text:
Do animals other than humans have different blood types?
Humans have the ABO and Rhesus blood typing systems. I have two questions about it:

Why have we evolved these blood types?
Do other animals have different blood types as well?

The answer to this question can be found by searching the Internet.

For some blood types, evolution and environmental selective pressures
  are clearly important for their persistence. For example, the Duffy
  blood type includes a receptor that allows certain types of malarial
  parasites to enter the red cell. Thus, in some malarial areas of
  Africa, populations with Duffy-negative blood types have a distinct
  survival advantage because absence of the Duffy antigen provides a
  measure of protection against malaria. The percentage of people
  lacking the Duffy antigen is much higher in these locations than in
  areas not endemic for malaria.

more here http://www.scientificamerican.com/article/why-do-people-have-differ/

Animals and bacteria have cell surface antigens referred to as a blood
  type. Antigens from the human ABO blood group system are also found in
  apes and old world monkeys, which have inherited the same system.
  Other animal blood sometimes agglutinates (to varying levels of
  intensity) with human blood group reagents, but the structure of the
  blood group antigens in animals is not always identical to those
  typically found in humans. The classification of most animal blood
  groups therefore uses different blood typing systems to those used for
  classification of human blood.

more here  http://en.wikipedia.org/wiki/Blood_type_%28non-human%29

So somebody really did write on Wikipedia that "…bacteria have cell surface antigens referred to as a blood type". But that's nonsense. I'll go and edit it now.

Blood group systems occur where there are multiple alleles of a gene which produces polymorphism in a surface component of the erythrocyte such that the different forms of the component display different antigenicities. This can cause haemolysis of transfused blood that has a different antigenicity to that of the erythrocytes of the recipient, whose immune system consequently regards it as foreign.
The major ABO blood group system of humans involves the gene for a glycosyltransferase which catalyses the addition of particular sugars to glycocoproteins or glycolipids. In addition to inactivation of the gene (giving blood group O in homozygotes) there are two forms of the active gene, encoding enzymes  transfering either N-acetyl galactosamine or galactose (1):

The ABO system is found in non-human primates, although with AO, BO and AB as variants in different species (2). Various other animals have polymorphism in this system — pigs, for example, are AO (3). Most animals possess the ABO gene (4), although it may or may not be expressed, and, if it is, may or may not give rise to polymorphism.
Blood group systems exist in other animals that involve different genes. The confusingly-named AB system of cats, for example, involves the gene for an acetylneuraminic acid hydroxylase, which catalyses the formation of the activated precursor for addition of N-glycolylneuraminic acid to cell-surface glycans (5).  This gene is inactive in humans (6).

Not all such blood group systems involve changes in the sugars of glycoproteins or glycolipids, but those involving mutations in proteins (e.g. in dogs (7)) tend to be less well characterized at a molecular level.
A common answer to the question “Why have we evolved these [ABO] blood types?” is that the ability to change the sugars on the erythrocyte membrane provides resistance to pathogenic organisms (parasites, bacteria and viruses). This could be because the pathogens bind the sugars to gain entry into the cells, or because they have similar sugars on their own cell surface and so do not provoke an immune response from the host. However the counter-argument of non-functional genetic drift (@CactusWoman) is difficult to exclude if one focuses solely on the ABO system.
The functional argument becomes more convincing if one considers that the ABO blood types are just one example of the ability of animals to vary the sugars on their cell by selecting from a large repertoire of genes with the potential to specify different glycosylating enzymes (8). This is shown by the fact that different animals exhibit different sugar antigens on the surface of their erythrocytes (whether or not they display polymorphism). There are over 100 genes for glycosylating enzymes, but one example of this diversity is instructive. The ABO gene has undergone duplication and, of perhaps seven members of this family (9), the products of three are well characterized (10,11,12), although their genes are either inactive in humans or not expressed in erythrocytes (i.e. in their precursors). Like the ABO gene product, the enzymes are α-1,3-glycosyltransferases, but differ in the acceptor carbohydrate:

I know this is coming late to the party, but I became interested in the topic from a molecular and genetic viewpoint following a more recent post that was marked as a duplicate. Happy to be told of typos or errors. I'll reference the piece shortly.

One of your references (https://www.pnas.org/doi/10.1073/pnas.1210603109) in points towards selection acting on multiallelic balanced polymorphism as an explanation to the existence of the ABO system in primates, what's your take on that hypothesis?

@Ponce — Six years since I posted, and it's not my area. I certainly am not competent to criticize the hypothesis. What you can do if you are interested is find papers that have quoted this one and see what those in the field think.

To answer your first question; it is not necessary that every trait have an evolutionary advantage. Neutral traits can persist in the population without having any adaptive value, or they can persist as a byproduct of another trait that does have adaptive value. Even a slightly detrimental trait can become fixed due to genetic drift. Take a look at this rather famous paper critiquing the "adaptionist programme" if you're interested.
That being said, I personally don't know for sure whether or not different blood groups have an adaptive advantage. Someone else can probably provide a better answer to this portion of your question.
However, to answer your second question: yes, yes they do. Indeed the Rhesus blood typing system was named after the rhesus monkey.


text:
If a person is infected with an RNA virus what percentage of the RNA in the blood of the person contains RNA of the virus?
Karius uses DNA sequencing of everything that's contained in a sample to detect all bacteria and DNA-viruses in the sample. Given the way that costs of sequencing are falling this approach seems to be the future of detecting bacteria based infections.
It would be great if the same approach would also work for RNA-based viruses. For it to work it would of course be necessary that there's enough RNA of the virus in comparison to the other RNA.
How much virus RNA is there in a person who's infected by an RNA virus in comparison to the other RNA?

You didn't get an answer to your specific question, though @de_novo answered a related one. It's not possible to give an answer to How much virus RNA is there in a person who's infected by an RNA virus because it's too general; RNA viruses are wildly diverse and include viruses that are highly localized and don't enter the blood at all, as well as some that are blood-borne and can reach fairly high concentrations. So the answer to your question would be cover at least a billion-fold range if not more, which isn't helpful.

I think your question is:

Can you diagnose someone with an RNA virus by looking for that RNA in their blood?

The use of nucleic acid tests, or NATs in diagnosis has been around for a long time. The specific for profit company you mention is not the first to use them. Almost all NATs work by first amplifying the genetic material with PCR or other methods, so there does not need to be a large proportion of pathogen RNA vs total RNA in a sample in order to use a NAT.
NATs, rather than culture or antigen/antibody based tests, provide the definitive diagnosis for many viruses, RNA viruses included. As the CDC describes, NATs (among other tests) are also used to screen donated blood for RNA viruses (HCV, HIV, and West Nile).
Incidentally, the for profit company you mentioned does NOT detect all bacteria and DNA-viruses in the sample as you said. It screens for a large number of specific pathogens in their

proprietary micro-organism reference database

If there's a new bacteria in the blood of patients then if enough of the bacteria is in blood samples that are given to Karius, Karius automatically gets the DNA of those bacteria through their process. Snippets of all DNA in the blood are picked up by their process even when the software analysis might not match all the snippets to organisms.
NAT's in the sense that Wikipedia describes the term you actually have to know what organism you are looking for to choose the right primer. More importantly it's price increases linearly if you are looking for more organisms.

@Christian you still have to know what you're looking for in the Karius test. It matches the non human DNA in a sample to its "proprietary micro-organism reference database." If it's not in the database, it doesn't get identified.

@Christian moreover, you don't have to have a large proportion of a nucleic acid for this same type of test to work. Karius's methods are a change in scale from standard of care, not type. If you read the studies from their group, they are not using a novel amplification or detection technique.

There test is based on next generation DNA sequencing. That's a technology that recently got a lot of cheaper. The Wikipedia page on NAT speaks about probe-target binding and not about next generation sequencing.

source: Stack Exchange

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

sort: votes


text:
Is the serum concentration of calcitriol different at different times in the day?
Given that calcitriol has a relatively short half-life in adults it would be possible that the serum concentration is at different times of the day different if it gets produced in different quantities at different times of the day.
Is this the case or is the level relatively constant over the day and doesn't follow a daily rhythm?

Calcitriol, or 1,25-dihydroxyvitamin D, is produced in the kidney by 25-hydroxyvitamin D-1α-hydroxylase from it's precursor, 25-hydroxyvitamin D.
Calcitriol has a plasma half life of about 6 hours. It is tightly regulated. This regulation involves a negative feedback loop on its own synthesis and via an inhibitory effect on PTH synthesis, and control by downstream effects (plasma phosphorus, calcium, FGF-23 and others).
25-OH-D, the precursor, has a plasma half life of about 2-3 weeks, and except in chronic deficiency or other pathologic states, is in plenty of supply for the appropriate production of calcitriol. Because of this, it is unlikely that, for example, daily changes in sun exposure or nutritional intake would propagate down to production of the active metabolite.

The image and a good review of Vitamin D can be found in this NEJM article
References ranges at my lab and in Lange's guide to diagnostic tests do not include any interpretation suggestions for plasma or serum 1, 25-dihydroxy vitamin D (calcitriol) at different times of day. Notably, though, this test is not often done clinically. It's primarily for the case where a patient has high calcium, low PTH, and no malignancy has been found.
Despite this (reference ranges do not distinguish between times of day), there may be a circadian rhythm within that range. Regulators and downstream effects of calcitriol do show a circadian rhythm, as is demonstrated in this classic 1972 study:

Is the tl;dr: We don't really know, both are plausible?

@Christian tl;dr: it isn't relevant for interpreting clinical values, but it is plausible (likely?) that there is some circadian variation.

@Christian I'd be surprised to not see some regular variation, along with those calcium, PTH, and phosphate levels.

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


text:
Difference between Fulminant and Acute Meningococcemias
Fulminant seems to mead rapid.
There is however some articles with both phrases: "fulminant meningococcecemia" (about 5000 Google matches) and "acute meningococcecemia" (about 3000 Google matches).
I am thinking Neisseria meningitidis and its pathogenesis

Portal entry nasopharynx (pili)-> attach epithelium cells -> bloodstream (bacteremia); upper respiratory tract infection -symptoms; may be asymptomatic in transient flora; fulminant meningocococcemia (regardless of meningitis)

What is the difference between the two diseases?

When we say "Fulminant meningococcemia" we mean failure of adrenal glands due to haemorrhage of infectious origin, or Waterhouse–Friderichsen syndrome
and acute is related to time of signs appearance, opposed to chronic disease.

Can we say that all fulminant diseases are acute? In this case, the fulminant disease seems to acute.

in medicine there are not 100%, so we only can say that most of fulminant infections are acute, but sometimes chronic bacteremia or chronic wounds can lead to fulminant deterioration in the host

This answer is incorrect. Fulminant does not refer specifically to adrenal hemorrhage. It's a general adjective describing the explosive course of a disease process.

Both fulminant and acute are adjectives that describe a disease course. The previous answer by @ilan is incorrect. Fulminant does not specifically refer to adrenal failure, despite the association between meningococcemia (which often has a fulminant course) and adrenal hemorrhage.
Fulminant relates to onset, speed of progression, and severity. A fulminant disease process is sudden, rapidly progressing and very severe. Diseases processes described as fulminant are often lethal if not immediately treated. Meningococcal bacteremia, classically described as purpura fulminans, is one example.
Acute relates mostly to onset. Here the earlier answer by @ilan is correct. Acute, as opposed to chronic, refers to a disease process with a short course, or a short term phase of a disease process with a longer course (as in an acute exacerbation of a chronic disease process).
All fulminant disease processes are acute, by definition. When referring to bacteremia with Neisseria meningitidis, the use of the descriptor acute or fulminant does not indicate a different disease. So I suppose the direct answer to this question is that there is no specific difference between fulminant and acute meningococcemia. They are not separate diseases, and both terms could correctly be used to refer to the same case.

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


text:
What parts of the visual system could be responsible for a fixed, monocular scotoma?
Light enters the cornea, crosses the lens, hits the retina. Electric sinal travels from retina through the optic nerve, reaches the chiasma, crosses and makes its way to the visual cortex.
My question is: given a fixed, absolute scotoma in one of the eyes, what parts of the vision could be at fault?
Initially, I believe the cornea/lens couldn't be, otherwise the scotoma wouldn't be absolute and fixed. Moreover, I suspect that, after the chiasma, signals from the same visual position are joined, so, the problem couldn't be after it, otherwise the scotoma would be binocular. As such, am I right to conclude that a fixed monocular scotoma could only be caused by issues on either the retina, or on the optic nerve?

Yes. You're right.
A scotoma only affecting one eye (i.e., one that is not perceived when one eye is closed) is diagnostic of a lesion upstream from the optic chiasm.
See Brust's Practice of Neural Science, Fig. 3-2. The figure demonstrates a full cut, with complete blindness in one eye, but the principle is the same for a scotoma.

Great answer! But could I ask just a quick confirmation? Notice this image. By the way it is drawn, we could conclude a small lesion on the highlighted area would cause a monocular loss of the right field of the right eye. That was the source of my confusion. Can I just assume this image is misleading in that sense, and that any lesion that far would result in binocular vision loss?

@MaiaVictor Yes, the image you link to in your comment is misleading. Any lesion at or downstream from the optic chiasm is going to present as a binocular loss. The optic radiations (from the LGN of the thalamus to the visual cortex) are not structured in such a way that a lesion would impact only one eye. This is one of the few absolutes: a monocular loss must be upstream from the chiasm.

Actually, I think this may be a counter-example to the answer, although seemingly extremely rare.

By the way, do you happen to be a doctor? If so, is it reasonable to ask here for a recommendation? It has been very hard to find competent doctors.

@MaiaVictor that is a fascinating article. Thank you for sharing. I appreciate the trust in asking me for a recommendation, but it wouldn't be appropriate on this site. Most doctors are quite good, but we all make mistakes every once in a while.

I agree. In the case you're willing to make a recommendation, please update your profile here with your professional contact info! Thank you very much again.


text:
Why is Cacao a stimulant?
As I write this I've just eaten a fair amount of cacao (not cocoa) powder and it's given me quite a buzz. I've googled the effects and the Internet seems to think it's somehow psychoactive although it's hard to find a reliable source for the details.
Some sites describe the ceremonial preparation of cacao but I'm wondering if someone here knows the actual science behind the effects of cacao.
Can you please help me understand the underlying processes better?

I'm voting to close this question as off-topic because it is not about biology as defined here.

@BryanKrause Seems on topic to me. Is there a known systematic mechanism explaining active compounds in Cacao? TLDR: yes, flavonoids.

@James OP is asking about how to prepare cacao to maximize those effects, not about the biology.

@BryanKrause Good point, I removed that from the question. Hopefully, that should stave off further close votes. OP feel free to roll back if that's your real question.

Cacao and products made from cacao contain a number of bioactive compounds. As far as the subjective sensation of a "buzz", there are three related alkaloids present in cacao that may account for this effect. Theobromine is present in the highest concentration, but is probably less potent of a stimulant. It's not well researched. Theophylline has a number of effects, and is well studied. It has CNS stimulant effects, with a similar mechanism of action to caffeine, as a competitive antagonist at adenosine receptors. Caffeine is also present in cacao. The stimulant effects of caffeine are known generally, but if you'd like to read more about the pharmacology this is a good review.

There are probably over a hundred compounds in cacao that might possibly have effects on humans. I don't want to speculate on the ones that are not known.  One that is known is theobromine.
I have seen a claim that cacao does not actually have caffeine, but I haven't checked it. Cacao might not have theophylline either. The link did not work for me.
no caffeine in cacao
Here is a picture of the structure of adenosine.
.
Here is a picture of the structure of theobromine.
.
Theobromine is kind of similar to a part of adenosine. Adenosine causes your heartbeat to slow etc. There are four known receptors for adenosine which cause different cells to do different things. It's complicated.
what adenosine does
So it's plausible that theobromine might interfere with adenosine attaching to those receptors, and might cause the result you'd get with less adenosine in your bloodstream.
Salsolinol is kind of similar to dopamine. It is created in the human brain and some gets excreted. It might possibly have some use itself and not be a waste product of something that matters. Here's one link from 2006 speculating about that.
salsolinol
The link I gave which appears to show serotonin up to 5% by weight is probably extremely misleading. Other sources have that in micrograms per gram. Serotonin in food is emetic -- you shit it out fast. Likely serotonin in cacao doesn't give you a lot of serotonin in your bloodstream. But it could be worth a better lit search.
serotonin effects


text:
How it happened that in cactuses the difference between the fruit, the leaf and the stem so much blurred if they were normal plants in the past?
Looking at a cactus may make impression that they evolved separately from other plants, which usually have stem, leaf and fruit.
But the fruit in cactuses has the same structure and surface as the leaf and stem, and grows from leaves. How this could come? Cacti are flowering plants, so should had evolved from normal plants.

cactus have stem leaves and fruit, the needles are modified leaves, the big flat green parts are the stem.

It makes sense if you think of it in terms of water conservation.  Cacti are adapted to environments where there's plentiful sunlight, so growth is limited by water.


text:
Are there life forms that freely fly in the atmosphere?
Are there (unicellular) Earth lifeforms that most of their life fly high in the atmosphere without contact with surface? For instance, in clouds, etc?
If so, at what max altitude have they been detected?

From @jakebeal's keyword "aeroplankton" you could go to https://scholar.google.ca/scholar?hl=en&as_sdt=0%2C5&q=aeroplankton+altitude

Are you only interested in unicellular examples, or do you mention that just as a suggestion?  If you’re interested in multicellular examples too, then common swifts (and some related species) seem to qualify.  They nest and roost at the surface during their brief breeding season, but barely if ever during the rest of the year: “Our data show that swifts are airborne for >99% of the time during their 10-month non-breeding period; some individuals never settled […]”— from https://doi.org/10.1016/j.cub.2016.09.014

@PLL but what do they drink and eat? They need to land.

@Anixx: Unless you’ve seen other research contradicting the paper I linked (which all sources I’ve found seem to agree with), it seems clear that they don’t need to land during the non-breeding months.  They feed on insects in flight; I don’t know whether they get their moisture requirements from their food, or clouds, or dipping into ponds/rivers while in flight (some birds do that, but I’ve not heard of swifts doing so), or something else.  EDIT: quick searching suggests they get moisture mostly from rain/clouds aloft, and sometimes from skimming surface water.

In response to answer the max altitude part of the question: https://www.space.com/microbes-fungi-space-station-identified.html although I couldn't say for certain that this is the maximum they have been detected.

@Frog this is irrelevant

@Anixx Consider fish, most of them are denser than the medium that they live in but many never "land" (while alive). Air is just an edge case.

@Anixx how so?  It seems entirely relevant.

It sounds like you are talking about aeroplankton, a general term for a wide range of tiny life-forms borne on the wind.
While some of these are essentially passive while airborne (e.g., pollen, spores), others like arthropods and microbes are quite capable of being active in the air as well. In essence, anything that can be easily swept up by the wind can be swept up as high as the wind will take it, often all the way to the jet-stream, and kept aloft for a potentially long time before being deposited elsewhere in the world.
For many of these species, this is a key part of their life cycle and dispersal strategy, and as such they are well adapted to survival at altitude.
The density of available resources at altitude, however, is extremely low, and thus, to the best of my knowledge, there has not yet been any species discovered that primarily lives high in the air, as opposed to merely transiting at altitude before landing elsewhere.

Pollen, spores, and their like do not "fly" and being "swept up by the wind" isn't like "flying…" particularly not "freely…"
How could "flying" - even "gliding" - not involve wings and how could "wings" not rule out anything "unicellular"?

@RobbieGoodwin: The OP explicitly suggested “unicellular” in the question, so they clearly meant “fly” in a very general sense.

@PLL That's a big leap of faith and if you have that strong a belief in your powers of assumption, leap away!

Apparently yes. Caveat: the experimenters are are potentially biased because they believe in panspermia (the idea that life came to Earth from outer space), which is clearly fringe. However, I don't think that invalidates the detection of the three new species, only the interpretation.

(PhysOrg.com) -- Three new species of bacteria, which are not found on Earth and which are highly resistant to ultra-violet radiation, have been discovered in the upper stratosphere by Indian scientists ... In all, 12 bacterial and six fungal colonies were detected, nine of which, based on 16S RNA gene sequence, showed greater than 98% similarity with reported known species on earth. Three bacterial colonies, namely, PVAS-1, B3 W22 and B8 W22 were, however, totally new species. All the three newly identified species had significantly higher UV resistance compared to their nearest phylogenetic neighbours.

The samples were collected at 20km to 41km altitude.
The article doesn't say if the bacteria land. Most probably, we don't know.

Is panspermia "clearly fringe"? I am not an astrobiologist, but my (admittedly limited) understanding is that it is a perfectly valid, if unproven, hypothesis that is taken seriously as a possibility in the field. I see 103 results for "panspermia" in the International Journal of Astrobiology, a perfectly respectable peer reviewed journal published by the Cambridge University Press.

@terdon as far as I know, it's fringe compared to abiogenesis. Some of the scientists involved (Chandra Wickramasinghe & Jayant Narlikar) also have a rather spotty reputation, being behind theories such as the quasi-steady state cosmology and the COVID-came-from-space hypothesis which are also fringe.


text:
Were any brain fusion experiments ever conducted?
Did anybody ever conduct experiments on fusing living brains?

You mean this? http://www.huffingtonpost.co.uk/2013/02/28/inter-continental-mind-meld-rats_n_2781469.html

@dd3 no. this seems not to be fusion, but rather a crude transmission of some signals. I am interested in attempts to grow the brains together.

The odds of that are really very slim. "Growing brains" in vitro is rather difficult, and it appears that no one has created the brain of a real organism, but they have created "brains" from cultured dissociated neurons.
Fusing brains is complicated by the fact that you need to make the appropriate synaptic connections between neurons, and what exactly are the appropriate connections is still being worked out.  As a side note, this is one of the goals of the BRAIN Initiative.
The closest I believe people have come to anything approaching fusion are brain transplants in non-human animals.  This might be the closest thing to an in vivo fusion, especially if it is only a partial brain transplant.  This is discussed a bit here.

I did not find anything about brain fusion following your link to the brain initiative...

No, the point is they are working out the behavioral circuits in the brain. Any sort of fusion is dependent on making the right connections. We don't know what most of them are, so that makes it hard to make successful fusions.

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


text:
Why do we yawn?
I've read a new study which suggests that yawning may help you keep a cool head. Also, the findings might hold some hope for sufferers of insomnia, migraines, and even epilepsy.
Is there any conclusion about what the function of yawning is and why do we yawn?

In an abstract, Brainerd at al. (2004) report the presence of yawn-like behaviors in "cartilaginous and ray-finned fishes, a lungfish, salamanders, caecilians, mammals, turtles, lizards, an alligator and birds".
So clearly the motor patterns necessary for this behavior evolved before air breathing and apparently have been conserved for ~400 million years. They reject the increased oxygen delivery hypothesis and associate yawning with stretching:

Yawning also has been thought to serve a similar physiological
  function to stretching. We measured the stretching movements of fins
  and limbs in association with yawns, and found that they follow the
  same movement pattern as jaw opening and closing. This lends support
  to the existing hypothesis that yawning and stretching serve a similar
  function, but the detailed nature of this function remains unclear.

I know it's only an anecdote, but as a kid I thought it would be a good idea to learn to yawn while keeping my lips together. (No need to put my hand in front of my face! Yay!)
Today I get a cramp every time I open my mouth too far. Great for eating burgers, visiting the dentist and yes, yawning. (May contain sarcasm.)


text:
How to find Exons in mRNA Computationally
I'm having trouble finding a method to find exons in the original DNA sequence used to create the mRNA, even given the sequence of the mRNA, as I cannot find a way to reliably identify the beginning and end of introns and exons. Is there an algorithm or method that I can use to do this? What information am I missing to be able to find the beginning and end of exons and introns?
Thanks in advance for answers.

The only information you are missing is a way to identify the splice sites. There are many ways of doing what you need. The simplest, assuming you are sure of the origins of the mRNA, is to use a BLAST flavor, either plain BLASTn or, even better, BLAT, to compare your mRNA sequence to the genome of interest. BLAT really should be all you need if the mRNA comes from the genome you are aligning it to.
BLAT however, has no knowledge of splice sites and will simply cut your mRNA so as to maximize local alignment scores. If you need something more sophisticated than BLAT, use a specialized aligner as @SteveLianoglou suggested. These programs include a model of splice sites (both canonical and non) and will align exons correctly. My personal favorite is exonerate.
Assuming you are using Linux (which you should be if you are planning on doing a lot of this type of analyses), you can install it on a Debian based distribution (such as Ubuntu and its variants) with this command:
sudo apt-get install exonerate

Then, to align the mRNA to its gene do:
exonerate -m est2genome -n 1 mrna.txt dna.txt > out.txt

-m is the model that exonerate will use to align your two sequences. Since the important thing in your case is to correctly model splice sites, you should use either est2genome or, if you are comparing different species, coding2genome, or if you have a full length cDNA including UTRs, cdna2genome.
-n 1 means find the best match only. Assuming you are aligning an mRNA to its coding gene, this is all you are interested in.

I realise that this is not a very biological answer. I did mention splice sites though, four times!

You should ask this question over at biostars.org -- and could use a bit more clarity.
Do you actually have RNA-seq data that you want to use to find the exon/splicing structure of an mRNA?
First step would be to use a splicing-aware aligner. A few free ones are:

STAR
TopHat
GSNAP

Let us know why that wouldn't do what you want when you re-ask this question over at biostar.


text:
How the lungs clear themselves?
Looking at my computer's fan I can say that a lot of dust is collected on it not less dust should be collected in the lungs, not to mention some inhaled parts of food.
How the lungs clear themselves from dust, smoke, food particles?

nuhcole is mostly correct.
Airborne particles first pass through the nasal passageways and/or mouth and throat and many are caught, but those that enter the lungs become trapped in mucus.
Your cilia act like a constant escalator, bringing up that mucus from your lungs 24/7.  You reflexively swallow it without even realizing it.  That is why when you are healthy, you might not even notice.
If you are sick (or asthma/allergies), more mucus is produced.  That is when you may notice the increased quantity coming up, and may need to cough to bring more up.
If your cilia are damaged (like in smokers), then mucus does not clear well from the lungs. In this case, people must cough more in order to bring it up.

Our respiratory tract is lined with cilia, which are hair-like structure that extend from the outside of the cells. They wave back and forth and act like brushes to catch dust particles before they enter the lungs.
Some particles do get past these cilia and enter the lungs, however. The lungs will secrete mucus that collects the dust. You then cough up the mucus to get rid of the dust particles.
The mucus your lungs excrete also help against pathogens you inhale. Bacteria and viruses are also collected in the mucus, and then removed via coughing. This is why you may cough up phlegm when you're sick.

I do not cough when I am not ill.

@Anixx of course you do, try going into a dusty room and breathing deeply, you will sneeze or cough.


text:
Does difference in expected life duration between men and women have biological nature?
It is known that men in most countries live less than women. I wonder whether it is due to different life conditions or because male and female organisms differ?
For example, I heard that testosterone may cause cardiovascular deceases. Is it true? Are there other biological mechanisms that can shorten men's lifespan?

There are several explanations. Probably these are all true to some degree and thus combine to give the general longer life expectancy of females.
Most of these statistics are from Annex 2 of the WHO Health Report 2004 (found through Wikipedia)

Males are more likely to get lung cancer, liver damage and other drug-related illnesses (implied would be that males are more often alcohol/tobacco/drug users).
Males also die more often as a result of work-related injury, especially as soldiers
Males are usually larger. There seems to be a small inverse correlation between size and life expectancy
Mitochondrial DNA is passes from mother to child. As such, mutations harmful for men are less effected by natural selection.
Men have one X chromosome, while women have 2. The y chromosome is very small and contains almost no genes. Thus if there is a genetic defect on the X chromosome the female might have a healthy X chromosome to compensate while the male does not have one. Among others this makes males more likely to have hemophilia or color blindness.

Does it mean that hormones do not affect the lifespan?


text:
Do violet potatoes contain more or less solanine than normal potatoes?
What is the solanine content of the violet potatoes? Is it more or less than in the normal potatoes?

What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

@theforestecologist I have googled the Internet for violet/black potato solanine

and what did you find? What websites did you look at? Have you tried Google Scholar?

Seems to be about the same.
In Effect of Genotype and Environment on the Glycoalkaloid Content of Rare, Heritage, and Commercial Potato Varieties, Tables 1 and 2 list 60 different potato varieties showing glycoalkaloid concentration (solanine and chaconine are shown separately); Table 1 indicates the skin color, and Table 2 indicates the flesh color.  "Violet" is not an option, but "Blue" is, and there doesn't seem to be any particular correlation between skin or flesh color and glycoalkaloid concentration. (The potato with the highest concentration of glycoalkaloid in the flesh was a blue one, but other blue varieties were fairly low; the variety with the highest in the skin was "yellow".)


text:
Do all mushrooms have the same multicellular ancestor?
Do all mushrooms have the same multicellular ancestor? Did that ancestor feature common mushroom elements such as cap, stem, sporofore, vulva, bulb, etc.

All fungal species within the kingdom have the same common ancestor, which is unicellular (thought to be protistan). This common ancestor is the point at which it is thought that animals diverged, as suggested by this article.
In their words:

It is now well established that animals share a common single-celled ancestor with fungi, and that in the two sister lineages multicellularity arose independently

A fungal phylogenetic tree is shown below, which originated from this paper.
Note: all colored areas represent different phyla of fungi.

EDIT:
I will respond to a few questions addressed in the comments.

Is there a unique multicellular ancestor to all mushrooms?

I am rather sure (but can't explicitly confirm with a reference) that multicellularity in fungi only evolved once. If this were true, I would also hypothesize that mushroom-like characteristics also evolved only once, thus indicating that there is a multicellular ancestor to all mushrooms.

Are there multicellular fungi outside dikarya?

No. One branch of dikarya seems to consist of only unicellular organisms, suggesting that multicellularity evolved at some point within organism under only one dikaryan branch.

Was the common ancestor of Dykarya multicellular?

No. See previous answer.

Are those unicellular dykaria secondary unicellular or not? Given that the both branches of dykaria show similarities in fruiting bodies, it seems to be plausible that the common ancestors of dykaria had a similar structure.

I am not exactly aware of the similarities in fruiting bodies in both branches, but if the physiology behind fruiting bodies are similar, it is very likely because the dikaryan common ancestor had a similar mechanism.

Is there a unique multicellular ancestor to all mushrooms? Are there milticellular fungi outside dikarya? Was the common ancestor of Dykarya multicellular?

By mushroom, do you mean fungi in general, or specifically those having a stem, bulb, etc? PS. Not all Dikarya are multicellular: some are unicellular. http://en.wikipedia.org/wiki/Dikarya.

And as far as I know, there are no multicellular fungi outside of Dikarya, but I cannot confirm that statement.

Are those unicellular dykaria secondary unicellular or not? Given that the both branches of dykaria show similarities in fruiting bodies, it seems to be plausible that the common ancestors of dykaria had a similar structure.

Please see the edited question which adresses most of your questions.

Your new version is contradictory: you say that the common ancestor of Dykaria was unicellular yet you believe that multicellularity evolved only once. An image of fruiting body of a fungus belonging to ascomycota (sac fungi): http://upload.wikimedia.org/wikipedia/commons/8/82/Morchella_conica_1_beentree.jpg A fruiting body of a mushroom belonging to basidiomycota http://salavat.spb.users.photofile.ru/photo/salavat.spb/200388730/xlarge/208364390.jpg You still believe that the last common ancestor of these mashrooms was unicellular?


text:
Confusion related to gene expression
I have a set of gene expression data downloaded from http://www.ncbi.nlm.nih.gov/geo. I have two sets of data, one is the raw probe intensity data set in the form of CEL files. Another is processed txt file.
Here is a link for example
http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7904
I don't know what kind of processing is done to generate the processed data from the raw CEL files. For example in the above link, I have processed data like
SOFT formatted family file(s)
MINiML formatted family file(s)
Series Matrix File(s)
I don't know what sort of processing is done to generate those files. Any suggestions? I can read the raw CEL files in matlab but what sort of preprocessing am I supposed to do?
I also want to map these probe its to gene ids and get the corresponding gene. How can I accomplish this? I know matlab. But I am bit confused about the terminology and all. Any suggestions?

this website converts affy id's to various gene id codes if this is the sort of thing you are after

@rg255. I didn't get how the processed data is generated. As you can see here http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7904 there are two data sets. One is raw CEL files and the other is Series Matrix File(s). How is this processed data generated. Also if I look at the number of rows. In the case of Cel files, the number of probes is huge 1354896. But when I look at the series matrix data it is around 50000. I didn't get it. Any suggestions?

@rg255. Also I didn't get the link you said this website. I didn't find the link attached

oops, http://david.abcc.ncifcrf.gov/conversion.jsp - as for the rest of your question I wouldn't like to answer as I am not an expert

If you click through to some of the samples in the study, eg. GSM194397, GSM194398, etc. it mentions under the "Data processing" section that "The data were analyzed with dchip with default normalization settings".
You can learn more about dChip over at the dChip website.

Thanks I will try that. However it looks like I will need some CDF files as well. Where can I get them? In particular I need the CDF files for chip type HG-U133_Plus_2 and HG-U133A. Any suggestions? I looked a couple of places but looks like I have to pay for it. It was supposed to be free I guess

I suggest you use the limma package in bioconductor to analyze the data. I'm not sure why one study has data from two chips -- it's unfortunate. You'd first have to study each batch separately, then do some meta-analysis to combine the results from each together. If you're not comfortable programming, you might try Gene Pattern, though I've never used it. Lastly: you should likely post bioinformatics related questions over on biostar.

I need to get the gene id for the corresponding probe it. For that I need the CDF file. So I was actually wondering where I can get them?

There are other ways to convert id's to genes. I'd be surprised if you can't query BioMart to get that answer (look in the ID Converter tab). It also looks like the DAVID website has a conversion tool that may get you what you need.

The methods used for the processign of the date should be mentioned in the Methods section of the paper the data come from (here it is Richardson AL, Wang ZC, De Nicolo A, Lu X et al. X chromosomal abnormalities in basal-like human breast cancer. Cancer Cell 2006 Feb;9(2):121-32. PMID: 16473279). I quote from the paper:
"RNA extraction, cRNA synthesis, and hybridization to Affymetrix Human Genome U133 Plus 2.0 Arrays were performed as described previously (Signoretti et al., 2002 and Wang et al., 2004). Raw expression data obtained using Affymetrix GENECHIP software was normalized and analyzed using DNA-Chip Analyzer (dChip) custom software (W.H. Wong and C. Li, http://www.dChip.org/). Array probe data were normalized to the mean expression level of each probe across a sample set. Where indicated, tumors were classified as BLC or non-BLC on the basis of their expression array characteristics, using dChip hierarchical clustering analysis as previously described (Matros et al., 2005 and Wang et al., 2004). Comparisons between results obtained on BLC or BRCA1 tumors, non-BLC tumors, and normal breast samples were performed using the dChip “Compare Sample” function. A threshold of 1.2-fold overexpression in BLC and BRCA1 tumors was applied with 90% confidence. Of 1271 gene probes that map to the X chromosome, 60 satisfied these overexpression criteria with a range of fold difference from 1.35 to 5.11. The false discovery rate (number) of 1000 permutations was as follows: median, 0% (0); 90th percentile, 3.3% (2). Of the 60 probes, 19 were redundant (two or more probes mapping to the same gene) and excluded, leaving 41 gene-specific probes for use in the expression plot of Figure 5B. The complete gene expression array data set is available on the NCBI GEO database (accession no. GSE3744)."
Since this is a standard Affymetrix human genome chip, it's CDF should either be embedded in most packages used to analyse this kind of data (limma is an industry gold standard example ;-), or downloaded from the Afymetrix website. Please note that the CDF itself may be quite old and it's annotation not always accurate any more (I have no experience with human data), so it's worth using an updated CDF (see Dai et al 2005).


text:
Confusion related to the use of PCA to determine the background network
I was reading this paper related to use of gene expressions for predicting the drug response. I have this confusion, the paper has used PCA on the covariance matrix formed by the genes to get what is called the background network as they say.
I don't know the essence of background in this case. I know PCA gives us components which preserves the greatest variance and used for dimension reduction. What they mean by background network. Is it pathways ?

For reference, previous question regarding this paper: http://biology.stackexchange.com/questions/7800/confusion-related-to-a-term-probe-by-background-interaction

Could you include a bit more information on the paper so we can understand more easily?

Perhaps, the background is the set of genes which are not represented by the first few principal components

I am by far not an expert, but I read the paper and maybe I can help clarifing things a bit.
Let's start with the simplest answer to your question:
In the last paragraph of the Introduction paper the authors say

"Throughout this manuscript [...]'background networks' and principle components are used interchangeably." ([1] Torkamani and Schork, Genetic background and drug response, The Pharmacogenomics Journal (2012) 12, 446-452; doi:10.1038/tpj.2011.35)

So they did not "use" PCA to get the background networks, they just call the PCs background models to indicate how they interpret it: As stated earlier in the introduction

"...interacting networks cannot be expected to correlate strongly with drug response, as their influence may only be observed when the major determinant of drug response and the interacting network complement one another or are both at a synergistic state. A major problem with identifying these interaction partners [...] is the extremely large number of possible partners [...] and [...] that individual genes are unlikely to accurately represent the overall state of a biological network." [1]

As far as I understand the article, they suggest PCA as a kind of compromise: Ignoring interactions would miss associations of all networks lacking a single gene representing the network's state accurate enough. Including all interactions is infeasable due to the huge number of gene-pairs. By PCA, the number of interactions can be decreased by orders of magnitude while keeping a maximum on information (as in variation): Instead of using the interaction (as in product) of all probes with all probes, they only consider those of all probes with the first six PCs.
I think, in this context 'background' is not used in the meaning of 'background noise' but of 'cultural background' - instead of assesing individual interactions, genes are assigned a 'background'. Since this corresponds to a) the biological network(s) they belong to and b) the principle components(s) they contribute to, those two ideas are used synonymously by calling PCs 'background networks'.


text:
RNeasy Mini Kit low 260/230 ratio -- can I purify this RNA for further use?
I used Qiagen's RNeasy Mini Kit to isolate RNA from 5*10^5 C28/I2 (immortalized human chondrocytes). However, my yield is low (~25 ng/ul), but my 260/280 ratio is great (~2.3), and my 260/230 ratio is tragic (~0.06). I have already thrown the spin column away, but I would like to know 1) if I could raise my 260/230 ratio for the 40 ul of RNA I extracted, and 2) if I could precipitate the RNA out of solution so as to make a more concentrated solution.
Please let me know if further details are necessary.
Thanks!

You can easily precipitate the RNA using either Ethanol or Isopropanol. I would do a Phenol-Chloroform extraction before that, too. But does this make sense? When you are working with a cell line, I would rather make a fresh prep than wasting time and money into saving the poor quality RNA.

These cells grow really slowly and I have some simple PCR that I need to run within the next couple days, so I'd ideally like to spare it. I've just never had these issues before. How do I precipitate the RNA using ethanol?

did you modify the amount of RLT buffer in the Qiagen RNAeasy mini kit? If yes, how much did you use?

RNAeasy kit will not usually give phenolic contamination. Your poor 260/230 is perhaps because of low yield; check the absolute absorbance values. Low 260/230 (and low yield) also happens because of improper lysis. I would advise that you do the cell lysis using more effective methods. I would not advise another phenol-chloroform or alcohol precipitation step- you will lose your RNA. With what you have now, run a little bit on the gel to see the integrity. Also try heating the dissolved RNA at 65-70deg for 10-15min and measure OD again (use nanodrop or a similar device)

The low 260/230 ratio is indicative of guanidine contamination I believe. The RNeasy "RLT buffer" contains guanidine to my knowledge.

It does. but column based purification generally doesn't leave these contaminants..

How did you lyse them? WYSIWYG is probably onto something here.


text:
How does a TOPflash/FOPflash assay work to detect beta-catenin protein expression?
I am reading an article (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596711/) wherein a TOPflash/FOPflash assay is used to detect beta-catenin protein levels in a COS-7 cell line. I can't find a good explanation in the article, or in any other article, as to how this assay works. I understand the cells are transfected with TOPflash/FOPflash reporter plasmids, but that's about it. Any insight or redirection would be much appreciated.

From what I can understand, TOPflash is a luciferase reporter plasmid that contains two sets of 3 copies of the wild-type TCF binding regions. If the canonical Wnt signaling is activated, beta-catenin will translocate to the nucleus to associate with TCF/LEF transcription factors to activate transcription of Wnt target genes. Since this is a luciferase plasmid, you should see an increase in relative luciferase activity when substrate is added. If Wnt signaling is inhibited, you will see loss of luciferase expression. The FOPflash is used as a negative control because the TCF binding regions upstream of the luciferase gene is mutated so even if beta-catenin translocates to the nucleus to activate TCF-mediated transcription, you should not see any luciferase activity.
Hope this helps.

Would you please provide a reference or two that supports your otherwise good answer. Good references helps to improve the overall quality of Biology.SE. :)


text:
What metabolic activities are performed by a developing human fetus's liver?
I understand that organ function varies with the stages of development. Does a fetal liver EVER perform lipogenesis, gluconeogenesis, make bile, etc? Or does it only begin performing these actions postnatally?
I have heard that a fetus delivered between 24-26 weeks can potentially be "okay" with proper care and monitoring in a hospital. I would assume (please correct me if I'm wrong) that this implies the fetus's liver has developed at this time. So in the case of a fetus that was not delivered at 24-26 weeks, does it spend the remainder of the pregnancy in a fully functioning state? Or at least, which functions does it begin to perform?
I've been trying to find an answer on Google, but one walks a fine line when searching for human development information -- either the results are oversimplified "expecting mothers" websites, or journal articles speculating about the effect of X on the development of Y in the mouse/chick/zebrafish/giraffe/et cetera other nonhuman model.

It's old and I can't get access to this issue of the Annals of the New York Academy of Science, but it looks like it has some relevant information. Sifting through the abstracts it seems the vasculature of the fetal liver is completed at around 8 weeks although is still different to the adult vasculature because of the umbilical vein. The growth of the organ itself goes through different stages with each lobe growing different amounts:

They start the same size
12 weeks the left lobe is twice as large as the right
36 weeks the left is 10% larger than the right
at birth they are the same size
5days after birth the right is 10% larger
adults, they are the same size

And, studies have been conducted with dyes to look at liver function in both its capacity to concentrate the dyes and secrete it into the bile. The fetal liver can carry out bile acid synthesis, despite lacking digestive purposes, from very early on (Suchy et al. 1987). The fetus does however require help in removing the toxic cholephilic organic anions (COAs), which is done via the placenta. This review describes more.
There is also evidence to suggest the newborn's liver is not performing all the usual metabolic processes of children or adults (from looking at drug toxicity and delays in excretion/detoxification), as would be expected. More recent literature notes the fetal liver lobes (right and left) as having differnt biochemical capacities and independent function due to the right one getting less oxygen. Also, a layer of drug metabolising enzymes normally present in adults is missing in the fetal liver, although its capacity for drug metabolism is still better than that of rodents.

In the adult liver, there is a clear zonation of metabolism of carbohydrates, proteins, lipids, and bile salts. In the livers of fetal rats, mice, and humans, this heterogeneous distribution of enzymes and metabolic function does not exist initially. Towards the end of gestation, the adult pattern of heterogeneity for these processes begins to emerge, and after birth, the adult pattern is rapidly established (Ring et al. 1999)

There is in vitro evidence for the activity of glutathione S-transferase and sulfotransferases in the human fetal liver. Returning to the asymmetry of fetal liver function (albeit in sheep..) it was found that levels of malondialdehyde, an index of lipid peroxidation, oxygen consumption, and CYP levels (a family of oxidative enzymes), are higher in the left lobe than the right lobe of the fetal liver which evens out after birth.
So in conclusion, looks like a variety of metabolic enzymes are present in the human fetal liver from very early on after the organ is formed. We know a varitey of metabolic enzymes are present and the drug/dye metabolism studies show there is some fetal liver activity, albeit reduced from that of an adult or child. The limitation with many of the studies that have been done is that they have to use in vitro data and extrapolate to the in vivo situation, so I guess we still don't really know for sure how metabolically active it is. It is clear though that it remains inefficient and unable to carry out all the functions required of it during childhood/adulthood until after further development after birth when it has stopped growing and adapted to ex utero conditions.
References
Ring JA, Ghabrial H, Ching MS, Smallwood RA, Morgan DJ. Fetal hepatic drug elimination. Pharmacol Ther. 1999 Dec;84(3):429-45.
Suchy FJ, Bucuvalas JC, Novak DA. Determinants of bile formation during development: Ontogeny of hepatic bile acid metabolism and transport. Semin Liver Dis 1987; 7(2): 77-84

I found that a search through Google Books was helpful...
While without the excretion of feces, it might seem as if the liver would not be active, but the liver tissue is not only active in development and tissue generation but serves direct physiological function as well.
After initial phases of development, the liver produces fetal red blood cells which is normally a function carried out by specialized bone marrow hematopoietic cells.
Over the course of fetal development the liver develops its typical functions.  It breaks down old red blood cells and stores their iron, and pushes the waste bilins and other waste products to the umbilical cord to keep the fetus clean.  The liver also synthesizes and stores fats.

Thanks for the Google Books link ("develops its typical functions"). I was most curious about whether the fetal liver functions in response to nutrients obtained through the placenta, but this is the most informative source I've seen so far. Thank you!

The key thing to remember is that the liver cleans out the blood - esp chemical toxins and cells that are past their prime - that function can't be performed by the mother as the blood of the fetus does not mix with the mother's directly.


text:
Heterocyst function in cyanobacteria and its localization
1.What is the function of heterocyst?
2.Where it is present?
A heterocyst I think may be a protecting organ in cells!

Welcome at Biology SE! If this is meant to be a homework question, then please share your effort on the subject. If you need help please take the short tour, or read the guidelines at our help center. If you can please elaborate and put your question into context. Have a nice day!

They help in nitrogen fixing . Ex nostoc of and anabaena

According to wikipedia :

Heterocysts are specialized, pale-yellow,thick-walled cells with disputed function nitrogen-fixing formed during nitrogen starvation by some filamentous cyanobacteria, such as Nostoc punctiforme...

Thus by definition these are not within the cells, but differentiated cells themselves.
This is a good paper that can give you details on nitrogen fixation in the cyanobacterium Anabaena variabilis.
In general: cyanobacteria are photosynthetic prokaryotes, and many of them are capable of fixing nitrogen (that is the ability to use and incorporate nitrogen from the air as N2 gas). The enzyme called nitrogenase is oxygen sensitive thus either temporal or spatial separation of nitrogen fixing must be done to avoid damage to the enzmye from oxygen produced by photosynthesis.

In Anabaena spp., aerobic nitrogen fixation is confined to differentiated cells called heterocysts that form in a semiregular pattern in a filament in response to nitrogen starvation. Fixed nitrogen in the heterocysts is transported to vegetative cells in the filament, while vegetative cells supply carbon and reductant to heterocysts

So as you can see spearate cells work together to supply each other with necessary nutrients. It is important to note that when sufficient fixed nitrogen source is available the number of such specialized formations is low due there is no need for extra nitrogen to be fixed
There are plenty of details on heterocysts and nitrogen fixation in the linked article. Also this paper hold details of regulation of nitrogen fixation and also has a thorough image of the process:

Though perhaps not relevant to the question, and certainly not true about any cyanobacteria that I know of, but just because something is a "cell" or single celled organism, does not mean it can't be contained within other cells.  Mycoplasma, for example, do it all the time.  Admittedly it doesn't normally end well for one group of cells, but it happens. +1

First of all the short and sweet definition of heterocyst are the specialized cells with homogeneous protoplast. Both the ends have thickenings called polar nodules.  Polar nodules are provided with minute pores.  Heterocyst help to fix the atmospheric nitrogen compounds.
In some species of Nostoc like N.commune heterocysts function as resting pores. The protoplasm of the heterocysts become functional and germinate to form a new filament.

Hi Christina. Welcome to [biology.se]. Can you add some references to your answer. You can have a look at the other answer. In general, if you post an answer make sure that you are not exactly repeating the stuff already said in the other answers. You can of course provide a better answer than the previous ones by adding additional supportive references. That is not the case here.


text:
What causes muscle spasms?
What causes muscle spasms with muscles that are not in the heart  ? Could it be some sort of stimulus overload that causes a massive contraction?

According to wikipedia and MedlinePlus muscle cramps can be caused by muscle overuse or injury or dehydration and lack of minerals (eg. potassium or calcium). In this wikipedia page you can read about the mechanism of muscle contraction. I'd emphasize and quote the most important parts here:

ATP binds to myosin, allowing it to release actin and be in the weak binding state (a lack of ATP makes this step impossible, resulting in the rigor state characteristic of rigor mortis). The myosin then hydrolyzes the ATP and uses the energy to move into the "cocked back" conformation. In general, evidence (predicted and in vivo) indicates that each skeletal muscle myosin head moves 10–12 nm each power stroke, however there is also evidence (in vitro) of variations (smaller and larger) that appear specific to the myosin isoform.
  Steps 9 and 10 repeat as long as ATP is available and calcium is freely bound within the thin filaments.

As you can see ATP is essential in the release of myosin from actin. In case of muscle overuse and dehydration ATP is depleted from the muscle cells and may cause the muscle to cramp.
Also according to this site it is said that repetitive firing of motor units with high frequency is associated with muscle cramps, although tehe origin of this is yet not clear. It can be either from the central nervous system or the peripherial.

Can the repetitive firing of any group of muscle tissues be 'dampened' by the local addition of certain biochemicals like endorphins ( if that's an appropriate molecule for 'dampening' ). Or maybe having certain receptors related to 'firing cells' blocked somehow.

To be honest, I do not know by heart, but I think you should post this as new question, to attract other people, and hopefully get an answer.

There was a story recently in the CTV news from Toronto ,Canada ; about a woman in great pain who had an electronic device implanted on her spine. This device sent signals to her brain area 'responsible' for the pain signals. Now she feels no pain. They said it was an underused technology. Maybe a similar device could send signals to the brain areas to do with the heart. Maybe if a chaotic spasm in the heart muscle was imminent signals 'could' be sent to the heart system through this 'device' to 'overwhelm' any chaotic signals and 'normalize' the heart rhythm.


text:
Are all protein composed of all the amino acid (in animal) or are there less diverse protein?
I have a question about amino acid composition of proteins: Are there proteins in animals that are made up only from a small subset of amino acids? So instead of all 20 amino acids let's say only 6-14 ( or any arbitrarily small subset) amino acids are used in a particular protein. Could you give me an example (or maybe a few examples) of such protein(s).

Welcome to Biology SE! I took the liberty to reformulate the body of your question. You can revert to your original version at any time if you wish.

This may interest you: http://www.nature.com/srep/2013/131010/srep02919/full/srep02919.html

Trp-Cage is a protein found in Gila monsters, and it is only 20 amino acids long and there are plenty of repeated amino acids so this does not use all 20. But there must be plenty of other examples, there is no reason why physically a protein must use all available amino acids.


text:
Why don't all bacteria have F-plasmids by now?
Some bacteria can undergo gene transfer by conjugation. Conjugation is a form of horizontal gene transfer, meaning from one (unrelated) bacterium to another (in contrast to vertical gene transfer, which is from predecessor bacterial cell to successor (daughter) cells). Conjugation is initiated when one bacterium has an F-plasmid (Fertility plasmid) and forms an F-pilus, connecting the F+ bacterium with an F- bacterium, initiating transfer of the F-plasmid.
Why is it that during evolution not all bacteria have acquired this F-plasmid?

Conjugation occurs between cells of the same species too. For this to occur cell have to be close to each other. Now, if you have an isolated population of bacteria that never gets in contact with an F+ bacteria then this population would stay F-. Also not all conjugation events are successful, mechanical perturbations can disrupt the pilus through which genetic material is transferred.
This old article can give you good details:
THE ORIGIN OF BACTERIAL SPECIES - GENETIC RECOMBINATION AND FACTORS LIMITING
IT BETWEEN BACTERIAL POPULATIONS ARNOLD by W.RAVIN

F+ shares, however, an important property of bacteriophage: after infection
  it behaves as though it were an addition to the bacterial genome. As an addition, it can furthermore exist in one of two forms: in one form, it
  is an unintegrated part of the bacterial genome, and may be  replicated either more or less rapidly than the "chromosomal" or linked genes (being
  infectious or lost through dilution, respectively); in its other form, it
  is integrated in the sense that its replication is coordinated with the
  replication of the host's genes, as though attached to them. In this latter form, found in Hfr bacteria, the F+ factor is incapable of infecting other bacteria (while permitting conjugation with them) and also prevents
  superinfection of its host bacterium by a nonintegrated F+ factor.

Taken from the linked paper. So you can see that are situations where conjugation occurs yet the F- won't become F+.
Also :

What is particularly interesting about the F+ factor is the fact that there
  seem to be a number of different  kinds. An F+ factor making a bacterium
  fertile with some  F- cultures does not necessarily  make it capable  of conjugating with others (49).

So not every F+ cell can conjugate with another F- cell.

Thank you for your answer. Also I was wondering if there are mechanisms that limit the amount of times conjugation and F-plasmid transfer can happen. E.g. "a bacterium can only transfer his plasmid once during his lifetime".

To be honest I've never thought about that question, might worth asking it.

Alright, will do. Do I just create a new question for this? (I am new to this site :-))

Yes, that is the right way.


text:
Change solvent of bacterial solution
I have to perform an RNA extraction that should start with 900 uL of 2%SDS bacterial solution. The problem is that the sample is in 900 uL of PBS.
I thought about centrifugation of the sample at 5ºC, remove PBS and then add the 2%SDS.
DO you think bacterial RNA quantities will vary?
Thanks!

PBS is isotonic to most cells, so in this buffer your bacterial cells are intact. Centrifuging them to remove PBS won't harm them it is quite standard procedure. You have to be careful after adding 2% SDS because it will lyse your cells and then the RNA contained within them will become "free" and RNAs are fragile molecules.

I'm assuming that you have a solution of bacteria in your buffer directly after growing them for some time, and without performing a lysis step yet. The 2% SDS step looks like it is for lysis of your cells.
In that case, centrifuging the bacteria and resuspending them in lysis buffer is a very common step in many protocols. Separating whole bacteria from medium or buffer by centrifugation is pretty easy and should just work. But if at any of your previous steps you already lysed your bacteria, this won't work because the cells aren't intact anymore.


text:
Does hypothalamus regulate posterior pituitary gland?
We have the hypothalamus-anterior pituitary-endocrine axis, but is there a similar chain of command for posterior pituitary gland such that oxycotin and vasopressin are regulated by some tropic hormones?

The difference between secretion of ACTH  and neurohypophysial hormones is that the prior is a two step process, with CRF from hypothalamus stimulating the anterior pituitary. The latter is produced and secreted from the same cell, only in different organs! Magnocellular neurons stretch from the hypothalamus to the posterior pituitary, where they have their neurosecretory endings packed with hormone storing large dense-core vesicles. The same neurons are osmosensitive, regulating their secretion themselves as physiological need arises. Also, they apparently do dendritic secretion as autocrine signalling. Some reading about this: http://www.ncbi.nlm.nih.gov/pubmed/24265070
and
http://www.nature.com/nrn/journal/v7/n2/full/nrn1845.html
Hope it helps.

This is a complete citation from the paper and not well liked here. Please answer the question in your own words and use the reference to back up what you say.

Sorry, error due to being new to the format. Edited appropriately.


text:
What does it mean for a hormone to be "active"
In my textbook it is stated that the T3 hormone produced at the thyroid gland is 3-5 times more biologically active than T4.
How is being active defined and how can this effect be measured?

This is quite a general question (and bit too broad). Activity of bioactive molecules such as hormones can be defined as how much change do the make to the receipient cells. For eg. let's take two growth hormones A and B. If they are given to some cells at equal concentration but hormone A induces proliferation 5 times more frequently than hormone B, then  A is 5 times more active than B. This is not the best definition / example but I think you can get the point from this.

This question is not broad and pretty well focused. I did a literature search and it is actually hard to find! In all a good question from my point of view +1.

@AliceD - I have to disagree with you on this one. I think we both agree that the effect of a hormone or any biologically active molecule can be measure in several ways, eg gene expression by RT PCR, flurescent riporter gene, riporter gene activity assay etc. and that's just one thing and few examples. This in my view is too broad. But on the other hand I might interpret the question in the wrong way....

If you think about a jackhammer, the better effector is the one that can chip away the most concrete. If the jackhammer had low power or no power (T4), we can safely imagine you'd have lower efficacy than the full-power jackhammer (T3). We can measure the activity of a jackhammer as a function of the work done vs. power provided. In much the same way, we can measure biological activity as a function of concentration vs. catalytic/binding activity. All they're saying is that T3 has more activity at comparable concentrations to T4. Plasmon surface resonance can help measure binding/interactions.

Activity of a hormone represents the efficacy of the hormone in causing the intended effect.
In case of T3 vs T4, though T4 is the majority fraction, T3 is more active, meaning it is much more efficacious in effecting the results.
The concentration of T4 is 30 - 50 times higher than T31. Though T3 is produced by thyroid it is in minority. The majority of T3 is produced by peripheral conversion of T4 into T3.
Thyroid hormones are transported in the blood vessels by albumin, thyroxine binding prealbumin (also called transthyretin). T4 binds more tightly to these transport proteins than T3. In other words T3 constitutes the majority of the free fraction (unbound to carrier/transport proteins). Only the free form of the hormone is metabolically active. So T3 is 3 to 5 times more active than T4.

T3 - triiodothyroxine
T4 - tetraiodothyroxine
1: pg. 312, Essentials of surgery, Sanjay Azad

Biological activity has a range of definitions, but in this case I believe it to mean that the T3 hormone is produced at a rate 3-5x that of T4. This can be measured with fluorescent tags. Typically, fluorescent tagging uses a reactive derivative of a fluorescent molecule, called a fluorophore. The fluorophore selectively binds to a specific region or functional group on the target molecule and can be attached chemically or biologically. Using technologies, such as microscopes, fluorescence can be viewed/imaged; this allows scientists to count, track, and/or monitor molecules over time.

Thanks for answering! Could you back these figures up with a reference or two?

It is unclear what you mean by "produced at rate 3-5x of T4" because 90% of all hormonal output from thyroid is T4, but T4 later get converted to T3 at liver and kidney. Do you mean the net total T3 present in the body at any given time? The sadly text is also unclear what it means by "biologically active", it is as if T3 has little legs and sprints while T4 crawls, not a very helpful image

In my opinion, activeness of a hormone is more about its effect than its production rate. Cortisol and Aldosterone are both adrenal hormones, yet as a mineralocorticid, aldosterone is the active one by great margin (due to intracellular degradation of the glucocorticoids).


text:
Is it in principle possible to revive an extinct species having no living relatives?
Is it, in principle, possible to revive an extinct species having no living close relatives but whose DNA and other tissues have been preserved?
What about the case where there are no living individuals of a species but there are some living somatic cells?
What about the case where only individuals of only one sex are alive?

This may absolutely be possible. Check this for some info. But really it appears that using somatic nuclear transfer, using the same principle used to generate Dolly, we may be able to recreate an extinct species by swapping in the genetic material into a new cell. One current problem that we face with this is that while the genetics should be fine in nuclear transfer, controlling proper epigenetic programming is difficult.

How would one go about raising the zygote if this processed occurred? With no living relatives, what would you use as a surrogate mother?

It depends, if there are close enough relatives its possible that the zygote could then be implanted in them. For instance it may be possible to regrow a woolly mammoth using an elephant mother to carrier the embryo. But this has not been done, this is now getting in to current leading edge science.

I only ask because the question specifically references "having no living relatives"

yeah that is true. honestly in that case who knows, I'm sure somebody at some point will be able to figure out how to grow an organism entirely in-vitro.

@TheNightman http://www.huffingtonpost.com/2015/04/27/woolly-mammoth-genome-video_n_7137764.html?ncid=fcbklnkushpmg00000010 we will see soon :D

"...controlling proper epigenetic programming is difficult" might be an understatement...

authors: Татьяна Третьякова


text:
What does a read simulator do?
There are various software for simulating reads for Next Generation Sequencing. Can anyone tell what exactly is done by a read simulator software

Welcome at Biology SE! Your question is interesting althoughI fear it is more related to informatics than biology. The actual algorithms and the internal workings of a software is off topic here.

I'm voting to close this question as off-topic because algorithms and internal software mechanism are not related to biology.

@poka.nandor it is not in a true sense about a general algorithm; it is a algorithm that simulates a biological experiment and so it should be on-topic. Likewise, mathematical models for biological experiments are also on-topic and we do have many questions on that subject. However, I think that the OP could have put in some more effort.

@WYSIWYG perhaps you're right, I agree with you that bioinformatics and mathematical biology should be on topic. I think it depends on how deep the OP is interested in the software. As a programmer I may have jumped to the point to assume that the OP is interested in exact algorithm implementation instead of general features. In the first case I think it's off topic, the latter case could pass as on topic. Until further clarification I'll uphold my close vote, but as always I'm willing to retract....

In general, a read simulator does the following:

Selects regions from a reference sequence with some sort of predefined or user-specified size distribution.
Converts the sequence from those regions into single or paired end reads with quality scores. The quality scores and read lengths are typically user defined.
Introduces errors into the aforementioned sequences, typically with more at the 3' end, which matches what comes from a sequencer.

A simulator may also try to reproduce the uneven coverage that you'd see in real data. In any case, most simulators will place the original coordinates of the simulated reads in the read names so that the quality of the resulting alignments of the reads can be assessed.


text:
Hopeful Monsters in Plants?
Does anyone know of any research/examples on Hopeful Monsters in Plants?
I define Hopeful Monsters as organisms of a species that have macroevolutions to prompt new speciations. These macroevolutions being themselves, prompted by smaller gradual microevolutions in the species. See this paper for more details. I'm interested in a plant based example, or any good recent example, if plants can not suffice. Ideally research that is easily read and recent, and useful for arguing the existence of themselves?

Could you please add more context to your question? I'm not particularly familiar with the term Hopeful Monsters.

I found a review on the topic for those who are also not familiar of the different versions of evolution theories: http://www.evolocus.com/publications/Theissen2006.pdf

@poka.nandor       I define Hopeful Monsters as organisms of a species that have macroevolutions to prompt new speciations. These macroevolutions being themselves, prompted by smaller gradual microevolutions in the species. I want a plant based example, or any good recent example, if plants can not suffice.

I didn't the term "Hypoeful Monsters" before. From Wiki, the term "hopefull monsters" designate a concept (a hypothesis) and not an organism. In the same logic, the term "macroevolution" has a meaning that depends only on the observer and not on the underlying evolutionary processes. It means "evolution observed at a scale of separated gene pool". In any case, the term "macroevolution(s)" as a noun don't have any meaning to my knowledge. What do you mean by "macroevolutions"? Also, what do you mean by "microevolutions"?

I've edited these extra info along with the paper I found into your question, so it has all these details and don't get lost in comment section. You can roll back at any time if you wish.

Is your question "Can you give examples of plant lineages that underwent major mutations (such as chromosomal rearrangement or hybridization or change in ploidy level)?" or maybe it is something like "Can you give examples of plant lineages which fundamental niche has suddenly and drastically changed in response to a single (or few) mutations?" or stated differently is would be "Do you know examples in plants lineages of mutations that had a major impact on the ecology occupied by the species?"

What do you mean with a species having "macroevolutions" that are "prompted by smaller gradual microevolutions"? This doesn't make any sense to me.

@fileunderwater   Sorry, I am not too great with biology( im a stupid undergrad). Can a species have macroevolution happen to it? Am i phrasing it wrong? If a species can have macroevolution happen to it, can then this macroevolution be caused by microevolution(small, gradual, changes in  allele freq in a population).

@RoSiv Macroevolution is mostly a label describing a level of studying evolution (macroevolution ~= evolution above the species level), and not a type of evolutionary change. Most evolutionary biologists would find it rather meaningless to talk about macroevolutionary changes "happening" to  a species. Macroevolution is the accumulated  result of many small evolutionary changes (i.e. microevolutionary changes). So in that sense, macroevolution is caused by microevolution. Sure, some  single mutations can have larger effects than others, but this is not macroevolution.

@fileunderwater   Can I ask you then how you would define and relate the four terms, Hopeful Monsters, Macroevolution, Microevolution, and polyploidy? So that I can get a solidified view on this, because to be honest I have some confusion with the concepts now. Thank you.

@RoSiv A starting point for the relationship macroevolution and microevolution (or simply just evolution) can be found in my previous comment. I hadn't heard about "Hopeful monsters" before, so I cannot really say anything about that. Polyploidization is a full genome duplication (polyploidy is just the state of having more than two homologous chromosomes), a common cause of speciation in plants and a good example of a single event that can have large evolutionary consequences.

I am not sure what your question is but here is an example that may interest you.

The three sunflower species Helianthus anomalus, H. deserticola, and H. paradoxus are all of hybrid origin of the same two "parent species" (H. annuus and H. petiolaris).

Major ecological transitions in wild sunflowers facilitated by hybridization is a paper that will likely interest you. This paper has been written by L. Riesberg and colleagues. You may want to read through some of the work of L. Rieseberg (CactusWoman already linked one of his articles).

One example of what you may consider to be a macroevolutionary change is a whole-genome-duplication, or polyploidy event. These are not uncommon in plants, and can promote speciation due to a reproductive barrier arising between the polyploid progeny and the diploid parents. You can find many papers about this topic, here is one from 2009: http://www.pnas.org/content/106/33/13875.short


text:
What is the difference between intrinsic and extrinsic apoptosis?
Hello my Professor has been teaching about apoptosis and sometimes makes the distinction between extrinsic and intrinsic. I am not sure if I know for sure what this means. Does this just refer to intrinsic is a cell doing itself while extrinsic refers to Fas ligand? Thanks.

In both pathways 'the cell does itself' the difference is in the reason.
In short:
Intrinsic apoptosis is a response to 'internal damage' eg. damaged DNA, chromosom rearrangement, hang ups in division, hypoxia, etc. that the cell senses itself and 'decides to commit suicide'. This is done by the mitochondrial pathway - release of cytochrome C from the mitochondria activates the caspase cascade that results in programmed cell death. This is like "I'm too damaged, I must die".
In the extrinsic pathway as you have mentioned is indeed related to the FAS ligand (and Fas/FasL being the main pathway for apoptosis), but that is not the only external signal as TNF (also known as TNA-alpha) binding to TNF-R1 (tumor necrosis factor receptor 1) may also lead to apoptosis. These pathways are usually activated by the immune system for example in cellular immune response. This is like "You're abnormal / dangerous / infected, you must die".
Both pathways activates the caspase cascade at some point that results in apoptosis. Either way the actual process of apoptosis is carried out by the cell itself in a programmed, regulated manner.
Source: http://en.wikipedia.org/wiki/Apoptosis
This papaer offers a great review on the topic, including both pathways:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117903/
I'd like to quote few  important parts to support my answer:

The extrinsic, intrinsic, and granzyme B pathways converge on the same terminal, or execution pathway. This pathway is initiated by the cleavage of caspase-3 and results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells.

(...)

The extrinsic signaling pathways that initiate apoptosis involve transmembrane receptor-mediated interactions. These involve death receptors that are members of the tumor necrosis factor (TNF) receptor gene superfamily

(...)

The intrinsic signaling pathways that initiate apoptosis involve a diverse array of non-receptor-mediated stimuli that produce intracellular signals that act directly on targets within the cell and are mitochondrial-initiated events.

Note that the TNFR superfamily is quite large - in this Cell paper from 2001 (sorry, not open access), it lists 26 known receptors binding to at least 18 known ligands.

Absolutely true, I've added that TNF-alpha bindig to the TNF-R1 may lead to apoptosis. The quote is there to justify the general idea that some members of the TNF superfamily play role in apoptosis. Thank you for your remark!

I would actually change the example to Fas/FasL, as that interaction almost always leads to apoptosis. While TNFα is pro-apoptotic in some circumstances, there are many cases where it isn't, as it is mostly regarded as a pro-inflammatory cytokine, helping to activate cells responding to infection. However, when cytotoxic cells express FasL and bind to a target cell expressing Fas (the receptor), that (almost) always leads directly to the induction of apoptosis. I just think it would be a more clear-cut example. Your choice, though :)

I wnated to point out that not only Fas/FasL can induce apoptosis, but I'll emphasize that Fas/FasL is the main component.


text:
Are both (partial) copies of DNA transcribed in S and G2 phases of cell cycle?
For a little less than half the cell cycle, a significant number of genes are represented twice (just before dividing).  Does the cell differentiate between these DNA in any way or are transcription rates limited by the amount of polymerase anyway?

I can't unequivocally say, at least without further literature review, that both sister chromatids are transcribed equally everywhere, especially since the cell does have mechanisms to differentiate between the old and new DNA strands (such as methylation state). It would be conceivable to expect, however, that the same regulatory factors that were present before replication have the same effect on newly synthesized DNA as they did on the old. Here are some electron micrographs showing transcription from both chromatids at some locus.
McKnight SL, Miller, OL Jr. 1979. Post-replicative nonribosomal transcription units in D. melanogaster embryos. Cell 17:551-563
Here you can see RNA (solid line in schematic, b) of increasing length branching from both sister chromatids (dotted line):

A similar image but this time showing the replication fork (arrow):

This image shows RNA free gaps (arrows) in a single transcription unit, which are symmetrical between the two chromatids:

From which they conclude:

The observation that fiber-free gaps often occur at symmetrical positions on sister chromatid transcription units suggests that the two identical transcription units respond similarly to the mechanisms that control RNA polymerase chain initiation. These cannot now be specified, but could include the local supply of RNA polymerase or other controlling molecules.


text:
Help identifying what this is in Crayfish gills?
this is my first time posting here. I was in my Zoology lab doing a dissection on a Crayfish when I noticed these hairlike structures within the gills. They were very "snappy" and fine, and would break off if I pulled hard enough. I put some on a wet mount under a dissecting microscope, but my Lab prof and the parasitologist could not identify it. We put it under a compound microscope and thought maybe it is an animal but we couldn't definitively say it had no cell well. My profs thought it was an animal, with setae, but I would really like to know what it is
Edit here are the images:

Were the hair things coming off the central tubes paired? It almost looks like they are, but I'm not sure.

I had to concede on this one after a lengthy query. If we had a look at either end of whatever it is it'd make identification a tad easier.

My best guess would be Trematoda which is a fluke worm that infects mollusk. I would think this is the larval stage of cercaria which is free swimming and develops in the mollusk and then moves on to infect others.
Here are some different images of a cercaria:

In this YouTube video you will see what is known as a "Rat King" which is just a ball essential of Trematoda. Here is a screenshot

It would be nice that the images from the question have some scale. The first picture of a trematode cercariae has a view of 0.267 mm across according to the source. From the average size of trematode cercaria, perhaps it's a little too small compared to the 'hair' structure on the (visible fine structures of) crayfish gills?

@SYK If you click edit, you will find the sources to the images. There was no scale provided. I just made do with what was available. The size of the rat king is appears to be an equivalent size.

@dustin OK, not that your image is not cool. I was just looking at the seemingly identical image at http://www.networlddirectory.com/blogs/permalinks/7-2006/parasites-form-the-thread-of-food-webs.html

I know this post received a bounty 4 years ago, but I really am not at all convinced this is a correct answer...

@theforestecologist if you read the first sentence I wrote, I state it is a guess. With the available information giving, that was my best guess.

You asked this question 4 years ago, but i randomly noticed this only now. Whell, that not parasite, not Rat King or someting. This is "setobranchies" - crayfish's cleaning organ. They struggle when crayfish move his legs, and cleaning gills from dirt and sand. I hope this information may be usefull for you, even so many years later

Welcome to Biology.SE! Your answer is plausible, but you are much more likely to get a positive response if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


text:
Father with mutated mtDNA- why isn't his offspring at risk?
Mothers transmit their mitochondria (and therefore mtDNA) to their offspring and fathers don't. Lets assume that father had a mutation of the gene that encodes mtDNA, would then be his offspring at risk? Why?
I also found the following statement:
"The current genetic advice is that fathers with mtDNA mutations are at no risk of transmitting the defect to their offspring."
How can that be true? Is it because of gene silencing?
Thank you in advance!

For that matter, the mitochondria replicates on its own unlike other cell components

...would then be his offspring at risk? Why?

No. Generally speaking, fathers do not pass on their mtDNA (Mitochondrial DNA).
Why? Because the mitochondria present in oocytes (egg cell) is the mother's, as every oocyte directly inherits the mother's mitochondria when they are made in the reproductive organs. The mitochondria that the sperm from the father carry to the egg do not enter the egg cell or are destroyed in the process.
It's also worth mentioning that, in general, mtDNA does NOT reside in the nucleus of cells, but in the mitochondria itself. It is not condensed during cell division, it is not spliced during Meiosis II, and it does not undergo recombination with another cell's mtDNA. Instead, when a cell divides, each cell takes about half of the mitochondria present in the cell and maintains them. That way only the mitochondria present in the cell before division will be inherited by the daughter cells, and thus only the maternal mitochondria present in oocytes (egg cells) before sperm instigate cell division will be inherited by any offspring.

Can you please cite references for the absence of mtDNA in fertilized cells? You have no references at all.

@anongoodnurse "Paternal Inheritance of Mitochondrial DNA in Mice" - Nature 1991. The truth is that some paternal mtDNA is passed along, but the undergrad level generalization is that "no" paternal mtDNA is passed because the amount is practically non-existent outside of rare cases. In those rare cases then mtDNA can cause metabolic issues, like the 28 year old case study by Scwhartz in 2002.

TL;DR: Ubiquitin.
Occasional occurrence of paternal inheritance of mtDNA has been suggested in mammals including humans. Clearly, spermatozoa have mitochondria; they make the energy needed for motility. Paternal mitochondrial DNA (mtDNA) does enter oocytes. It is a persisting fallacy that only maternal mtDNA is present in humans because only oocyte mitochondria are present in the product of conception.
This has been known for some time. According to an article in the Proceedings of the National Academy of Sciences, Nov. 1996, under Evolution:

In vertebrates, inheritance of mitochondria is thought to be predominantly maternal, and mitochondrial DNA analysis has become a standard taxonomic tool. In
  accordance with the prevailing view of strict maternal inheritance, many sources assert that during fertilization, the sperm tail, with its mitochondria, gets excluded from the embryo. This is incorrect. In the majority of mammals — including humans — the midpiece mitochondria can be identified in the embryo even though their ultimate fate is unknown. The "missing mitochondria" story seems to have
  survived — and proliferated — unchallenged in a time of contention between hypotheses of human origins, because it supports the "African Eve" model of recent radiation of Homo sapiens out of Africa.[1]

So, what happens to paternal mtDNA if it is indeed present in embryonic cells? Paternal mitochondria are targeted and destroyed.

While some confusion may still persist in popular science, research data clearly document that the paternal sperm-borne mitochondria of most mammalian species enter the ooplasm at fertilization and are specifically targeted for degradation by the resident ubiquitin system. Ubiquitin is a proteolytic chaperone that forms covalently linked polyubiquitin chains on the targeted proteinaceous substrates....Prohibitin, the major protein of the inner mitochondrial membrane, appears to be ubiquitinated in the sperm mitochondria.[2]

A finding of a patient with severe exercise intolerance in whom the mutated mtDNA in muscle was shown to be paternally inherited challenged the concept of strict maternal inheritance of mtDNA (the mtDNA harboring the mutation was paternal in origin and accounted for 90 percent of the patient's muscle mtDNA.)[3]

Paternal mtDNA inheritance may have gone unrecognized in cases of mitochondrial disease with no clear maternal pattern of inheritance because mitochondrial haplotypes are rarely investigated in diagnostic analyses.

However, a small study of 12 patients with mitochondrial myopathy failed to show Paternal mtDNA.[4]
It is too simplistic to say paternal inheritance of mtDNA does not occur. It has been shown in mice and other mammals.

The mitochondrial DNA of 172 sheep from 48 families were typed by using PCR-RFLP, direct amplification of the repeated sequence domain and sequencing analysis. The mitochondrial DNA from three lambs in two half-sib families were found to show paternal inheritance. Our findings provide direct evidence of paternal inheritance of mitochondria DNA in sheep. A total of 12 highly polymorphic microsatellite markers, which mapped on different chromosomes, were employed to type the sheep population to confirm family relationships. Possible mechanisms of paternal inheritance are discussed.[4]

We should not believe everything we read without more investigation.
[1] Misconceptions about mitochondria and mammalian fertilization:
Implications for theories on human evolution
[2] Degradation of paternal mitochondria after fertilization: implications for heteroplasmy, assisted reproductive technologies and mtDNA inheritance
[3] Paternal Inheritance of Mitochondrial DNA
[4] No evidence for paternal inheritance of mtDNA in patients with sporadic mtDNA mutations
[5] Further evidence for paternal inheritance of mitochondrial DNA in the sheep (Ovis aries)