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Which human cells have the longest and shortest lifespan?
Which cells in a human have the longest lifespan? Which cell has the shortest lifespan?

Neuronal cells do not divide. Mature ones anyway

The time a cell spends before it divides should be considered its lifespan in the sense of the question? As it is often heard: cells that divide are immortal (see comment above). The question is not about the shortest span between cell devisions; there might be related questions.

If we define lifespan of a human cell to mean the period during which the cell survives with the same function in a human then..
LONGEST (LIFETIME)
Stem cells. Many types of stem cell form during embryogenesis and persist with the same functionality through to death. would be the longest lived (e.g stem cells that form blood cells such as lymphocytes, red blood cells and platelets).  Stem cells are found in many tissues including self-renewing ones such as the blood/bone marrow, gut epithelium and skin.
VERY LONG (YEARS-DECADES)
Neurons are long lived and are generally non-mitotic.  However, recent studies are raising questions about the degree of cell division in the 'mature neurons' of the brain.
Memory T-cells and memory B-cell (which can be activated and secrete antibodies as 'plasma cells') can provide long-lasting immunity from exposure to antigens in the environment and vaccines.
LONG (FEWER YEARS-DECADES)
Oocytes (eggs)..which are present at birth but which become functionally mature in waves  during puberty.
RACE FOR THE SHORTEST
Labeling studies show that mature gastric epithelial cells live for a few days.
The top layer of skin epithelium is sloughed off every few days.
Sperm cells live for days and are expended or re-cycled.
Mature neutrophils have a circulating half-life of around 8 hours but they can persist as mature forms within the bone marrow for a few days before entering the circulation and they may exit the circulation into depots such as the lung.  So the 8 hours is too short for their actual lifespan.

Some mature neurons can last a lifetime.  Gastrointestinal cells such as those in the colon might be shortest-lived, and skin may give them a run for their money.  However, depending on how you define lifespan, egg and sperm cells could beat those numbers.  Also, some immune cells only last a few days under certain scenarios, such as the aptly-named short-lived plasma cells.


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Identification of this fly?
So I find these flies every year in my mulch, and I've never seen them anywhere else. The mulch becomes full of their larvae, which I feed to my toad and lizards. There are so many that you can hear them moving. The adults are black, look like a wasp or hornet, and have a curious green patch on the underside of their abdomen, which is a clear patch showing some kind of liquid. The larvae are brown and have a little hair on them.

It's about one inch I think maybe a little less. I hope the quality is good enough, because I used my iPod for the picture and you can't do macro with it. Also, I live in Hillsboro Oregon. I am near a small forest and in the suburbs.

A picture (but I think you need more reputation first so I've upvoted) and location would both be very useful for this. also some idea of size.

Hi Keivn, to show us the pictures you have first upload them to a website such as imgur.com and [edit] your post to include the links the site gives you.  Once you have 10 reputation you will be able to this in one step on this site.

You now have more than 10 reputation and can include images in your post.

This should be a comment, but rep is too low. Question: what do you put in your mulch pile? That would help ID the fly.

These links might help: Wasps and BugGuide.

Black soldier fly Hermetia illucens. http://en.wikipedia.org/wiki/Hermetia_illucens
There is a good key to the Dipteran families here. Although it is for British families, it is very thorough.

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Mechanical cause of loss of consciousness
Consciousness is an electrical and chemical interaction in the brain, caused by neurons firing and chemical interactions. How does a mechanical "force" cause this to stop working?
i.e. How does a mechanical action (such as a punch to the head) cause this electrical/chemical system to stop working (leading to unconsciousness)?

One basic point I can offer is that any proteinaceous structure is force-sensitive. Neurons are soft matter and they're intrinsically sensitive to mechanical forces, right down to the chemical level. So if you picture what an ion channel is, a gate that can be opened or shut through thermal energy, it's easy to see how a density fluctuation (like a sound wave) could flip it between states.

Mechanical force can compress neurons and cause action potentials as you probably experienced in the form of hitting the funny bone. Strong enough acceleration of the brain tissue may be causing massive excitation of neurons as indicated by animal EEG study. It suggests that the loss of consciousness is due to generalized epileptic seizure. However, it is not fully agreed upon: quoting wikipedia entry on Concussion:

It is not known whether the brain in concussion is structurally
  damaged or whether there is mainly a loss of function with only
  physiological changes.[14][needs update] Cellular damage has
  reportedly been found in concussed brains, but it may have been due to
  artifacts from the studies.[15] It is now thought that structural and
  neuropsychiatric factors may both be responsible for the effects of
  concussion.[16]

And following quote is from this

The brief loss of consciousness that characterizes concussion appears
  to be the result of rotational forces exerted at the junction of the
  upper midbrain and thalamus that cause transient disruption of the
  functioning of the reticular neurons that maintain alertness.
  (Allan H. Ropper, M.D., and Kenneth C. Gorson, M.D.; N Engl J Med 2007; 356:166-172 January 11, 2007)

so are you saying that the process is not actually well understood? There seems to be alot of unknown about the process?

@TheShiftExchange Unfortunately, that seems to be the case.

Loss of consciousness, or syncope, can be caused by a number of factors, almost all of which relate to lack of proper blood flow: high G-forces, low blood pressure, low blood sugar, cardiac arrhythmia, and vasovagal responses, such as when I give blood.  These all make sense and are moderately well understood.  The mechanism of loss of consciousness due to mechanical trauma, however, is less well understood, in part because it can be tricky to study.  It almost definitely has to do with lowered blood flow as well, and in particular direct trauma to the brain stem, which regulates consciousness.
Basically, you need to rattle the brain inside its cage, slamming it against the skull.  The easiest way to get knocked out from a punch is usually to the chin; the rotational force is much harder for the brain to cushion against, and is a very sharp force.  The displacement of the brain from such a force can compress blood vessels, cutting off blood flow to the brain.  There's also some evidence that the higher brain and the brain stem can twist around each other, which certainly worsens things.  There's even a theory that consciousness is rooted in the neurological structure, which might support the idea that unconsciousness is caused by parts of the brain inhibiting each other.

ETA This isn't exactly a reliable source, but the guy writing this piece for Deadspin is board-certified in internal medicine, and had this (uncited) to say:

Researchers have examined the brain waves of recently concussed animals and determined that their brains resemble that of an animal suffering an epileptic seizure. This comes as a bit of a surprise, because the brain waves (measured by an electroencephalogram) show hyperactivity, which implies that when a fighter is glassy-eyed and unable to answer the referee's questions appropriately, his neurons might actually be overactive, not underactive.
But a hyperactive brain is not the only problem. When the head is hit at high speed, shearing movements within the skull can cause micro-hemorrhages of the blood vessels within the brain tissue. If the shearing force is large enough, or if the head is it hard enough, a large bleed can occur. This becomes a medical emergency because the skull is fixed, enclosed space. As blood accumulates, usually in the form of a subdural hematoma, it can squish the brain and potentially compromise critical neural functions like breathing; death becomes imminent.

A hit can break blood vessels, produce inflammation and exert pressure in the brain tissue. Pressure in fact can alter the composition and distribution of the cerebrospinal fluid. Since the nervous cells are very sensible to oxygen deficit and the composition of their surroundings, phisical damage can lead to loss of brain function. Moreover, while it's true that cerebral activity is due to chemical reactions, it's also true that this activity must be focused in very specific points (synapses), wich may be damaged by an strong hit.

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Does the use of RNA as a primer affect the accuracy of DNA replication in E.coli?
DNA polymerases have proof-reading ability, but RNA polymerase does not. Does the use of RNA as a primer affect the accuracy of DNA replication in E.coli? Explain

E.coli use DNA polymerase for DNA replication too. Primase creates a short oligonucleotid (primer) in the start of string and DNA polymerase continues in work. RNA polymerase is using in synthesis of RNA molecules.


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Is saturation of olfactory cells able to create a feeling of another odour when it stops?
I'm looking for at least one scientific study about how odours could impact human olfactory system and create some phenomenon that could be loosely compared to retina remanence.
As an example, with standard eyes, when you look at a cyan area for a long time and then look at a white paper, the paper looks yellow for a while (see some fun experiments here). This seems to be called an afterimage.
In the type of study I'm looking for, if it exists, the olfactory cells would be involved instead of the retina.
Being exposed to a strong odour for some time would make the subject smell an other odour (a complementary odour?) when the strong odour disappear even if nothing casts this new "complementary" odour to the nose. We could call this an "afterodour" or a "complementary ordour".

The problem with odors is that no known odorant hits only one olfactory receptor. A saturating concentration of compound X for receptor A might be saturating another receptor B, but not receptor C. If you now decrease the concentration, receptor A is still saturated, receptor B is only partially activated and receptor C is not activated at all. Since smell is perceived as the sum of inputs from all olfactory receptors, the smell at the different concentrations will be perceived totally different because of the different receptor activation. Exposing a nose to a strong stimulus will always stimulate more than one receptor, so saturation will occur at more than one receptor.
Perception of light on the other hand depends on finely tuned receptors which are specific for a certain wavelength range. Once the receptors were tuned to have few very specific receptors and once they were tuned to have a lot of unspecific receptors. I like the idea but I doubt it can be confirmed in the lab, also I couldn't find any reports supporting, not that this is any proof.


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Fruit identification
On the way from school to home, I came across this strange looking fruit that looks similar to a potato and it grows on a tree. Can you identify it?

Where is this image taken?

it looks like medlar. Medlar is a fruit sized about 4cm (1 1/2 inch). it must be common medlar.

You can find out more about this interesting fruit here at Wikipedia.

The medlar was already being cultivated about three thousand years ago in the Caspian Sea region of northern Iran and Azerbaijan. It was introduced to Greece around 700 BC, and to Rome about 200 BC. It was an important fruit plant during Roman and medieval times. By the 17th and 18th centuries, however, it had been superseded by other fruits, and is little cultivated today.

Looks like that to me too. +1. Don't know exactly why you got a down vote. Don't think this correct answer deserved it. Perhaps because it is heavily link-dependent, and link rot can destroy it? I'll edit the picture in for you.

first answered "it looks like medlar but dont sure about details i dont even touched before" i was trying to say "i saw multiple times but never look that close" i guess first answer deserved that down vote. edited and added wikipedia image link because of that down vote :) there is also another fruit called japanese medlar or loquat but it is in different genus. and there is a nice coincidence have to tell, yesterday went to grocery for buying some potatoes and saw medlar went back to home and after surfing little bit saw question when just asked. and i hardly remembered what was its name :)


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Resting stage of primary oocytes
In my biology textbook, I read that the primary oocyte gets arrested in the early stages of meiosis in prophase I (diplotene stage). I wanted to know why this is so. I searched google, and this phenomenon is known as dictyate. Furthermore the source was talking about translational arrest after transcription. Why does it occur during cell division? Moreover, what's so necessary about this phenomenon?

Could you provide a link to the article from your google search?

http://www.embryology.ch/anglais/cgametogen/oogenese01.html

I am not sure if I can answer the question of why the primary oocyte gets arrested during meiosis (and finishes after fertilization), but the stage of growth the egg is arrested at does vary widely between species; it's not always primary oocyte. This might suggest that the reason is species-dependent.

In sea urchins, it's the fully mature ovum that gets fertilized.
In humans, it's the secondary oocyte (arrested during this stage of meiosis) that gets fertilized.
In the majority of mammals (dogs, etc.), it's the primary oocyte that gets fertilized. In both of these last two, the oocyte finishes meiosis after fertilization & the entry of the sperm nucleus into the egg.

The translational arrest of the egg you mentioned is because the egg is in a "dormant" state until it is fertilized, and it is "activated" by fertilization. Until fertilization, the mRNA's are present in the cytoplasm, but cannot be translated because they are missing poly-A tails (translational arrest); free levels of calcium in the cytoplasm are low; and respiration and oxygen levels are low. This is because the egg is "primed" for the explosion of activity necessary during early development (taking place after fertilization); the mRNA's code for proteins that are used at that time, but they are not translated until fertilization.
Source: http://www.ncbi.nlm.nih.gov/books/NBK10029/ (see the second paragraph under "Late Responses")


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House sparrow or something else?
These little flying fellows seemed to have made themselves a small nest in the crevices of the roof of my house (I live in Poland). I don't know if this makes a difference, but I do live near a small park.
I'm wondering if this is a house sparrow or something else.
On one of the photos I could swear these look like common sparrows, but on another (the one where the wings are apart) it seems like a different species. It also seemed larger than a sparrow, but is hard to tell due to the distance at which I've seen the birds and the photos were taken. One other notable feature was that they seemed very loud...
Any help?

Based on your image I would rather identify it as an Eurasian Tree Sparrow. They are pretty similar to the House Sparrow, but have a distinct black spot below their eyes which is missing for the House Sparrows (image from the Wikipedia):

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Why is there a seeming dichotomy between mobility and photosynthesis?
At least among more complex organisms, I cannot think of any examples of highly mobile species (like animals) that also incorporate photosynthesis. Perhaps there are examples that I'm unaware of, but even so it seems to be exceedingly rare.
Is there some good reason for this, or is it a mere chance of evolution?
I could speculate, perhaps, in that photosynthesis just doesn't provide enough energy for the relatively high metabolism of mobile species; but even then, there seems there should be a "sweet spot" where some level of mobility would still be "worth it" for a photosynthesizing species, rather than the strict dichotomy that seems to be observable, so I naïvely find that explanation somewhat dissatisfactory. There just seems to be little reason for animals to not practice photosynthesis, if only to be able to eat less than they need to without it.

Interesting question. I would think that if you are mobile, and able to eat other non-mobile organisms that can't run away, then there's a pretty strong reason not to do photosynthesis: it's way faster to just swallow a bunch of carbohydrates in one bite rather than synthesize them all from scratch.

@Roland, I think nature shows that it's not always easy to "just swallow a bunch of carbohydrates". ;)

The difference in energy requirements of a motile species make photosynthesis an unsuitable form of primary energy generation for them.
Since plants are sessile, their energy consumption rates are lower. Plants have approximate respiration:photosynthesis rates of 0.35-0.9, as can be seen in this table (click to enlarge):

Once the energy consumption rates exceed 1, the organisms will, by definition, no longer be full autotrophs, as they will need to obtain their energy from alternative sources. Therefore, the relative low energy content of sunlight makes it impossible for motile animals, which have a larger energy requirement, to survive fully via photosynthesis.

Why be mobile? To follow the sun?
Plants are mobile. Their seeds are. We have plants living on other plants.
Once they have a spot on the sun though moving does not necessarily improve your situation, being stationary and defending your territory though does. (Growing taller, deeper roots, wider crowns)

There is at least one species of highly mobile animal that can photosynthesize, depending on your definition of "highly mobile":
Sea Sheep? This Adorable Sea Slug Eats So Much Algae It Can Photosynthesize
The catch is that this animal does not produce its own chloroplast.

There are unicellular eukaryotes that photosynthesize and are very mobile.
Many are in the phylum Chlorophyta.
This one mentioned below is used for research and protein production, and can live on eating organic compounds in the dark. In the lab you dont need to stir small containers growing them - they move themselves to the light.
https://en.wikipedia.org/wiki/Chlamydomonas_reinhardtii

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How do mosquitoes orientate in the darkness?
An annoying mosquito (Culicidae) which kept me awake nearly the whole night lead me to this question.
I have heard that mosquitoes can smell CO2 which could help them to orientate in the darkness, but how do they avoid obstacles and know where to land? I was browsing the wikipedia article but did not see an explanation for this, can somebody explain this to me?
I also wonder about the purpose of their loud, annoying sound (afaik only females produce it), which i would think as an evolutinary disadvantage, but this would be another question...

What is the purpose of their loud, annoying sound?

Both males and females produce a sound when flying but not at the same frequency. I would think of the male sound as mainly an artefact of flying and don't really know if it has any usefulness. I would note though that before mating both gender tend to synchronize their sound (Gibson and Russel 2006). On the other hand males are very attracted toward the sound of females.
In nature, mosquitoes make swarms. Male's job in the swarm is find find female, courtship and mate. This means that males need a cue to detect them from far away and this cue is their sound. Males evolved large and fluffy antennas (with which they hear) while females only have small antennas Charlwood and Jones 2008.

How do they avoid obstacles?

They have eyes! It is never complete darkness and they just move around, see things and sometime bump into something and keep flying until they reach their goal.
I can't offer you a citation for that but as I worked with mosquitoes in the past, I think it is a good description.

Thank you for the answer. Do mosquitos have a very high light sensititvity? Because I can see barely nothing add night in my room, but they seem to navigate quite good. And when i turned on the light, they stop flying and hide till i turned it off again.

You might get the info in Gabriella 2008 (I can't access the paper for the moment). I know that mosquito have a range of vision that is narrower than ours (they can't see red).

Some researchers found that they may sense obstacle in the dark from the sound of their wing beating against the obstacle and modifying the air flow around them:
"Nocturnal mosquitoes exhibit a behavioral response to divert away from surfaces when vision is unavailable, indicating a short-range, mechanosensory collision-avoidance mechanism. We suggest that this behavior is mediated by perceiving modulations of their self-induced airflow patterns as they enter a ground or wall effect"
About the purpose of their their loud sound, indeed it is a disavantage for the female when flying close to their blood host, but it is believed to be a way to be heard by the male in the mating swarm. In addition, there is an auditory mechanism in mosquitoes which allow to use its own flight sound to amplify the sound of the nearby mate (ref1, ref2). The "harmonic convergence" theory (ref3; saying that mosquitoes actively changes their wingbeat frequency to harmonize between each other) starts being out of date (ref4).


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Cut strand of hair longevity?
Quick and useless question : what can be the longevity of a cut strand of hair, assuming we kept it in (good) normal conditions ? Any idea ?

"assuming we kept it in (good) normal conditions" - your definition of normal matters.I recently read that some of the dead from Herculaneum had intact hair. That was more than 2000 years ago. And that's far from the oldest hair specimens.

Fossilised hair can last over 200,000 years. http://www.telegraph.co.uk/news/earth/environment/archaeology/5299352/200000-year-old-human-hair-found-in-dung.html

In order to keep the hair from decomposing, my first assumption is you'd need it in an environment that inhibits decomposers, e.g. dry. We can see in the mummification process that hair may be preserved for hundreds of years. Hair is also composed largely of keratin, however, and in my own search of the literature: (1) we need microbial (bacteria, fungi) keratinases to decompose the keratin in hair [source], and (2) this process is slow. There's a really old article here, from the abstract:

Keratin, prepared from horn meal, was added to moist field and garden soil and allowed to decompose in the laboratory. The keratin was found to undergo a decomposition resulting in a slow, but steady accumulation of ammonia and nitrate. 35–40 per cent, of its nitrogen was transformed into nitrate after 120 days.

More recent numbers to shed light on a rate of degradation for keratin are either obscure, or untested. This is more so for hair specifically as I couldn't find much more.


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How to identify a pseudogene to a specific protein coding genes?
Pseudogenes are those sequences in the genome that bear similarity to specific protein coding genes, but nevertheless are unable to produce functional proteins due to existence of frameshifts, prema- ture stop codons or other deleterious mutations (Mighell et al., 2000). While I doing some research on protein PLEKHA7, I use the PseudoPipe(an automated pseudogene identification pipeline)(Zhang et al.,2006) to find out the pseudogenes of PLEKHA7. But I am confused that the DNA sequence is 226929bps in length, its pseudogene is only about 100bps long but with a much higher identification like 41.1% and 71%. (chr = chromosomes,start = start position,end = end position,query =  parent protein,frac = fraction of the parent protein that is overlapping with the pseudogene,ins = number of insertions in the pseudogene sequence,del = number of deletions in the pseudogene sequence,shift = number of frame shifts in the pseudogene sequence compared to parent,stop = number of stop codons in the pseudogene sequence,expect = e-value for the sequence identity between parent and pseudogene,ident = sequence identity  between parent and pseudogene,polyA= presence of polyA signal,type = pseudogene biotype : PSSD =  processed, DUP =  duplicated, FRAG = ambiguous )
So how does these pseudogenes have such high identification to the parent gene as they are only very short sequences?

It would probably much easier for us if you could paste the relevant lines in plaintext and also add a link to the specifications of the output file.


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What is the difference between phylogroup and subclade?
Looking for clarification in terminology, examples would be greatly appreciated!
Not sure how this is off-topic. It is a general question about the difference between biological concepts defined in the field of bioinformatics.
"Questions are from students, academics and active researchers in biology and closely related fields, including:

general questions about biological concepts
questions about the biological mechanisms behind medical conditions
questions about techniques in a biological or biochemical laboratory

Questions on interdisciplinary subjects like bioinformatics are also welcome, as long as they focus on the biological part of the subject."

The homework policy, which is linked to in the close reason, should tell you why people voted to close your question.

@canadianer this isn't homework ..... I genuinely do not understand the difference. Not taking any courses right now.

First off, I didn't vote to close. Second, some people around here have decided that "homework" includes any question that the asker does not show effort in researching themselves. This is in the homework policy as: "A question that addresses a basic biology concept that may seem trivial to biology professionals". The policy also directs you to "Research it yourself ".

PS: If you think this question was unjustly closed, you can create a post on [meta].


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If all bacteria in human gut are dead, can they be there again?
If someone likes to eat chocolate, she may have gut bacteria which like chocolate according to some articles that I have read.
http://www.theatlantic.com/health/archive/2014/08/your-gut-bacteria-want-you-to-eat-a-cupcake/378702/
If I do not eat chocolate for a long time, would their number be decreased and other (bad) bacteria dominate the gut?

I think I heard of procedures to innoculate bacteria into guts of humans.

@RoSiv - oh yeah - sterilally referred to as fecal transplantation - I will refrain from going into answering this question O.o

@AliceD From the title I totally thought they were going for Antibiotics... silly me.

@AMR - I got fooled by the title too. I also thought it was about antibiotics - and how to re-populate the intestinal microfauna. I didn't read further and commented. Luckily without answering.. It seems a bit of a twin question, and quite an unclear one too.

The article ( as far as I understood from quickly scanning over it) is more about bacteria in your gut generating cravings for different types of food. The ones "liking chocolate" are more likely to like high-sugar food. If you wouldn't eat any sugar at all, some of them might die out, but others will be able to utilise other nutrients. (Very, very basically said.)

I got a good answer from someone but he deleted it. I think this to be helpful for others, too. http://biology.stackexchange.com/questions/35887/what-are-the-most-important-factors-influencing-a-person-s-gut-microbes?rq=1

So the question your essentially asking is "Do certain types of bacteria like a specific nutrient, and if so will they dissipate or die off if I do not acquire that nutrient?"
Let's give a specific example for comparison. Lactose intolerance is a prevalent disorder among many people and those who do have the intolerance, if aware, tend to steer clear from lactose containing foods. Some studies have been shown that correlate lactose consumption to amount of lactose-containing bacteria in the gut.
So I would say if your asking if you remove a nutrient from your diet will a particular bacteria suffer i.e die then yes. Although be aware that many bacteria are able to break down a variety of different nutrients, and in the case of a cupcake which is loaded with sugars, and fats, I would say a large majority of gut residing bacteria are able to use that as energy in one form or another.
Here's an article comparing lactose-tolerant, and lactose intolerant individuals, not chocolate, but a good start. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898492/

Lactose is a better example than chocolate, thanks.


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Why isn't water decompose well like food, although bacteria need water?
Fruits are decomposed by bacteria well.
Although bacteria need water more than other foods,
why isn't water decomposed well like food?

-1, this question makes no sense. What do you mean by water decay? I wouldn't define water as a 'food', do you have a reference that does?

Perfectly good question, for any adult teacher, to understand and answer. Pontification is not the mission of moderators. Clarification IS. Fruits contain cells and sugar which can be eaten by millions of organisms. Water is like rock, an element, and it can only give food to as many animals as it has CO2, N2, Mg, Ca, And other cell constituents dissolved in it. If the water is rich in dissolved rocks and nitrogen, it will produce a lot of life. Stagnant water is older and gives life an easier place to live, and is less filtered by algea.

I agree. The web site is not like a book or Wikipedia. In the original web site, Stack Overflow, users help each other even if the question is duplicated or unclear, by trying to understand what the questioner wants to know, also the answerer shows the link of other answers, when it is duplicated. So I believe that kind of behaviour is needed in this biology section.

It is unclear what you mean by "decay".
Water is not an organic compound (it contains no carbon). It is just $H_2O$. Water cannot rot! Water is typically not considered as "food" as it is not a source of carbon.
Living organisms can split water molecule (through photosynthesis typically, see wiki > water splitting) and synthesize water molecule (through formation of carbon polymers typically) but I doubt this is what you were thinking about.
Note that if you leave water with a source of carbon (dirty water) somewhere, many organisms will be happy to colonize this environment.

-1, I can't see any value in answer a question that is totally unclear.

I've got another answer from other site, water has no nutritious value. So as you mentioned, in dirty water, bacteria can colonize. Hence we can leave a bottle of water on a desk for a long time. Probably dirty water can be decayed. But the bottled water has also an expiration date, right? I was curious for it. Thanks anyway.

@Michael_A An answer should not be judged based on the question. It is not easy to ask clear questions on subject you know little about. I have asked a lot of unclear questions and comments and short answers have helped me even if the question ends up being closed. It would be silly to rebuke any attempt at helping someone just because (s)he failed to formulate a clear question (except maybe when the post clearly shows lack of effort).

@Remi.b, I agree with your reply but I don't think it's relevant to this question + answer. Many very useful answers correct a false premise in the question, I have read, and enjoyed, a number of your answers that were very useful in that regard. It's not clear that you have corrected any false premises with the answer. The comment from Solek indicates that another site provided an answer to whatever the question was. I think this question shows a very clear lack of effort.

I agree there might have more helpful answer in explaining the basics of organic chemistry and why water will not rot. Note btw that I did vote to close the question as unclear right after you did (as it will become obvious if it eventually ever closes).

@Solek Based on your comment, I feel like you are still thinking that water can be decayed. That expiration date on the water bottles is for the plastic that starts leaching chemicals into water. Example can be found in this paper here. Water can be contaminated with waste but not decayed.

I don't think not being an organic compound is the relevant factor here.  After all, you could say that iron 'rots' when it rusts.  What's important is that rot is a bunch of exothermic reactions, so breaking down those organic compounds supplies energy to the microorganisms responsible for it.  Splitting water is an endothermic reaction: you have to put a good bit of energy in to split the molecule.

@Remi.b actually, answers should be judged based on the question. From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.

@Remi.b it's actually one of my canned comments that I posted on Meta a while back. It's meant for the occasions when people try to answer god-awful questions where nothing is clear, or there's no research effort whatsoever and the question could be answered by googling the question title, or whatever.

@MattDMo, that was the section I was thinking of with my initial comments. I couldn't locate it.   I remember reading that and thinking, those are some wise words.

I thank Remi.b much for answering this question, especially when I see other comments.


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Genetic coding question, amino acid to base relationship
I'm studying for a test and I am confused by these problems/statements.

How many amino acids will 18  bases code for? Answer: 6. I got this right.
If a certain complete protein has 33 amino acids that compose it, then exactly how many bases will it take to code the entire thing?

The answer to 2. is 105, but I'm confused on how we arrived at this answer. If possible or if necessary, please explain the related concepts to me!

Think I figured it out.

I don't think that's right.  I think 102 would make sense, because you want 99 nucleotides to code for 33 amino acids and more more triplet to code for stop.  Maybe the question writer didn't quite realize that the starting methionine counts as one of the 33 amino acids.

I realized my own question after a lot more mulling, but yeah, you need to account for the Start and Stop codon. According to my teacher, the Start codon = Start codon when it's the first in the sequence and it codes for Methionine if it's not the first.

No.  It codes for methionine when it's the first.  The first amino acid of virtually every protein is methionine, at least before any post-translational modification.

@biologyflair your teacher is incorrect. Met is START, as well as being the first AA in many proteins. Take this Entrez Protein search for the ribosomal S6 protein, which is conserved across pretty much all species. Pick entries at random and look at the FASTA sequence - the first letter of the second line (beginning of capitalized sequence) is always M. Or, try here for all the proteins in the E. coli chromosome.

Then the question is, should I listen to her and pass the test or listen to this for long term benefit?

Do you have a textbook?  I'd be surprised if the textbook was wrong.  You could try and point out that your teacher is wrong, if you don't think that will work, give them the answer they wnat, but remember the real answer for the future.  That link to all the e.coli proteins is proof.

@biologyflair bring it up after class. Heck give her my contact info, it's not hard to find from my profile. I'm a Real Scientist™, I don't mind talking to her :)


text:
Was the dodo a dinosaur?
I've always believed that the dodo was a dinosaur, I don't know exactly why. I've done some searching on the internet, but except for toy stores selling "Dodo the Dinosaur's" I didn't find anything very useful of which I could conclude if the dodo was a dinosaur or not.
So, was the dodo a dinosaur or not? And if the dodo wasn't a dinosaur, why do people say it's a dinosaur?
(I couldn't find a related tag, I think 'palaeontology' was the closest to what I needed)

It was a bird, and is now extinct. Typing 'dodo' in the Google search engine yielded the Wikipedia entry as the number 1 hit.

I've read the wikipedia page, but it doesn't say anything about it being a dinosaur or not. Which could point to the direction that the dodo wasn't a dinosaur. But I'm wondering why stores say it's a dinosaur. Where does that come from?

Perhaps you would have more success posting your query in ToyStores StackExchange, or PeopleWhoSayThings StackExchange? In this forum for Biology StackExchange I don't think you will encounter anyone with the appropriate expertise.

Yes, dodos were dinosaurs, but that probably doesn't quite mean what you think it does.
Dodos were birds, closely related to pigeons. All birds are dinosaurs.

Thanks! Now I get it. Never knew I've seen so many living dinosaurs ;)

@snake This post will probably help to understand the possible confusion with the term dinosaur.


text:
Why are segments/parasegments in fruit fly embryos staggered?
I'm reading my developmental biology textbook and I don't understand this concept. I can see how concentrations of Eve and Ftz determine each parasegment. However, I don't understand why the length of one parasegment isn't equal to the length of one segment on the actual embryo. Parasegments and segments are staggered from eachother.
Could anyone clarify?
Edit: I've gone back and re-read a bit. Is this staggering because parasegments are established while the embryo is still syncytial? So parasements are established, and afterwards cell division begins. But the daughter cells cant line up perfectly with the parasegments so segments and parasegments end up a bit staggered.
Edit2: Bit more reading. I think I got it. After parasegment establishment by Ftz/Eve, further segment polarity genes Engrailed and Wingless are expressed, with Engrailed expression being induced by either eve/ftz. The posterior side of the first engrailed cell determines where the boundary for a segment will be determined.
Can anyone confirm?


text:
Is there an organism which is "The Opposite of Hydra"?
My understanding is that if hydra is cut into pieces, each piece can evolve into a new hydra. What I'm looking for is whether there exists an organism with a this property reversed, that is, if two or more such organisms meet, they would form new organism with the same property.
UPDATE: I do not mean the mythical creature, but this one. I should also have stated that I'm (obviously) not a biologist, so my terminology and information about the Hydra genus might be wrong. Despite that, I hope the question is still valid.

Not that it really matters, but the hydra myth involves its heads, specifically.  Cut one off, and it would grow two (or three or more, depending on the myth) from where the first used to be.  The whole creature wouldn't duplicate.

@Nerrolken, sorry, should have been more clear. Updated my question.

Perhaps sea sponges might satisfy your criteria? There were some classic experiments where two distinct sponge colonies were dissociated individually into small clusters of cells, and then the two suspensions were mixed. As I recall like sorted with like.

Siphonophora (these are close relative of hydra). They are considered to be a colony of zooids. I am not sure if that is what you are asking. You an also think of Dictyostelium. They can aggregate to form fruiting bodies.

Possible duplicate of http://biology.stackexchange.com/q/37473/3340


text:
Can any enzyme be produced?
After reading about how recombinant insulin is produced, the following question occured to me. Does the current level of technology allow any enzyme to be produced in a similar way?
As I see, producing amino acid sequences is not an issue. A possible difficulty I can think of is modifying the amino acid chains. In the case of insulin the problem has been solved. Are there some generally applicable solutions available to this problem, or do they have to be researched on a case-by-case basis?
Are there any other limitations to producing enzymes?
EDIT: As pointed out by P. Jay, the question might seem to suggests that insulin is an enzyme which it is not.

Anything can be produced, the problems lie in producing large amounts with high quality.

No, not all enzymes (or other proteins for that matter) can be obtained in functional form by recombinant expression with today's methods. As you suspect, problems arise when complex post-translational modifications are necessary to obtain the correct function.
Direct modifications to peptide is one potential problem. Some of these can be resolved by expression the recombinant protein in the right cell type: for example, expression in a bacteria may not provide the right modification, but expression in yeast or a mammalian cell might. CHO cells are a common mammalian cell type used in such cases; antibody production in hybridomas is another well-known example. But there are plenty of posttranslational modifications that are poorly understood, and most likely there are still many completely unknown types; new ones are still being discovered.
Another posttranslational event is association with cell membranes. Membrane proteins (including membrane-embedded enzymes, for example in lipid metabolism) can be very difficult to express properly, as not only the peptide but some surround membrane structure must be reproduced in the expression system to obtain correct function. This is also a major hurdle in obtaining structures for membrane proteins, notably many cell surface receptors. This article is a summary of the current challenges and unsolved problems in this area. And you can imagine the problems with proteins that need to form large superstructures to be functional --- large protein polymers, respiratory chain complexes, ribosomes, DNA replication forks ...
So there is no universal method; all proteins are different, some are easy to express, some are extremely hard.

If you are talking about the possibility, the answer is yes. However, you might have some difficulties in producing some proteins. In some cases, the reasons could be obvious--sugar modification and phosphorylation which can not happen in E. coli. Although phosphorylation is involved, if you do not know if your protein is phosphorylated, you would never find the reason why you can not get the active protein.
Polypeptide folds in the correct way or incorrect way in E Coli. Sometimes, it is difficult to fold proteins correctly in E coli expression systems. In addition, if your proteins has multiple polypeptide chains, it could be more difficult.
There are mammalian, yeast, insect expression systems, and these systems could be better if you have problems in producing proteins in E coli. But it is not always that these systems work.

Yes enzymes can be produced and even be optimized like restriction enzymes which are now mostly recombinant thou to low efficiency or biosafety level of source bacteria leaving that behind ,the greatest problem here is the size of protein and it's gene as when you produce artificial bio products you've got a prokaryote host to do that in cases which they do it out of cells then it's completely different but for sure possible the greatest problem is efficiency of production....and by the way insulin is not an enzyme


text:
Assays to determine competitive binding versus non-competitive
I'm looking for both simple and complex assays or technologies than can be used to determine if two competing molecules are competitive or noncompetitive.  I figure xray crystallography is a clear one, but say I can't get crystals to form.  What other techs or assays could I use to determine this?
It's a protein-protein interaction with a small molecule competing with one of the proteins.  This particular set has not been done before. All interactants are purified.

Can you please describe your setup in a little more detail? Are your ligands small molecules, proteins, or something else? Do you have the purified target protein? Is it a receptor or some other kind of enzyme? Has anyone worked with it in the literature before?

If you've got an enzyme and a good activity assay and you want to test if the molecule is an inhibitor, try building Lineweaver-Burke Plots. It can take a lot of work though, because each plotted point is a reaction rate, and determining each reaction rate can take significant effort. Because the plots are reciprocal measures, small errors are easily magnified, so you have to be very very careful to minimize any error whatsoever. But if done well you can determine competitive, non-competitive, or mixed inhibition.

http://www.ncbi.nlm.nih.gov/books/NBK92001/ has some good guidelines for mechanism of action studies.

Now that I see you are looking at protein-protein interaction, would fluorescence anisotrpy help? If you labeled one protein with a fluorophore, you should be able to observe a change in tumble rate as the other protein binds or falls off.

I'll have to edit the question, I'm looking for label free methods.  Sorry about that!


text:
What are the chances that two children of the same couple will have the same genes without being identical twins?
If I randomly select half the chromosomes of the male and female eventually I will select the same exact half for both a second time. How often does this occur? Is this considered a twin if it is born at a different time as in years apart?

Just because the poster might not have an intuition for why this is obviously very low doesn't make this a bad question. In fact, this is interesting.

The chances are effectively zero.
Even in the absence of recombination, this calculation involves choosing the correct member of a pair from each of the 23 chromosomes, from both the father and the mother.
223 × 223 = 246 = 70,368,744,177,664
So, less than a 1 in 70-trillion chance. For some context, only about 117 billion humans have ever been born in history.

A more accurate calculation would include recombination, which occurs on all chromosomes (except the XY in males). Incorporating this would require knowledge of the recombination profile and number of genes for each chromosome. It would make the above probability many, many orders of magnitude less likely. (Like, it's very possible there are more potential combinations of two parents' chromosomes than there are atoms in the universe.)

If this were to occur, I personally wouldn't call them twins. That term is consistently used to reference a single pregnancy, regardless of whether the children are genetically identical.

There is a one in 1/(0.5)^46 = 70 trillion chance of this happening in theory without accounting for recombination. However, there is a 6% chance of this happening when there are 4 chromosomes, which is applicable to real plant and animal species! With real human data, which takes into account recombination, hotspots, etc., there is a one in 4.771 * 10^39 chance of this happening. This is one in a 5 thousand billion billion billion billion chance, and only 100 billion humans have ever lived.
Extra information:
Theoretically, there is a one in 17.59 trillion chance of independent assortment happening so that the exact autosome combination is the same (0.5^44).
There are chromosomes A and B. Uppercase: from mom. Lowercase: from dad
Mother: A1 A2 B1 B2
Father: a1 a2 b1 b2
1st step: assort chromosome A. 4 options. (A1 a1, A2 a1, A1 a2, A2 a2)
2nd step: assort chromosome B. 4 options. (B1 b1, B2 b1, B1 b2, B2 b2)
Now, there are 16 options for the child for 2 chromosomes.
Imagine a pairwise matrix of these options; the top left to bottom right diagonal represents the pairs in which two children have the same chromosome combination. This is 16 children out of a total 16*16, or 0.0625 = ~6% chance of happening. This means this must happen regularly for some animal species! https://en.wikipedia.org/wiki/List_of_organisms_by_chromosome_count
If we increase the chromosome count to 22, there are 4 options for each chromosome, so there is a one in 1/(0.25)^22 or 1/(0.5)^44 or one in 17.59 trillion chance.
Different-sex siblings can never be 100% genetically identical.
For men, the Y-chromosome will always be the same and brothers will have a 1/2 chance of having the same X chromosome. For women, the X chromosome from the father will always be the same and there is a 1/2 chance of getting the same X chromosome from the mother. Since they have to be both the same sex (50% chance) and get the same X chromosome, this increases the odds by 4 to (1/(0.5)^44)*4 = 70 trillion. This is why the sex chromosome acts like an autosome.
For full siblings, there is an observed mean of 0.50146 relatedness with an SD of 0.03761 (from the supplementary table). To get this halfway to twins, we would need 0.25/0.03761 = 6.6471683063 SDs above the mean. This occurs, on average, once in (1 / (1 - norm.cdf(6.6471683063))) = 66,937,665,852 events. To go the rest of the way to full twins, we will need to be (1-0.50146)/0.03761 = 13.2555171497 SDs above the mean, which is one in 4.771 * 10^39 events!
Since about 100 billion humans have ever lived, and a “chance” half-twin half-sibling occurs once every 67 billion humans, this has probably happened before. Interestingly, this 75% genetically related sibling pair, derived from empirical data, has about the same probability of about 75% of the chromosomes happening to assort the same way.
More extra information:
Darlingtonia's answer is good. However, there is recombination, which makes it extremely more unlikely than it already is. The existence of inbreeding helps with this a bit, as sequences might be exactly the same between mother and father already.
Let's look at some data.
This paper used real allele frequencies to generate a relatedness distribution for full siblings.
https://academic.oup.com/beheco/article/20/2/410/219031
Another paper looked at relatedness of full siblings had has standard errors available.
https://academic.oup.com/beheco/article/29/2/468/4819097
But this isn't fine grained enough. Let's make a simulation. Also, let's assume the siblings will both be women or both be men. Since this only happens half the time, the real odds are halved. We will also ignore recombination hotspots, discussed here: http://adamauton.com/adam_auton_thesis.pdf
23*2 chromosomes. 1.6 recombinations per chromosome (we are ignoring variation between different chromosomes): https://book.bionumbers.org/what-is-the-rate-of-recombination/.
Length of the average chromosome: 6.3 Giga-base-pairs divided by 46 = 136,956,522. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391780/
136,956,522 base pairs make up each of the 46 chromosomes. Recombination happens 1.6 times on each chromosome.
137 base pairs make up each of the 46 chromosomes. Recombination happens 1.6 times on each chromosome. Allow two parents to produce 10 offspring in this way. Then, calculate the average relatedness coefficient between the children.
We could use the infinite allele model but adjusted for the baseline relatedness we’d expect due to chance, which, for four alleles, is 0.25. However, this would incorrectly classify genetic twins as only 75% related.
Therefore, we could use chunks. The length of shared chunks can be used to estimate genetic relatedness. We would also need to use SNPs, not total base pairs, as most base pairs will be the same for all mammals.
At this point, we are making way too many assumptions for this simulation estimate to be realistic.
Instead, let’s look at real data:
“IBD sharing between pairs of full siblings in the SAMAFS and Hemani20k data, which have mean IBD proportions of 0.501 and 0.502”
https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1007979
We want both homologous chromosomes in one individual to be identical by descent to make “twins.”
For full siblings, there is an observed mean of 0.50146 relatedness with an SD of 0.03761 (from the supplementary table). To get this halfway to twins, we would need 0.25/0.03761 = 6.6471683063 SDs above the mean. This occurs, on average, once in (1 / (1 - norm.cdf(6.6471683063))) = 66,937,665,852 events. To go the rest of the way to full twins, we will need to be (1-0.50146)/0.03761 = 13.2555171497 SDs above the mean, which is one in 4.771 * 10^39 events!
Since about 100 billion humans have ever lived, and a “chance” half-twin half-sibling occurs once every 67 billion humans, this has probably happened before.


text:
Breeding laboratory mice with cancer; how does this work?
It has recently been brought to my attention that live laboratory mice with specific cancer strains can be readily purchased for medical research.  For example, the Jackson Laboratory sells mice with a wide range of strains of cancer (with price depending heavily on the type of cancer desired).

Question: What is the general process behind breeding laboratory mice with specific cancers for medical research?

I could imagine a) they inject a few cancer cells from an in vitro culture which, being cancer cells, find a niche to proliferate; or b) the genes causing the cancer type are known and they produce a local knockout/knockin/knockdown in order to get the cancer started.

It really depends... for instance we have transgenic mice with a specific mutation in a protein controlling cell cycle that spontaneously develop certain tumours when adult/old. Other tumours can be induced by giving specific substances.

Cancer is a highly genetic disease, and much is known about how different genetic mutations contribute to the generation, growth, proliferation, metastasis, and control of tumors. Jackson Labs (commonly known as Jax in the research community) provides literally thousands of strains of mice, each bred/genetically engineered to have certain genotypes and/or phenotypes, a good proportion of which can be used for various purposes in cancer research.
I'll take a very basic example to walk you through the creation of a "cancer mouse." Say I've been doing research and have found through studying the DNA of many patients that the ABC123 gene seems to be associated with a certain type of cancer (skin, for example). I want to know more how ABC123 works, so one of the first things to do is to find out what (if anything) goes wrong when it isn't there - when it gets "knocked out." Using genetic engineering techniques, I create a sequence of DNA (called a vector) that matches the "wild-type" (WT) or normal mouse ABC123 gene sequence at the ends, but in the middle has a certain selection gene called Neo instead of the rest of the ABC123 sequence:

Neo makes cells that it is in resistant to a certain antibiotic called Neomycin or Geneticin, also called G418. I take my targeting vector and electroporate it into mouse embryonic stem cells (ESCs) that, if implanted into an appropriately-prepared female mouse, could develop into a normal mouse embryo. I then culture these ESCs in the presence of neomycin, which will kill any cells that haven't taken up and incorporated the vector into the genome.
Once I have some cells that I know have taken up the Neo part and are missing the targeted part of the gene (the exons marked 1, 2, and 3), I inject a few cells each into mouse blastocysts, where they divide and differentiate to form various parts of the new mouse.

This is a chimeric mouse, with different cells coming from different origins, either wild-type or ABC123-mutant. I try to generate a number of different chimeras to breed together in the hopes that at least some of my original injected mutant cells went on to form the gonads, and the mutant gene can be passed on to its offspring. I then breed the various chimeric mice to WT mates in hopes of producing heterozygous offspring, which have one copy of the WT-ABC123 gene (from one parent), and one copy of the mutant-ABC123 gene (from the other parent). These mice can then be bred together to produce homozygous "double-knockout" mice, which I can then use to study my gene's effects and its possible relation to skin cancer. This is the type of animal typically sold by Jax, although this depends very strongly on the gene being studied.

Now, there are many issues that can arise along the way, such as the mutation being embryonic-lethal, causing sterility, or other defects that don't allow you to produce true knockout mice. Much can still be learned, though, and scientists have gotten very inventive in producing functional animal models of previously-difficult mutations. For example, it is possible to engineer a strain that only becomes a knockout when you feed it a certain chemical in its water, or is only knocked out in certain cell types or tissues. Some gene functions are only apparent when two (or more!) genes are knocked out at the same time. Genetics is incredibly complex, but fascinating, and more and more complex tools are being developed all the time to assist scientists in their research and ultimately help people overcome illness and disease.

Just a very minor correction: although geneticin and G418 are the same antibiotic, neomycin is a different molecule (although they are both aminoglycosides). Resistance to both is conferred by an aminoglycoside 3' phosphotransferase, and the gene encoding this enzyme is often designated neo


text:
Where can I find a list of diseases and their incidence?
Say I am studying a particular disease and I know that its incidence is 0.8 per 100000 children below the age of 18, how would I find the incidence of a whole bunch of other pediatric diseases (or even not just limited to pediatrics)?
Essentially I want to find diseases that would be familiar to a medical audience and provide an example of a disease with an incidence of about 0.8 per 100000, another one that is one tenth the incidence and another one that is ten times the incidence.

About diseases in general, that would concern the health dept. of the respective country government, and the govt. is the most probable source for such numbers.
However, orpha.net has two reports with numbers concerning hereditary diseases, have a look at http://www.orpha.net/consor/cgi-bin/Education_Home.php?lng=EN#REPORT_RARE_DISEASES

Pretty good. The list details prevalence. I would prefer incidence but if prevalence is all I can get then I will settle for prevalence.

The Center for Disease Control is a great source for disease statistics. I didn't find a chart with common disease incidence on their website, but if you search for a specific disease you should be able to find the incidence.
http://www.cdc.gov/nchs/

Nice resource but not for what I am trying to find. I specifically am looking for a listing of incidences across many disease all in one place. I could search for any disease in pubmed (or even better I could start my search from MESH headings) and specify that I am looking for statistics or incidence.

A couple resources that might be of use:
If you subscribe to it (annoyingly, I cannot get at my copy), the American Academy of Pediatric's Red Book may contain incidence figures. I don't recall, but it contains a remarkable amount of information in it.
For viral diseases, most if not all entries in Fields Virology have an Epidemiology section, and many of these touch on the incidence rate, especially for more common diseases.
In addition to the CDC (listed in another answer), take a look at the Agency for Healthcare Quality Research (AHRQ)'s Healthcare Cost and Utilization Project (HCUP) data. While this will only give you incidence in terms of hospitalizations rather than all cases, it may be potentially useful.
Beyond that, I'd suggest looking for particular papers, or search for "DISEASE OF INTEREST" meta-analysis in Google Scholar or PubMed for overall incidence figures.
Additionally, a useful formula:
Prevalence = Incidence * Duration. Which in turn means Prevalence/Duration = Incidence. If you can find those two pieces of information, you can calculate the incidence for what you want.
There's also a way to extract incidence from a mathematical modeling paper about a disease which reports an R0 figure, but that may be a touch technical given your stated desires.


text:
Easy derivation of Kimura's approximation for the probability of fixation of a mutation
Kimura's approximation for the probability of fixation of a mutation under selection finds recurrent use in population genetics models till date. I am trying to understand the mathematical basis of this equation but none of the textbooks or online resources that I have checked, provide an easy derivation of this approximation but rather simply cite Kimura's 1962 paper.
$$P_\text{fix} \approx \frac{1-e^{-4Nsp} }{1-e^{-4Ns}} \qquad (1)$$
So, I was reading the original paper but the provided derivation doesn't appear clear to me.

Details
Kimura starts with definition of probability of change in allele frequency as:
$$u(p,t+\delta t) = \int f(p+\delta p; \delta t)\ u(p+\delta p,t)\ d(\delta p) \qquad (2)$$
where (quoted exactly)

$u(p,t)$ is the probability that an allele will be fixed in a time interval $t$ given that it's initial frequency is $p$.
$f(p+\delta p; \delta t)$ is the probability density of the change from $p$ to $p+\delta p$

Then he uses Taylor series approximation to obtain an equation of this form:
$$\frac{\partial u(p,t)}{\partial t}= \frac{V}{2}\frac{\partial ^2u}{\partial p^2}+M\frac{\partial u}{\partial p} \qquad (3)$$
He defines $M$ and $V$ as mean and variance of change of $p$ per generation. These are formally defined as:
$$M=\lim_{\delta t \to 0} \frac{1}{\delta t}\int (\delta p).\ f(p+\delta p; \delta t).\ d(\delta p)$$
$$V=\lim_{\delta t \to 0} \frac{1}{\delta t}\int (\delta p)^2.\ f(p+\delta p; \delta t).\ d(\delta p)$$
($V$ actually should be just the second moment as per the mathematical definition and not variance)
Then he solves equation 3 at steady state with boundary conditions $u(0,t)=0$ and $u(1,t)=1$ to obtain this:
$$u(p)=\frac{\displaystyle\int_0 ^p G(x) dx}{\displaystyle\int_0 ^1 G(x) dx} \qquad (4)$$
where:
$$G(x)=\exp\left(-\int \frac{2M}{V}dx\right)$$
I understood the derivation till this point.
Then he just puts:
$$M=sx(1-x)$$
$$V=x(1-x)/2N$$
and obtains equation 1.

In short
Is there an easy derivation for equation 1?
If not, can someone explain me how M and V were approximated as above?

nice question! It might be worth tyring to ask this on math stackexchange (or whatever its called), since most biologists probably don't get the math behind this (I'm including myself here, and I probably have more math background than the average)

@Nicolai Perhaps the mathematicians may know these methods really well but I am afraid without context, just knowing the mathematical methods won't be of any use. I'm trying to read Kimura's book which is more detailed. I think I'll find an answer there. When I find it, I'll post it.

Presumably you've solved this, but, in case not, it's because the PDE is a Kolmogorov backward equation, so the first and second order coefficients are the mean and variance of the underlying stochastic process being modeled.
In detail, consider a stochastic differential equation (which has a solution given by an Ito diffusion process):
$$ dp_t = \mu(p_t,t) dt + \sigma(p_t,t) dW_t $$
then the following system holds (under some conditions):
$$ -\frac{\partial}{\partial t} u(p,t) = \mu(p,t)\frac{\partial}{\partial p}u(p,t) + \frac{1}{2}\sigma^2(p,t)\frac{\partial^2}{\partial p^2} u(p,t) $$
where $u$ is the density of $p$ at $t$.
Note that the drift (infinitesimal mean) $M=\mu(p,t)$ and diffusion coefficient (infinitesimal variance) $V=\sigma^2(p,t)$ are as in the paper (except for the negative sign, which I assume is ignorable since he mostly seems to care only about the case when $\partial_t u\approx 0$ anyway).
Indeed, they are equivalently written:
\begin{align}
\mu(p,t) &= \lim_{\delta t\rightarrow 0}\frac{1}{\delta t} \mathbb{E}\left[ p_{t + \delta t} - p_t \mid p_t=p \right] =: M \\
\sigma^2(p,t) &= \lim_{\delta t\rightarrow 0}\frac{1}{\delta t} \mathbb{E}\left[ (p_{t + \delta t} - p_t)^2 \mid p_t=p \right] =: V  \\
\end{align}
as Kimura writes.
Note that a useful approximation of the transition density is given by:
$$ \mathbb{P}[p_{t+\delta t} \mid p_t] \approx
\mathcal{N}(p_{t+\delta t}\mid p_t + \mu(p_t,t)\,\delta t, \sigma^2(p_t,t) \,\delta t) \tag{TD} $$
Ok, so everything above is just basic stochastic processes theory. Thus, if we have a stochastic model for the population dynamics, we can derive values for $M$ and $V$ from it (by computing its moments), and those will carry over to the backward Kolmogorov equation, upon which Kimura's work rests.
Here is where my ignorance of population dynamics shows. However, since Kimura mentions Fisher and Wright, I looked up the Wright-Fisher model.
It seems like Kimura is using the diffusion process approximation of the Wright-Fisher model.
This appears to be a well-studied and storied model that I cannot fully describe here; instead, I found the work by Tataru et al, Statistical Inference in the Wright–Fisher Model Using Allele Frequency Data to be an excellent description of it, though I do not pretend to understand much of it.
What's important, however, is that the change in genes (transition density) can be described by a binomial distribution. This can be approximated by a normal distribution:
$$ \mathbb{P}[p_{t+\delta t} \mid p_t] \approx \mathcal{N}(p_{t+\delta t}\mid p_t + a(p_t) \delta t,\, p_t (1-p_t) \delta t ) $$
using the standard approximation to the binomial.
This then gives us a forward Kolomogorov equation (not backward) written:
$$
\frac{\partial}{\partial t} u
=
- \frac{\partial}{\partial p}\left[a(p_t) u(p_t) \right]
+
\frac{1}{2}\frac{\partial^2}{\partial p^2} \left[ p_t(1-p_t)u(p_t) \right]
$$
This basically implies that $V=p(1-p)$.
( I noticed that another way to prove this is to notice that the Wright-Fisher approximate diffusion (without any selections, etc... so $a\equiv 0$) has an infinitesimal generator given by: $ \mathfrak{G} f(p) = p(1-p)\partial_{tt} f(p) / 2 $. This immediately implies $V=p(1-p)$. But may be less straightforward to understand. )
Confusingly, however, the paper has changed timescales (variables), so that $\delta t \leftarrow \Delta t / (2N)$, and then set $\delta t$ to $1$ (probably so that they would not have to write $2N$ everywhere).
If we undo this transform, we get
$$ \mathbb{P}[p_{t+\delta t} \mid p_t] \approx \mathcal{N}(p_{t+\delta t}\mid p_t + a(p_t) \delta t,\, p_t (1-p_t) \delta t/(2N) ) $$
If you compare this to our approximate transition density above (equation (TD)), you will see that this implies: $$ \sigma^2 = V = p(1-p)/[2N] $$
as desired.
Now, what is the infinitesimal mean, i.e. $a$ or $M$? Clearly this depends on the selection model, since it controls how the "environment" deterministically affects the process. Kimura describes this as a "constant selection advantage" with coefficient $s$.
The Tataru paper notes that the diffusion approximation to Wright-Fisher under genetic drift, mutation, and selection is given by:
$$
a(p) = -\nu p + \xi(1-p) + 2N\tau p(1-p)[h-(1-2h)p]
$$
If we (1) ignore mutation by setting $\nu=\xi=0$, (2) remove allelic dominance effects by setting $h=1/2$, and (3) define $s:= N\tau$, we get:
$$
a(p) = s p(1-p) =: M
$$
which of course we see by noting $M=a(p)$ matches $\mu$ in the equation (TD) above. (Note that the $2N$ transform also occurred here, but it was hidden inside $s$).
Thus, we have derived where Kimura's $M$ and $V$ come from, albeit probably not in the simplest possible manner.
All that remains is to derive the (steady-state) equation for $u$. I guess I'll do it for completeness.
Ignoring the steady-state subscripts, we get:
\begin{align}
G(x) &= \exp\left( -\int \frac{2M}{V} dx \right)
     = \exp\left( -\int 4sN dx \right)
     = \exp\left( -4sNx\right) \\[0.15cm]
u(p) &= \frac{\displaystyle \int_0^p G(x) dx}{\displaystyle \int_0^1 G(x) dx}
     = \frac{\displaystyle \frac{1}{4Ns}\left[ \exp\left( -4sNx\right) \right]_0^p}{\displaystyle \frac{1}{4Ns}\left[ \exp\left( -4sNx\right)
\right]_0^1}
     = \frac{\displaystyle -\left[ \exp\left( -4sNp\right) - 1 \right]}{\displaystyle -\left[ \exp\left( -4sN\right) -1
\right]} \\
&= \frac{1 - \exp(-4Nsp)}{1 - \exp(-4Ns)}
\end{align}
as required.

Apologies for any errors. (I am neither a population dynamics modeler nor a mathematician, so please point out any problems).

Thank you very much. I don't really understand KBE very well. I remember reading about Fokker-Plank equation but I am not familiar with it in the context of diffusion. I have no background in SDE, so it may take me a while to understand.

@WYSIWYG No problem. The main idea I think is that the allele freq can be modeled by a differential eq with noise (SDE), which approximates Wright-Fisher, then the KBE falls out of that. Let me know if there's anything I can expand on.


text:
Examples of prey predator interactions where density of predator is very low and prey form groups when the predator attacks the prey for food

Examples of prey predator interactions where density of predator is very low (has a threat of extinction) and prey form groups when the predator attacks the prey for food.

I have searched this in net but not get examples. Please help me to supply some examples with a brief interaction of type discussed above.
EDIT
Specialty of predator:
Predator population has a threat of extinction due to their low population. They have the difficulties in locating acceptable mating partners for sexual reproduction during their receptive period due to low population densities.

This sounds like a homework question. Look up bait fish ball.  Use what you learn there to guide other searches.

@akaDrHouse Thanks. In that case which one is the engendered predator mostly feeds on the bait fish. Please provide me more such examples of prey and predator pairs having such interaction.

Homework questions are off-topic on Biology.SE.

This post might help you to understand how prey-predator interactions affect population size. The post does not contain examples though as it focuses on the theoretical aspect.

@Remi.b This is not a home work question.

@Remi.b I am not interested to understand "how prey-predator interactions affect population size". I know this. But I am in need of a very special type of interaction that I have discussed above. Please don't think this search is for solving a homework question or homework-type question.

@user1942348 If it's not homework, can you then provide a better background? Describe your problem, what you know, what kind or interaction you are interested in and why? By doing so, you are much more liklely to get useful answers.

Are you asking for cases where the flocking behaviour is used specifically against low-density predators, or flocking against predators in general? At the moment, it's unclear why are asking specifically about low-density predators,and bring the risk of extinction of the predator into the equation.

@fileunderwater I am asking examples about group defending behaviour is used by prey against engendered predator (who have the risk of extinction due to low breeding or mating for their low density).

@fileunderwater Please reply if my question is not clear.

You are only restating exactly the same thing that is already in the question. Why is it important that the predator is potentially endangered? The flocking behaviour will probably have been selected for when the predator was more common. And as I wrote earlier, add more information and background to your problem. Why are you interested in this?

@fileunderwater I have to study about the feeding behavior of engendered predators.  This is required for my higher studies. I got some information. But I am in dark if the prey are of special type for example prey tries to defend the predator in group. If I get this information, then I can study further. I have to collect all information for engendered predator only, as my topic is for engendered predators.

The endangered Canadian Lynx interaction with Snowshoe hare.

A low predator density is not synonym with "threat of extinction". Of course large predators are more prone to extinction because of lower numbers, but they usually exist in lower densities than prey (look, for instance, Lotka-Volterra equations and graphics, and also biomass and food pyramids). The risk of extinction is usually caused by fragmentation of habitat, that reduces population and gene flow.
Many preys form groups to avoid predation. That happens with schools of fish, caterpillars that walk as a multi-organism mass, grasshoppers that change behavior into locusts, bovids and related mammals, that make a circle with the horns to the outside to defend against predators.
So, it's not clear what you're asking. Is there any special case of low density of predator/modified prey behavior?

EDIT: If you want a more concrete answer, it will depend of the geographic region. But everywhere the largest predators are usually the most endangered. They usually prey on large mammals (but not only, since a jaguar can eat an anaconda or an alligator, etc.).
Here is an example from Alaska:
http://www.nps.gov/gaar/learn/nature/muskox-circle-defense.htm

If there is one predator—a lone wolf for example—the defense strategy
  is to form a line. If a wolf pack surrounds the group, the muskoxen
  will form a tight circle, all facing outward, forming a phalanx of
  heads and horns.

https://www.youtube.com/watch?v=pb6Rke7jiTc
http://www.iucnredlist.org/details/3746/0
Although IUCN has no data about the subspecies Canis lupus arctos, they say:

Originally, the Grey Wolf [Canis lupus] was the world's most widely
  distributed mammal. It has become extinct in much of Western Europe,
  in Mexico and much of the USA, and their present distribution is more
  restricted; wolves occur primarily but not exclusively in wilderness
  and remote areas. Their original worldwide range has been reduced by
  about one-third by deliberate persecution due to depredation on
  livestock and fear of attacks on humans.

It may not be the case in Alaska, though.
Another example from Africa are zebras. There are many species from two different subgenera, but if Equus zebra is endangered, what we may think about their predators! Lions, for instance. They flock in groups so the stripes may confuse the predators about where one individual ends and the next begins - making a successful attack more difficult.
http://animals.howstuffworks.com/mammals/zebra-stripes.htm/printable

"Is there any special case of low density of predator" - Answer is yes. Special case is predator population has a threat of extinction due to their low population. They have the difficulties in locating acceptable mating
partners for sexual reproduction during their receptive period due to low population densities.

Not sure if its a "special case" or just a usual low-density predator worsened by other causes of extinction, such as deforestation. Still, not clear what the question is.

Ok. It may be just a usual low-density predator worsened by other causes of extinction, such as deforestation. Only thing is that predator should have threat of extinction.

May I get more concrete answer that I need?

In any example given you can add a theoretical extinction risk.  That's very common nowadays.  You can look at iucnredlist.org, for instance.

Many species of animals use flocking/ schooling/ shoaling/ etc as a mechanism to confuse predators. A few examples are tuna, starlings, goldband fusiliers. tuna and goldband fusiliers use their reflective scales to blind and confuse the predator, whereas starlings use sheer numbers to overpower and throw off their predator. The large groups tend to scare away far away predators.
The act of grouping is not dependent on whether or not the predator is endangered or not, but there would be cases where both the predator is endangered and the prey uses grouping. For example, several species of owl are endangered, which prey on starlings.
https://en.wikipedia.org/wiki/Collective_animal_behavior#Protection_from_predators
http://www.fcps.edu/islandcreekes/ecology/european_starling.htm
http://rsif.royalsocietypublishing.org/content/10/85/20130305


text:
Gene and Protein isoform
What is the relationship between term "Gene isoform" and "Protein isoform"?
Say a gene can make 3 isoforms, will it produce only (maximum) 3 isoform protein?

where are you seeing these terms - context will help answers

The term isoform has become a little ambiguous over the years (see http://blogs.cornell.edu/collinslab/2012/05/30/protein-isoform/)... still some things are consistent:

In some genetics literature 'isoform' has been used in the place of allele when talking about the allele states at a locus for a gene
Typically a gene isoform is equivalent an alternate transcript. The gene isoforms are the set of mRNAs that can be produced by a gene.
Protein isoform commonly refers to the set of proteins produced by a gene, this can include variations produced by alternative splicing and post-translational modification. Note that in some contexts the set of products from closely related gene duplications can also be included.

Note that databases will typically have a specific definition in mind for their use of isoform in their annotation, check their documentation for details (e.g. in UniProt see What is the canonical sequence? Are all isoforms described in one entry?)


text:
Generating custom human DNA sequences based on traits such as eye colour?
I'm wondering if it would be possible to create software (unless some already exists, but I couldn't find any) to generate human DNA (the base pairs on the double helix) containing genes representing specific permutations (eye colour, hair colour, etc.)?
Basically, something like the "character builder" from those "Saints Row"-style video games, except with actual human chromosomes, enabling you to essentially create a 'custom' human.
Of course, that is assuming that all human DNA has a common structure, and that the entire sequence can either be assembled from individual chromosomes, or by using a reference genome and modifying specific genes/chromosomes according to user input. Is this the case?
One setback here, of course, could be the number of bases in each chromosome, which ranges between 100 million and 250 million, and the (approximately) 23000 human genes - a lot of data to manipulate.

A major limiting factor in such an exercise is the complexity of the biological process under question (eye colour etc.,) and thus, our nascent understanding of these. What I mean is that there is not a single gene that determines a given characteristic, rather it is the complex interaction of a set of genes in different conditions responding to environmental cues and such. We are barely at the level of scratching the surface when it comes to understanding the mechanisms that underlie such outputs. And so, we are long ways off (maybe hundreds of years?) before we can even start thinking about coming up with feasible approaches to such objectives.

We may be long ways off- but really? Hundreds of years? I don't think so. :-)

"maybe" is the keyword ;-)

I'm pretty sure 23&me could already do something pretty accurate for many traits.


text:
How many agarose gel bands are typical for circularised DNA
I am aware that circular DNA can be both relaxed and super coiled. However when running an agarose gel of the circular plasmid along with singly digested plasmid with BamHI and HindIII, I see 1 band for the linearized plasmid (lanes 2-5) (as expected) but 5 bands for the circular plasmid (lanes 6 and 7).
What are these various conformations?

I don't have hands on it, but I will not be surprised if supercoiled DNA migrates at different distances according to some inner topological conformation (i.e., more or less coiled AND/OR more or less nicked). Similarly, this picture highlights >8 conformations. What is run in the gel is circularized phage DNA with some degree of knotting due to the circularization (phage DNA is otherwise linear).

Figure from: Arsuaga et al. 2005, PNAS 102 (26) 9165-9169 (free on PubMed Central)
Another theoretical possibility is that two or more plasmids of different sizes were grown in the same maxiprep because of some contamination. But in this case, you will spot the problem also in the digestion, so it does not seem to be your case.

I think these answers have all missed the most likely explanation of the multiple bands in the uncut sample. I agree that you are likely to see supercoiled, linear and relaxed (open) circles in that order going up the gel. But then all of those higher forms are the same thing being repeated for dimers, trimers etc. formed by recombination between plasmid molecules. So, for example, I think the 10 kb band in the uncut lanes is a supercoiled dimer. I have a dim memory that you see more of this sort of thing if the DNA is prepared from a recA strain of E. coli.
update
Here is someone who I think would agree.


text:
Death because of no radio waves
I read somewhere that a man dies if he is isolated from natural electromagnetic fields and waves. (I imply fields of radio frequencies and below.)
Is it true?

note that visible light and infra-red are also EM waves. Humans can survive in total darkness for a while though....it would be pretty cold too!

@Memming: certainly light, UV, and infrared don't count in my question

what frequency of EM wave, then, are you talking about? Without the magnetic field of earth, there would be too much solar wind/cosmic ray as well.

@Memming: I am about radio frequencies and below. I do not ask on indirect effects of EM on survival of human (such as about Earth field protecting from Sun rays), only about direct effect of EM on human body.

I see. So less than GHz range? Could you update your question to clarify this? :)

I never heard of anybody dying in a Faraday cage, so I don't think lack of EM or natural electric field has any effect, at least short term.

This question appears to be off-topic because it is based on an unreferenced claim

@porton I think your right, we all know that every body above absolute zero dissipates energy as em waves, so if a person is isolated from all em waves it implies that there is no em wave coming to him, so the person dies because hi will be at absolute zero temperature at that moment. Hope it answers your question.

I've never heard of such a thing, and a quick Scholar search didn't yield anything significant. In fact, artificial radio waves are used in things that usually save lives, like MRIs.
If we were truly agnostic about this, we could say that it might or might not have an effect on human survival due to the general lack of evidence or even indication of a claim, but like the orbiting teacup, it's safe to assume that given our current extensive set of knowledge of biology, radiowaves do not affect human at all, and that as it has not been observed, the claim doesn't have a scientific basis.


text:
Why some seeds are mucilaginous (chia, rucola)?
Why some seeds are mucilaginous (chia, rucola)?
It is not obvious what kind of preferences that can bring to them. What is a role of mucilage in seeds cultivation?
P.S. The cultivation in germination cup shows only "difficulties": more affected by micro-flora, harder consequences after become too dry...


text:
Could be an union/synergy between Math, Computer Science and Marine Biology?
I'm studing for my bachelor's degree in Natural Science and I have to chose the path for my future life. I have to chose the right kind of graduate studies. Since I love computer science, maths and marine biology more in details I love the tropical ecology especially that of the coral reefs and atols in the pacific ocean, the whales (e.g. the humpback whales and their migrations), the computer simulations and mathematical models. Thus, I want to ask you if is there a branch of marine biology that allow me to study and specialize myself in tropical ecology and in math & computer science too, because in my current course we don't have any exams of computer science and only one of maths, and I'm feeling sad for this. The right path coul be the computational biology? Exist in biology, some field called "Computational Marine Biology" or "Computational Marine Tropical Ecology"? One last thing, what about Ecoinformatics?

You won't find a field as such, but knowing how to do computational biology can be applied to any field. You just need to find a group that works on a subject you like and then offer to do their modelling. That's the great thing about groups, they consist of different people, each of whom has different knowledge and abilities.

This is a very open-ended question, and you could come a long way by just searching Web of Science for the keywords that you have mentioned. I dont know about "Computational Marine Biology" as a defined field, but in population or community models of marine life mathematical models are certainly used and computational skills are clearly useful. To guide on particular topics is almost impossible, and not the subject of this site. GO with what you find interesting and try to find suitable research groups.

I have the intuitive feeling that it may be easier to specialize in computer sciences and then apply this to marine biology than specialize in marine biology and then learn the computational tools. It may be easier to learn the tricky technical aspects with a younger brain, and later acquire the necessary knowledge to apply your technical skills to marine biology. Of course, it would be better if you could study both at the same time, but it may be difficult to arrange this.

This advice is America-centric; graduate programs in other countries may be different, especially in regards to assigned course work, etc. But this should more-or-less be solid. Also, I'm assuming you're interested in a PhD.
I don't know if what you're looking for is a proper field, but that doesn't matter.  Ideally, grad school is where you do research on your own terms, and what lab you join is the single most important consideration. What you want is a competent program that:

gives you the flexibility to create your own subfield
has supportive and knowledgeable faculty that you can work under
has excellent computer science AND marine biology programs (or analogs)

First, find faculty who are doing research you are interested in, and look at the programs available at their schools. Since they're the most important consideration, everything else will fall into place after that.
Next, email 5 of those professors with an introduction of what you're interested in, particularly about their research.  Ask them what programs are most appropriate at their university, and how flexible you can be in taking appropriate coursework.
At some point, you'll probably want to decide if you want to be more of a marine biologist or a computer scientist. Your diploma at the end of the decade is only going to say one of those things.  That shouldn't make a huge difference as to your job outlook, but is worth thinking about.  Practically, the question is whether you want to get your hands dirty, go out on a boat, and collect your own data.  Alternatively, if you join a CS program, you are more likely to be analyzing large datasets collected by other scientists.
At most universities, you'll likely only have the option to join a biology program. But there are certainly excellent CS programs with biology oriented faculty.  Even then, the CS faculty is more likely to be doing genomics and such.
For practical recommendations, the University of Washington in Seattle would probably have something appropriate to your interests. While I was there, my lab was adjacent to an Oceanography lab that had a video wall for visualizing ocean currents and such. Not precisely marine biology, but UW has a very collaborative faculty and I'm sure the two departments work together.
UW also has a strong computational biology program that you can go into either through CS or through one of the many biology programs. You should also check out the Institute for Systems Biology at UW. I saw a presentation there specifically about DNA exchange between marine microorganisms.  I'm not saying UW is your best option, I just know that school because I did my PhD there.
A final word of advice. Once you're in a program, it's very likely your interests will change as you learn about other research going on. And also, it's quite possible you won't get into the lab you want simply because of money or logistics. With both of these in mind, be flexible about where you're willing to go. What you do during your PhD isn't really that important anyway.  If you're going to be research scientist, it's what you do during your Postdoc that will establish your career. Just take the opportunity to learn everything you can and see what's out there.
Hope this helps.  Good luck!

Alexander's advice is excellent in the general case, but since I faced a very similar problem when I applied to grad schools last year, I wanted to offer my perspective on this specific union of fields. Many people (including me) believe that this intersection is about to be a really important field - ecologists are starting to recognize the need for scientists with these skills, but there is not yet a lot of infrastructure in place to train such scientists. This presents a challenge to people like you and me right now. On the other hand, it means that if we can find a way to acquire these skills, we should be pretty well set up to help establish this field (bonus: we should be pretty well set up to get jobs).
I am personally of the opinion that if your interests are truly interdisciplinary, it's a really good idea to go somewhere that has a framework in place to support interdisciplinary work. Otherwise, you can end up in a situation where your adviser doesn't feel equipped to offer guidance on large portions of your projects, which can strain your working relationship and stymie your progress. Despite the lip service paid to the importance of interdisciplinary research, however, programs that are set up to provide interdisciplinary mentoring can be hard to find. The best course of action depends very specifically on how you want to combine these fields.
If you want to stay rooted in biology and use computer science and math as tools without doing research that furthers them as fields, you're in luck. There are a lot of labs with PIs who do this kind of research and many more who are interested in finding people who can, as terdon said, "do their modeling." I would be careful of the latter scenario while you're still in the learning phase of your career, however. As a student, your goal should be to learn how to best do the research that you want to. If you are the lone modeler/math person in a group, you may be in high demand but your rate of learning will probably be a lot slower than if you had an adviser who was actually doing what you are interested in. If these are your interests, your options are pretty varied but take a look at UC Berkley, and UC Davis. Also UW, as Alexander suggested. There are indeed good collaborations between biology and computer science there. I found it helpful to search for people who were studying macroecology, but that might be a label that is used more for terrestrial systems.
However, if you want to do research that actually furthers computer science in addition to biology, things get more complicated (I don't know if there are people who do both math research and biology research so I can't speak to that). Don't constrain your thinking by believing that you have to get a degree in one or the other; dual degree programs exist (and that may sound intimidating, but they aren't necessarily more work, just different work), although they are so few and far between that you might decide that it makes the most sense to just choose one field. If this is what you want to do, take a look at UC Santa Barbara - they do a ton of marine bio research and are home to the National Center for Ecological Analysis and Synthesis. Also, again, UW. I'd recommend my program too, but it's neither marine nor tropical.
In general, if you want to get a feel for how open a lab is to you doing interdisciplinary research, I found that it was best to just ask explicitly. If a place offered joint appointments (i.e. the ability for me to be co-advised by professors in two departments), dual degrees, or even just had research groups that involved people from multiple departments, I took that as a great sign.
In summary, don't start out with low expectations for finding a match for your interests. That said, it will ultimately be valuable to be flexible, as both finding a perfect match and getting accepted to it definitely requires a lot of luck. The considerations that I've brought up here won't make or break your grad school experience or your eventual career. They're just things to keep in mind if you have the option. I also apologize that it's probably a bit late in the application season for this to be useful to you, but I had such a horrible time grappling with these same issues that I just wanted to put what I learned out there in case it can help anyone.
EDIT: I forgot to address ecoinformatics! Ecoinformatics can fall into either the "computer science as a tool" category or the "furthering both computer science and biology" category, although it falls into the latter category much more frequently than modeling does. It still all comes down to what exactly you want to do. Look at research in computer science journals. If doing that sort of thing appeals to you as much as biology research, then you should be thinking about trying to pursue both fields. I found doing some pure computer science research helpful for figuring this out, but you probably don't have time for that.

"Despite the lip service paid to the importance of interdisciplinary research, however, programs that are set up to provide interdisciplinary mentoring can be hard to find." - This is sad, but very true. Even in programs that are set up for this, individual professors may not be comfortable sharing students. It is definitely best to talk directly to faculty that interest you (this applies to any field) and see what kind of mentoring style they're willing to offer.