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What's the effect of oxygen deficit on plants?
As I know all cells require oxygen. So my question is how efficiently can plants operate in no-oxygen atmosphere? Do all plants produce enough oxygen for themselves? Can they consume their own oxygen or the oxygen will be quickly lost to the air? Is there a plant that consumes more oxygen than they produce?

During the daylight, the plant is photosynthesising faster than it is respiring so there is no net uptake of oxygen (the oxygen of course being produced in the as part of the photosynthesis).
Of course, this only applies for tissues where photosynthesis is occurring.  In the roots of the plant, oxygen must always be present in the surrounding soil/growth medium for respiration.  Therefore if there is no oxygen in the roots then the root cells will be unable to produce ATP from respiration and consequently die.  This will eventually lead to the death of the entire plant as it is unable to take up nutrients due to the lack of a functioning root network.
This is the cause of plant death when soil is waterlogged - the water fills spaces in the soil that would otherwise contain air (i.e. oxygen).
Certain plants (often crop plants), rice being given as an example in the comments below, are able to survive being waterlogged and the resulting low oxygen supply. However they can only do so in the short term.  Rice plants in particular have adaptations that allow the transport of oxygen from the aerial parts of the plant down to the roots.  This does of course mean that the rice can not survive being totally submerged for an extended period of time.  Plants such as rice may have better adapted anaerobic fermentation pathways that become the main producer of ATP when aerobic respiration has arrested thus allowing them to better cope when transiently submerged than other plants.
Molecular strategies for improving waterlogging tolerance in plants

still there are plants that feel well in water-flooded environment, as rice for example.

Can you address @Anixx's point?

@Abe plants that routinely encounter saturated soils have adaptations to get O_2 to the roots.  The "knees" of Cyprus trees are an example as are the "air roots" of Mangroves.  Wetland monocots can also have hollow stems that allow them to transport air below the air-water interface.  Offhand I don't know how rice does it but adaptations to saturated soil are not uncommon.


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How do PLINK files and HapMap Phased files differ?
I know that PLINK and HapMap files show the same information, but can you give a thorough explanation of how exactly they differ.

Better ask this question in biostars :-)
http://www.biostars.org/

According to http://pngu.mgh.harvard.edu/~purcell/plink/data.shtml#ped:

The PED file is a white-space (space or tab) delimited file: the first six columns are mandatory:
 Family ID
 Individual ID
 Paternal ID
 Maternal ID
 Sex (1=male; 2=female; other=unknown)
 Phenotype

[...]
Genotypes (column 7 onwards) should also be white-space delimited; they can be any character (e.g. 1,2,3,4 or A,C,G,T or anything else) except 0 which is, by default, the missing genotype character. All markers should be biallelic. All SNPs (whether haploid or not) must have two alleles specified. Either Both alleles should be missing (i.e. 0) or neither. No header row should be given. For example, here are two individuals typed for 3 SNPs (one row = one person):
 FAM001  1  0 0  1  2  A A  G G  A C
 FAM001  2  0 0  1  2  A A  A G  0 0
 ...

And here is what I find in the begining of a HapMap .ped file I got a few years ago (hapmap3_r2_b36_fwd.YRI.qc.poly.ped):

 Y001    NA18488 0       0       2       -9      C C     T T     ...
 Y014    NA18519 0       0       1       -9      C C     T T     ...
 ...

So far, it seems to me than this is plain .ped format: the number of "header" columns is the same, and seems to conform to the specifications given in the above-mentioned web page.
Now let's have a look at the .map files.

By default, each line of the MAP file describes a single marker and must contain exactly 4 columns:
 chromosome (1-22, X, Y or 0 if unplaced)
 rs# or snp identifier
 Genetic distance (morgans)
 Base-pair position (bp units)

[...]
Note: Most analyses do not require a genetic map to be specified in any case; specifying a genetic (cM) map is most crucial for a set of analyses that look for shared segments between individuals. For basic association testing, the genetic distance column can be set at 0.
[...]
The autosomes should be coded 1 through 22. The following other codes can be used to specify other chromosome types:
 X    X chromosome                    -> 23
 Y    Y chromosome                    -> 24
 XY   Pseudo-autosomal region of X    -> 25
 MT   Mitochondrial                   -> 26

The numbers on the right represent PLINK's internal numeric coding of these chromosomes: these will appear in all output rather than the original chromosome codes.

Here we have something that may be different.
The end of the .map file corresponding to the HapMap .ped file looks like this:

 26      rs28357376      0       15825
 26      rs2853510       0       15925
 26      rs2854125       0       16149

The HapMap .map file uses "plink's internal numeric coding" for the chromosome instead of the letter code (MT).
Otherwise, it looks a pretty standard .map file, with no genetic distance indicated.

I should have specified, I meant the HapMap phased/legend/sample files as compared to map/ped files

source: Stack Exchange

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How can cabbage worms (Pieris brassicae) smell/see cabbages from a distance?
Recently I did post a question on gardening stackexchange asking if cabbage worms could smell their way back into my cabbages after I moved them away outside my fence. Answers says yes they do, but it seemed to me opinion-based and I cant find anything to support this answers.
Can this type of worm smell/see or have any other type of sensorial navigation thing that can lead them towards cabbages?

Yes, caterpillars have antennae that provide an olfactory sense. I don't know how well this particular caterpillar can smell and if it can travel long distances, but it is able to identify its food source.

I don't understand why you are asking about the caterpillar? The most important way the caterpillar ends up at your plant is because the butterflies deposit their eggs.

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Can a person be infected with HIV viruses without contacting them by person-related stuffs?
We know that a person can be infected with HIV viruses when he/she has sexual relationship with those having HIV viruses (and very, very, very rarely, urine/defecation-related transmission) - but I wonder if there are other sources of HIV transmission - so for example, let's say during sexual relationship, some cuts on body (for example, inside vagina) occurred. Then even if the partner did not have HIV viruses, and a person afterwards does not sex with partners with HIV viruses, is there a chance that he/she may get HIV viruses, still?

let's say during sexual relationship, some cuts on body (for example, inside vagina) occurred. Then even if the partner did not have HIV viruses, and a person afterwards does not sex with partners with HIV viruses, is there a chance that he/she may get HIV viruses, still?

No, because there is no virus present in any of the people involved to be transmitted in this scenario.  HIV doesn't spontaneously occur in people.  It should also be noted that HIV is also highly transmissible in the blood.

The virus must be present in one partner's body for transmission to occur.

Also, HIV can be transmitted through blood to blood contact.

There is currently a similar question/conversation that I have provided a link for here. It may provide some slightly more scientific answers than what I can:)
How does a person get AIDS?


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Is there an advantage to linear chromosomes
The DNA replication enzymes are unable to copy to the end of a linear chromosome. A portion of DNA is lost from the end of the chromosome after each replication. Because of this, eukaryotes have telomeres at the ends their chromosomes.
In most cells of a multi-cellular organism, the telomere is slowly reduced in size after each replication, leading to apoptosis. Cells that need to reproduce indefinitely such as germ and stem cells have to employ special mechanisms to replenish the telomere.
For multi-cellular eukaryotes I can see how this might be useful (for instance as a mechanism to counter cancer). However, I cannot see a purpose for apoptosis in the unicellular eukaryotes from which multi-cellular organisms evolved. Yet unicellular eukaryotes (e.g. yeast) have linear chromosomes with telomere caps. This problem does not exist in the circular chromosomes of unicellular prokaryotes from which unicellular eukaryotes are assumed to have evolved.
What advantage did linear chromosomes provide single-cell eukaryotes to offset the extra investment in reparing the telomere?

Related questions

What is the advantage of circular DNA in bacteria?

@MCM that was my first guess, too... especially with the other big difference between pro and euk being the tight space of nucleus. However, I couldn't think of why folding a very long circular genome would be fundamentally more difficult than a linear one (in fact it would make certain kinds of knots more difficult, avoiding potential damage). I also know a negative amount of biology so couldn't think of how to start the literature search myself :D.

@MCM if you could work that into an answer, I think it would be a decent one and I would enjoy reading it in detail. I was hopping for a more subtle answers (maybe related to life-histories), but I am happy with this, too :D.

Linking number? I think this goes with @MCM's torque issue.

I don't think the problem is torque. mainly because at the DNA level, water is very viscous. And DNA of a chromosomes being a very long molecule (tens centimeters long), a linear molecule would behave like a circular one, removing torque would be very difficult. My guess, is that organism with linear chromosome tend to be ones which under go meiosis. Chromosomes pairup, form chiasmata and exchange chromosome segments. On a linear chromosome, both odd and even exchange events resolve fine. In circular chromosomes, odd exchange lead to chromosome fusion. Even chiasmata resolve to two chromosomes

I think it is the wrong question. You assume that eukaryotes developed from a single-cell organism with circular DNA. Then, clearly, there must have been an advantage of (newly) developing a linear genome. But eukaryotes could have developed from an organism with linear DNA, too. There are still a few bacterial species with linear chromosomes, so this is not unlikely. We don't know, however.
On the other hand, if linearisation developed independently, you can learn from bacteria why it might have occurred:
J. N. Volff, J. Altenbuchner: A new beginning with new ends: linearisation of circular chromosomes during bacterial evolution. In: FEMS microbiology letters. 186, 2, May 2000, 143–150, PMID 10802162. (Review).
Abstract:

Bacterial circular chromosomes have sporadically become linearised
  during prokaryote evolution. Unrelated bacteria, including the
  spirochete Borrelia burgdorferi and the actinomycete Streptomyces,
  have linear chromosomes. Linear chromosomes may have been formed
  through integration of linear plasmids. Linear chromosomes use linear
  plasmid strategies to resolve the 'end-of-replication problem', but
  they have generally retained from their circular ancestors a central
  origin of replication. Streptomyces linear chromosomes are very
  unstable and at high frequency undergo amplifications and large
  deletions, often removing the telomeres. At least in Streptomyces,
  chromosome linearity is reversible: circular chromosomes arise
  spontaneously as products of genetic instability or can be generated
  artificially by targeted recombination. Streptomyces circularised
  chromosomes are very unstable as well, indicating that genetic
  instability is not confined to the linearised chromosomes. Bacterial
  linear chromosomes may contain telomere-linked regions of enhanced
  genomic plasticity, which undergo more frequent genetic exchanges and
  rearrangements and allow differential evolution of genes, depending on
  their chromosomal location.

I think its related to structure, like the noncoding (junk) DNA contributes to structure my guess would be that the Linear genome "just happend" and there was no way of going back.
That could have been because of Phage/Viral predation radical changes in genome structure will make it certainly very hard for viruses to adept. So in the early days of the eukaryotes the different genome would have provided a very strong protection against viral predation and thus would have allowed those organisms to reproduce nearly inhindered from the selective pressure of viruses. Which allowed for evolution to take place structures developed that make a step back impossible.
but yeah those are just WILD guesses

An interesting theory! Could you expand with sources?

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Do male mammals other than humans have nipples?
When I grew rabbits, I had a pair, one male and one female. And while the female's nipples were quite prominent, especially after giving birth, I don't remember the male having any nipples at all.
Do males of other mammal species, have nipples like human males, or is it a trait that's unique to Humans?

You never heard the old saying "worthless as teats on a boar hog?"

At the very least, I know that male primates also have nipples like female, though they are very close relatives to human. On the other hand, in some of my dissection labs, I noticed that male pigs also have nipples just like the female ones. It seems to be the case that most male mammals have nipples, which probably has to do with mammals being breast-feeder and their developmental pattern.
There is a page on Wikipedia that I found about this topic:
http://en.wikipedia.org/wiki/Nipple#In_male_mammals

I can also testify as to the presence of nipples on male dogs and cats (or, at any rate, my male dogs and cats).

u dissect pigs in ur lab?

Most mammalian males have nipples. The duck-billed platypus does not have nipples but you begin to see development of nipples in marsupials (Park and Lindberg 2004) like the opossum and kangaroo.  Development of a complete nipple begins in the eutherian (placental) mammals.
The mammary glands develop early in the embryo along a pair of ridges called the mammary ridge, mammary lines, or milk line (shown in an adult human in the figure below, taken from Wikipedia). The nipples form along this line. In humans, this happens during the fifth week of development. Within a few days, nipples begin to form. The number of nipples pairs that form is characteristic of the species (e.g., 1 pair in humans to 9 pairs in pigs). The development of nipples occurs before sexual differentiation begins which, in humans, is during the sixth week of development. That's why both males and females have nipples. This same order of develop occurs in other mammals, revealing our common ancestry.

However, because the process is under genetic control, mistakes can happen. Occasionally, humans (and other mammals) can develop extra nipples, the so-called supernumerary nipple(s). The most common places that humans develop one or more supernumerary nipples are identified by the circles in the figure above. The actor Mark Wahlberg is not shy about showing his.

For a general overview of mammary gland development, Dr. Jacqueline Veltmaat has a nice web page that highlights her research in this area. For those interested in the more technical genetic aspects of mammary gland development, a paper by Watson and Khaled (2007) reviews the genetic processes that regulate development of the mammary gland in mammals, based on the mouse model system. The article covers all stages of mammary gland development, from the embryo through puberty to pregnancy. Their Figure 1 shows one row of embryonic mammary buds (labeled MB1 - MB5) in the embryonic mouse. In the case of the mouse, all of the mammary buds will develop into fully functioning mammary glands.  Another paper by Robinson (2007) discusses the signalling pathways during development of the mammary glands.
Literature Cited
Park, C.S. and G.L. Lindberg. 2004. The mammary gland and lactation. pp. 720-741 in Dukes' Physiology of Domestic Animals, W.O. Reece, ed.  (Publisher not identified.)
Robinson, G.W. 2007. Cooperation of signalling pathways in embryonic mammary gland development.  Nature Reviews Genetics 8: 963-972.
Watson, C.J. and W.T. Khaled. 2008. Mammary development in the embryo and adult: a journey of morphogenesis and commitment. Development 135: 995-1003.

Yes, almost all male placental mammals have nipples, typically the same number of nipples as the females.  Notable exceptions: male horses and males of most mice species do not have nipples.

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Flora and fauna of early Homo sapiens environment?
Where can I find as much detail as possible on the flora and fauna (and perhaps geological structures too) between the time of the origin of Homo Sapiens say ~300kya to their "out of Africa" migration?
I haven't been able to find much research on the topic. I am looking for the types of predators they would have had, the foods they would have eaten, the plants and animals and bugs they would have encountered, etc.. If at all possible.
To put it another way, what are the flora and fauna of the Great Rift Valley.
https://en.wikipedia.org/wiki/Ethiopian_Highlands#Ecology

It's a bit outdated, but Quézel (1978) suggests the flora of the Mediterranean region of Africa is not much different than today:

It is concluded that the Mediterranean flora is relatively old and goes back at least as far as the middle Miocene.

See here for a scale of Geologic time. The middle Miocene would be ~10mya, so the above quote encompasses your time of interest.

However, I personally find this claim to be difficult to believe, especially due to documented variability at smaller scales: (e.g., Moreau 1963, Carlo et al 2009, etc.).
Other literature, unsurprisingly, points toward the fact that humans very likely modified their surroundings in noteworthy ways once on the scene. For example, Thompson et al. 2021:

Archaeological data and principal coordinates analysis indicate that early anthropogenic fire relaxed seasonal constraints on ignitions, influencing vegetation composition and erosion. This operated in tandem with climate-driven changes in precipitation to culminate in an ecological transition to an early, pre-agricultural anthropogenic landscape

Perhaps Gardner (1935) would also be of interest (I don't know, I don't have access).
Conclusion: I don't know the answer and only compiled the above in about 5 minutes of Google Scholar searching. I would guess that both the flora and fauna were likely somewhat dynamic across the time period you're asking about, and certainly, spatial physiognomic heterogeneity exists even today.
To narrow further searching, make sure you're using technical terminology where possible (e.g., late Pleistocene, Chibanian, etc.).

Citations:
 Carto, S.L., Weaver, A.J., Hetherington, R., Lam, Y. and Wiebe, E.C., 2009. Out of Africa and into an ice age: on the role of global climate change in the late Pleistocene migration of early modern humans out of Africa. Journal of human evolution, 56(2), pp.139-151.
 Gardner, E.W., 1935. The Pleistocene fauna and flora of Kharga Oasis, Egypt. Quarterly Journal of the Geological Society, 91(1-4), pp.479-518.
 Moreau, R.E., 1963, September. Vicissitudes of the African biomes in the late Pleistocene. In Proceedings of the Zoological Society of London (Vol. 141, No. 2, pp. 395-421). Oxford, UK: Blackwell Publishing Ltd.
 Quézel, P., 1978. Analysis of the flora of Mediterranean and Saharan Africa. Annals of the Missouri Botanical Garden, pp.479-534.
 Thompson, J.C., Wright, D.K., Ivory, S.J., Choi, J.H., Nightingale, S., Mackay, A., Schilt, F., Otárola-Castillo, E., Mercader, J., Forman, S.L. and Pietsch, T., 2021. Early human impacts and ecosystem reorganization in southern-central Africa. Science Advances, 7(19), p.eabf9776.

Early human migrations may have gone through Yemen. The Red Sea rift has become salt flats multiple times because of the ice age, if you find studies of the salt strata please write a new answer.
The science keywords are Pleistocene fauna, flora and Pleistocene ecology.
There were a lot more species/varieties of elephants, hippos, homo, deer, zebra, birds, bears, felines, with large mammal species enduring 1+ million average roughly depending on taxonomic precision. The plants were 90% the same, and plants can move roughly 100km to 10,000km per 1000 years conditions permitting. The green zones moved in a patchwork mosaic that was also tended by herbivores and dependent on climate. Tree species also change in more than 1+ million year ranges, perhaps 5-20, I don't know.
The mountains change yearly by 1cm for granite, 1-10cm limestone 10-50cm flysh and schist, 10-100cm for chalk, and 1+ meters for unconsolidated volcanic. The major changes were therefore climate changes
The rift valley is 5500km long, so It's too complicated to answer.
Here's animals from the holocene:
https://en.wikipedia.org/wiki/List_of_African_animals_extinct_in_the_Holocene
Here's some info about pleistocene, it's not very a very good list though, best to look at other sources.
https://en.wikipedia.org/wiki/Pleistocene_megafauna#:~:text=Pleistocene%20megafauna%20include%20the%20straight,and%20the%20leopard%20in%20Europe.


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Difficulties understanding a pathway
I am not a biologist and I would love to understand what is going on with this pathway.
I went to the description but it's still complicated, and I couldn't follow. Can someone please help me with it? Is this a comprehensive pathway or is it based on specific details? How do i read this pathway?

your link doesn't work...

@MattDMo thanks I updated it and should work now

Your question is pretty broad. What specifically do you want to know about this pathway?

@CactusWoman my main question is how can we come to such conclusion that a pathway is very important or one is not! how to interpret such pathway shown in the link? and what can I understand from it? to be honest it is very complicated for me to understand it

Please remove the link and make it a stand-alone question. I vote to close as unclear what you are asking.

I'd make sure to go over exactly what it is that confuses you, instead of simply stating the entire diagram couldn't be followed. These are proteins interacting with each other with a result of the interactions noted at the end, among other information.

So if you're reading the flowchart, understanding the notation of the arrows is important:

We have rectangles around the gene products
There's a circle, denoted by DNA, noting that the proteins are expressing the product that follows through interaction with DNA
The solid line with an arrowhead means there's some sort of interaction
The solid line with the blunted or T head means this pathway or interaction has been abrogated somehow
The solid line with the slash through it means there's some missing interaction that we don't see
The +p means phosphorylation
The double solid line to the left is the plasma membrane, whereas the dotted line central to the figure is the nuclear envelope
The dotted line means an indirect effect

Source: http://www.genome.jp/kegg/document/help_pathway.html
The pathway is kind of broad but it provides some mechanisms for tumorigenesis from two standpoints: chromosomal instability, and microsatellite instability. The pathways we're seeing promotes the tumor development by upregulating proliferation signals, and downregulating apoptosis pathways. There's bound to be more to it, especially since we see other players involved when we get into cases like metastasis like snail1/2, Met, Src, etc. Below is a survey of apoptotic pathways from Nature, with pro-apoptotic in red, and pro-survival in green:

Source: http://www.nature.com/reviews/poster/apoptosis/index.html
Ignoring the therapeutic targeting jargon, you can see that when growth factors bind, the cell generally pushes towards a survival state. When death factors bind or something goes wrong, the cell pushes toward an apoptotic state. Cancers, however, are intrinsically disregulated:

They have methods of overstepping their boundaries as cells, which is what makes them problematic. The general conclusion I'd draw from that KEGG pathway, though, is that many pathways need to be disregulated to end up with colorectal tumors, and the method of disregulation is (a) downmodulated mismatch repair, and (b) chromosomal aberrations due to duplication, etc. Andkeeping in mind the box of oncogenes vs tumor suppressors in the corner: "An important difference between oncogenes and tumor suppressor genes is that oncogenes result
from the activation (turning on) of proto-oncogenes, but tumor suppressor genes cause cancer when they are inactivated (turned off)"

Pathways in biology are very hard to interpret without being an expert in the subject. Here a link to The Standard Graphical Notation for Biological Networks that might help you understanding the notation used.
Pathway are generally based on evidences of links between the players. These links do not require to be found using one particular technique. Those evidences could come from genome-wide association studies (GWAS), RNA-seq, functional assays, receptor based assays, clinical data etc.. just to cite a few.
For example The MAPK pathway was linked to colorectal cancer via gene expression experiments as shown here. The MAPK pathway is known to influence cell proliferation and therefore contributes to colorectal cancer development but if you don't know what the MAPK pathway is doing at first it is hard to comprehend the full picture.


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Spermatogenesis question
I found this diagram in my textbook regarding the process of spermatogenesis. But, I doubt if the labelling done is correct or not. Especially, I can't figure out any difference between the cells labelled as spermatids and those as spermatozoa. Also, I doubt the labelling of Sertoli cells.
Please help me clarify my doubt.

As per my textbook,

The spermatids are transformed into spermatozoa (sperms) by the process called spermiogenesis. After spermiogenesis, sperm heads become embedded in the Sertoli cells, and are finally released from the seminiferous tubules by the process called spermiation.

I edited your question to convert the image of text to actual searchable text.

Notice the cell labeled "spermatid" is still attached to the Sertoli cell. Once released from the Sertoli cell, spermatids are called spermatozoa.
This process (release of the spermatid to form a spermatazoon) is called spermiation
EDIT
The text you added is still correct, but not well explained. Spermiogenesis is the development of the spermatid, the haploid 1N gamete produced by the second meiotic division, into a cell with a long flagella with a small amount of cytoplasm. Spermiation is the release from the sertoli cell. Both spermiogenesis and spermiation are involved in the development of a spermatid to a spermatozoon, but the specific point where we stop calling them spermatids and start calling them spermatozoa is release by the Sertoli cell, or spermiation, a substantial process in its own right. Both spermiogenesis and spermiation are important steps in the conversion of the haploid 1N gamete to a motile, free spermatozoon.

Your answer does not match at all to the theory in my book. Please see my edited question again and help me out. Thanks.

@DJKoustav your text is still correct, but not well explained.

@DJKoustav If my answer doesn't fully answer your question now, let me know. Otherwise, please mark it the answer by checking the gray checkmark next to it. See someone answers. Thanks!


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Why should collected blood from patients be analyzed as soon as possible?
I'm looking for the possible factors influencing blood samples. What happens to the blood cells esp. WBCs/PBMCs after 8 hours of blood draw? For example, I know that granulocytes may cause oxidative stress and that may affect the viability of WBCs. What else could have an effect on blood samples that we can't store them for a long time at room temperature?  Thank you.

Biological samples, including whole blood, are not at equilibrium. Biological processes, e.g., cellular metabolism, continue. Cells interact with their environment and a tube is not the same thing as the human vascular system. For one, in humans, on average, the entire volume of blood recirculates once every minute (see Costanzo Physiology Ch 4). Recirculation, with the associated access to nutrients, waste drop off, and exposure to various different compartments doesn't happen in a specimen tube. Nutrients are consumed, waste collects, cellular stress occurs, intracellular components leak out, cellular morphology changes... You can slow this down by putting samples on ice and collecting blood in a tube with components that preserve the sample for the specific test. There's a nice discussion of this in Lange's Guide to Diagnostic Tests, Chapter 1.
Given ongoing biological process in a very different environment, you can understand how interpretation of a particular test result depends on consistent collection and storage methods. Different tests are going to be more or less sensitive to time since collection and storage methods. There's a good deal of data on this for whole blood in this review.

@biologist you're welcome. If this answered your question you should mark it the answer by clicking the gray check mark next to it and turning it green. See someone answers


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İrreversible dopamine antagonist vs. Dopamine agonist
Can a dopamine agonist reverse the effects of an irreversible dopamine antagonist?

What do you mean by reverse?  Do you mean withdrawal?  The brain is altered by medications which would do not always understand.

İ mean unblock.

Can you clarify whether you're talking about an inverse agonist or an irreversible antagonist? Your question title says inverse antagonist, which isn't a typical term. The body says irreversible antagonist.

William so they both block dopamine receptots then ?

No. Irreversible antagonism is, by definition, inhibition that cannot be reversed by the agonist. Let me summarize the basics. You can read about this in Goodman and Gillman's The Pharmacological Basis of Therapeutics, Chapter 3, but there are many basic biochemistry textbooks that will cover the same ground.
When an interaction between a ligand and a receptor is said to be reversible, it means that it can associate to form a ligand receptor complex, and then dissociate, leaving the system with free ligand and free receptor. In the most general case, when the ligand is bound, it changes the conformation and activity of the receptor, and when it dissociates, the receptor returns to its original conformation and activity. The effect of the ligand in the biological system is related to the proportion of bound receptors.
Irreversible ligands typically involve covalent bonding (e.g., aspirin, alkylating agents). When the ligand interacts with the receptor, it irreversibly alters the conformation and function of the receptor. Cell or tissue function is only returned to the free receptor state when the particular receptors that have had a ligand receptor interaction have been degraded and replaced by a new receptor.
One of the ways to test whether an interaction is reversible is to try to reverse it. Let's look at how you would do this.
Start by looking at the effect when an agonist binds. The agonist is reversible. When you add it to an assay that contains the receptor, it associates and dissociates from the receptor, but at any moment, some proportion of receptors is bound to agonist. This binding produces an effect you can measure. The effect is related to the overall proportion of receptors bound to agonist at any given time, which is related to the concentration of the agonist. When you increase the concentration of an agonist, more agonist binds and you can measure a greater effect. In this figure from Goodman & Gillman Chapter 3, you can see the log concentration of the agonist on the x axis and the effect measured in an assay on the y axis:

Now consider the effect of an agonist in the presence of an antagonist. Classically, a competitive reversible antagonist binds the same site as an agonist. When the antagonist is bound, it doesn't allow the agonist to bind. So run the same experiment as you did above (by increasing the concentration of the agonist and measuring the effect), but start with a solution that contains some fixed concentration of antagonist. Because an antagonist is competing for those same binding sites, there will be fewer receptors available for agonist binding, fewer receptor/agonist complexes, and a smaller effect.
If the antagonist is reversible, though, you can still get the same effect you got in the first experiment. You just have to increase the concentration of the agonist until it binds the same proportion of receptors. Since both agonist and antagonist are constantly associating and dissociating with the receptor, increasing the concentration of one of them will out compete the other.  In this figure (same source), you can see that in the presence of an antagonist (here, i, for inhibitor), it requires more agonist to get the same effect, but the maximum effect is still the same.

If the antagonist is irreversible you can't get the same effect you got in the first experiment, even by increasing the concentration of the agonist. The receptors have been permanently altered by the presence of the antagonist, and whatever portion of them had some interaction with the antagonist will either not bind the agonist, or will not produce an effect when bound. What you see in the assay here is that increasing the agonist concentration in the assay may increase the measured response, but you are unable to reach the same maximum response. Note here, the figure describes a pseudo-irreversible inhibitor (antagonist). This is just a term for an irreversible inhibitor that doesn't covalently bind the receptor, but has a strong enough affinity for the binding site that, based on the measurements, it looks like it covalently binds. Effectively, the inhibitor is going to sit there on the binding site until the receptor is degraded and will not be outcompeted by the agonist.

Thank you. Do you know how long it would take for receptors blocked by a irreversible dopamine antagonist to degrade?

@user57928 You're welcome! Your other question about how long it takes for receptors to degrade, asked here is a lot more complicated than it may seem. Try editing it, though, as suggested by my comment there, and we'll see if we can't get some answers.

@user57928 As far as this question is concerned, take a look at the help page for someone answers. If  this answered your question about irreversible antagonists, you should mark it the answer by clicking the gray check mark next to it. Once you have the upvote privilege, you should upvote useful answers as well.

But in practice I have yet to find any irreversible dopamine antagonists on any commonly prescribed drugs today(if Wikipedia is a valid source).

There's Haldol off course.


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How does vasodilation slow blood flow?
During inflammation, cytokines and histamine cause vasodilation to increase blood flow to the inflamed area. However, it is also said that vasodilation slows blood flow which facilitates the adhesion and movement of leucocytes through the blood vessels and into extravascular tissue. My question is how does it slow blood flow? To me it would seem that there would be less drag force for a given volume of blood which would increase the speed of flow. There would also be less resistance.

The measurement that decreases during vasodilation is flow velocity, $v$, or a change in distance over change in time $\frac{\Delta x}{\Delta t}$. Prior to a reflex response, the same rate of flow, $Q$, or $\frac{\Delta V}{\Delta t}$ enters the capillary bed (here we use a capital V to represent volume, where $\Delta V$ is a change in volume, and $\frac{\Delta V}{\Delta t}$ is the change in volume over change in time. Because volume is area times a third distance dimension (e.g., if we say area is height times width, then volume is area times depth or thickness), we can describe flow as flow velocity times cross sectional area ($Q = A \cdot v$, or  $Q = A \cdot \frac{\Delta x}{\Delta t}$). If you increase the cross sectional area, $A$, and maintain the same flow, $Q$, then flow velocity, $v$, has to decrease.
A more intuitive explanation would involve turning on a garden hose and covering part of the end with your thumb. The smaller the opening you allow, the greater the flow velocity through the end of the garden hose. The same volume of water leaves the hose per unit time. It's just moving at a faster flow velocity if you decrease the cross sectional area (and at a slower flow velocity if you increase the cross sectional area).
This is discussed in Chapter 4 of Costanzo Physiology, in the section on hemodynamics.
The actual physical measurements end up being more difficult to predict in a situation with parallel capillary beds and reflex responses. $Q$ does not stay constant, for both the specific capillary bed, and for the entire circulatory system. However, you can say that, as a general rule flow velocity, or $v$, will decrease when cross sectional area, $A$, increases. As @BryanKrause points out in particular, provided the series resistance for a capillary bed doesn't change, the initial $Q$ for the capillary bed won't change, which means this caveat isn't relevant.

You might improve the answer by considering an entire branch of the vascular tree from artery to capillary. Because resistance does not occur in one cross-section, local vasodilation has a bigger effect on velocity than flow, even when the overall pressure is distributed in a parallel configuration with other branches of the tree.

@BryanKrause could you be more specific with your suggestion? This is textbook level material, and I'm honestly not certain if in a local (vs. systemic) inflammatory response there are good measurements that show resistance clamped upstream of a dilating arteriole, enforcing a constant $Q$.

It doesn't have to be upstream or downstream specifically, if there is any part of the vascular tree that is not affected (or less affected) the effect on velocity in the affected area will be bigger than the effect on flow, because flow is dependent on the series resistance whereas velocity depends on the local cross-sectional area.

I don't have time to grab a reference but I think the important vasodilation for leukocyte infiltration is on the venous side.

@BryanKrause local mediators of inflammation have different actions on venules than on arterioles, but the question is about the relationship between dilation (i.e., increased cross sectional area) and flow velocity. If you have a specific suggestion for how to change the answer, I'd be happy to incorporate it, or you can feel free to edit. I trust your physiology knowledge.

@BryanKrause incidentally, I just looked it up in Robbins, and histamine, at least, does appear to clamp resistance upstream. I'm not sure that an increase in resistance downstream would hold flow to a capillary bed constant, at least initially, since there is an low resistance path out of the capillaries into the tissue


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What do cells do when they aren't creating proteins?
I've always thought that the majority of the "work" in a cell is protein production, until I read the following.
The Wikipedia article on the central dogma of molecular biology states this:

80% of the human genome is transcribed even though only 1% codes for
  proteins.

and this:

Current research focuses on investigating the function of non-coding
  RNA, that is, RNA that does not follow the dogma trend and does not
  code for polypeptides.

If 99% of what's transcribed isn't used for creating proteins, what is it used for?  If it's not known - are there any hypotheses?

in short, some of it is regulatory, like miRNAs, and a bunch of it we don't really know why...

...and of course, even regulatory RNAs are ultimately concerned with the core activity of "creating proteins".

...and from another angle, red blood cells don't make any proteins.

So what do the Ribosomes do in red blood cells?

Red blood cells lose their ribosomes when they develop from reticulocytes. My comment was only meant to point out that not all cells are typical.

OK - I didn't know that, I'm learning a lot - thanks.

As indicated in the comments there are several non-coding (untranslated) RNAs, that the cell produces. Most of these perform gene regulatory functions.
However, widespread transcription is known to take place throughout the genome (pervasive transcription), but the functions of these RNAs are not clearly understood. It has been suggested that in certain cases the event of transcription, rather than its product, is responsible for chromatin regulation.

Untranslated RNA is incredibly important. As mentioned it regulates gene control, siRNA or miRNA for example can cut up mRNA preventing it being translated. Others can cause an increase in expression like enhancer RNA. Then RNA can act as tRNA or ribosomal RNA in protein translation. RNA can be enzymatically active, RNA also acts as a primer for initiation of replication. Then theres retroviruses that have inserted into our genome but have lost the ability to exit and are now part of our genome: the endogenous viruses. There are genes that are redundant duplications of functional genes that are free to evolve. As mutations occur silent parts may regain the ability to be transcribed.

When cells are not producing proteins they are performing their specialized functions.  Consider red blood cells carrying oxygen.  Or gut epithelial cells aiding in your digestion.  The list goes on...liver cells have a different role than the keratin cells in your hair.  There is a lot of transport that goes on as well in an certain cells that is carried out by motor proteins such as myosins, kinesins, and dyneins.  Cells are producing ATP to power these motors and many other integral functions. Also, consider cell replication and the machinery needed for that to occur.
You may visit Wikipedia for more information on motor proteins.
https://en.wikipedia.org/wiki/Motor_protein


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How does a cell sense its size?
Cells come in all sorts of sizes. How do they regulate their cell size to the point where similar cell types have a fairly mono-disperse size distribution?
Reasked from http://www.quora.com/How-Does-a-Cell-Know-Its-Size

Of particular interest to this question might be the latest issue of Curr Biol that has a special section devoted to this topic: Curr Biol, Vol 22 Issue 9 (http://www.cell.com/current-biology/issue?pii=S0960-9822%2812%29X0009-5)

This is a question that has been the focus of study for the last century (e.g., Amodel of cell size regulation - Ycas et al, J. Theoret. Biol. (1965) 9, 444-470). Cell size regulation may be in part determined by ribosomal activity (through mTor regulation) and is a critical checkpoint in cell division.
How the cell senses its size, however, is not understood. In 2009, two reports suggested that protein gradients could be responsible for the sensing of cell size. You can read a commentary about those articles in Cell size control: governed by a spatial gradient. - Almeyda and Tyers, Dev. Cell. (2009) 17(1), 3-4:

The phenomenon of cell size homeostasis, whereby cells coordinate
  growth and division to maintain a uniform cell size, has been an
  outstanding issue in cell biology for many decades. Two recent studies
  in Nature in fission yeast demonstrate that a gradient of the polarity
  factor Pom1 is a sensor of cell length that determines the onset of
  Cdc2 activation and mitosis.

These articles demonstrate one way in which cells may sense their size, but most probably several other mechanisms are also in place.

Rebecca Heald and her group at Berkeley do very interesting work looking at how organelle sizes are controlled by comparing two Xenopus species, very much related to the question here. Check out Nuclear size is regulated by importin alpha and NTF2 in Xenopus


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How do infectious bacteria determine when their numbers are high enough to attack a host?
When you get sick, you generally don't contract enough bacteria at once for them to succeed in battling your immune system, right?  Their numbers must gradually increase in the host's body before they know that they can attack.  How does that work?

I think the current answer to this for bacterial infections is quorum sensing.  Quorum sensing is a signalling pathway in bacteria which senses a molecule that the bacteria themselves secrete.  When the concentration of the quorum signal reaches a certain level, the bacteria interpret this as their population density reaching some threshhold.
Bacteria are always around - even infectious Staph, as described in the other answer, the bacteria are always being cleared out by the immune system, but when they find the right place where they can get critical mass, they dig in, form a biofilm and secrete toxins, which can help them divide more successfully.
This is a description of the process from a paper on Staph infection, a common bacterial infection in humans.

S. epidermidis is considered part of the of the normal human microbial flora, while S. aureus is usually regarded as a transient member. Colonization by either species usually does not lead to adverse events. However, when these organisms or their extracellular products are allowed to breach the epithelial layer, serious disease can result (1). S. aureus has many cell surface virulence factors (such as protein A and clumping factor) and secreted exotoxins and enzymes that allow strains to cause a myriad of infections. These diseases range from relatively benign furuncles and subcutaneous abscesses to scalded skin syndrome, sepsis, necrotizing pneumonia, and toxic shock syndrome (TSS). While no single cell surface virulence factor has been shown to be uniquely required for mucous membrane attachment, once colonization occurs, numerous secreted exotoxins, including the pyrogenic toxin superantigens and exfoliative toxins, definitively cause serious human disease. Other secreted exotoxins, such as the four hemolysins (α, β, δ, and γ) and Panton-Valentine leukocidin have also been suggested to contribute to significant illnesses. S. epidermidis does not possess the array of extracellular toxins that S. aureus does, and its primary virulence factor is considered to be its ability to form biofilms.
To improve their ability to cause this variety of human disease and to occupy numerous niches within the host, staphylococci have developed quorum-sensing systems that enable cell-to-cell communication and regulation of numerous colonization and virulence factors.

Viruses are typically simpler - as @MattDMo describes. They seem to rely on finding an environment where they can infect more cells at such a rate greater than the immune system can clear them out.  For influenza, this is more of a 'shock and awe' offense where they infect and multiply quickly, trying to outpace the immune system.  Another virus like HIV will actually multiply so slowly that the immune system can't find the host cells, allowing HIV to slowly spread over the host cell population.
Here's a bonus topic... When they were looking a cholera in the 1990s they found that V cholerae bacteria actually take up phage with toxins in them that convert benign bacteria to virulent ones (that cause dysenteric cholera).  They do this by conveying both the pili that attach to human cells and the toxin that causes the violent G.I. reaction of dysentery.  I think this is not unusual for bacterial diseases.  (the reference is Science 272, 1910-14 BTW).
This has lead to a suspicion that bacteria might be even adapting to infectious phenotypes through genomic changes.  This study had sequenced the genome of C difficile from 486 patients and found that relatively few of them really were capable of patient to patient infection:

The results of the study indicated that, although transmission between patients is likely to occur, it actually happens at relatively low frequency. In particular, concerns that healthcare teams were spreading infection between different hospitals seem to be misplaced. One exception to this general finding is that there were a large number of cases of infection from one particular strain that does appear to have been due to patient-to-patient transmission, emphasising the epidemic nature of this lineage. Notably, this strain has declined in UK hospitals in the last five years.

Great!  Thanks a lot -- this is what I was looking for.  Here is a very interesting TED video about the subject matter: http://www.ted.com/talks/bonnie_bassler_on_how_bacteria_communicate.html

@Hypoxide this is a great talk - highly recommend it too.   There is another topic of interest regarding bacteria - they modify themselves to become virulent.  I've added a note to the bottom of the entry above...

Infectious agents like bacteria, viruses, fungi, etc., don't know when to "attack" or produce pathogenic substances, they just do it under their preferred conditions, and your body's immune system either succeeds in fighting them off immediately, or it doesn't and you get sick. Your body is constantly confronting and clearing potentially dangerous microorganisms without your ever being aware of it. Every breath of air, mouthful of food, or contact with your mucus membranes is a possible infection, if not for your innate immune system.
However, sometimes pathogens get past the first line of defense, or are otherwise able to evade it, and in the time it takes for the adaptive immune system to engage they are building up their numbers and gradually getting to the point where you realize that you are sick or otherwise infected.
Interestingly, many of the symptoms of sickness you often feel - being tired, feeling sore, having a fever or localized redness/inflammation - are actually caused by some of the effector chemicals or cytokines released by your own immune system, and not by the infective agents themselves.
For example, lipopolysaccharide or LPS is a major component of the cell wall of Gram-negative bacteria, including such pathogenic species as E. coli (food poisoning, urinary tract infections), Neisseria species (bacterial meningitis, gonorrhea), H. pylori (stomach ulcers), and Salmonella species (food poisoning, typhoid fever). LPS on its own does not cause fever or inflammation, for example, but when bound by certain immune cells (B-cells and macrophages, mostly) it rapidly and overwhelmingly promotes the generation and release of pro-inflammatory cytokines like TNFα and IL-1β. These proteins then act on target tissues to allow the inflammatory response - swelling, pain, increased temperature, redness, etc. - and recruit immune cells to fight whatever invaders must be there.

I would have thought this was the universal answer, but shigeta gives some fascinating examples of bacteria that do use environmental information to "choose" a stealthy vs. aggressive strategy. I would imagine your answer is still applicable in most cases.


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Anaerobic respiration choice in E. coli
Under anaerobic conditions E. coli has two options to generate ATP: fermentation (substrate-level phosphorylation), and respiration (proton gradient, chemisomotic phosphorylation). Which is favored? What determines the choice? If availability of enzymes required for anaerobic respiration is decisive, what regulates them under anaerobic conditions?
I looked into the web but did not find the answer.

E. Coli is not simply aerobic. Nor is it anaerobic. It is facultative, meaning that it thrives in both environments, and can breath with or without oxygen.

Let me first clarify the difference between anaerobic respiration and fermentation.
Literally respiration refers to breathing, but its definition has been extended to include cellular metabolism that leads to ATP generation.
Fermentation, as you said depends on substrate level phosphorylation. Anaerobic respiration on the other hand just means ATP synthesis in the absence of oxygen- in other words anoxic. This happens in several cases in which the terminal electron acceptor is not oxygen but some other chemical species such as $Fe^{3+}$ or fumarate.
E.coli can carry out ETC mediated ATP synthesis both in the presence and absence of oxygen. At high oxygen concentration it uses $O_2$ as electron acceptor, mediated by cytochrome-d. At low oxygen concentration other kinds of cytochromes accumulate and the cell uses fumarate or nitrate as the terminal electron acceptor with the help of fumarate reductase and nitrate reductase respectively. This is an old article but is still quite informative. Check it out.
Fumarate and nitrate reductases are regulated as a part of what is known as FNR regulon. FNR is an oxygen-sensitive transcription regulator. In the presence of oxygen it is inactivated. In the absence of oxygen it activates the fumarate and nitrate reductase genes.
Perhaps in the absence of these alternate electron acceptors, the bacterium totally depends on SLP.


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Cell Respiration and Oxidative Phosphorylation
Why and how does the proton travelling through the stalked particle in the inner mitochondrial membrane, cause a conformational change in the ATPase?

The passage of protons through the FO (membrane) portion of the molecule (driven by the electrochemical gradient of protons across the respiratory membrane) generates torque at the interface between the a and c subunits. This mean that the ring of 10 c subunits rotates relative to the a subunit. The γ subunit in the stalk rotates along with the ring of c subunits, while the ring of α and β subunits in F1 is constrained to remain static with respect to the a subunit because of the interaction with the δ and b subunits (forming the peripheral stalk). So we have two portions of the molecule the "static" a-b2-δ-α3β3 part and the rotating c10-γ-ε part. The γ subunit rotates within the α3β3 part of F1 and drives a three-step cycle of conformational changes (via intersubunit interactions) which are linked to the phosphorylation of ADP.
There is a useful animation here illustrating the three step catalytic cycle being driven by the rotation of the γ subunit.
(image from Aksimentiev et al. (2004)
Insights into the molecular mechanism of rotation in the FO sector of ATP synthase. Biophys J. 86:1332-44)

For me, ATP synthase is one of the most remarkable features of the cell. Beautiful.


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How were the first primers made?
I keep reading about how primers are useful in pcr -- they allow you to select a specific dna region. Similarly, in NGS or Sanger sequencing they give you a starting point. The primers I see are about 20-30 bases long.
However, how were the first primers developed? Somewhere, someone needed to come up with a 20-base sequence that bound to a specific part. Aren't there 4^20 such combinations? That's a lot of potential options to test.
How was that done?

When you don't know what primer to use, you can use random hexamer primers. They have a rather low specificity but they make it possible to get some information that you can use as a starting point. Alternatively you can also use the known parts as a poly-A tail in mRNA and start from there. Or you add an adapter to your DNA to be sequenced with a known sequence and use primers from this adapter (this is what is done for NGS).

The process of sequencing was, and can be, assisted by cloning a DNA fragment into a plasmid and using primers that bind to known sequences (in the plasmid) that flank the cloning site.  (and what @Chris said)!

+1 for PlaysDice - this is why the primers that were used in Sanger sequencing were called universal primers. @PlaysDice you should write this as an answer.

@PlaysDice I want to understand more about it! Please write it in an answer.

@AlanBoyd.  By popular demand..added ;)

The MIT synthetic chemist Gobind Khorana won the 1968 Nobel Prize in Chemistry for his work which successfully was able to make chains of Ribonucleic acids.  The chemistry was difficult at the time but he won the prize for making specific sequences of RNA bases which were then fed to cells, resulting in specific amino acid chains, which ultimately deciphered the specific base to amino acid correspondence of the genetic code.
Khorana was only one of the chemists who worked on nucelotide synthesis, but the technique overall is simple and since nucleic acid polymers are only unbranched polymers,
any sequence combination is easily obtained.  Each sequential reaction adds one base.  Repeat the reaction as many times as needed.

The chemistry Khorana devised was refined and easily extended to DNA polymers since the linkages are identical, the difference between DNA and RNA is only a single alcohol (-OH) group, which is not directly involved in the bond between the nucleotide bases.
By 1983 when Kary Mullis concieved the idea of PCR, short sequences of DNA and RNA could be synthesized on commercially available machines.  In fact Mullis was responsible for just such a machine at Cetus Pharmaceuticals and had been trying to find a way to increase demand for his services.
The PCR oligos were the easy part of the operation.  To prove the concept, the team at Cetus used a conventional DNA polymerase and add it to the PCR mix after every cycle.  By 1986 the Cetus team had succeeded in performing PCR a heat tolerant DNA polymerase from Thermus aquaticus, a bacterium from a hot spring, which basically made it the technique we still use today.

The process of sequencing was, and can be, assisted by cloning a DNA fragment into a known site in a plasmid designed to help sequencing. That cloning site is flanked by a known sequence(s) that can use standard primers

In the figure "A" and "B" are just reference points on either side of the Cloning site.  Of course, the plasmid extends on either side of the shown region.  The plasmid is first cut open at the cloning site (upper step) and the unknown DNA fragment ligated in (middle step). Then the known 'forward' sequence can be used, with a complementary primer (shown as the arrow), to prime a sequencing reaction (lower step, dashed line).
Additional modifications include (per @Chris) preparing the insert with adapters or using a plasmid with sequence that binds a 'reverse' primer (on this figure, that would be an arrow on the right hand side of "B" and pointing to the left).   The reverse primer allows sequencing of the opposite strand to the forward primer and gives access to the 3' end of the inserted unknown sequence.   In the early days of Sanger sequencing read lengths were quite short and often were unable to run the length of a larger insert.
Sequencing plasmids are designed so that their forward and reverse primer binding sites are unlikely to contain any sequences that may be found in the insert.   Because these known primers can be used in this manner to sequence almost any insert, they are often called Universal Primers (per @AlanBoyd).


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What kind of event would cause the current Mitochondrial Eve to be replaced by a new one?
Apparently all living humans are matrilineal descendants of a single woman who lived 200.000 years ago. She is called Mitochondrial Eve.
But at the time she lived there was a different matrilineal ancestor that all living humans shared. And between then and now I imagine many other women have been Mitochondrial Eves of the human population that lived at a particular time.
What I'm wondering is what kinds of events would cause a different, more recent matrilineal ancestor to become the Mitochondrial Eve of all living humans?
One scenario I can image is that the human population is on the brink of extinction and literally only a few people survive. Because there are so few people alive, I imagine that the chance that they share a more recent matrilineal ancestor is high.
Are there other scenarios possible? Does the chance of a new Mitochondrial Eve emerging decrease if the human population is large (billions) instead of small (hundreds or thousands)? Suppose that the human population will not decrease, is it likely future human populations will ever have a different Mitochondrial Eve than the current population? Does it depend on the amount of people that migrate?
The same questions could be posed for Y-Chromosomal Adam and the most recent common ancestor of all humans, I guess...

An mathematical solution to this question is the Galton-Watson Process. It is formulated in terms of surnames and this situation is very similar. http://en.wikipedia.org/wiki/Galton%2DWatson_process

It looks like the genetic Adam just got replaced... so there you go. http://www.newscientist.com/article/dn23240-the-father-of-all-men-is-340000-years-old.html

The new mitochondrial eve is alive right now.
When humans reproduce, mothers pass their mitochondria to their offspring without a contribution from the father.  As a result, each human can trace back their mitochondrial lineage as an unbroken chain to a single individual woman in the past.  Through random chance (genetic drift) or natural selection women in some mitochondrial lines will pass offspring to the next generation, while others will not.  If a woman fails to pass offspring to the next generation then she represents the end (i.e., extinction) of a particular mitochondrial lineage.  As time progresses more and more of the original mitochondrial lineages will go extinct until all humans represent one remaining linage.
Note that this is a continual process since lineages accumulate differences through mutation of the mitochondrial DNA.  This mutation is the source of the different lineages that that will go forward.  Based on the estimated rate of mitochondrial DNA mutation we can estimate how long  it would take for extant mitochondria to have developed the genetic differences we now see.
If you take a snapshot of this process at one point in time (e.g., contemporary humans), you can use this estimated time to say how long it would take to accumulate the present differences - that is when the line began.  Due to the continual extinction of extant mitochondrial lines, there is some point in the future where if we were to take the snapshot we would estimate that the mitochondrial eve was alive right now.
EDIT based on comment:
The rate that a new mitochondrial eve would be formed is based on the accumulation of mutations in non-coding regions of the mitochondrial DNA (i.e., the molecular clock) which is dependent on the population size only in so far as the probability that a given mitochondrial line will survive when all others go extinct is basically its initial frequency in the population. So in a large population with more initial diversity each line will have a lower probability of succeeding.
Also, if there is no selection for or against a given line then changes in frequency are due to chance (genetic drift). In a large population the effect of drift is smaller than it is on a small population.  So if the population size is small, then the likelihood that a mitochondrial line will go extinct is greater and the rate of a single mitochondrial line succeeding to be the mitochondrial eve is greater.

True, I hadn't thought it fully through...  I edited my answer to remove the references to speciation.

This sounds fair, but I'm left wondering if the rate of extinction of mitochondrial lineages is dependent on the total population. At what rate do humans get a new M-Eve, and which factors influence that rate?

@molf I edited my answer to address your comment.  Hope that helps.

it sounds like you expect all the mitochondrial lineages to disappear in the future.  why would that happen? It has never happened in the past.

@shigeta it has happened in the past.  Mitochondrial lineages are continually going extinct but new diversity arises due to mutation.  Using the rate of neutral mutations we can estimate how long it has taken the population to accrue that amount of diversity, which is the time since that diversity was 0, which is when that lineage arose, which is the estimate of the age of mitochondrial eve.

the question is what would it take before the mitochondrial Eve to be replaced.  there are 7 billion people on the planet.  You are right it might have happened before our current Eve, but do you really believe it will happen at some time in the future?

The mitochondrial eve after the one we have now is probably not alive right now. If the species is around long enough, someone born today might become the new eve, or might not.  Imagine killing off all the women in the world bar two native american ladies. That pushes mitochondrial eve forward to maybe 15 thousand years ago, 'skipping' 185 thousand years of history. We could be 'skipped' in the same way.

One possible scenario would be that a particular woman develops a mutation rendering her much more 'fit' (in the evolutionary sense) than her peers. For the sake of argument, lets take the very simplistic case of an X-linked recessive mutation causing the women who bear it to have say 10 children at each birth. If this mutation is then transferred to the offspring, it will very quickly spread across the entire population.
If this continues for a few generations, the crushing majority of the earth's population will be the descendants of that one woman who carried the original mutation, she would be the new mitochondrial Eve.
I want to stress that this is nothing but a very simplistic thought experiment. Such a mutation is i) very unlikely, probably impossible, ii) likely to render the carrying individual less fit rather than more as each birth would be exhausting, increasing the chances of dying during child birth.

Update:
I have specified that the mutation has to be X-linked and recessive. This means that it will only present a phenotype in women who are homozygous for it, women both of whose parents carried the mutation. This is because, as mgkrebbs very correctly pointed out in the comments below, otherwise her sons would mate with women who are not their sisters and their children would have the mutation but not her mDNA. If the phenotype is only expressed when the mutation is homozygous, only women whose mother carried the mutation (and Eve's mDNA) would show it and only then would a new mEve arise.

Not correct, as such a mutation would pretty much have to be in the nuclear genome, not the mitochondrial genome.  Being on a nuclear chromosome, it would spread to offspring of women who are not her mitochondrial descendants, and thus she would not become  a mitochondrial eve.

@mgkrebbs, huh? Of course the mutation would be in the nuclear genome and of course, by definition, it would pass to her descendants only. What exactly are mitochondrial descendants? Each female egg contains both the mitochondria and the genome of the parent. Yes, the mutation would not be carried by her mitochondria, however, her mitochondria would be carried by her descendants, therefore, she would be the new mitochondrial Eve (although, as shigeta points out, she would still be dcendant from our MEve herself).

But these mutations can ultimately also be transferred to the offspring through patrilineal descendants, right? What factor makes it likely that this woman would become a M-Eve? Was our M-Eve really so different from other women alive at the time?

@molf, not necessarily no. The point is that mitochondria come from the mother not the father. Therefore, if one female has a much greater reproductive success than her peers, and that female's offspring do so as well, eventually ALL individuals will be the descendants of that one female. Since mitochondria come from the mother exclusively, all individuals will have the same mitochondrial genome. Their nuclear genome will be different as it is also affected by the father but that is irrelevant to the point discussed.

This is true but it is not necessary that one woman have much greater fitness.  Even if fitness was equal drift would produce a mitochondrial eve with sufficient time. Just like one player will wind up with all of the money if the poker game goes on long enough, even if they are equal players.

@DQdlM, I'm not sure... Drift will affect the spread of genes through the population. I see no reason why it should afect MEve.

This is how I see it:  if the population has 10 M-lines at equal freq. and fitness.  At each generation the lines will be perpetuated based on their freq.  W/o drift the freq. wouldn't change and no lines would go extinct but drift can raise or lower the freq. of a line by chance so over time some lines will become less frequent and more vulnerable to extinction and others will become more frequent and less vulnerable to extinction.  Given enough time only one line will remain. This is MEve.

@DQdlM, OK, yes, I see your point. However, I am still not sure whether drift is applicable here. Even if the M-lines have equal freq. and fitness, the nuclear genomes of the hosts will not. Therefore, the fitness of the nuclear genotype will affect the spread of M-lines much more than drift. The only way I can see mitochondrial genomic drift producing a new MEve would be if the both nuclear  and mitochondrial genomes were free of any selective pressure and governed by drift alone.

Agreed.  In nature, both selection and drift are going to be acting in concert and it would be very difficult to tease them apart.  My understanding of the MEve concept though is that the estimate is based on the accumulation of neutral mutations in the mito. DNA, so the estimate assumes no selection and only drift.  Selection should speed up the process and MEve would be more recent (assuming it doesn't change direction during the process) - as you point out in your answer.

@terdon, since you say "Of course the mutation would be in the nuclear genome", the scenario would not be likely to make the particular woman a Mitochondrial-Eve.  Suppose she has 5 sons and 5 daughters, then the offspring of the 5 sons are just as likely to carry the advantageous nuclear mutation, and thereby be likely to have surviving descendants, yet the sons' children do not carry her mDNA. The population will not especially favor female-only descendants of the original woman, hence not favor her mitochondria, and not favor her becoming a M-Eve.

@mgkrebbs, I see what you mean, however, even if the mutation is caried by her male offspring, it will make no difference. Since the females of each generation that carry the mutation will consistently have more offspring, eventually the vast majority of the species will carry the mutation. Therefore, her male descendants will mate with her female descendants, thereby spreading her mDNA.

@terdon, yes, "the females of each generation that carry the mutation will consistently have more offspring, eventually the vast majority of the species will carry the mutation" is true, but it is not true that these females need have her mDNA.  Her sons mated with non-sisters, so all their offspring, sons and daughters, will not have her mDNA, yet will have the advantageous mutation to the same extent.

@mgkrebbs, I understand now, you are absolutely right. I have changed my answer to make the hypothetical mutation X-linked recessive.

That would increase the probability that she could become a M-Eve, but does not assure it.  First off, being recessive, none of the woman's children would have any advantage carrying the mutation, since they will mate with non-carriers and so not show the advantage.  (Assume for discussion both her X's have the mutation.) Now note that of her grandchildren, one half of them will be carriers and one half of them not.  Note also that all of the sons' daughters will be carriers (the X coming from her), while [continued in next comment]

...while only half of the daughter's daughters will be carriers (plus half of the daughter's sons).  This means that the most likely first appearance of the fertility advantage is between cousins: a daughter's son and the daughter of either sex child of the original women (excluding unlikely brother-sister matings). Two-thirds of these latter granddaughters are (probalistically) via sons; the other third via daughters.  Thus, 2/3rds will not carry the original mDNA, and thus the original woman is not so likely to become a M-Eve.

What's a more realistic scenario that could happen to allow only one lineage to survive ?

What would need to happen for a single woman's mitochondrial genome to be in all living humans ?
All other women would suddenly or gradually need to be eliminated from the gene pool.   No other woman could enter the gene pool of this future humanity.  So the most likely scenario is one where we would have to be reduced to a single woman at some point.
Genetic isolation was brought up, but the words 'all living humans' doesn't really say 'isolation'.  In isolation, there are other people still carrying on somewhere else.   Here we are talking about only isolation in the sense that the breeders are the only ones left to reproduce.
Even so, any human woman will still be descended from MEve.  That original Eve would still be the mitochondrial Eve, though the genomic record pointing to her would have disappeared.
A completely New Eve could happen if there were a woman unrelated to MEve were to come along, and her offspring were so much more successful than all other women that over time only this woman's daughters were chosen as mothers.  She would be incredibly successful- like all her children were 6'6" and much smarter, attractive etc etc, then the rest of the gene pool could dwindle leaving only 'new Eve'.  This could happen say if we got some Neanderthals going.  They don't seem to be particularly likely to take over though.
This is similar to the scenario where one female lineage simply out-competes all other female lineages to assume the mantle of M-Eve.  This seems less likely to me.  This lineage would have to enjoy an advantage would have to out-weigh all over variants that exist at the time and would ever emerge over the following generations before our new M-Eve's final domination. Given the number of genes and possible variants, in the entire genome, that is statistically really improbable.
As far as a new Y Adam, this sort of thing nearly happened for men.  Just to remind, the Y chromosome is transmitted exclusively from father to son, so a Y Adam would be the only ancestor of all men on the face of the planet.
A national geographic sponsored survey of genomes found that in central asia 8% of all men have the same Y chromosome.  Over all humanity, 0.5% of all men have the same Y chromosome.  The genetics point to the Mongol Warrior King, Genghis Khan whose campaigns across Asia to the doorstep of Europe included him bedding with one or more different women from the conquered peoples every night, one of whom is reputed to have killed him.  Not incidentally killing many men too, eliminating much future competition for his progeny.
Still, all this is a mere fraction of the sort of effect you are talking about.  100% replacement by a single individuals descendants is hard to imagine in less than an extinction like scenario.  Or a new race of superbeings coming from a single individual.  Hard to imagine given the billions of people on the face of the planet now.
Its a little easier to imagine in the case of a new Adam only because a one man can have hundreds or even thousands of offspring in his lifetime.  Even then, Male psychology seems to bring it up more than is rational. Its still extremely improbable (not going to happen).

Its also worth noting that few species have been able to come back from such a small gene pool and number...
Here's a tree of human Y chromosomes. You can see that fat grey blob which are descendants of GK.

Based on the comment to my answer I removed the mention of isolation so I edited out your reference to the part of my answer that no longer exists.

I was also editing - i think i ran over your changes, but i took the reference to you out.

This notion seems to conflict with the hypothesis that our current M-Eve was not the only woman alive at the time. Isn't it so that other contemporary women of our M-Eve do have living descendants, just not matrilineal?

If there were a group of women that were not at all related at the time of origin of the human race, we should see it in the mitochondrial version of the above diagram - more than one tree.  It seems as the human race (and speciation) started with just one event.  On the other hand its interesting that there are theories that neanderthals and denisovans mated with humans after leaving africa, but it doesn't seem to show up here. http://en.wikipedia.org/wiki/Denisova_hominin#Interbreeding_with_modern_humans

It isn't required that all other women be eliminated from the gene pool but rather that through time the individual lineages of mitochondrial DNA (based on some initial variation at a specified time in the past) go extinct.

How do you make a single chromosome go extinct while the rest of the chromosomes breed?

The point is that you do not need to be reduced to a single woman at any point.  If there are x different mitochondrial lines extant right now.  Through time, the proportion of descendants from each of these lines will vary (n/x) and some lines will go extinct (0/x).  Given enough time all lines but one will go extinct (either from selection or drift) and all of the individuals in the population will be the descendants of a single line.  Note that background mutation will mean that the extant variation need not decline through time.

That's true - though I did not really mean say that all the women would need to be removed at the same time, but eventually they would have to exit to achieve the scenario depicted. I think this is what I said though its true not at the top of the entry. This parallel competitive MEve is a lot less likely. I can amend my answer to describe how much less likely that is, although all these scenarios are the stuff of science fiction - more thought exercise than at all likely to happen.

I don't really think it is science fiction as much as a way to think about genetic drift.  It is basically just genetic drift in reverse.  The MEve is just an estimate of how long it took for drift to eliminate the genetic diversity of the population.

let us continue this discussion in chat


text:
Which kind of mushroom is this?

I'm in Western Arkansas, and these are red, hollow mushrooms with a brown slimy coating that popped up in our mulch, roughly a half an inch in diameter and they have grown several inches tall. Is there anything specific that I can/should do to these things? I have young kids and pets that I assume I don't want eating these things.

This looks like a type of stinkhorn fungus.  They commonly pop up in urban settings, including mulched areas, and can come in many different appearances.  The slime on these mushrooms is used to attract insects and flies which will disperse their spores. They are found in North America including in temperate and north-temperate climates.  According to MushroomExpert.Com these mushrooms will not hurt you, your children or pets.
Specifically, the stinkhorns in your photo look like Mutinus elegans to me.

Source: http://www.projectnoah.org/spottings/635556012


text:
Probability for a megafauna specimen to exhibit a gene not present in either parent
What is the rough probability for a megafauna specimen to exhibit a gene not present in either parent?
I'm looking, ideally, at the chance for one specific individual to be the first in a breeding population to have a given gene.

So similar : https://biology.stackexchange.com/q/86138/38451

Not similar at all.

@Christos Similar to what iayork's answer has expressed, when do you think a mutation results in a new gene? If you had a protein with one function (e.g. kinase activity) that gradually evolved another function (e.g. trafficking), where is the cutoff between them? Which is the kinase gene and which is the trafficking gene? For this reason, your question is incomplete and cannot have a definite answer.

well for scale every single human carries around ~100 mutation in is sequence. but this is going to depend a lot on the size of the genome.

@Jam See my comment on iayork's answer. If you think about it, a gene duplication occurs, if the gene is functional that event produces an extra copy. If at some stage a mutation occurs or mutations accumulate to give the gene a new function (including a dormant mutation gene acquiring a promoter) a new gene has arisen. It has to happen during evolution at some stage, so it is reasonable to wonder about rates and probabilities, although unreasonable to expect anyone here to be able to answer.

@David I completely agree that when the question is expressed in terms of rates, it is answerable but in terms of instantaneously switching from one gene to another, it is incomplete.

The rate of evolution (as a result of germline mutagenesis) depends on many environmental factors. Scally (2016) suggests that germline mutation rate is approximately $0.5 \times 10^{-9} \text{bp}^{−1} \text{year}^{−1}$ in humans. You may be able to calculate the probability from here. It may be different for other organisms. Moreover, evolution can also happen because of gene duplication (as David said) and horizontal gene transfer, transposition etc. So you may narrow your question down a bit.

You need to define “gene” for your question to make sense. In humans, each individual has roughly 100 novel mutations (that neither parent had) (Human mutation rate revealed). However, those are not necessarily “new genes”, since many occur in non-functional DNA, even those that occur in functional regions may not alter any function, and even those that alter function may not be part of a gene, depending on your personal definition.

I wouldn't think the poster needs to define gene. It's evident that he's talking about new genes, not mutations that change existing ones. Most new genes appear to arise by duplication, and it's possible to compare species and identify differences e.g. in gene families like globins or blood group antigens. If someone has some figures for differences between rodents or primates and estimates of time of evolutionary divergence this would give a rate. To calculate a probability you would probably have to estimate the number of generations and the population of each. So this is not an answer.


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Estimate for number of genes changed in speciation between a megafauna parent and child species
At least in terms of a back-of-the-envelope calculation, what is a believable range for the number of gene changes between parent and child species to represent speciation between species of megafauna?

Why duplicate this : https://biology.stackexchange.com/q/86139/38451

To paraphrase an old saying, gene changes should be weighed not counted. There are a plethora of types of gene changes, and they vary by orders of magnitude in their impact. In particular, which genes are affected has a huge impact. Some point mutations (change in a single or a few nucleotides) can be lethal. On the other hand there are trisomies where an entire chromosome is duplicated. These may cause severe health problems but don't result in a different species.
As is discussed in many other questions on this site, the definition of a species is fuzzy and context specific.

What you say is all very well but it does not seem to be an answer to this question. The poster's question may be unclear and naive, but he seems to be interested in the rate at which new genes appear as species diverge to something different. The fact that the definition of species is fuzzy is irrelevant. The sort of answer that would be useful (but which I am not able to provide) is an estimate of the number of different gene between two species with a common answer (mouse and rat?) and the evolutionary distance between them. This would give some sort of approximate rate.


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Does anyone know good software for producing tanglegrams?
I'm trying to look at relationships between parasite and host phylogenetic trees. I have done a bit of searching for software with which to do this, and I have tried using Dendroscope and TreeMap, but can't get to grips with them.
I want to produce something along the lines of this;

Treemap and Dendroscope are the only ones that I know of. Can you start small? Search for examples like: http://ib.berkeley.edu/courses/ib200b/ib200b_2009/Labs/15%20Biogeography/15%20Biogeography%20and%20Treemap.pdf and try to work through.

I think that I may have underestimated the complexity of the matter. That run through is very useful, however it is the very earliest stage that I am struggling with. I have two phylogenetic trees (one host and one parasite). Both are in newick format. In this manual it says "This file contains two trees,
one for the host and one for the parasite, and a description of which hosts are associated
with which parasites.". I think the lack of description of association is the problem. I assumed the software would take the associations from the information in the trees? I'm not an expert!

how to use dendroscope3 for making phylogenetic tree?

The word "software" is uncountable in English so cannot take the indefinite article. I have corrected this in the question.

Dendroscope
Using Dendroscope, I opened the provided example file trees.new. This opens a new window with 16 trees in it.

Shift click on the first two trees (Tree1 and Tree2).
Choose Algorithms $\rightarrow$ Tanglegram...
This will compute the tanglegram and open a new window.

At this point, I get:

There is nothing special in the trees.new file, just 16 Newick trees. So it looks like all you need is to have your trees in the same file or use File $\rightarrow$ Add from file.
I think that the tricky part is that your trees have to have the same tip labels, so that they can be lined up optimally. So in your example, Phalacrocorax pygmaeus and Pectinopygus excornis must have been named the same in the original Nexus file and then modified to produce the final figure.
TreeMap 3
TreeMap requires some preliminary setup. Basically you create a Nexus file manually. Using the 4taxonmatch file from the examples, you can get the basic layout. You have a HOST block and a PARASITE block. Within each one of those is a TREE block, which contains the Newick formatted tree.
The RANGE block inside the DISTRIBUTION block contains the mapping table. Here p maps to u, etc. This is the connection between host and parasite.
#NEXUS
BEGIN HOST;
TREE * Host1 = (u, (v, (w, x)));
ENDBLOCK;

BEGIN PARASITE;
TREE * Para1 = (p, (q, (r, s)));
ENDBLOCK;

BEGIN DISTRIBUTION;
RANGE
    p: u,
    q: v,
    r: w,
    s: x
;
END;

In contrast, you get the correctly labelled tree directly. See below.

Brillian,it was the tip labels in Dendroscope. I understand how these work now, thank you!

I have to confess that I know nothing about phylogenetics and the associated software but according to the abstract of this article it seems that they used BEAST to map coalescence of co-evolving hosts and parasites.
Also this article is probably of highest interest to you as it compares the efficiency of different software to construct tanglegrams

That makes two of us! I shall try and use dendoscope again with that article in mind. Thank you!

You can try the R package dendextend. The function tanglegram can do the trick.  Several associated functions are also available for getting plots with minimum entanglements such as untangle_step_rotate_2side.

Jane 4 (software for cophylogeny reconcilation) has a tanglegram viewer with an interactive editor.  (https://www.cs.hmc.edu/~hadas/jane/)

I recommend mesquite, which I've used to create phylogeny trees with.
There are some intricacies with using it, but there is plenty of documentation on its webpage!
https://www.mesquiteproject.org/