an answer just for the sake of statistics.

so, when a whole chromosome is replicated, the process is carried out from one point following the two opposite directions always, or is there any other scenario?

let us continue this discussion in chat

If you are talking about prokaryotes - yes, if about eukaryotes - no. Eukaryotes have multiple origins of replication to increase speed. So the telomere problem is going to arise at only the "last" origins of replications at both the ends. (No telomeres in middle as there will a 3'end available from the replicated dna from  either side. Do you understand this ? It's a little tricky. Try to visualise it with the help of the image I linked)

By the way there are no telomeres in prokaryotes.

In replication, both the chromosomal halves (which are simultaneously threaded through the replication complex) have a lagging and a leading strand. A part of the segment will be replicated as leading and a part as lagging.

i think you are a little confused.. the strand that is in the direction of the fork  (5'->3') is leading strand . The other one is lagging. It is so because the DNA polymerase holoenzyme complex has two polymerases in the same orientation. So the 3'->5'strand has to be first bent to make it locally 5'-> 3' and then replicated.

Since replication can be bidirectional, a strand of a chromosome will contain both leading and lagging elements (was that what you were trying to explain ?). If so, you should elaborate in your answer. The concept of leading/lagging strand is confusing because it is just a local structure, not the entire chromosome.

@WYSIWYG Yes I meant the second thing. Please feel free to edit it.


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Which mountain range was formed first (historically) and which the pedigree is correct?
Source 1:

Source  1 shows a map of a particular area. In this map you will find the  mountain ranges 1 and 2, the species P, Q and R. Two possible pedigrees of  the ancestral history of the species P, Q and R are drawn .
Which mountain range was formed first (historically) and which  pedigree is correct?

1 might have formed first and I think pedigree 1 is correct.

If mountain range 1 was formed first, pedigree 1 is correct.
If mountain range 2 was formed first, none of the two pedigree seem correct.
If mountain range 1 was formed first you would first have the split of the initial population into population P and the population Q+R. Then, the formation of mountain range 2 split the population Q+R into Q and R. Therefore, Q and R are more closely related than they both are to P. Therefore Pedigree 1 is correct.
You can apply the same kind of reasoning by guessing that mountain range 2 was formed first and you will realize that you would expect a pedigree different than Pedigree 1 and Pedigree 2. If mountain range 2 appeared first then, the correct Pedigree would display the population/species/lineages P and Q more closely related to each other than they both are to R.

Could you elaborate on why you think so?

@user4847 Update! Does it make sense to you?

I approve it....


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Will I grow taller? How can i tell?
I'm 17 and I'm about 160 cm and my weight is 47 kg . I just want to know if I will still grow taller ?

Two things might help here... The height of your parents (and possibly any older siblings), and your gender. As the answers below show there is sex specificity in timing of growth spurt, and height (and timing of growth spurt) is heritable from parents. Don't give up hope, I grew 30 cm after turning 18!

By the way this question in it's current format is a personal medical question and is more suited to your GP, not suitable for BiologySE. I suggest you rewrite it in a general biological framework, perhaps along the lines of... "How heritable is height, how does the likelihood of significant growth decrease with age, at what age can someone expect to have achieved their maximum height?"

Simpler answer (although I like Remi.b's):
Probably.
If you want to know for sure go to a doctor and have them look at your Epiphyseal Plates in your long bones (Femur, Tibula, Fibula). If they've fused, you won't grow anymore. If they're still distinct then you'll continue to grow until they fuse.
For males that can happen as late as early-20's. However, depending on genetics, you might not gain that much height.
Here's a graph you might be interested in:

You're at the tail-end of probably your last growth spurt. You have probably 2-3 years' worth of growing left, but don't expect miracles. You've got maybe another 1-2cm.

wow. that is a great find.

I guess there are two main solutions:
1) From the science of antropometry you might find some clues of the probability that you have of growing taller. For example, if your body (hairs and stuff) already look like an adult body, then you would probably not grow much more. See @MCM's answer who gives a solution that will be way more useful to you than my answer!
2) Knowing the size of your parents you can infer your expected size. Below are some comments on this question.
Any phenotypic trait has shows some part of variance. This variance is explained by genetic variance, environmental variance and the variance due to the interaction of genetic and environment. In equation it gives:
$$V_P=V_G+V_E+V_{GxE}$$
Dividing the genetic variance by the phenotypic variance gives the heritability
$$H=\frac{V_G}{V_P}$$
Estimations of heritability (in the narrow sense, see this for more info) can also be realized with selection experiments or parent-offspring.
The heritability of height in humans is around 0.6 (Welcome to anyone who can give an accurate value and a good reference) which is quite high. It means that more than half of the variance in height among humans has to be accounted to genetic variance. If your parents are tall, don't lose hope, you have quite a good probability to grow tall.

I think your answer is perfect but the "asker" seems to be looking for a simpler answer as he does not seem to be from a scientific background.

Wow! Real Good! Is this sentence correct? "Any phenotypic trait has shows some part of variance"

I guess that all phenotypic traits should show some variance in a population (as soon as the population is larger than 1 individual!), just because there is internal noise (proteins degrade a ta given rate for example). However, not all phenotypic traits shows some underlying genetic variance (that is, not all phenotypic traits are heritable).


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How is RNA of retrovirus converted into cDNA?
The retrovirus (oncovirus) contains RNA. It also has a molecule called reverse transcriptase. This molecule transcribes RNA into cDNA. This cDNA is the DNA copy of viral RNA genome
RNA has Uracil instead of thymine and DNA has thymine instead of uracil. So, how can RNA be converted into DNA? Where does Uracil go and where does thymine come from?

RNA has Uracil instead of thymine and DNA has thymine instead of uracil. So, how can RNA be converted into DNA?

I think you may want to ask a more basic question.  DNA and RNA are extremely similar, with only an oxygen being the difference.  This has vast consequences for organisms, and life as we know it uses DNA and RNA for very separate purposes.  DNA stores the genome providing the instructions for life, and RNA in a nutshell is how that message gets converted into protein for a useful action.  RNA is generally less stable than DNA, so this arrangement works out well.
DNA is regularly and constantly transcribed to RNA, so Thymine is regularly used in favor of Uracil.  There is a fantastic answer here on Biology.SE already dealing with why so I suggest reading that.  The how is pretty straightforward, there are different molecules used!  DNA polymerases incorporate Thymine whereas RNA polymerases incorporate Uracil.  The reverse transcriptase that is encoded by the retrovirus does just this: it transcribes RNA to DNA, using Thymine instead of Uracil.  Both Uracil and Thymine are present in the cell and are thus available for use.

Does reverse transcriptase CONVERT rna to cDNA or is cDNA transcribed from RNA just as RNA is transcribed to DNA in cells ?

Transcribed, of course; sorry for the lack of clarity, fixed.

I think it might be of use to show you the difference between uracil and thymine

They are very similar structures. The part that is involved in base pairing is actually the Nitrogen and the  oxygen furthest from the sugar. See below:

So having an extra methyl group on the other side of the molecule does not interrupt basepairing. And remember, with DNA/RNA synthesis you have a template, and the new strand is based on the template. So, when the RT enzyme Medhat mentions encounters an adenine in the template RNA, it will pair it with a thymidine. And when it encounters a uracil, it is able to pair it with an adenine. The enzyme is structured specifically to only allow in thymine and not uracil, which is how it makes the distinction.


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What is the best way to orally administer a water insoluble powdered drug to macaque monkeys?
They typically need to be given ~150mg, once a day, and it'll last for two weeks. The drug is very water insoluble, becomes almost like a paste, not suitable for tube feeding. And yes, this is for for real lifesaving medical research.
The best we can come up with right now is putting them to sleep, mixing the powder into Nutella, and putting it under their tongue. The idea being they'll wake up and swallow the mixture.

I'd give this a veterinary tag, but it doesn't exist, and I don't have enough points.

So what's it soluble with? Could you dissolve it in oils, like coconut oil? I suppose it tastes too bad to just mix it with mashed bananas?

Can you mix it with food? Especially something what your macaques like?

Could you not suspend it in some liquid?

If it is not water-soluble (lipophobic or hydrophilic), the only other alternative would be that it is fat-soluble (lipophilic or hydrophobic). Consider adding the powder to fatty solids or liquids which can be absorbed from the GI tract into the vascular system, if that is where you'd like the drug to go to be distributed throughout the body. Ideally, you would need to look up the target concentration of the drug within the blood in order to be effective, its volume of distribution, its bioavailability, its half-life, mechanism of metabolism, and calculate from there how much you would really need in order to last the full 2 weeks.

Thing's aren't always water or oil soluble, I've tried to dissolve indigo dye in several organic solvents with no luck. Of course any drug as insoluble as indigo would have terrible pharmacological properties.


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Genetics - Is this hybridization possible?
Suppose you hybridize two plants - One has a red flower and a long stalk, the other has a pink flower and a short stalk. This resulted in these 4 type of plants, with ratio 1:1:1:1

Long stalk red flower
Long stalk pink flower
Medium stalk red flower
Medium stalk pink flower

What possible genotype could the parents have that would result this way?

Do you mean "genotype"? Unless I'm missing something, it seems like you've already described the phenotype (red/long and pink/short) of the parents in your first sentence.

Flower Color
A Heterozygous (Rp) x Homozygous recessive (pp) cross can produce the distribution:
         p      p

   R    Rp     Rp  = Red, Red

   p    pp     pp  = pink, pink

Stalk Length
To me, there appears to be another allele involved or a lack of allele, and definitely Co-Dominance. The only way I could think of a way to get the ratio of stalk lengths in the question after a few minutes thought is if one of the plants are missing a gene before the cross (akin to Turner Syndrome) - the example that follows puts the missing gene on the Short-stalked parents:
SS = Short
TT = Tall
ST = Medium
SX = Short
TX = Tall
X = Missing Gene / Nothing
         S      X

   T    ST      TX = Medium, Tall

   T    ST      TX = Medium, Tall

So ultimately the cross would look like this:
        Sp     Xp

   TR   STRp   TXRp = (#3), (#1)

   Tp   STpp   TXpp = (#4), (#2)


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How do scientists create specific mutations?
Suppose I want to create a mutant like Antennapaedia how will I go about accomplishing it ?
I know that radiation and certain chemicals are mutagenic. So do scientists subject animals to such mutagenic chemicals and then wait for their progeny to see what mutation it has got ? Are there any specific protocols to create a specific type(for eg.homeotic) of mutant or is it pure luck ?
Sorry if I am being too naive!

Thats basically the oldest method to induce such mutations. For this purpose either radiation (x-rays) or mutagenic chemicals (like Ethylnitrosourea) have been used for this purpose. This method is undirected, so you never know what the outcome will be untill you see the off-springs. Using this method to get specific mutations is relative difficult. Its used for the detection of genes which deliver visible phenotypes (for example it has widely been used for the analysis of pigmentation in mice, since you can easily spot mutations).
Newer methods can target genes directly and either introduce or remove sequence areas. These techniques make use of homologous recombinases. In short you bring in you gene of interest in the modified version on a plasmid into the cell which you want to change. The plasmid also expresses the recombinase (this can be under a cell specific promoter to target specific cells) which then recombines the DNA between the plasmid and the genomic DNA.
An example for that is the FLP-recombinase system (image from the Wikipedia article on it):

Other examples for site specific altertions are the Cre-LoxP-System or the Crispr/CAS-System.


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Refractory period in action potential

I know that the part E in this graph is definitely the part of refractory period.
My question : Will there be any effect on B,C or D if a stimulus is given at  time B,CorD respectively ?

If there is a stimulus at E, there will be depolarization (membrane becomes relatively more positive). It is just that no action potential is fired. Therefore, if a strong stimulus does arrive, it will depolarise the membrane to an extent depending on its strength. It will increase the height of the succeeding B phase or decrease the dip of E phase. If it is strong enough, it might persist above the threshold till the refractory period is over, and then an action potential can be fired.

@SatwikPasani I'd say that's a great answer, would you like to add it as one?

If there is a stimulus at E, there will be depolarization (membrane becomes relatively more positive). It is just that no action potentials are fired. Therefore, if a strong stimulus does arrive, it will depolarize the membrane to an extent depending on its strength. It will increase the height of the succeeding B phase or reduce the dip of the succeeding E phase. If it is strong enough, it might persist above the threshold till the refractory period is over, and then an action potential can be fired.


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Why does the stability of YAC increase with size?
From Lehninger Principles of Biochemistry :

The stability of YAC increases with size (up to a limit). Those with
  inserts of less than 100000 are gradually lost during mitosis.

Why does this happen ? (YAC refers to yeast artificial chromosome )

just guessing: perhaps small YACs have problem during mitotic segregation (too small for the cohesin and kinetochore assembly)

From The world of the cell by becker : Infact, YAC must carry at least 50000bp to be reliably replicated and segregated. This supports @WYSIWYG guess.

@user137 :P Edited it !

This is a question which is not easy to answer, especially the 50.000bp number (which I haven't found anywhere in there literature). However, I found some evidence, partly derived from plant and mammal artificial chromosomes (references 1 and 2), partly from the original publication from Murray and colleagues (reference 3).
The problems with small chromosomes seems to be their passage through mitosis and meiosis, where smaller artificial chromosomes tend to get lost. They are also not controlled very well in their number.
Murray states that YACs of 55kB in size are relatively stable in the yeast cells are relatively stable, but have a lower stability than natural chromosomes. When you are interested in the deeper details, I recommend reading the article.
References:

Construction of mammalian artificial chromosomes: prospects for
defining an optimal centromere
Alteration of chromosome numbers by generation of minichromosomes –
Is there a lower limit of chromosome size for stable segregation?
Contruction of artificial chromosomes in yeast.


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RNAi in nematode resistant plants
Background : Certain plants have been genetically engineered to have sense-antisense gene of a parasitic nematode. The dsRNA produced by the plant then inactivates the mRNA produced in the nematode, who, then isn't able to synthesize the corresponding protein and dies as a result.
Question : How is the dsRNA from the plant transfered to the nematode's cell ? By transformation ?

Apparently it is transferred by simply feeding. C.elegans feeding on E.coli producing dsRNA can produce the siRNA. C.elegans seems to have a lot of RNA transporters such as SID1.

Yes, in vitro you can simply soak the worms in a solution that contains the dsRNA (i.e. in a large-scale microtiter dish for HTP screening)--this is not the same as ingestion because the worms won't eat if there are not small particles  in the liquid.  For the bacteria the E. coli express the RNA hairpin in response to an inducer (IPTG) and then after ingestion the cell contents are released after the cells pass through the pharyngeal grinder, and the RNA is taken up by the gut cells, and then transferred to other cells by the transporters.

@wysiwyg thanks. Pls see my comments on Ilan's answer.

The question is little bit unclear: is in vitro or in vivo introduction in question?
In vivo:

As the nematode feeds on the plant during its parasitic phase, it
  consequently assures the introduction of dsRNA and/or siRNA molecules
  into the nematode’s digestive system.

in vitro introduction etc  ->
The status of RNAi-based transgenic research in plant nematology

Why does it feed on it ? Even if it does, won't the RNAases in its digestive system break down the RNA ?

@biogirl They feed on the plants for nutrition. RNAses should break down the RNA but I couldn't find much information about exoribonucleases in nematode digestive system. Apparently the RNA transporters are far more active. Perhaps an evolutionary adaptation.

@biogirl it is a part of a parasitic evolution. The mechanism of dsRNA introduction includes enzymatic interactions: dsRNA is introduced into the nematode digestive system by feeding on dsRNA-expressing E.coli. The dsRNA spreads to neighborhood (the SID-2 and SID-1 proteins actions), followed by cleavage of dsRNA by the RNaseIII, Dicer, in the cytoplasm. Attachment of siRNAs to the RNA-induced silencing complex (RISC) separates the strands of siRNAs and incorporates the siRNAs into the active RISC. These siRNAs target mRNA molecule and the RISC cleaves them and a gene is silenced.

@wysiwyg Thanks ! How are active RNA transporters evolutionarily advantageous ?

@biogirl That I cannot comment about. It could have been advantageous for some reason. There is too much to speculate here


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Size of DNA in phage
I have read that DNA(after recombination) is packaged in bacteriophages lambda only if it's between 40000 and 53000 bp long. This constraint can be used to ensure packaging of recombinant DNA.
I don't understand why shorter DNA can not be packaged.
Source : Lehninger Principles of Biochemistry

Does the Lehninger explicitly state that it is not possible?

These values relate specifically to lambda phage.

@Chris Yes. And as Alan Boyd states, this values are applicable only for bacteriophage lambda. (Edited my question)

For lambda:

If the distance between the two cos sites is less than ~37 kb, the resulting phage particle will be unstable. When the DNA is inside the capsid, it exerts pressure on the capsid. Likewise the capsid exerts an inward force on the DNA. If there is not enough DNA inside the capsid, it will implode from the inward force of the capsid. If the distance between the two cos sites is too far (~52 kb), then the capsid will be filled before the second cos is reached. The tail cannot be added because the DNA hanging out of the capsid is in the way and no infectious phage particle is produced.

http://www.microinmuno.qb.fcen.uba.ar/03-Bacteriophage.pdf
In contrast filamentous phage like M13 have no upper size limit, but since they get longer with more DNA they become physically fragile.


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Pedigree analysis : autosomal or mitochondrial

I have tried a to decide if this is a autosomal dominant, recessive or a mitochondrial disorder.
Is it possible to know for sure, or do you have to use probability?
(English is not my native language)
No other pedigrees have had carriers marked so I did not expect this one had it either.
Auto dominant.
I:1 aa I:2 A-
II:1 aA II:2 aa II:3 aa II:4 aA
II:1 children could have got a from him and a from her the the disorder would be gone.
III:9 children got her dominant A
Recessive
I:1 A- I:2 aa
II:1 aa II:2 A- II:3 A- II:4 aa
Mitochondrial disorder
I read "transmission only accours through females"

Could you please share your findings/rational so far on the matter and what makes you think it is autosomal or mitochondrial? This will show that you have thought about the question and will encourage others to contribute and point you to the right answer.

Since other pedigrees we have used have not had carriers marked I presumed this would not either.

Mitochondrial because all the offsprings have the same trait as that of the female parent. Lets go through the possibilities one at a time. Assuming you have no carriers (you do not have any carrier symbols) we can work out the following.
Autosomal Recessive?
This might be the case if we assume the male in the first generation is a carrier.
Autosomal Dominant?
This might be the case but it is unlikely. Looking at the first generation possibly yes, as 50% of offspring have the trait. Looking at the second generation however only 3 out of 9 offspring have the trait. Making autosomal dominant unlikely (but it is still a possibility.)
In the test, if you have to go with one option, mitochondrial inheritance is the best because there are no assumptions at all but if multiple options may be correct, you can have any of them.

Actually, all offspring of females with the trait are affected ...

ah yes sorry my mistake, i read the female in the first generation as a daughter not a wife. so it is mitochondrial. Thanks

As Rory has pointed out, there is no incomplete penetrance if we accept it as a mitochondrial trait. Besides that, your "Sex-linked?" point seems to be incorrect. In this case we can rule out the case of a dominant X-linked locus based on the observation that males didn't pass the trait to their daughters (decisive argument) and that sick heterozygous mothers transmitted the trait to all of their progeny (in statistical terms).

It cannot be X linked dominant. If it were then the male in the top left corner would always have daughters who had the trait as they need to inherit one X from their mother and the other trait X, X_T from there father. Resulting in XX_T and if X_T was dominant they would show the trait.

Please read my comment again. Your argument was: it's not a sex-linked locus, "because both males and females are effected."


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Do body lotions enter into bloodstream of people? And how do they do it?
I found this

very disturbing: bombastic tabloid-style writing in capital and the content is doubtful. If it was correct or close "does it really take something like 26 seconds for a body lotion to enter into bloodstream?", you select a lotion with very high level of fat -- now your heart will pump  blood with a very high-level of fat, possible source for heart failure. If you have a dry skin and you put 40%-fat lotion to your skin, it makes it more flexible. I am very-very skeptical whether any fat gets into your bloodstream. I am new to things such as blood lipids (blood fats) and mechanisms how the body lotions really penetrate into the skin. How? And which factors determine the time and does any get actually into bloodstream and after which kind of processes by the body? Is this just a hoax?

Surely they go in, that is the principle by which topically applied drugs work!

Lotions, like any other drug, can effectively enter the blood system. However, the fraction of the applied lotion that actually enters is really small, and it only achieves a significant concentration in the zone near the application. The skin, if healthy, offers a very high resistance to the passage of substances. Moreover, the bloodstream actually dilutes even more the little fraction it achieves to enter, further reducing its effects. If the skin is damaged the penetration is greater, though you'll never be able to get drunk by dropping booze in an injury.

To complete, I would add that the issue here is that the skin is composed by a mix of hydrophilic (="water-loving") and hydrofobic (="fat-loving") layers, so a water-based lotion will pass easily through the former and much less easily through the latter, and the opposite is true for a fat-based lotion. PS: just a little note on your first sentence: lotions are not drugs, they are formulations, like a pill or a spray. You can use lotions as a formulation for drugs.


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Improving myopia
I have a friend who no longer needs glasses. He previously had myopia in both eyes but over the years it has improved until he no longer needs glasses clinically. He's had glasses for over 30 years since he was around 20.
Based on the above, I'd like to know if myopia can be improved naturally. Specifically whether not using glasses helps the underlying architecture of the visual system compensate in someway, or perhaps if nutrition can reduce myopia or finally if aging is known to decrease myopia. I'm interested in any biological mechanism at play.
I have a good understanding of Opthalmology and additionally would like any answers to be evidence based.

Apparently reduction of myopia with age is fairly common. It is thought that the improved vision comes from relaxation of the ciliary muscle as the person ages. Since the lens changes shape the aberrant myopic focusing of light can be corrected to the correct location. While age was found to be the strongest factor influencing myopia progression, other factors like ethnicity and sex also play a role.
http://archopht.jamanetwork.com/article.aspx?articleid=417134#
For additional info see:
http://www.iovs.org/content/41/8/2103.long
http://www.improveeyesight.org/can-myopia-near-sightedness-improve-with-age

Thank you! I read your reference which said improving beyond 1 diopter is rare. Perhaps there are more factors at play or certain factors tilt the balance such as genetics, nutrition etc. Could you explore these also?

I'll give you an answer based on my personal experience. I know that presbyopia usually increases with aging, so presbyopia and myopia can compensate each other with time. That's maybe what happened to your friend. But I don't know if myopia is related to nutrition or the use of glasses..


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What is the evolutionary advantage of regret?
Some motivational speakers may say that regrets are only useful to learn something from.
What are the other advantages?

Regrets (as an Emotion) have fair equally it's disadvantages. And in this question of your's, did you intentionally avoided talking about it's disadvantages? Please make it clear. Also regret on a long-term leads to self loathing, chronic stress. it's a negative emotion, isn't it?

Very interesting question.
First I'd like to highlight that this question relates to a very hypothetical field of evolutionary biology which is evolutionary psychology. This wikipedia article on evolutionary approaches to depression might be of interest as well. One sentence says: "Feelings of regret associated with depression also cause individuals to reflect and analyze past events in order to determine why they happened and how they could have been prevented". It basically says the same thing than you said in your question.
What other advantages might "regrets" have? Before trying to answer it, I'd like to ask : is it necessary that it has advantages? A behavior or a feeling might as well be a by-product of selection for big brains. It might therefore not be selected for but it exists only because there is not much selection against this by-product trait.
Our brain are often considered to have evolved for social purposes. I would hypothesize that if someone express "regrets", he might benefit from other's care and pity. And the best way to express "regrets" is to feel the "regrets". Robert Trivers would maybe say that in order to fool someone else (make someone else think we regret) the best thing to do is to fool ourself (make ourself feel "regrets"). See his book, the folly of fools.

Very good. I am thinking of regrets for things we do to ourself.