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Linkage disequilibrium with multiple alleles and loci
Linkage disequilibrium $\left(D\right)$ for two bi-allelic loci is defined as:
$$D=X_{11}X_{22} - X_{12}X_{21}$$
where $X_{11},\ X_{12},\ X_{21},\ X_{22}$ are the frequencies of the haplotypes $A_1B_1$, $A_1B_2$, $A_2B_1$, $A_2B_2$ respectively (the subscript number correspond to the two different alleles and $A$ and $B$ correspond to the two different loci)
My questions are

How is $D$ defined for more loci and a greater number of alleles?
How is $D$ defined when the number of alleles differ from locus to locus?

Let me know if my answer is making sense to you

LD describes the associations among alleles at different loci. For anything more than two bi-allelic loci, you need more than just one number to fully describe the associations. For instance, if we have three bi-allelic loci 1-3, we need the three pairwise LD coefficients, plus one extra three-way coefficient. In general, if we have $K$ loci, and the $k^\text{th}$ locus has $n_k$ alleles, there are $\prod_k n_k$ possible haplotypes, so to fully describe the state of the population we need $\prod_k n_k-1$ haplotype frequencies. If we instead want to use allele frequencies and associations, we'll therefore need $$\prod_k n_k-1-\sum_k(n_k-1)=\prod_k n_k-\sum_k n_k+k-1$$ LD coefficients. (Note that each locus is described by $n_k-1$ allele frequencies.) This means that things get complicated pretty quickly with many loci! If you want to dive into the details, check out Barton and Turelli (1991) and Kirkpatrick, Johnson, and Barton (2002).

Being a typical molecular biologist, I am a little uncomfortable with classical genetics terms. I might redefine some symbols (perhaps to mean the same) [It is like talking to oneself while thinking].

There are four DNA-blocks : A1, B1, A2 and B2. Ak and Bk are adjacent blocks. [Perhaps this is same as what you defined the symbols as]. A and B are contiguous DNA regions whereas 1 and 2 are different chromosomes (homologous regions). See the figure below.

The formula:
D=X11X22 - X12X21
basically means that the difference between the probability that the loci are in configuration I (11 & 22) or configuration II (swapped) (12 & 21). Lets say there is a third region (3) which is homologous to the two alleles which has DNA-blocks A3 and B3.
As LD is defined it is a difference in probabilities. Depending on how you define, it will take a negative or a positive value. When you have 3 recombinationally feasible alleles then there can be six cases:

C1: [A1B1] [A2B2] [A3B3]
C2: [A1B1] [A2B3] [A3B2]
C3: [A1B3] [A2B2] [A3B1]
C4: [A1B2] [A2B1] [A3B3]
C5: [A1B2] [A2B3] [A3B1]
C6: [A1B3] [A2B1] [A3B2]

In this case there is no single measure for difference. You can also do something like this:
LD1' = P(C1) + P(C2) - (P(C3) + P(C4) + P(C5) + P(C6))
Where LD1' is LD of region 1 and P(Cm) is the frequency of mth configuration.
Now, if there are 3 or more adjacent DNA blocks, you can only define LD, pairwise. It however, makes sense because linkage reduces with distance and you can calculate LDAC = LDAB x LDBC (A,B and C are contiguous in alphabetical order. If A and B are not linked then A and C cannot be linked.)


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Which chemical and hormonal effects on heart are by metabolites?
I am thinking which hormonal and chemical effects from:

catecholamines
thyroxin
corticosteroids
sex hormones
prostaglandins
Ca2+
Na+
K+

can be be regarded as metabolites i.e. intermediates or products of metabolism.
I got this question

Account for chemical and hormonal effects on the heart.

and I am thinking if I should include metabolites as a factor as

Metabolites by intrinsic autoregulative system locally

because the autoregulation of heart is very important factor in the physiology of the heart.
Can you regard some metabolites as having hormonal and chemical effects?

Strictly speaking, hormones are either steroid derivatives or peptides, which transduce their effect in specific ways (e.g., diffusion into the cell to bind a target in the case of steroids,  or signalling through a surface receptor for peptides). Catecholamines are neurotransmitters and not considered hormones by the classical definition. The effects can either be autocrine, paracrine or endocrine depending on the distance of action. Ions will typically affect the electrical conductivity of the myocardium and can be considered passive in nature, but ions are not metabolites.

Ions are not hormones. Ions are not metabolites either.
Technically, anything that is not directly absorbed from environment but is synthesized/modified in the body is a metabolite.
Even if you don't consider polypeptides as metabolites (which for some reason are not classified as metabolites in scientific parlance), all the molecules that you mention are metabolites with known biosynthetic pathways.

You are right about ions. I missed the word "chemical" in the whole discussion.

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Effective population size when the population sizes varies from season to season
Let's think of a species which has four generations per year and which population size changes from season to season so that the population size is 100 in summer, 200 in spring, 50 in autumn and 20 in winter for example. In such case, the effective population size $N_e$ can be calculated by:
$$N_e = \frac{n}{\sum_{i=1}^n\frac{1}{N_i}}$$
where $n$ is the number of generation per year (4 in my example) and each $N_i$ correspond to the population size in one season.
My question
Can you please provide an explanation of why this formula (based on the harmonic mean) holds true to define the effective population size?

source

This is derived from studying how heterozygosity changes over time. The standard equation for change in heterozygosity ($H$) with constant population size ($N$) is:
$H_t = \left(1 - \frac{1}{2N}\right)^tH_0$
When $N$ varies between generations you use the product of this formula:
$H_t = \left(1 - \frac{1}{2N_0}\right)\left(1 - \frac{1}{2N_1}\right)...\left(1 - \frac{1}{2N_{t-1}}\right)H_0 = \prod_{i=0}^{t-1}\left(1 - \frac{1}{2N_{i}}\right)H_0$
To get the overall $N_e$ you need to find the population size that gives the corresponding decrease in heterozygocity over t generations i.e:
$\left(1 - \frac{1}{2N_{e}}\right)^t = \prod_{i=0}^{t-1}\left(1 - \frac{1}{2N_{i}}\right)$
Rearranging gives:
$N_e = \frac{1}{2\left[1-\left[\prod_{i=0}^{t-1}\left(1 -\frac{1}{2N_{i}}\right)\right]^{1/t}\right]}$
This expression can be approximated by the harmonic mean, which is easy to verify with some toy data (you get small deviations if yearly population sizes are very small). The explanation given above can also be found in Hedrick (2009, p217ff), along with some nice examples that integrates the effects on effective population size from several factors.

That was simple! Thanks a lot for this very good answer!

Yes, and not very difficult to instead use the exact expression to calculate Ne when you have yearly population sizes.

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How to calculate the effective population size ($N_e$) with overlapping generations?
From this Source: If generations are overlapping, then the effective population size $N_e$ does not equal the population size $N$.
I know mathematical formulations in order to find the effective population size $N_e$ when the sex-ratio is biased $\left(N_e = \frac{4N_mN_f}{N_m+N_f}\right)$ or when the population size varies cyclically through time $\left(N_e = \frac{n}{\sum_{i=1}^n\frac{1}{N_i}}\right)$.
What is the effective population size in a population with overlapping generations?

Some info on this can be found in Hendrick (2010, p 234), and if you follow the reference there (Laikre et al, 1998) you might find a more complete answer.

Moved misposted answer (see below) from http://biology.stackexchange.com/questions/23098/effects-of-selection-on-effective-population-size

There are many different ways to do this, depending on what assumptions you make on e.g. stable age structure, distribution of offspring, haploidy/diploidy, population growth etc. As you probably know, there are also two main approaches to effective population sizes, namely ones based on:

the rate of inbreeding ($N_{e,i}$)
the increase in variance of allele frequencies ($N_{e,v}$), and they can sometimes differ a bit from each other.

An early attemp to calculate effective population size with overlapping generations comes from Felsenstein (1971), which is based on life table information. This paper includes several derivations, both on inbreeding $N_e$ and variance $N_e$. As an example, the formula of inbreeding $N_e$ for a diploid population is:
$N_e = \frac{N_1T}{1 + \sum_i^\inf l_i s_id_i v_{i+1}^2}$
Here, $T$ is the generation time, $l_i$ is the survival up to age i, $s_i$ is the survival from age i, $d_i$ is the probability of death at the end of age i (i.e. 1-$s_i$), and $v_{i+1}$ is the reproductive value of individuals in stage i+1. However, this is assuming a constant population size and a stable age distribution, so some rather restrictive assumptions. The paper also includes models for haploid populations, and I haven't gone through it carefully.
A couple of more recent papers that calculate $N_e$ for overlapping generations are Engen et al. (2005) and Engen et al. (2007). These papers use diffusion approximations to derive several formulas for $N_e$ under different assumptions, for age-structured density independent populations. One model for a haploid population in a fluctuating environment is:
$$\begin{align}
N_e & = \frac{N}{\sigma_d^2T} \text{, with} \\
\sigma_d^2 & \approx \sum_{i=0}^k \frac{\lambda^{-2}}{u_i} \left[\left(\frac{\delta\lambda}{\delta b_i}\right)^2\sigma_i^2 + \left(\frac{\delta\lambda}{\delta s_i}\right)^2 s_i(1-s_i) + 2\left(\frac{\delta\lambda}{\delta b_i}\right)\left(\frac{\delta\lambda}{\delta s_i}\right) c_i \right]
\end{align}$$
where $T$ is the generation time and $\sigma_d^2$ is the demographic variance. In the lower equation, $\lambda$ is the deterministic growth rate (dominant eigenvalue), $u_i$ is the proportion of the population in stage i (a component of the stable age distribution), $b_i$ is the expected number of offspring with variance $\sigma_i^2$, $s_i$ is the survival rate of stage i (with binomial variance), and $c_i$ is the covariance between reproduction and survival. You really need to dive into these papers to fully understand how these equations are derived and how the variables are defined (will take up far to much space here). However, at its core, it is using a diffusion approximation on an allele at a selectively neutral locus.
There are many other papers out there deriving effective population sizes, under different assumptions and restrictions, but the ones cited above should be a good starting point, and by looking at citations to and from these you should get a decent overview of the topic. Many textbooks also cover ways to calculate effective population sizes with overlapping generations, e.g. Hedrick (2011) and Felsenstein (2013, free pdf).

Ha ha I actually didn't even notice either that it was under the wrong post!

@Remi.b Yeah, I didn't at first either. Also, upvote if you find it useful, so that the Q is removed from the unanswered queue.


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Meaning of the word Oleracea
What does "oleracea", as appears in numerous plant species (scientific) names, mean? Examples: Euterpa oleracea, Brassica oleracea, Portulaca oleracea, Acmella oleracea, Spilanthes oleracea.

It means "vegetable".
I think it's because people use those plants for food

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Conserved proteins are non immunogenic
I read that proteins that have been highly conserved are non-immunogenic.
Why is it so ? What is the special thing that makes it non immunogenic(antibodies against them are hard to make) ?

Immunogenicity has nothing to do with how conserved a protein is. As nico already pointed out, it is a mechanism to prevent autoimmunity. But this is only valid for proteins which are similar to human proteins.
If you design a vaccine, you try to choose proteins as vaccine candidates, which are as conserved as possible. This makes the vaccine more universal (since conserved proteins are shared between different strains of a bacterium or a virus) and also prevents it from getting ineffective when the target protein mutates. An example would be the flu virus where you need to predict the strains which will be in circulation to formulate a vaccine. If it would be possible to find a conserved protein, which is shared between all viruses (and of course has no similarities to human proteins) than you would have a universal flu vaccine.
Antibodies can (and are) be designed artificially, this is for example done for capsulated bacteria like Menningococcus B, where so far no vaccine was available. These vaccines are either relatively short peptides or single proteins from the from the pathogen. The proteins for the vaccine are then usually made in a biotechnological way, purified and can be used as a vaccine. This approach is called reverse vaccinology.

Hi! Please see my comment to nico's answer.

@biogirl I expanded my answer. Does this answer your question?

Immunogenicity is

the ability of a particular substance, such as an antigen or epitope, to provoke an immune response in the body of a human or animal. In other words, immunogenecity is the ability to induce a humoral or/and cell mediated immune response.

If a protein is highly conserved between species it means that its epitopes will be recognised as self by most species, hence the organism will avoid producing antibodies against them to prevent autoimmunity.
You may want to read about central tolerance to see how T cells and B cells are rendered non-reactive to self.

Hi! thank u . I read this not in relation to living organism but artificially trying to make antibodies. Do artificially made antibodies also always involve living organism ? Can we make antibody(just like we make some chemicals) that can not be induced to be made in a living organism ?

@biogirl: most commercial antibodies are generated by injecting the antigen into an animal. Most used speciars are rabbits, sheep, goats, chicken, guinea pigs, rats and mice. You can get antibodies synthesized in bacteria as Chris pointed out, but I would say that is not the most common way nowadays.


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Telomerase in tetrahymena
In this amazing video, at 26:03 we see this image
We now know that the telomerase contains a sequence complementary to the telomere sequence and so is able to do what it is capable of doing in this image.
My questions : What if we make a piece of dna with  five GGGGG at the 3' end ? Will the telomerase not work, as the RNA in telomerase has the sequence AACCCC and so won't be able to form complementary strand ? If so, has such a mutation been detected in any organism ie it's telomerase is unable to work just because it has a random insertion(maybe during replication) of one of the nucleotides in the telomere at the 3' end ?

Anyone who wishes to understand telomere and telomerase and want to know more about them from the discoverer of telomerase HERself please see the video I mentioned in the link! It's enlightening.

This is speculation, as I haven't done or read of the required experiment. However, I imagine that this would not be a problem.
You're right that the RNA template (TERC) would not hybridize with a poly-G sequence, and so the telomerase would not be able to add more telomere repeats. You can imagine that the poly-G sequence is a cap, preventing telomerase activity.
However, without the telomere repeats other proteins are likely to recognize the chromosome end as a DNA break. Exonucleases would likely chew at the end of the chromosome until they got to the actual telomere sequence, which is bound by protective proteins (namely Shelterin). With the poly-G region degraded, the end of the chromosome would now have the true telomere repeats, and telomerase would be able to add even more repeats.
Even if the poly-G region was bound by protective proteins, the telomeres naturally shorten with each replication cycle, due to the nature of 5' to 3' DNA replication. Therefore, the poly-G region would eventually be removed revealing the true telomere repeats and allowing telomerase to extend the chromosome once again.
In a worst case scenario, rather than degrade the poly-G region the cell undergoes recombination between poly-G regions on multiple chromosomes, leading to either massive chromosomes or circular chromosomes. However, I'm sure these cells would die with some kind of massive mitotic failure.


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2 types of telomerases?
As telomerase works by adding new nucleotides complementary to the RNA it contains, it cannot work for the complementary strand.
Say telomerase X has RNA complementary to the 5' to 3' strand it cannot elongate he telomere for the 3'to 5' strand.
So does a cell have 2 types of telomerases ? One for 5' to 3' and another for 3' to 5' ?

A second telomerase is not necessary, as the lagging strand is filled in by the DNA-Polymerase, see this figure:


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What stops telomerase?
The telomerase is an enzyme that adds telomeres.
What stops the telomerase from adding too many telomere sequences ? What's the regulating mechanism ?

Telomerases are tightly controlled on all level: Expression, post-translational modifications and by external factors. I think for this the external factors, a protein class called telomeric proteins. They bind to the end of the telomere and regulate the telomerase.

The figure is from this paper, which looks into the topic quite extensively:

Regulation of telomerase by telomeric proteins.


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spinal cord lesion and result in somatic sensation
Jimbo suffers a lesion to the entire right half of the spinal cord at the T6 level. A few weeks after his injury, his doctor tests his right and left legs for somatic sensation and tone.  fill out her chart concerning the absence or presence of different sensations and muscle tone in the lower limbs.
Mark a for absent, P for present
Right leg: Light touch, Pain, Proprioception, Temperature, Hypertonicity, Hypotonicity
Left Leg: Light touch, Pain, Proprioception, Temperature, Hypertonicity, Hypotonicity
what about if the lesion is in C1 or L5? where would it affect (leg/hand..) and fill out the above chart?

Is this a homework question? If so, please use the tag and show how far you got with an answer so far.

it's a practice question. I have no clue how to proceed...

For the sensation aspect, dermatomes are a big hint.  They will give you a rough idea of some of the motor neuron projections.  I'd recommend trying to fill in all that you can and ask specific questions about the portions you don't understand (in the form of "Okay, I know that X ascending tract has been likely damaged, so there's likely to not be any information about Y propagating above a certain level...so, will this mean...") rather than just dropping off the assignment. This is a very useful exercise :)

This is a classic Brown-Sequard syndrome well- studied in the field of neurology. To answer your question, you would need to know what tracts are being severed and what sensations each tract is responsible for. A clean R hemi-section of the spinal cord at the level of T6 would affect the 1) R lateral corticospinal tract, 2) R spinothalamic tract, and 3) R dorsal columns.

The R lateral corticopsinal tract is an upper motor neuron (UMN) pathway, which relays messages from your brain to the periphery. If severed, it would lead to paralysis of muscles below the lesion on the ipsilateral side. This would result in UMN signs such as increased reflexes, increased spasticity, and muscle weakness.
The spinothalamic tract is a sensory pathway connecting peripheral sensations and bringing them up to the brain. Specifically, it communicates sensations of pain, temperature, and gross touch. If severed on the R side, these sensations would be lost on the contralateral side a few levels below the site of the lesion. The reason for this is due to the decussation, or crossing over, of the tract at or slightly above the level of entry of the nerve fibers into the spinal cord from the periphery.
The dorsal columns are similar to the spinothalamic tract, except the sensations communicated are vibration, fine touch, and proprioception. If severed, this would cause loss of these sensations below the level of the lesion but on the same side. A patient would not be able to balance himself/herself without support.

Regarding what areas of the body would be affected based on a lesion in T6, C1, or L5, just as mentioned by jonsca, one would need a dermatome to understand what areas of skin sensation would be affected, and know the nerve root origins of different nerves of muscles. A great book to read to locate these answers in a table format is Neurology BluePrints.
Otherwise, feel free to open any Neurology textbook for a reference, and look for Brown-Sequard Syndrome to read in more detail.


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Neuroscience: zapping an axon connected to thermoreceptor
Let’s say an experimenter has an electrode that can give a shock to a single axon. She takes that electrode and zaps an axon connected to thermoreceptors in the hand of her subject.
I) What would the subject’s perception of the stimulus be?
II) Why?
III) If she zaps that axon AND ONLY THAT AXON so hard that it destroys the axon, would the subject feel pain?

Hi! Welcome to the site. The question you have asked is classified as homework question. You need to show your efforts - what you thought, what you tried to search, etc. You should write what you think can be the answer.

I and II depend on the type of electrical signal applied to the axon. for III, most receptors can perceive other sense as well, so for example striking a vision receptor may produce the perception of light (even in complete darkness) - my guess is the you would feel pain, even if you could isolate the destructive signal away from nearby pain receptors.
search "action potential" in duckduckgo.com, it will get you going.

Can you please add some references?


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Which inflammatory response with Cytomegalovirus infection?
I am thinking about inflammation process with Cytomegalovirus infection.
I first thought it is about chronic inflammation, but then changed my mind because of virus infection.
I think cytokines must be there in activation.
I am thinking which of these is right mechanism for both of these

mononuclear cells and granulocytes (I think this must be chronic inflammation)
granulocytes with scar formation (I think no scar)
cytopathic cytoproliferation inflammation

I think the cytopathic cytoproliferation inflammation is the right one because cytokines are activating the inflammatory response in virus infection.
However, I am not sure if this inflammation is of chronic type.
Which type of inflammation can cytomegalovirus infection lead to?

According to this paper the virus triggers the innate immune system and induces inflammatory cytokines as well as interferon stimulated genes (which is a response to a viral infection).
It seems to be recognized by the cells via the Toll-like receptor 2 and CD14, which subsequently trigger the cytokine production. A schematic view comes from the second paper:

These two articles are interesting in this context, the first addresses CMV in special,
the second is a pretty recent review about how viruses are recognized and how cytokines are involved:

Human cytomegalovirus activates inflammatory cytokine responses via
CD14 and Toll-like receptor 2.
Learning from the messengers: innate sensing of viruses and cytokine
regulation of immunity - clues for treatments and vaccines.


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How much of your stock solution should you take to make the 1000 cells/mL mixture?
You need a solution containing 1000 buccal cells/mL. You count that you have 125 buccal cells in 50uL, from a total solution of 8 mL. How much of your stock solution should you take to make the 1000 cells/mL mixture? How much solvent if you would like a total volume of 5mL?
I don't even know how to approach this!!!
Help??

You should try to find the concentration of your stock solution which contains the same amount of cells as required and then dilute it. Have you tried anything yet?

welcome to cell culture & dimensional analysis
125/50µl or 2.5 cells/µl is your concentration (better way of expressing it)
2.5 * 8000µl = 20,000 total cells you have. 1000µl in 1ml that's why the 8000µl
20,000 cells / 1000 cells/ml = 20mls final culture volume to reach desired concentration
20mls - 8mls = 12mls   so you need to add 12mls of medium / saline / whatever to your 8mls to dilute it to the correct concentration.
when you ask about solvent to ADD to make 5mls. Prob with this question is you don't state the desired concentration. So assuming its still 1000 cells/ml kinda go backwards,
1000 cells/ml * 5mls = 5000 cells is what you want to get
to get it:
5000 / 2.5 cells/µl = 2000µl or 2mls of your culture.
So take 2mls of your culture and mix it with 3mls of solvent / medium  (5mls - 2mls).
I'm quite certain chris below is not correct.

OMG! You should be a teacher!!
It's crystal clear now!
I'm in love with this answer :)
Thank you very much. I wish you luck and success
I sincerely do

Oh, come on, thats simple math.
First calculate how many cells you have per ml: 50$\mu$l are $\frac{1}{20}$ of 1 ml. So multiply 125 with 20 to get the concentration per ml: $125 \times 20 = 2500 \frac{cells}{ml}$
If you want to know how many cells you have in total, multiply by 8 (for the 8ml you have) and you come to 20.000 cells in your 8ml solution.
When you want to know, how much of your solution you need, you calculate: $\frac{2500 \frac{cells}{ml}}{1000 cells} = \frac{1 ml}{x}$.
This can be transformed into $x = \frac{1}{2,5} ml = 400 \mu l$.
So you need 400 $\mu$l for each ml of your final cell solution. So if you want to have 5ml with 1000 cells/ml you need $5 \times 400 \mu l = 2000 \mu l = 2 ml$ of your cell solution. To reach 5 ml add 3 ml of your solvent/media.


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Hela live cell confocal laser scanning - reccommendations for good fluorophore that will show good movement
I've been doing a lot of live cell imaging lately mostly using hela cells expressing some EYFP based chimeric proteins. I'm building a video library for an art student here at the university who is going to create an exposition using the videos. I need a lot of content to make this sucessful and rather than requiring much scientific merit these videos need to be "busy" and look good. I'm looking for suggestions as to any dyes or fluorophores, drug treatments or conditions someone has worked with that will show significant movement/change of/in the cell, change in intracellular localization....doesn't matter it just needs to be a significant alteration for the cell.
I'm still really optimizing the system with the CO₂ etc.. and the longest aquisition i have taken is about 8 hours - after that either the cells are dead or the focal drift becomes too much of a problem. I am hoping to see some division once I can get the system recording long enough. Until then was looking for some suggestions as to other possibilities.
The various dyes I have been using include:  hoechst, dapi, mito-tracker, draq5, er-red, rox-red. also eyfp/tubulin, eyfy/mito, eyfp/golgi, draq5. These dyes aren't cheap and I'm only one i know doing this so I'm checking here.

I am not really sure, what you are asking for. You are looking for a fluophore that is nicely visible in confocal microscopy? Or do you want to tag a protein, which moves a lot? Or do you want to see whole moving cells?

Thank you Chris, I added a lot of needed info to the original question.

You could think about tagging proteins, which are imported and exported from the nucleus.

MitoSOX looks pretty cool. I've never used it myself, but I'm sure you could see some cool mitochondrial dynamics going on. Its a bit pricey though, but all dyes are going to be.
Even at only 8 hours you should probably be able to see a few divisions, which would be cool with hoechst.


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What errors can occur during DNA replication?
When there is an error in copying DNA (a mutation), what exactly goes wrong?
If G goes with C and A goes with T, I don't see how that part can mess up.
Is the idea that when the double helix is split, an A gets ruined and replaced with a G by mistake, which then pairs with a C in one of the copies? So something that was supposed to be AT is now GC.

The Wikipedia entry for DNA repair might be helpful to understand the types of damage and errors that can occur. http://en.wikipedia.org/wiki/DNA_repair

There are many way in which DNA can be damaged. As already pointed out in the comment by @skymninge, the Wikipedia page on DNA repair, as well as the mutation page detail some of the things that can go wrong.
You say:

If G goes with C and A goes with T, I don't see how that part can mess up.

This, however, would imply that the four bases are completely different so that mispairing cannot exist. This is (may I add luckily?) not true.
Indeed the chemical structure of the bases is very similar, and changes between one base and another (transversions and transitions) are common.

These can result for instance from exposure to external agents such as ionizing radiation and alkylating agents, or from exposure to endogenous products such as reactive oxygen species.
Furthermore, the enzyme synthetizing DNA, called DNA polymerase, can insert the wrong base, although most of these errors can be corrected by its "proof-reading mechanisms". However, it is estimated that

the frequency at which human DNA undergoes lasting, uncorrected errors range from $1 * 10^{-4}$ to $1 * 10^{-6}$ mutations per gamete for a given gene.

Source: Nature Scitable
So, in summary, the system is not perfect, and mutation can be introduced even endogenously. This may seem bad, but, at least for relatively small rates of mutation, is not, as it allows change in the population, which is the basis for evolution.

just to clarify, youre saying a C can transition into a T sometimes? or, are you saying a C can pair with a T sometimes? or both? btw, thanks!

Transitions are transformations between purines or between pyrimidines (that is C becoming a T or viceversa and A becoming a G or viceversa). Transversions are between a purine and a pirimidine (the red arrows in the picture). You can also have so called "wobble pairings" or "non Watson-Crick pairings" such as C-C, T-G, A-C.

Pyrimidine dimers are another example that cause errors is replication. Though this generally results in premature attenuation of replication, and not mispairing. Still a messup, and the primary cause of the skin cancer melanoma. Another is the incorporation of 8-oxo-Guanine residues. This paper is a good review of DNA mutations http://www.ncbi.nlm.nih.gov/books/NBK22525/
8-oxo-Guanine wiki https://en.wikipedia.org/wiki/8-Oxoguanine


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Dimensional analysis Question
So I'm new to the dimensional analysis world and I'm little confused and the answers I'm getting are not convincing :(
if the concentration of hemoglobin in a 5ml sample of blood is 34 g/dL. and red blood cells are 31.45 hemoglobin, what is the mass of red blood cells in the sample?
So.. any thoughts on how to do it?
Thank you so much

It doesn't seem like you need the 31.45 hemoglobin number (which is good because no units are given:
5ml * 34g rbc /dL * 1 dL/ 100 ml = 1.7 g rbc
would fall out from unit analysis

Thank you!! hemoglobin's unit is percentage. 31.45% so should i just multiply your number it with that?

Shigeta's equation should have used "hgb" instead of "rbc".  To turn 1.7g hgb into rbc, you multiply it by the .3145 hgb/rbc value. Note the dimensional units work out.


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Is urine dirty as soon as it leaves the human body?
Human urine is sterile as long as it is in the human body. But is it dirty after leaving the human body? Could you get sick from it, if you drink it or don't wash your hands, for example?

It was believed for a long time that urine stored in the urinary bladder is sterile. However, Wolfe et al(1). recently found evidence of bacterial presence in the urine extracted from bladders of healthy women. In an article just published, Hilt et al. found that at least some bacteria found in the bladder of healthy women are viable and can be grown in a laboratory after extraction from the bladder).2 (Paywall). They expect that the same is the case for men.
From the Hilt et al. paper:

Thirty-five different genera and 85 different species were identified
  by EQUC. The most prevalent genera isolated were Lactobacillus (15%),
  followed by Corynebacterium (14.2%), Streptococcus (11.9%),
  Actinomyces (6.9%), and Staphylococcus (6.9%). Other genera commonly
  isolated include Aerococcus, Gardnerella, Bifidobacterium, and
  Actinobaculum.

Note that these species for the most part (Actinobaculum being one exception, as a possible uropathogen) appear to be part of the normal microbiome (collection of microorganisms) in healthy people in the same way as bacteria inhabit other parts of healthy persons. Additionally, the recovered organisms required special care to achieve growth:

Most of the bacteria isolated required either increased CO2 or
  anaerobic conditions for growth, along with prolonged incubation, and
  they often were present in numbers below the threshold of detection
  used in routine diagnostic urine culture protocols.

Thus, fresh urine is non-sterile but probably unlikely to cause infection in healthy persons.
In the process of leaving the body, there is a chance of contamination from organisms living in the urinary tract or on the surface of the body. However, if organisms picked up from the urinary tract made you sick, I except that you would already be having symptoms of an urinary tract infection, as the stomach is hardly a more forgiving environment. The risk of contamination from the surface of the body would depend on personal hygiene.
See also this question on https://outdoors.stackexchange.com/questions/264/is-drinking-urine-safe
Edit: This might go without saying, but apart from possible pathogens, there are of course other aspects of urine which makes it unfit for general consumption.


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Quorum Sensing in Vibrio cholerae

This is a figure summarising the quorum sensing mechanism in Vibrio cholerae.
In this video by Bonnie Bassler, she explains how quorum sensing can be targeted to control infections.
At 15:09 she explains why cqsA- mutants show more dramatic effect when external CAI1 is added - because we are not fighting against the endogenously produced autoinducer1.
My question : But won't endogenously produced autoinducer help in controlling virulence, as the more the auto inducer lesser the virulence ? Why should we be fighting against endogenously produced autoinducer 1 ?

I haven't watched the video and I don't know the details, but doesn't induction of virulence depend upon auto-inducer in these systems?

its true the compound (homoserine lactone?) is produced by the individual cells already.  but yes we can engineer the bacteria to be non virulent, but in general the problem is not the stuff coming out of the labs, but the stuff that's out there already.

@AlanBoyd Yes it is usually that, but Vibrio Cholerae has exactly the opposite mechanism - it switches off virulence when in large numbers and activates genes that help it go out of the body via diarrhea.

@biogirl but isn't diarrhea = virulence in this case since it is the main pathological effect?

@Alan yeah you are right but when it is in large number it activates a gene for chopping off the protein by which it was attached.

@Alan i feel i havent answered your question and to be honest i really dont know. Does it cause diarrhea and then suddenly switch off its vir genes and on the prot cutting genes ? Is there some way of continuing diarhhea while it is detaching ? I couldnt get the exact mechanism from the video. So i am not sure.

First of all I find quorum sensing to be generally facinating, so I'm happy to see the topic brought up here.
Dr. Bassler has many papers on the subject, but I think one of the most relevant ones to this question is here.
Regarding your question, you have the right idea, but you're missing the point of her comment.  The Western shows a more dramatic difference in cqsA- bacteria because they are not inhibiting themseleves (as you suggested).  Thus the lower concentrations have much higher levels of the toxin produced because the only CAI-1 being provided is the synthetic one.  This makes the ramp up in administered CAI-1 seem more drastic because you start at a higher level.
I hope that makes since, if I can find an open writes version of the Western, I'll come back and give further analysis on it.
Regarding @AlanBoyd 's comments, V. cholerae is different because it seeks to create an acute infection, not a persistent one.  Cholera toxin is what causes the majority of diarrhea and virulence from cholera.  V. cholera produces the toxin until it's inhibited by ether auto-inducer (which should be after the pt already has massive diarrhea), then it switches to produce enzymes which detach it from the gut.  The pt still has diarrhea at this point, cholera just doesn't need to make any more toxin for it to continue.  To do so would probably waste energy, and not help the bacteria make it back to a water supply.

Thanks u ! And to add to your last point , if it secrets excessive toxin it might also kill the host before it has chance to escape.

i would want to add a point that V. cholerae  is not an obligate pathogen.. Being a mild alkalophile, it cannot tolerate the stomach acidity. Infection happens only if there are too many bacteria.


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X Linked Hardy Weinberg Equilibrium Problem

In a given population under Hardy Weinberg equilibrium, 40.0% of men have hemophilia. What is the probability that a random man and random woman will have a daughter with haemophilia?

I think the answer is 16%, but the answer given is 9.6%. According to  Hardy-Weinberg principle, p2 + 2pq + q2 = 1. In order to inherit the disease, the mother must either be a carrier of have the disease, which occurs with probability 1-q2 = 0.72
Therefore, the odds of having a child with the disease is (0.84)(0.4). Since it asks for the probability of a girl, the total must be divided by two, so the answer is 0.168
Where am I wrong?

I think it is a case of the wording in the question: 'will have a daughter' still means we must consider all the offspring in ou probability. This means we must look at all the children they could have an including boys and girls and the probability that the daughter has haemophilia (with all of your working). If they had said: What is the probability that a random man and random woman's daughter has haemophilia? your answer would be correct, as we would have excluded the males from the offspring (as a conditional probability) which you had done correctly.

I make it 8%. Here is my reasoning.
The gene is X-linked.
40% mutant males, so freq(mutant allele) = p = 0.4, and freq(wt allele) = q = 0.6
To get a mutant female we have to have a mutant male parent, probability = 0.4
Of these matings one half will produce a female offspring so 0.4*0.5 = 0.2
i.e. 20% of matings derive from a mutant male and produce a female offspring.
Now look at the female mate:

probability(mutant) = p2 = 0.16
probability(carrier) = 2pq = 0.48
probability(wt) = q2 = 0.36

so our 20% of matings that have the potential to produce a mutant female offspring partition as:

mating with a mutant female: 0.2 x 0.16 = 0.032 mutant female offspring
mating with a carrier female: 0.2 x 0.48 = 0.096 of which:
0.048 mutant female offspring
0.048 carrier female offspring
mating with wt female: 0.2 x 0.36 = 0.072 carrier female offspring

(sanity check - 0.032 + 0.096 + 0.072 = 0.2)
Thus the probability of random mating producing a mutant female is 0.032 + 0.048 = 0.08 (8%)
Incidentally there is another way of thinking about this. Note that the H-W frequency of mutant females in the population is 16%. One of the assumptions of H-W is random mating. So the probability of a random mating producing a mutant female = p(female) * p(mutant if female) = 0.5 x 0.16 = 0.08
So - where have I gone wrong?

I get the same result. These type of questions can throw people off very easily, apparently including the people writing the answer keys!

In a given population, 40% of men have hemophilia – an X-linked recessive disorder. What are the odds that a random woman and a random man from that population will have a daughter with hemophilia?
Hemophilia is X-linked and recessive, so the frequency of males having the disease = q. So, q = 0.40. To determine the frequency of the dominant allele in the population, use…
p + q = 1
p + 0.4 = 1,
p = 0.6
Use these allele frequencies to calculate the genotype frequencies in the females using the Hardy-Weinberg equation:
            P2 + 2pq + q2 = 1
            0.36 + 0.48 + 0.16 = 1
Now use these frequencies in two separate Punnett squares
1)  All of the offspring from a homozygous recessive woman and a hemophiliac man will have hemophilia. Thus, (0.16)(0.4) = 0.064. Half of these offspring will be daughters, so 0.064/2 = 0.032
2)  Half of the offspring of a cross between a heterozygous woman and a hemophiliac man will have hemophilia. Thus, (0.48)(0.4)(.5) = 0.096. Half of these offspring will be daughters, so 0.096/2 = 0.048.
3)  Add the two possibilities together, so 0.032 + 0.048 = 0.08, or 8%

Frequency of allele for Haemophilia (q) = 0.4
Frequency of normal allele (p) = 0.6
Cross between Heterozygote female and hemophiliac male
by punnett square:
Probability of hemophiliac daughter = 0.5
P(hemophiliac male) = 0.4
P(heterozygote female) = 2pq = 2 × 0.4 × 0.6 = 0.48
P(hetero female+hemophiliac male+hemophiliac daughter) = 0.5 × 0.4 × 0.48 = 0.096
Hence 9.6%

In a given population, 40% of men have hemophilia – an X-linked recessive disorder. What are the odds that a random woman and a random man from that population will have a daughter with hemophilia?
Hemophilia is X-linked and recessive, so the frequency of males having the disease = q. So, q = 0.40. To determine the frequency of the dominant allele in the population, use…
p + q = 1
p + 0.4 = 1,
p = 0.6
Use these allele frequencies to calculate the genotype frequencies in the females using the Hardy-Weinberg equation:
            P2 + 2pq + q2 = 1
            0.36 + 0.48 + 0.16 = 1
Now use these frequencies in two separate Punnett squares
1)  All of the offspring from a homozygous recessive woman and a hemophiliac man will have hemophilia. Thus, (0.16)(0.4) = 0.064. Half of these offspring will be daughters, so 0.064/2 = 0.032
2)  Half of the offspring of a cross between a heterozygous woman and a hemophiliac man will have hemophilia. Thus, (0.48)(0.4)(.5) = 0.096. Half of these offspring will be daughters, so 0.096/2 = 0.048.
3)  Add the two possibilities together, so 0.032 + 0.048 = 0.08, or 8%


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Surrogacy Post Fertilization
The wikipedia page on surrogacy highlights two main forms of surrogacy: Traditional Surrogacy and Gestational Surrogacy. Traditional surrogacy inseminates the surrogate mother with sperm, while gestational surrogacy uses in vitro fertilization to form an embryo from egg and sperm, which is then transferred into the surrogate mother.
It does not discuss whether surrogacy is possible after a natural fertilization has already taken place, such as if a woman becomes pregnant and then wishes, for whatever reason, to have a surrogate take the baby to term. Is this biologically possible? If it is possible, what is the mechanism? Also, if possible, is heightened risk a major reason it is not more common?

No, it is not possible. The problem is the fertilization which takes place near the ovary. It takes the new forming blastocyst about 4-5 days to wander through the fallopian tube to reach the uterus and 8-9 days in total to implant itself into the uterine wall. See the picture below (from the Wikipedia article on fertilization):

You would have to get the blastocyst out of the right fallopian tube, make sure it survives the procedure and then implant it into the uterus of a woman which is about in the same phase of their period (otherwise the uterus is not ready to allow implantation).
It is already hard enough to do in vitro fertilization where you can control the environment.

in other words...have you ever tried to find a fertile zygote in a fallopian tube?  the physician would have to be in there with a light and a microscope and some forceps...and its 0.1 mm in diameter! yow that sounds impossible and painful and interminable!

Thanks for the short version :-) And you would have to choose the right tube as well...

There are different types of surrogacy, but as you said the most common one are traditional and gestational surrogacy.
Traditional surrogacy normally involves intrauterine insemination (IUI), so the eggs of the surrogate are used in the surrogacy process. Once the fertilization takes places it's not possible to extract the embryo.
On the other hand, in gestational surrogacy the creation of the embryos is done via an IVF process, and once they are created they are transferred to the surrogate. So in this process, the fertilization process take place out of the surrogate body.
So, in summary, while gestational surrogacy uses a IVF technique to create an embryo that afterwards is transferred to the surrogate, traditional surrogacy uses IUI to artificially inseminate the gestational carrier. IUI is less complicated than IVF, and this process can be repeated several times until a pregnancy is achieved. However, it's not possible to make the fertilization in one woman and afterwards transfer the embryos to the surrogate, that would be extremely complicated.
Here you can get more info about the different forms of surrogacy.

Hi, welcome to the site!  I'm honestly not sure what this adds to what has already been said... and in a lot of ways this looks more like a comment than an answer.  Sure, it does very briefly answer the question (1 sentence with no backup other than "that would be extremely complicated"), but the rest of the answer is totally incidental to the question posed.  In the future, please try to keep answers directed specifically toward the question posed.  Thanks!

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


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

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

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

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

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

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

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

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


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Do recessive alleles really exist?
This question may seem illogical to some, but I seriously have this doubt. I searched google for some proofs but they were extremely complex and I couldn't understand anything.
I was just wondering whether we really have recessive allele or not? Is it like there are only dominant allele present, and when dominant allele isn't present we consider it recessive.
Is it like there is a place reserved for dominant allele and if that place is empty it turns out to be recessive.
Although this thought is vague but then if you take this example, it probably would make sense:
Let's say there are two allele : T and t for tall and short respectively. Now, because TT, Tt, tT are tall, they all lead to the formation of specific hormone due to the presence of dominant allele. But the plant with genotype tt is short, hence the "extra" hormone for "excessive" tallness is missing in tt plant because the dominant gene isn't present. Can we say that that place for two allele (dominant allele) is actually empty in the plant with genotype tt?

A selection of related questions: what makes a gene dominant or recessive, why are some genes dominant to each other? and relative properties of alleles.

This is a good question. Firstly, let's get the terminology straightened out: The terms recessive and dominant are not actually used to describe genes, but rather alleles. The term allele is used for alternative forms of the same gene.(1) Many genes have two or more alleles, and some genes have alleles that can be described as dominant or recessive.
It is also useful to be familiar with the terms genotype and phenotype. Genotype refers to the form of the genetic material (DNA), while phenotype refers to the observed effect of the genotype.
Secondly, it's important to realize that the concept of "dominant" and "recessive" is a human-made abstraction. The concept of dominant and recessive genes were invented (or discovered, if you like) before we reached a good undertanding of how genetics works at the molecular level. Thus, genetics in the early days had a much cruder understanding of how different phenotypes depend on the genotype.
The dominant/recessive concept is useful in cases where there is a limited number of possible allele pairs and one or several alleles can mask the effect of other alleles. This is a very limited set of cases. Many genes have many different alleles, and it's hard to account for all of them. Many alleles also do not have a clear observable effect, in which case any "masking" effect is not prominent. To quote Wikipedia (2):

The most common basis of dominance and recessiveness is that the
  dominant allele codes for a functional protein and the recessive
  allele for a mutant, non-functional protein.

A further important point is made in the following passage:

Dominance is not inherent to an allele. It is a relationship between
  alleles; one allele can be dominant over a second allele, recessive to
  a third allele, and codominant to a fourth. Dominance should be
  distinguished from epistasis, a relationship in which an allele of one
  gene affects the expression of an allele at a different gene.

Let's consider your example: A single gene with two different alleles, T and t. Let's assume the T allele codes for a more powerful version of the growth hormone than the t allele, or that the t allele produces a non-functional hormone. Furthermore, we assume that production of the T hormone from a single allele is enough to make the plant grow tall, and that production of T or t from a second allele has no further effect. Then, we can say that the T allele masks the effect of the t allele. However, as you can probably imagine, one allele fully masking the effect of another is rather rare. So recessive/dominant allele pairs are rather the exception than the norm.
Thus, the that place for the two alleles in the genome of the plant is definitely not empty. Note that a mutation could in principle cause one of the genes to be deleted in its entirety from one of the chromosomes of the plant during reproduction. The "place" for the gene on that chromosome would then indeed be empty. This has nothing to do with how dominance and recessiveness usually works, except that a recessive gene could become expressed if the dominant allele is deleted.
So, at the molecular level there is no concept of recessive or dominant alleles. Some genes have allele pairs that can be described as dominant/recessive in relation to each other, most others do not. The effect of different combinations of alleles determines whether the relationship between the alleles is described in terms of dominant/recessive.

Yeah, I used wrong term gene over here. Thanks. But question still remains unanswered.

OK. I'm working on a bit more elaborate explanation.

Do we seriously have recessive allele or is it just the dominant one? Is it like when dominant allele isn't present we consider it (the allele's placeholder) to be recessive. This is want I am searching for. :)

I expanded my answer. Does it answer your question now?

Wonderful explanation Jarlemag. Thank you. :)

My pleasure. It's a concept that bugged me for a long time too, as the molecular details are often left out, and only a very simplified view of genetics is presented, when dominance/recessiveness is explained.

Great answer.  I sometimes wonder if the usual way Mendelian genetics is taught causes more confusion than it's worth.  People don't seem to get that that paradigm is only helpful for a small percentage of our observations, even though it spawns a huge number of easy-to-grade homework assignments

I'm having real difficulty understanding the original question. We know that a diploid organism has two copies of a gene because we can sequence them, and if they are different alleles we can point to the difference in their sequences. Then through genetic crosses we can follow the two alleles and look at the association between genotype and phenotype, thus deciding on the nature of any dominance.
Also we can create a mutation in a gene by inserting another piece of DNA with its own associated phenotype (drug resistance for example). In this situation we would normally see a dominant phenotype associated with the undisrupted gene, but we would know that the recessive (disrupted) allele was also present because of the associated drug resistance. Certainly this is done all of the time in yeast genetics.
I think the problem is that you are treating genes as abstract entities in some sort of 19th century theoretical framework, disregarding over a century of genetic studies and, as @jarlemag has so eloquently explained, the physical reality of genes (as DNA sequences).
Final thought: the situation that you are describing (a "space") does exist in the special case of  males for X-lined genes, where only one allele is present. This is the explanation for the genetic properties of sex-linked diseases like haemophilia.


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Dyes to bind to double stranded DNA?
Are there any commercially available fluorescent dyes that will bind only to double stranded DNA (not RNA, single stranded DNA etc.) for studying in vitro using confocal microscopy?

Most of the dyes used for visualization bind with a much higher affinity to dsDNA. This would be SybrGreen, EtBr (although this will bind RNA as well).
There is a pretty comprehensive website from Life Technologies about Nucleic acid stains that is worth a look.
There is as well a publication on this topic: "DNA Staining for Fluorescence and Laser Confocal Microscopy"

YOYO, TOTO join the list, I believe they have 1000-10000x binding/fluorescence efficiency in presence of dsDNA than ssDNA

You may also want to look at acridine orange.  It binds both single stranded and double stranded DNA, but fluoresces green when bound to double sided DNA, and orange when bound to single stranded DNA/RNA, making it very easy to see both in the same image.


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How does a fertilized egg form 23 pairs of chromosomes?
I am always confused about this...so when one cell which has 23 pairs of chromosomes undergoes the two meiotic divisions it produces four cells containing 1 chromatid of every chromosome pair so when this fertilizes the opposite gamete (of course it has also one chromatid of each chromosome pair) when they are fertilized they make one 23 chromosomes because 23 chromatid from one and 23 from other and they will form 23 chromosomes not 23 pairs of it, so my question is how they form 23 pair of it or to make it homologue..please clarify with some pics??...tnx

you've almost got me confused as well! 23 chromatids in each gamete: 23 + 23 = 23 pairs, no? the gamete chromosomes do not fuse or recombine in fertilization or anything like this.

I was confused by this for the longest time too...it's confusing how a both a single chromatid and a pair of chromatids can both be referred to as a chromosome.

After fertilisation the zygote has two copies of each of the chromosomes (not worrying about sex chromosomes). When each of these is replicated the cells will have chromosome pairs, which will then divide in mitosis.
The classical chromosome image of pairs of X-shaped chromosomes relates to the situation at mitotic metaphase when each of the chromosomes has replicated and consists of two sister chromatids. As anaphase proceeds the splitting of the centromeres means that each of the sister chromatids becomes a chromosome, and each cell ends up with a pair of each chromosome type, just like a zygote.


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What is the difference between intracardiac and extracardiac reflexes in cardiac regulation?
The primary parameters of heart pumping are

strength of contractility (inotropic positive; Frank-Starling relationship)
rate of relaxation (lusitropic positive)
heart rate (chronotropic positive)

which change the secondary parameters according to the marginals

Heart rate
Stroke volume

Contractility
Starling relationship

Which of these paramecers are controlled intracardiacally and which extracardiacally?

Rate is controlled outside the heart by the Vagus Nerve having parasympathetic activity on the sinoatrial nerve.
Stroke volume (taking contractility and Starling's law as one) are factors from the cardiac tissue itself - "intracardiac".


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Databases for metabolic pathways of human disease
Which databases contain the metabolic pathway of human diseases?
I have searched Metacyc and KEGG but didn't find the appropriate metabolic pathway.

What exactly are you searching for, and how specifically did KEGG and Metacyc fail to meet your requirements? Please [edit] your question with additional details so we can provide focused answers.

nearly any pathway can exhibit a disease if its damaged in the right way - disease is a dysfunction.  this is pretty difficult to answer in a way that makes sense.

NCBI BioSystems help file contains a list of their sources:
http://www.ncbi.nlm.nih.gov/Structure/biosystems/docs/biosystems_help.html#SourceDatabases
Please specify what you need as stated in the comments as it is almost impossible to give you more (relevant) information then this.

I need the details of Ubiquitin/proteasome pathways which is responsible for cervical cancer from E6 and E7 oncoproteins?

I've been doing some research but I couldn't find exactly what you're looking for. I'm not a cancer research expert but you might find what you are looking for from this page: http://www.ncbi.nlm.nih.gov/biosystems/?term=DNA+repair+Ubiquitin
I'll let you know if I know more.

I need the step wise rections of ubiquitin/proteasome pathway. I have to calculate its parameters for COPASI.

You can try Disgene package in Cytoscape.

please add some more detail if you can..


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How is a stem-cell induced to assimilate a knock-in DNA construct?
While looking at (daylight) color perception I came across a paper by Jeremy Nathans (et al., Proc. Nat. Acad. Sci., vol. 100 no. 20, 2003, full text here) in which he describes the creation of a mouse with genetically modified vision.
My threshold question is just about the mechanics of the process, which he characterizes as "site-directed mutagenesis." My understanding (a guess, really) is that embryonic stem cells are induced to assimilate homologous human DNA sequences and these cells are injected into mouse blastocysts.
In outline I understand the idea of the DNA construct but wonder physically how the stem cell initially acquires the knock-in construct.
Thanks for any enlightenment.
Edit: I see that there are several ways to do this and that the paper's "Materials and Methods" section focuses on the molecular genetic details. Maybe we can't get the information from the four corners of the document? If so I'd still be interested in whatever process seems likely given the sort of mouse they made. Thanks.

So, essentially your question is just "How is a transgenic mouse created?", is that correct?

@MattDMo: If I am correct about the injection into blast cells, my question is about what happens before that.

OK, I understand. Can you post a PubMed link to the paper so I can see what kind of mouse they made?

What is the title of the paper - "Genetically engineered mice with an additional class of cone photoreceptors: Implications for the evolution of color vision"?

@MattDMo: That's the one, yes.

The bounty is for an accessible explanation of the physical process of getting the human gene into the mouse. Thanks.

There are two ways to introduce genetic material past a cell membrane. Infection and generation of a porous cytoplasm. Viruses and bacteria generally are used. Retroviruses tend to cause leukemia so they are avoided however they are the only way to get past the nucleus in vivo of multicellular life. Electroporation and needles generate a porous cytoplasm allowing genetic material to seap or be inserted into the cell.
Once the genetic material is in the cell it has to have contained site specific oligonucleotides to hybridize with the strand of interest.

Procedure
The procedure for making mixed-genotype blastocyst.
Breeding scheme for producing knockout mice. Blastocysts containing cells, that are both wildtype and knockout cells, are injected into the uterus of a foster mother. This produces offspring that are either wildtype and coloured the same colour as the blastocyst donor (grey) or chimera (mixed) and partially knocked out. The chimera mice are crossed with a normal wildtype mouse (grey). This produces offspring that are either white and heterozygous for the knocked out gene or grey and wildtype. White heterozygous mice can subsequently be crossed to produce mice that are homozygous for the knocked out gene.
  There are several variations to the procedure of producing knockout mice; the following is a typical example.
The gene to be knocked out is isolated from a mouse gene library. Then a new DNA sequence is engineered which is very similar to the original gene and its immediate neighbour sequence, except that it is changed sufficiently to make the gene inoperable. Usually, the new sequence is also given a marker gene, a gene that normal mice don't have and that confers resistance to a certain toxic agent or that produces an observable change (e.g. colour or fluorescence).
Stem cells are isolated from a mouse blastocyst (a very young embryo) and grown in vitro. For this example, we will take stem cells from a white mouse.
  The new sequence from step 1 is introduced into the stem cells from step 2 by electroporation. By the natural process of homologous recombination some of the electroporated stem cells will incorporate the new sequence with the knocked-out gene into their chromosomes in place of the original gene. The chances of a successful recombination event are relatively low, so the majority of altered cells will have the new sequence in only one of the two relevant chromosomes - they are said to be heterozygous.
  The stem cells that incorporated the knocked-out gene are isolated from the unaltered cells using the marker gene from step 1. For example, the unaltered cells can be killed using a toxic agent to which the altered cells are resistant.
The knocked-out stem cells from step 4 are inserted into a mouse blastocyst. For this example, we use blastocysts from a grey mouse. The blastocysts now contain two types of stem cells: the original ones (from the grey mouse), and the knocked-out cells (from the white mouse). These blastocysts are then implanted into the uterus of female mice, where they develop. The newborn mice will therefore be chimeras: some parts of their bodies result from the original stem cells, other parts from the knocked-out stem cells. Their fur will show patches of white and grey, with white patches derived from the knocked-out stem cells and grey patches from the recipient blastocyst.
Some of the newborn chimera mice will have gonads derived from knocked-out stem cells, and will therefore produce eggs or sperm containing the knocked-out gene. When these chimera mice are crossbred with others of the wild type, some of their offspring will have one copy of the knocked-out gene in all their cells. These mice will be entirely white and are not chimeras, however they are still heterozygous.
When these heterozygous offspring are interbred, some of their offspring will inherit the knocked-out gene from both parents; they carry no functional copy of the original unaltered gene (i.e. they are homozygous for that allele).
  A detailed explanation of how knockout (KO) mice are created is located at the website of the Nobel Prize in Physiology or Medicine 2007.

-wikipedia

This is a rather bare-bones answer but I am upvoting because it is essentially correct. The bonus would go to something a lot more detailed. Since the author specifies ES cells in his paper I am guessing the method used plasmids vs. virus but maybe that's not necessarily true? Perhaps you can elaborate.

@daniel some functional changes are only possible during the embryonic stage before the evolution of a fetus has occured. That is to say once the expression of genes has come to fruition it doesn't matter how much modifications are made the substructures are already present. Thats the reason it happened with es as far as i know.

I think electroporation not viruses


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In biosynthesis of cysteine and methionine, where does the sulfur come from?
Methionine and Cysteine are the two amino acids containing sulfur. According to wikipedia, cysteine is built from methionine. However, the wikipedia also claims that methionine is synthesized from cysteine.
So, a chicken and egg problem (esp. since eggs are a rich source for those proteins). Where do living things get their sulfur to build these amino acids in the first place, in what forms is sulfur available biologically?

Microorganisms (and plants) make cysteine from serine using H2S as the sulphur source. Condensation of these two directly gives cysteine in some bacteria, but most often the reaction sequence is:

serine + acetyl-CoA >>> O-acetylserine + CoA-SH
O-acetylserine + H2S >>> cysteine + acetate + H2O

As you say, in terms of the sulphur, cysteine and methionine are interconvertible.
Animals rely upon their diet for methionine, and can make cysteine from that methionine.

+1 and accept: the key info was that H2S is a sulfur source.

Which plants use H$_2$S? I only found sources about microorganisms doing this and plants using soluble forms sulphur.

Apparently, a number of them can take up H$_2$S. http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0062048&representation=PDF.

First of all, the wikipedia article you quote states that methionine is synthesized from cysteine in plants and microorganisms, not in humans. In humans, both cysteine and methionine are essential amino acids which means that they cannot be produced by the human body but need to be acquired elsewhere.
Now, this is mostly done by eating proteins that contain these amino acids. The proteins are broken down and the amino acids (or their constituents, such as sulfur) are reused. In mammals, cysteine is produced from serine but the sulfur comes from methionine via homocysteine:

So, methionine comes from the diet and it is then used to produce cysteine.


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Lytic Viruses -- Cell lysis?
So in the video my instructor sent on viruses, he said that for lytic viruses, new viruses manufactured by the host cell could get out of the cell in one of two ways.

The new viruses would leave by exocytosis.
or,
The cell would be "ruptured" and the new viruses would "erupt out of the cell".

In the rupturing option, is the cell destroyed? The way he phrased it as well as his tone of voice brought to mind an image of the cell bursting and the viruses spilling out....but the diagram showed a little gap in the cell membrane, and the viruses leaving from that one exit point.
Which is more accurate?
Thanks!
evamvid

Yes, ruptured here means that the host cell is destroyed. The virus "hijacks" the cell anyway and uses its protein production machinery to make as much virus particles and its transcription enzymes to makes as many viral genomes as possible. If the ressources of the cell are exhausted, it get destroyed and the viruses are set free.
See this image (from the Wikipedia article on the lytic process). It actually doesn't matter, if the virus infects the cell from the outside or if it comes from the genome.

Adsorption of the virus to the cell.
Injection of its genetic material into the cell.
Production of new viruses (hull and genome).
Rupture of the cell and release of the viruses.

I understand now that the cell is destroyed either way. But is it more likely to be destroyed physically (ruptured) or because of exhaustion of resources?

Rupture and release of the virus happens, when the ressources are exhausted. So one event happens before the next. Then there are phages, which can leave the cell without destroying them before, the phage M13 is such an example. It expresses proteins which make a pore in the cells membrane which the phages can pass.

After the phages leave, what happens to the cell? Does it still have the viral DNA? Does it make more viruses? Or does it carry on with normal business like it was never infected?

Its dead. The membrane is destroyed, and it can not do anything anymore.

I'm confused...I thought you said that some phages can exit without destroying the cell by expressing proteins which basically open a hole in the cell membrane and let the phages out. Is that correct? If so, what I was trying to figure out is, after this process, does the undestroyed cell then carry on with normal business, or does it keep making viruses?

Sorry, I thought you were talking about the burst cells. The M13 infected cells will eventually die as well, since they are busy making viruses. It will probably last a bit longer, but not much. The virus pretty much shuts down everything what he doesn't need.


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Do lysogenic viruses only infect bacteria?
In the video sent by my teacher on viruses, the example he used for lysogenic viruses was a bacteriophage infecting a bacteria. When he was describing how the genetic material was incorporated into the host cell's genetic material, he said something along the lines of:

Now the genetic material is incorporated into the cell's chromosome.

My question is, did he describe it as one main chromosome because that was the example being used? Or do lysogenic viruses only infect bacteria?
I guess a better way of phrasing this would be, are bacteriophages the only type of lysogenic viruses?
Thanks!
evamvid

Bacteriophages are the only viruses where this phenomenon is called lytic and lysogenic cycle. There is a similiar phenomenon in humans (and other mammals as well) which is called "endogenous retrovirus" and is pretty common.
For humans, there are estimations that something between 5 and 8% of the human genome are made of endogeneous retroviruses. See these two references:

Long-term reinfection of the human genome by endogenous retroviruses.
Endogenous Retroviruses and Human Evolution

Otherwise I can recommend reading the article on "Endogeneous retroviruses" in the Wikipedia, it is pretty extensive and has a lot of references.

This is really a question of semantics. Yes there are endogenous viruses in eukaryotic cells, but is the term lysogeny used to describe this situation in practice? (I don't think it is.)

Now that you ask direct, no I don't think so. I think this was discovered with the Phage Lambda in bacteria. I will edit the answer.

I'm confused -- the terms 'lytic' and 'lysogenic' don't apply if the host cell isn't a bacteria?

Obviously it is not used outside the context of phage-bacteria. Although endogenous viruses in our genome are more or less the same.


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What happen's to a virus's capsid after it injects its genetic material into the host cell?
After a virus (one of the varieties which infects the cell via injection and not endocytosis) injects its genetic material into the host cell, what happens to its protein coat? I would guess that it just falls off. However, since it is now outside of a cell, there are no protein-digesting enzymes -- or are there?
What happens to it now? I'm guessing it doesn't just float around for all eternity.

Interesting question and actually I haven't found a real answer here yet. The phages seem to bind rather hard, since the need to be blended (subjected to relatively high forces) to shear off. This was used in the Hershey-Chase-Experiment to find out what the genetic material of the cell is. It doesn't matter though, since most of the cells which are infected get destroyed anyway. If not, they are most likely taken up and broken down inside the cell, as it happens with other membrane proteins.
This is only valid for viruses which inject their genetic material into the host cell, while the capsid stays outside. This happens mostly for Bacteriophages.
There are a few other possibilities for viruses to enter cells where this is no problem:
Viruses which have a membrane envelope can enter the cell via membrane fusion. To make the fusion happen, either the membranes have to get very close, or the virus first binds receptors on the cell surface and then fuses its membrane with the cell. This causes the interior of the virus to be released into the cell. The picture below shows the fusion (from the Wikipedia article on membrane fusion). An interesting article on this topic is: "Membrane fusion."

Another possibility for a virus to enter a host cell is via endocytosis. Here the virus uses the uptake of material from the surrounding of the cell to get inside. This can either happen together with resources inside a vacuole.
Or it happens via the binding of specific receptors, which are internalized into the cell upon binding of the specific ligand. Here the virus mimics the ligand of the receptor to get internalized into the cell.
In both cases the virus needs to escape from the vacuole before it get broken down because the vacuole is turned into a lysosome.

Thanks! I was talking about viruses which inject their genetic material; I just somehow forgot to mention that. =)

Ah, ok. I answered that, too. :-)

I think the external protein coat is degraded as the virus releases it's nucleic acid into the Host' cell. This is due to the fact that a protein is lifeless without the activity of a gene(one gene-one enzyme hypothesis).Since the nucleic acid is composed of genes, when it is injected into the host's cell, the capsid becomes useless and so it is degraded.

Can you add some references?


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In the lysogenic cycle, does the provirus split from the cell's main genetic material for replication?
In a diagram of the lysogenic cycle sent by my instructor in a video, it shows the provirus splitting from the cell's main DNA when the dormancy period ends and the viral DNA is "activated". Is this how it happens, or was he just trying to illustrate the activation?
I guess a better way of phrasing this would be, is the viral DNA replicated as part of the cell's normal DNA, or is it replicated separately?
Thanks!
evamvid

When the virus is integrated into the hosts genome (and becomes a provirus) it is replicated with the cell genome, since it is now part of it. When the provirus gets activated (this happens by changes in the host's environmental conditions or health), it will get transcribed.
This is followed by the translation of the viral proteins which then leads to a cell which exclusively produces viruses until its resources are exhausted and the cell gets destroyed.


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Is it impossible for a retrovirus to be lysogenic?
Is it impossible for retroviruses to be lysogenic? In the lysogenic cycle, the viral genetic material is incorporated into the host cell's DNA. Because retroviruses have RNA, it would be impossible for their genetic material to be incorporated into the host cell's DNA, unless the RNA is reverse-transcribed or something.
Is this the case? How does this work?
Thanks!
evamvid

Sorry! I phrased the question completely wrong -- I managed to confuse myself with my own question!

Both things are not exclusive of each other. Retroviruses are RNA-based viruses which need to reverse transcribe their RNA genome into DNA before they can multiply. This is done by the reverse transcriptase enzyme, which is part of the virus and is incorporated into the cell.
Once the reverse transcriptase has been active and made the DNA, this DNA can also be incorporated into the hosts genome. If you look into the Wikipedia article on Bacteriophages, you will find a list of different bacteriophages, with all kind of genomes, among them as well a number of RNA-based viruses.
RNA-based viruses which enter the lysogenic pathway are obviously either pretty rare or they haven't been discovered yet in bigger numbers. Two examples are the phages F2 and MS2 (which are closely related).

Are there any RNA phages that exhibit lysogeny?

Yes, there are a few. I added two references.


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What can thrombosis lead to?
I am thinking this question.
Thrombosis can result in

organisation of thrombus,
sepsis
thromboembolism,
fibrinoid swelling
adiposity.

I fibrinoid swelling (edema) (4) can occur.
Also, I think (3) thromboembolism can occur and also (1) organisation of thrombus.
What can thrombosis result in?

I am not sure I understand this question. First, you give the answer. Then, you ask the question. Please note that I am a layman in Biology, absolutely no expert.

@scaaahu this is a homework question. Masi is copying a question he presumably got in an exam and is wondering about it.

Fibrinoid swelling involves necrosis and swelling so no.
Organisation of thrombus refers to some very large space of organising thrombus in different ways - so no, since there is an exact mechanism under.
Based on my interpretation of Robbins -book.
The correct answer is 3. thromboembolism.
Thromboembolism is a combination of thrombosis and its main complication, embolism.


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What is ischaemia exactly?
I think it is decreased blood supply to organs and tissues.
I also think it is the stopped circulation.
However, both ones cannot be right, I think.
What is ischaemia exactly?

Is insufficient blood supply a better word?

I am asking this because we have too venous congestion which is decreased blood supply to tissue. So Ischemia and Venous congestion should be orthogonal terms.

As I understand it, venous congestion is one of several possible causes for ischeamia. So a venous congestion would lead to ischeamia, but ischeamia does not imply venous congestion.

Ischaemia is lack of sufficient perfusion to a tissue.  Reduced perfusion could therefore mean decreased blood supply to organs and tissues and could also mean a complete cessation of blood flow to an area - therefore both can be correct as they are on a continuum.  Infarction is tissue death due to hypoxia which can result from ischaemia that is not swiftly resolved.


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Can systemic venous congestion caused by tumor?
I am thinking, if 1) little compressed superior caval vena and 2) some vein compression by tumor, can cause systemic venous congestion.
I think this is only in rare occasions.
However, the question is if this is possible.
Can systemic venous congestion caused by these two factors?

No. They increase the risk, but are not the causes.
There must be other factors involved which triggers the systemic venous congestion.


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Does fat on our heart come from the fat that we eat?
If we eat fat:
Does the fat go into heart, arteries and fat cells.
OR
Is the fat digested, following which our body creates fat that goes into heart, arteries and fat cells.
Which one is right?

Fat is, in molecular terms, triacylglcerol. In order to be absorbed in the small intestine triacylglycerol molecules are broken down by lipases into fatty acids and monoacylglycerols. Once these have got across the enterocyte membrane they are reassembled into triacylglycerols and packed up into a special class of lipoprotein particle, a chylomicron, which enters the bloodstream via the lymphatic system.
The triacylglycerols in the chylomicrons are then able to be passed around through the system of lipoproteins (LDL, VLDL etc.) and pretty much can end up anywhere, including fat cells (adipocytes) or they can be metabolised as fuel molecules
So, because of that initial digestive step I would say that a single intact dietary fat molecule cannot end up as a body component directly, but complete metabolism of the components of the fat molecule is not necessary for these to contribute to body fat.

It's more of somewhere between then. So they are broken and then reassembled into the same molecul?

Yes, but the pieces that are reassembled are unlikely to have been derived from the same original molecule. It must happen occasionally I guess, just by chance.

Fat is digested just like any other food you consume, and eventually the energy you do not expend ends up as an energy reserve in shape of fat cells.
So, the second statement is right.


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Are there any forms of heart failure where cell size decreases?
I think hypertrophy happens in most of the cases. However, I am not sure if hypertrophy always happens. I started to think about wet lungs (pulmonary reason for the left-sided heart failure).
Can the decrease of cell size occur in the heart failure?

Literature covers only hypertrophy of the heart.
Atrophy not mentioned.
Theoretically atrophy of the heart would require some factors

mutations (which can destroy the gene to build up the organ),
poor nourishment,
poor circulation,
loss of hormonal support,
loss of nerve supply to the target organ,
excessive amount of apoptosis of cells, and
disuse or lack of exercise or disease intrinsic to the tissue itself.

Atrophy can happen locally in some part of the heart only, like in some parts of myocardial infarction.
However, the surrounding healthy tissue then undergoes hypertrophy so the total heart undergoes hypertrophy.
Some discussion about Cardiac atrophy here.


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RNA isolation from Drosophila head
I need to isolate RNA from Drosophila head. I basically chop the head off and first homogenize it with a homogenizer (similar to this: http://www.omni-inc.com/omni-tissue-homogenizer-th-package-p-11.html) and further homogenize it with 22G needle in TRIzol reagent. I use TRIzol RNA isolation for larvae brain a lot and have no problem with the method itself. However, with adult I got really low RNA concentration which is weird.
I thought that maybe I have problem with homogenization itself, or I overlook something (such as extra centrifugation or different kind of homogenization etc). Does anybody have experience with it?
Thanks.

You mean you have not a lot of RNA compared to whole larvae? Don't forget that in larvae a lot of gene expression is going on compared to the brains of developed flies. And the heads are a lot smaller, too. What does low concentration in terms of numbers mean?

I isolate RNA from larvae brain so not whole larvae. For example, from approx. 150 larvae after DNase treatment, I got more or less 120 ug RNA.
For the very first time I have tried with adult. I used 220 adult heads and after DNase treatment concentraion of RNA was 52 ug. For me this result indicates a problem.

Oh, then I misunderstood that. How is the quality of the RNA?

I measured with nanodrop and these are the ratios for adult RNA: 260/280= 2.17 and 260/230: 2.21
For larvae I usually get also more less these ratios.

That sounds not bad for me, at least you have no quality problem. Do the heads dissolve completely?

Good way to get heads off (if doing many flies of the same genotype/treatment etc.) is to put whole flies in a safe-lock eppendorf, put them in liquid nitrogen, drop the eppendorf on the desk a few times and the heads should have fallen off and you can collect them - ideal if you are putting them in liquid nitrogen anyway (as is common with RNA extraction).

Yes quality is ok but I need more RNA, thats the issue unfortunately. I also homogenize larvae brain with 22G needle and works well. This time after homogenizer, I did with 22G needle also, it was going up and down easily. After phase separation with chloroform, there was a huge trash phase.
I did not do any liquid nitrogen step before homogenization. Do you think it can be the problem? I simply make them sleep on ice and then got their heads.

You say that 150 larval brains give you ~120 ug RNA. Do you have an idea of the amount of total RNA that can be extracted from a single brain?
I have posted a question here:
http://biology.stackexchange.com/questions/28078/how-much-total-rna-can-be-extracted-from-drosophila-brain

It doesn't seem like a homogenization problem. Nonetheless you can try this:

Suspend the heads in trizol
Homogenize by passing through 30/31G needles (insulin syringe) up to 10-15 times.
Heating a little might help but I think it is unnecessary for these tissues.

Insulin syringe is much better than the hand held homogenizer. Freeze-thaw 1-2 times if you want (helps in homogenization).
During extraction you can add 5M LiCl (100µl) + Ethanol (1ml) to 400µl aqueous phase (instead of isopropanol), keep at -20⁰C for 1-2h before centrifuging. Alternatively you can add a little RNAse free glycogen to Isopropanol during precipitation.
PS: the liquid Nitrogen trick that rg255 mentioned is for quickly getting heads and avoiding the pain of dissecting each head.


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Does Yerba Mate contain Beta carbolines like harman and norharman?
I know that this is true of (roasted) coffee but haven't been able to find any reliable information about mate in its smoked or steamed state.  Thank you.

After a bit of research I can say that Yerba mate does not contain beta-carbolines. Now, I don't know if this makes you happy or sad but the tea has many antioxidant properties which makes it good for health. You can find a list of the components in Yerba mate in paper 1 and this article.

Hi. I'm the OP.  I just wanted to thank you for your answer.


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Many spermatozoa, but just one ovulum
Why do men produce so much spermatozoa, that will get discarded, but women, just one ovulum, which is a good one.
Couldn't men produce good spermatozoa as a limited edition?
Where is the evolutionary advantage of things being like they are?

The way which the spermatozoa have to travel is long and relatively dangerous. So you want to make sure that at least one is reaching its final goal. Having many ovums would mean that you get more than one embryo...

There surely some room for lower spermatozoa concentrations. But since there are reports about fertility problems in men with lower spermatozoa counts, I doubt there is much room.

I think the asymmetry allows for a stronger selection process.  Sperm competition is a powerful force in evolution.
This is useful since sperm vary wildly in quality - for healthy human males only 50% might not be normally motile. Other animals can have a higher percentage, but there are always a significant number of floaters... This means that the fertilization via sperm takes out a lot of the less functional sperm.  Since these are in many cases the same genes we use as diploid organisms later, sperm competition really tames a lot of problems which might be produced in meiosis.
Many animals have multiple mating events from multiple males at just about the same time - when the female is in heat.  This gives a larger role for sperm competition - literally different sires are competing as sperm to fertilize the egg.
In females it is a different process of choosing the cells.  Ova are mostly eliminated in women by the time they reach reproductive age.  I think that this is not well understood biologically... references are hard to find.
The differences in the morphology and roles of the gametes, which goes back to the most primitive of animals has a strong role in selection of healthy offspring through a diverse set of mechanical and biochemical conditions experienced during fertilization.
Added Note: I ran across this reference for how ova are selected for presentation by the ovaries.  Its not really a review, but maybe a lead reference on how selection works in the female reproductive system - its also picky:

In mammals, ovarian folliculogenesis is a process regulated by complex networks composed of various endocrine, paracrine and autocrine factors that interact coordinately.

Its no cake walk to being an egg either...

In addition to motility - up to 70% of sperm can be abnormal forms and this is still considered normal.

that's interesting!  I wonder if they end up fertilizing the egg?

I'm not sure to be honest, some definitely wouldn't (for example loss of the acrosome) whilst others could potentially make it with reduced chances (minor tail defects etc.)

morphology isn't always fitness, though for diploid human beings it seems to be important.

Shigeta's answer is excellent.  I also agree with Chris in his discussion of ova, upon which I want to expand.
This is in part speculation, but I believe that the answer to producing (usually) only one ovum lies in the development of animal viviparity.
Many animals (especially aquatic animals) currently and historically have reproduced via oviparity - the female producing a multitude of ova and allowing the male to shower them with spermatozoa.  The general style of males producing a large number of spermatozoa seems to not have changed greatly (aside from location of sperm deposition) through evolution.
However, viviparous animals must by necessity have some sort of limit on the number of simultaneous offspring, as the females carry offspring within their own bodies.
In animals who reproduce with hemotrophic viviparity, the embryos are provided nutrients from the mother through a placental organ that interfaces with the maternal bloodstream; the biological cost of having many offspring depends on how long they are carried and how large they are at term.
Most mammals carry a litter and develop small, underdeveloped young, but hominids evolved to carry (usually) one.  There's an interesting discussion to be had on the different reproductive strategies (very careful rearing of one versus attention divided over many) but I don't have sources at the moment for those.
But the cost of having more than one embryo must have been significant enough in our own past evolutionary process to have eliminated most women who produced multiple ova.  Maternal mortality rates have historically been MUCH higher than they are now, and risk is higher with twins (or more).  There are still times when more than one ovum reaches maturation and ovulates, resulting in dizygotic twins, but it's fairly rare (between 6 and 14 per thousand births).

As spermatozoa need to be transported therefore in order to increase the chances of successful transportation (and fertilization) the number may be high.
Also, there is only one ovum probably because more cytoplasm is required in the creation of an ovum, which is evident from its size.

i like the idea of the sperm are small and easy to produce and eggs are large and difficult to produce idea it seems relevant to the nature of us as a species rather than a pat quotation of evolution.


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Evolution from Mating types to different sexes
Imagine a lineage of multicellular organisms that had mating types and evolved their mating types into sexes. What are the possible mechanisms that might have brought this lineage to evolve sexes from mating types?
To my understanding of the definitions of sexes and mating types, the only diffenece between the two is that sexes imply gametes of different sizes. Is it correct?

Another important reason to have mating types is to prevent self-fertilization or self-polination that produces less capable offspring. Because of this requirement, mating types may evolve also for species that produce both types of gametes, or does not differentiate them into male and female gametes. Fertilization is only possible if gametes have different mating types.
It may be more than two mating types, but if there are only two, they are probably similar to "sexes" even if gametes do not look different.

Thanks for you answer. It is interesting so to explain the evolution of mating types. But I don't think it answers the question though in the sense that it does not address the evolution from mating types to sexes. In my question, I am mostly interested in the evolution of gamete size differentiation and of number of gametes from a lineage/species where there is different mating types but no difference in size of number of gametes.


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Organs lifespan out of the body
What organ can be conserved outside of the body for the longest time and still function when reimplanted?

you may want to be more explicit... this is hard to understand...  Do you mean when transported for transplantation for instance?

Yes it can be. I mean in the any best conditions.

this is really too vague to answer. I might say cervix since there is an immortal cervical cancer cell line.  It has never died.  really the question is not precise enough for you to get a satisfactory answer.  the cells may live but the organ can lose all its function..

Sure there are many immortal cancer cell lines. I read in somewhere in the internet mentions that before transplantation, organs lives 4 to 24 hours. I just couldnt find most durable one  on the internet. :)

It sounds like what you are really asking is "What organ can be conserved outside of the body for the longest time and still function when reimplanted?" - Is that correct? If so, please edit your question to reflect that and provide more detail!

Depends what you consider an organ. Typically though it's the cells which require the most metabolic activity which have the shortest life span. The kidney is the most of the major internal organs with up to 36 hours with liver coming second at up to 16 hours.

... on ice i think?

Yes in optimal preserving conditions.