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DNA replication and combination

"Each gamete is genetically unique because the DNA of the parent cell is shuffled before the cell divides. This helps ensure that the new organisms formed as a result of sexual reproduction are also unique."

Then why do we say that the DNA of the parent influences the characteristics of the child while the DNA of the child is formed as a combination of shuffled up nitrogenous and phosphate bases?

Welcome to SE Biology. Please provide a citation for your quotation.

To explain it briefly:
Lets take a human as example, you are diploid and you have a pair of 23 chromosomes (= total 46) and the sex chromosomes which I will exclude for this explanation.
Your gamete is haploid and has therefore only one of the two paired chromosomes. So for every chromosome pair there are 2 possible chromosomes. So in total you have 223 possibilites to arrange chromosomes. The gamete from the sexual mating partner also has 223 possibilites to arrange chromosomes. So in total a new diploid organism has (223)x(223) possibilites. So unique.
However, it is always the chromosomes of the parents. So yes, parents influence the children because the genetic information of the children can be found in one of the two parents.
Furthermore you have recombination, but you already asked another question about this. So I will not expand this answer.
There are relevant articles in Wikipedia on genetic recombination and meiosis that I would recommend.

Thank you for your contribution. I have reset your programming-style powers in html superscript tags and replaced * by x for general readability. I have also rewritten your reference links in a way that it is clear what they refer to.

Parents influens children's characters because the shuffeling (crossing over)  changes only few genes present on the parent chromosome and also these changed gene peices are also parental so actually we recieve a non parental chromosome (generated by shuffling)but the genes present on it are still parental..  Hope this helps


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Humans have tails?
Today in biology class, my teacher said that all chordates have all the necessary traits, at least during the embryo stage, and we humans are chordates. So, one of these necessary traits was that they should have tails. My question is, humans don't seem to have tails, so how can they be chordates?

Oops.... I am always surprised when my vote to close alone is enough to actually close a question. I think @kmm answer is good (+1), I just wanted to highlight that the question can be though as a duplicate of another one.

@MamaTank what I meant is that, a species can be called a chordate only if it has all the traits a chordate is supposed to have.

The chordate trait you are describing is more precisely termed post-anal tail. It is one of the basic characteristics of all chordates, along with, among others, pharyngeal pouches, a hollow dorsal nerve tube, and a notochord. Two other traits are less commonly considered chordate traits: segmented body musculature and a thyroid gland or endostyle (the latter particularly controversial).
These characteristics are present in all chordates at some point during their ontogeny. These traits are shown below.
We can see these most clearly in embryonic forms. For the post-anal tail: in humans, there is a short "tail" that extends past the anus (end of the yellow tube). This tail does not typically persist for very long. Similarly, the notochord is absorbed into the vertebral column, and remnants of the pharyngeal pouches are not externally visible.
The key phrase is "at some point during development." Non-embryonic humans don't have a tail, but that doesn't mean humans are not chordates.

What do you mean "non-embryonic humans"?

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What organelles are in an onion cell?
I was wondering what organelles are in an onion cell, because, based on the labs we are doing in my biology class, I only saw a nucleus and cell wall. My friends and brother say there are all the organelles that you would find in a typical plant cell, but I can't find any evidence anywhere. I need to create a model and it's due in a week.

what magnifivation was used to see it

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Neural signals amplitude
Can anyone explain me if there is a difference in amplitude of signals between extracellular recording and intracellular recording. I know that the amplitude of neural signals when an action potential occurs is from -70mV to 45mV for intracellular recording. The same results are for extracellular recording?Can someone help me?
Also, I have read a paper that refers:

Neural signals from extracellular recording are very weak (typically between 10 μV and 500 μV). As a result, amplification is needed before such signals can be processed further."

So my question is why neural signals are so weak (maybe author when he says 10μV refers to amplitude) when we know that an action potential has amplitude approximately 75mV(-70mV to 45mV)?

The edit to this post referring to signals between 10 and 500 Volts is definitely incorrect (unless you are measuring voltages in electric fish); maybe it was microvolts.

Possible duplicate of Why is extracellular measurement of action potentials so different from intracellular?

Those voltages refer to the difference between the inside and outside of the cell (i.e., -70mV means the cell is 70mV more negative than the outside).
You can't possibly measure that potential difference from outside of a cell. When you do extracellular recording, you are measuring spatial differences in ion concentrations that occur due to ions flowing in and out of cells. For example, when a cell fires an action potential, lots of positive ions flow into the cell; this makes the area just around the cell slightly more negative than an area further away. The magnitude of this potential as measured depends greatly on your recording configuration, the type of signal you are recording (i.e., population activity or just a single cell; synaptic currents versus action potentials), how close your electrode is to the signal you are recording, and where your ground is (or position of both of your electrodes if you are doing a bipolar recording).
Although it varies, in most cases the signals you record extracellularly are on the order of microvolts to a couple of millivolts.


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What is meant by "complexity of carbon sources"?
My biology book states

"life on earth depends upon carbon based molecules, most of these food sources are also carbon based. Depending upon the complexity of these carbon sources, different organisms can then use different kinds of nutritional processes"

Please explain this statement.

They mean complex arrangement of the carbon atoms in the carbon sources.

According to me Plants are autographs and they make their own food by the process called photosynthesis and they take Carbon dioxide and water directly from air and roots so Thor the simple diffusion is taking place so they are not that much complex than us so they use simple nutritional process

@Tanushka - On Stack Exchange we are looking for informed answers supported by citations, references or links. This allows users of the site to judge their validity. Please read the tutorial before posting or answering.

Consider all the different types of carbon molecules one can find on earth.
Proteins.  Sugars like cellulose and starch.  Alkanes like methane and tar.  CO2.  Alcohols.  A boatload of variety.
Now think of how each one is used or can be used by an organism.  I will chow down on a potato.  And some alcohol. Termites eat cellulose.  Anaerobic bacteria use methane.  Plants eat up the CO2.
One carbon nothing eats is CaCO3 or limestone.  I am not sure why.  Oh - also diamond.  Not many things can metabolize a diamond.  Although maybe they don't get the opportunity to try...

@gerardo Furtado  CO2 is also technically an inorganic compound.  But lots of things use it.   "Complexity of carbon sources" I think encompasses traditional concepts of inorganic and organic.

Consider that all the various carbon compounds mentioned can react with oxygen (perhaps including other things in the reaction) to produce energy and CO2.  CO2, OTOH, requires energy from sunlight for plants to turn it into more complex carbon compounts.  Simplistically, CaCO3 is like CO2 in that it would require energy to metabolize, but most of it sinks to the ocean floor where there's not a lot of sunlight.


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Origin of human intelligence and thought
I've been debating this topic with a friend of mine and we can't get to a common answer. She argues that we don't descend from any Chimpanzee or Orangutan because, if we did, they would also have the cognitive thinking ability that we have. I am arguing that a high protein diet allowed the first humans to have the possibility to develop a higher memory, intelligence and other mental procedures.
But after all, what would be the real origin of the intelligence? And if animals do have intelligence too, why isn't theirs as advanced as us.

Read https://en.wikipedia.org/wiki/Evolution_of_humans.  We did not evolve directly from chimpanzees or orangutans, but rather humans and chimps share a common ancestor more recently than most other species.

Ok, but what about cognitive thinking?

Could you make it clearer as to how these arguments can't coexist? It seems to me that (hypothetically) we could or could not have a common ancestor with chimpanzees and have become more intelligent thanks to a higher protein diet.

You're right. The main debate here is the origin of the thought. She replies that thinking is a faculty of the soul, and not a matter of biological evolution. My question would be, When does in the line of evolution humans/primates started to actually think. And why ?

I feel that a tighter set of definitions could help the discussion. What do you mean with thinking, cognitive thinking and intelligence? Intelligence/thinking is also not (in my mind) an on/off thing, and there is a continuum between 'pure' instinct behaviour and behaviour based on intelligent thought. Also, if your friend has the starting point of a mind(soul)/matter separation (dualism), where evolution cannot affect the mind, you will probably have a hard time convincing her.

I use them without difference, it's just for the matter of this. I know that they are completely different, but just for this discussion, I'm using them as the same besize they are completely different. The term that I should be using is Reason. The fact of recognizing myself as a human being.

I recommend watching the PBS documentary [The Human Spark] (http://www.pbs.org/wnet/humanspark/episodes/program-one-becoming-us/video-full-episode/395/ ) for a thorough look on this particular question, including this evolutionary approach to it comparing with chimpanzees and other primates. PS: I am not aware if everything is available for free, it will take maybe a little bit of browsing to find them, but I know I managed to.

How is

"we don't descend from any Chimpanzee or Orangutan because, if we did, they would also have the cognitive thinking ability that we have"

not equivalent to

"We are not related to the chimpanzee or orangutan because, if we did, they would also have [the same amount of body hair]/[the same sized mouths]/[the same muscular strength] that we have"

?
Any related species are going to differ in some respects (otherwise they would not be different species, after all), and it is plain to see that intelligence is one of the ways in which species can differ.
Regardless of that (if your friend thinks intelligence is special in a way that hairiness is not), you can make your argument even while sticking to talking about intelligence, and there is no need to go into the reasons for changes (increases) in intelligence to see that.
To make the point with your friend, it might be best to point to two different animals that

she recognizes as related, and that
she also recognizes as having different levels of "cognitive thinking ability".

In light of such an example, her argument falls flat (unless she further considers only human thinking ability special, in which case you will have a harder time!)

Actually yes, she does think that human race is the only one to think, being this good a faculty from the soul(again, which only humans have). I certainly don't agree with her, but with evolutionary theory. But, in which point do humans differentiated from the rest of the animals, (that means, stopped being like the rest of the animals by having cognitive thinking and self recognition as a being) and why?

All the evidence suggests that we aren't qualitatively different from other animals - most of our cognitive traits are present to some extent in other animals. For example, birds, primates and cetaceans can all solve abstract puzzles, and some aniamls apparently recognise themselves in a mirror.

Regarding self-recognition: https://en.wikipedia.org/wiki/Mirror_test#Animal_species_capable_of_passing ...in fact, according to the same wiki article, humans aren't capable of recognising their own reflection until around 18 months. By your friend's logic, do babies therefore have no soul?

@atrichornis Nice.  I was going to link to exactly that article.  +1  (at)Eric Frick, the fact that the list of animals who recognize themselves in the mirror is non-zero should be enough, but let's also consider that self-awareness can be present without understanding of the specific concept of image reflection, so the list is longer still.  Also, people who have their sight restored after being blind from birth can fail the mirror test, so your friend can't dismiss atrichornis' baby argument purely on the basis of babies not having all of their cognitive faculties yet.

@EricFrick The second part of my answer, which admittedly will probably not move your friend, is that the onus is on her to prove the existence of the soul, or that human thinking means a soul is there.  On that second part, if she does not want to end up concluding that some humans don't have souls, she will have trouble defining thinking that is present in all humans (including those with severe disabilities) but no animals (including the clearly intelligent ones).

Indeed. It seems the soul must be a temporary gift. It is given to toddlers who then become self-aware, and then taken away from a proportion of the elderly population who then sink into dementia and lose most of their higher cognitive function. Makes perfect sense!

One thing we haven't discussed much is emotion. While the science is somewhat anecdotal here, there is good reason to believe that emotions aren't unique to humans. Alex the African grey parrot, apart from having a better grasp of language than a human toddler, also seemed to have comparable emotions to a toddler (for example, he was prone to sulking and acts of kindness). http://en.wikipedia.org/wiki/Alex_(parrot)

@atrichornis I doubt you will find anyone who is not a crackpot who claims that animals do not have emotions. Try wetting a cat and telling me she is not pissed off.

Certainly, but @EricFrick's friend sounds like she might be a crackpot!


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What is the inbreeding coefficient for the female offspring of a sib-mating in a haplodiploid system?
The inbreeding coefficient of a sibling mating for a diploid organism is 0.25 (each allele has a 25% of being identical by descent in the offspring).
In haplodiploid organisms, males result from unfertilized eggs, so they don't have fathers (they get half of mom's diploid genome, and that's it). Females have both a mom and a dad, and are diploid in the standard way (dads give their daughters their entire genome).
What is the inbreeding coefficient for the daughter of a sib mating?

I think the answer is 0.25.
Here's how I arrived at it:
The only way a daughter of a sib-mating can have an IBD (identical-by-decent) genotype is by being homozygous for one of the two alleles belonging to her grandmother (her mother and father's mother).
There is no way for her to be IBD for the allele that her grandfather has, because that allele can never end up in her father (who only gets an allele from his mother, because he's haploid).
Let's trace the path of an allele from the grandmother to the focal grand-daughter:
This allele has a 50% chance of being passed from the grandmother to mother, and another 50% chance of being passes from mother to focal. It has a 50% of being passed from grandmother to father, but then a 100% of being passed from father to focal (it's the only allele that father has to give). So, the probability that ALL of these things happen is 50%*50%50%%100 or (1/2)^3 = 1/8 = 0.125 or 12.5%.
Since this can happen for EITHER allele from the grandmother, this must be multiplied by 2, giving our final inbreeding coefficient of F=0.25 or 25%.

From the same article on wikipedia:

The inbreeding is computed as a percentage of chances for two alleles to be identical by descent.

Now let's draw a family tree for such mating and sign chances for having each allele:

You can see, that the "brother" has a 50% chance of receiving A allele and the "sister" has a 50% chance of receiving A from their mother, but the "brother" will not have the C allele that the sister certainly has. Their daughter will have the allele from her father and one of mother's alleles. Therefore, her chances of having a C allele are 50%, and for a A or a B allele each 75% (remember, she needs two copies, so we need to end up with 200%; furthermore, she may have two A alleles but not more than one C allele). Chances of her having two A or two B alleles are 56,25% $$0.75 * 0.75 = 0.5625$$
Now we have the percentage of chances for two alleles to be identical by descent, her inbreeding coefficient is 56,25%.
The son will have only one allele, 50% for C, 25% for A and 25% for B. Because he does not have two alleles, by definition there is no inbreeding possible.

http://en.wikipedia.org/wiki/Inbreeding
I'm thinking that the answer is not defined as there is probably an explicit or implicit assumption about both parents having the same ploidy (brother (haploid) and sister (diploid) in your question) in both the path and tabular methods used for calculating inbreeding coefficient.


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Are humans still competing in the same way now that the first life forms did?
I'm not sure if this is actually a philosophical question, but I was reading a timeline of life on earth and I came to this:

4500-3500 Ma The earliest life appears, possibly at Alkaline vents
  with the creation of the Last Universal Common Ancestor, possibly
  derived from self-reproducing RNA molecules.[6][7] The replication of
  these organisms requires resources like energy, space, and smaller
  building blocks, which soon become limited, resulting in competition,
  with natural selection favouring those molecules which are more
  efficient at replication. DNA molecules then take over as the main
  replicators and these archaic genomes soon develop inside enclosing
  membranes which provide a stable physical and chemical environment
  conducive to their replication: proto-cells.

..and I thought to myself, are we still essentially doing that as we live our lives?  I think I'm trying to connect the idea of a human "being competitive" with "evolution".. is there any truth to that?

It's important to realise that evolutionatry competition and the common usage of the word competition do not mean quite the same thing. For example, you could talk about Usain Bolt competing in the 100m but this is only evolutionary competition with the other athletes in they are in competition in terms of evolutionary fitness. Evolutionary fitness encompasses ideas of survival, reproduction and the nurturing of offspring. The only thing that matters, from an evolutionary point of view, is how many successful offspring are produced1. Where human competition does not relate to this, it is not related to competition in the evolutionary sense.
People certainly do still compete in the evolutionary sense for mates, resources, etc. but in the West, in particular, much of human competition has become a very long way removed from anything that relates to evolutionary competition except in the most tangential of ways.
1 - my favoured definition for fitness is number of grandchildren.

If you have kids and set a horrible example they might be afraid of screwing their own offspring up and decide not to propagate.

Your question is a little vague, but if I understand it correctly yes.
The crux of evolution is that in essence the resources we need to survive and reproduce are in lower supply than necessary for all to survive- therefore there is competition for such resources.
Those who are more genetically adept to gain those resources are more likely to pass on their genetic material to the next generation.
If you're speaking specifically about Humans there is of course still competition between individuals for resources (money being a primary one now). Competition is just an entirely different game now. Beyond that level of answer it's a philosophical can of worms I don't feel equipped to properly answer, and arguably it doesn't belong here but over in the philosophy stackoverflow.
Hope this helps a bit...


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What in soy are people allergic to and will these allergens be passed along if an animal that has eaten soy is consumed?
I have two related questions about soy allergies and possible reactions.

What is it that are humans who have soy allergies actually allergic to? What is the allergen?
If an animal eats soy, are those allergens broken down or retained? Can the consumption of that animal cause an allergic reaction similar to direct soy consumption?

I think this is a worthy and interesting question. I've rewritten it to try and make to not personally medically related.

There are multiple soy protein allergens.  This has a pretty good review in the introduction.  Here is a list of some of the allergens (same paper).
Chickens on soy diets do lay eggs with higher concentrations of soy isoflavones than chicken on non-soy diets. (Edit: higher concentrations of soy isoflavones are also found in chicken tissues -- see ref 4 below.) References (originally found here) are:

Saitoh, S.; Sato, T.; Harada, H.; Takita, T. Transfer of soy isoflavone into the egg yolk of chickens. Biosci. Biotechnol. , Biochem. 2001, 65, 2220-2225.
Saitoh, S.; Sato, T.; Harada, H.; Matsuda, T. Biotransformation of soy isoflavone-glycosides in laying hens: intestinal absorption and preferential accumulation into egg yolk of equol, a more estrogenic metabolite of daidzein. Biochim. Biophys. Acta 2004, 1674 (2) 122-130.
Lin, F.; Wu, J.; Abdelnabi, M.; Ottinger, M.; Giusti M.M. Effects of dose and glycosylation on the transfer of genistein into the eggs of the japanese quail (Coturnix japonica). J. Agric. Food Chem. 2004, 52, 2397-2403.
Vargas Galdos, Dante Miguel Marcial. Quantification of Soy Isoflavones in commercial eggs and their transfer from poultry feed into eggs and tissues. Thesis. Ohio State University, Food Science and Technology Graduate Program, 2009; http://etd.ohiolink.edu/send-pdf.cgi/Vargas%20Galdos%20Dante%20Miguel%20Marcial.pdf?osu1236706764.

However, I do not know whether this is enough to cause an allergic reaction if consumed. (There's plenty of anecdotal evidence, but no clinical studies that I know of.)

Are soy isoflavones among the allergens listed, though?

@octern: they're not listed, but that table references only the major allergens (as per the authors of that paper, there are around 20, although only 7 are in the table). Hence, my last statement - anything I can find regarding this is anecdotal evidence from not necessarily reputable sources.


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What species of bird is on this coin?
What species of bird is depicted on this coin?

http://www.artic.edu/aic/collections/citi/images/standard/WebLarge/WebImg_000100/139651_846511.jpg
Thanks in advance for your help!

well I don't think this is really a biology question given that it is probably quite an "artistic" impression of the bird, but some clues as to the coins origin would help people hazard a best guess at most.

The coin shows Ptolomey I Soter I, a ruler of ancient Egypt c. 367 BC – c. 283 BC. This Source suggests that it is an eagle standing on a thunderbolt.  This is corroborated here and again here so this seems most likely.  This question isn't really answerable from within our site scope, however, see the species identification tag wiki.  Hope the above helps though!

It said to be an eagle.
It looks like a Ptolemy V (204–181 BC):
http://www.bonanza.com/listings/-DD-G-068-Ptolomy-V-Octadrachm-COPY/16293418?gpid=21297750541&gpkwd=&goog_pla=1&gclid=CMWBpbOaxrUCFYx_Qgod6TsA9w
it looks to be a pretty standard motif of that era:

From: http://www.worthpoint.com/worthopedia/alexander-iii-great-336bc-greek-coin-150614256
I agree that this is not really a biology question.. but what the hey.

this is why we need new answer notifications when writing comments!

I know a professional ichthyologist who once had to propose an identification for a fish painted on a cave wall. Surely it is more difficult than identifying from a real specimen, a photo or a scientific drawing, but in some case, artistic representations have a precise biological source of inspiration, and it is meaningful to try identifying it.
If we didn't already knew what species of bird is represented here:
http://en.wikipedia.org/wiki/File:Seal_Of_The_President_Of_The_United_States_Of_America.svg
I think it would make sense trying a identification.

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While someone's ears pops with pressure, can he/she hear other sound at the same time?
I know that after or before someone's ears pops because of pressure changes, he/she can hear the sound such as laughter. But can these two things ("her ears popped with pressure" and "she can hear the laughter") happen at the same time?

Yes, of course they can. What happens when your ears feel 'full' like on an aeroplane is that the air pressure in the middle ear is different from the air pressure outside. When you 'pop' your ears, you push open the Eustachian tubes that connect the middle ear to the throat and make the pressure equal. No matter what the air pressure, the air still conducts sounds. The difference is that your ear drum moves a bit less if the middle ear pressure and outside pressure is different, thus why sound is muffled before you pop your ears.

the air still conducts sounds---yeah, that's the key, thank you ! can we hear a sound like a "pop" when we pop our ears?

Sort of! it's kind of similar to the noise you hear when you swallow saliva as well as a gentle 'popping' feeling and relief.

aha!I see. and if the pressure of inside and outside is highly imbalanced, then the sound of a "pop" will not be gentle, and will be like a really "pop", right?

@Lincoln I guess so?

maybe having an extreme experience like this will know it...but the one will be deaf, right?...

@Lincoln well usually if the pressure on either side is different your hearing is a bit muffled. If there is an extreme pressure difference (from a combination of Eustachian tube blockage, infection & air travel, or more commonly a momentary difference caused by a huge sound like an explosion) your eardrum will burst. This is called 'barotrauma'

@Lincoln no problem! I'm guessing you've never felt your ears pop?

yeah, being seen through by you...  (hope you understand what i am saying... pardon my my bad english...not a native speaker).


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Determination of gene direction
I have one sequence that composed of sequences of three genes. I should determine the direction of each gene, but two of these genes are disrupted, and I can't determine the initial codon. Does anyone knows how I can determine the direction of genes?

I'd first try translating it and looking to see if there are big regions that jump out at you that do not have stop codons in them.  I normally use this tool for quick and dirty translations, it gives you all 6 reading frames.  Also, you could just try BLASTXing your sequence if it is short enough.  BLASTX translates your DNA in all 6 reading frames and will search the protein database for matching proteins.  Most anything will have a hit in there, and if you get a hit it will show you the DNA sequence and reading frame that got translated.  If your sequence is too big, break it down into smaller chunks until BLASTX works.  One of your chunks will have your gene in it, and it will get a protein hit.  You'll also need to break it up if you have two genes in one chunk, but you only get results for one of them because its longer and gives better hits.


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RNA-seq Data on domestic animal with different environment
I want to find the RNAseq data available on domestic animals in different environments. If microarray data is available, it would be more useful. If you know I would appreciate to inform me.

There is something called GEO, which is maintained by the NIH and is a massive collection of data obtained from RNA seq, microarray, etc. experiments. One thing you can do is search for a paper that has done what you are looking for. The paper may have a GEO accession number, and you can use that number at the GEO website to find the data you want. You may also search GEO directly but Im not too familiar with it. It may just be easier to find a paper with a GEO accession number.

There's also the ArrayExpress database maintained by the EBI.


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Is Homo sapiens the only species capable of prioritization?
Just what the title states--given an absurdly large number of assignments to perform in a limited time-frame we usually attempt to do the most important ones first. Is this ability to define and execute by priority a universal feature in all sentients, or is it a socially learnt behaviour of us Homo sapiens?

I think this is a tough question - how could you tell? Many animals are seemingly capable of 'planning' their lives (for instance mating and rearing offspring at the right time, keeping them fed, safe from predators, etc, might seem to have taken some planning) but that is not to say they do any such thing. I would have thought it's all instinct, but I look forward to any answers!

of course not - prioritization is necessary to survival.  I think this is not apparent because most living things don't worry about so many things as we do.  But social relationships vs mating relationships or the act of mating vs food vs avoiding danger have very clear priorities with most living things.

Both useful comments .. I also goofed in my question a little - the concept of time itself is probably not very well understood by other species. I wonder whether I should make that into a question, and ask too.

Animal behavior is not my field but I think the answer is "no, animal feeding / foraging shows optimization of the cost / benefits of finding and capturing different foods / prey", an ecological 'paradigm' as explained here https://notes.utk.edu/bio/greenberg.nsf/d9441c1523c0c69785257015006e1937/1c127b67e45523e4852575de006d4233?OpenDocument

There is a very simple experiment you can do that will demonstrate that animals prioritize. Give a dog two bones. Preferably one which is more tasty than the other. Say one has more meat on it. The dog cannot eat both at once and you will observe it choosing one over the other. This is a clear example of prioritization.
Again with a dog, try observing one greeting two people it is fond of. If you and a friend stand a few meters apart when the dog comes up to you, the animal will choose to greet one of the humans first. Prioritization.
Any animal, or plant, fungus, bacterium or archaeon for that matter, that is ever presented with a choice between two actions during its lifetime, will have to be able to prioritize in order to chose between them. Clearly they can as our world is not strewn with, for example, panicked, confused looking squirrels trying desperately to chose which tree to climb.

Good point! Sir Dumpty, when offered a second bone whilst he is already eating one, will invariably opt to snap up the new one first; perhaps knowing the one he eats at present will remain untouched by the rest of his 'human family'... I could be wrong about understanding what goes through his mind though

@Everyone, please tell me you also have a cat called Dame Humpty!

Afraid not (+: Sir Dumpty is all by his lonesome.
p.s. Did you realize you're on the 666 score?

@Everyone, shame, poor Sir Dumpty, and yes, I only just realized my rep and its all thanks to your upvote :)

All species of the genus Homo were able to plan stone tool manufacture in a way that suggests the ability to prioritize and follow steps to an envisioned end form.

Good point! too bad the other members of our genus are extinct.


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What makes a metal safe to use for an artificial joint?
What determines if a metal is suitable for transplantation such as in the hip? What I am most interested in however is why might some metals be toxic to animals once in the body?

There are a number of reasons why a given metal may be toxic to an animal:

Radioactive metals are the easy ones.
Some metals can affect the normal biosynthetic pathways within the body.  Lead is a good example of this, as it can take the place of calcium; I believe beryllium does the same for magnesium.
Some metals themselves are very reactive.  Hexavalent chromium ($Cr(VI)$) is highly reactive, and will cause damage through severe oxidative reactions, whereas $Cr(III)$ is largely okay.
A lot of metals are okay, even required, at some level, but become toxic at too high a concentration.  Iron, for example.
People can simply have allergies to metals.  Nickel in silver jewelry is a good example, although in my experience it can be overcome.

The basic gist is that some metals are required for life, some aren't but aren't too terrible, and some are completely toxic to it.  Different organisms can vary a bit in which metals are useful or not.  A good implant will of course not be toxic at all, and will be strong and long-lasting.  Titanium is often used, given its strength and general nonreactiveness, but so is cobalt, despite being toxic to some degree.

Ref: Metal Sensitivity in Patients with Orthopaedic Implants.  Hallab, et al. J Bone Joint Surg Am, 2001 Mar 01;83(3):428-428

If the question is why a transplant implant like an artificial hip may be made from a metal, then toxicity issues of the metals are not the main question.
I think it would be better to focus on metal sensitivity.
Metal sensitivity is not a specific immune response as with transplanted organs, but a non specific response to a foreign substance in contact with the body. While  Surgical stainless steel and similar hardened alloys which contain iron, nickel, chromium and molybdenum are popular for metal components of implants, even plastic coated pieces can cause scarring and irritation.
This reaction is highly variable from one individual to the next and can have no effect or cause further surgery or rejection of the implant.  the cause is poorly understood and so diagnosis is still in an exploratory state.
Since oxidation and rust seem to cause more irritation, it seems that corrosion resistance is an important part of implant metal choices.   Hardness, durability and Cost is also an issue since I'm sure gold and platinum would also be great choices from a cost perspective.

I think the question is specifically interested in what makes some metals better or worse than others.

i agree, though I feel that within the the set of metals that might realistically be chosen for implants might be a more focused answer.

I think  @Amory answer is a good one but I would like to add a new point for the last part of your question.
Our normal body cells can recruit the immune system when there is infection but the transplants can not. Some findings suggest that bacteria can form a biofilm over that part and  so can become difficult to treat with antibiotics.
Source : I read this in a book called Good Germs, Bad Germs by Jessica Snyder Sachs

yes this is i think more to the point. why is surgical steel better for transplants than say, iron or copper?  immune rejection is a big part of the problem, but i don't know the answer myself

@shigeta I don't know why surgical steel is  better but I can only say that whatever artificial material we use, biofilms are going to be a problem .

Biofilms can form on materials within body cavities exposed to fluids. But can it form on implant materials within tissues surrounded by tissue fluids? Are there any references?

then why do they bother to use some alloys of metal at all?  its not for the looks... lmgtfy  http://emedicine.medscape.com/article/1230696-overview

@shigeta I really don't know why.

ok i'll ad a bit on that below.


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Which cells will pass cancer to offspring?
Each of these types below contains a DNA mutation. Which type(s) will affect the children of the individual whose cell it is.

Red blood cell
T cell
Skin (epithelial) cell
Neuron from the brain
Sperm cell
Cell from lining of the uterus
Placenta cell
Stem cell

My attempt: I think it's only a sperm cell, because that is the only cell to get passed on.  Is this right?

(This should be a comment, but my reputation precludes me from doing that)
I just wanted to chime in and say that it looks to me that the last three are just Red Herrings that are supposed to make you think a bit.

Red blood cell
Will probably not. You inherit blood type, but not actual erythrocytes (though the mother's erythrocytes do interact with a fetus).
T cell
Will probably not. However, while in the uterus and for the first few weeks outside the uterus the Mother's immune system is effectively the newborn's immune system. While the mother doesn't pass on any myeloid progenitor cells, a disease affecting a leukocyte might also be passed on to the child (HIV).
Skin (epithelial) cell
Will not. You inherit many traits to do with skin (melanocyte activity resulting in melanin concentrations, for instance), but no skin cells are involved in the creation of the fetus.
Neuron from the brain
Will not.  Neurons are the last time of cell I'd expect to vertically pass on a mutation, not only because their environment is usually tightly controlled (Schwann Cells, Blood-Brain Barrier, etc.), but also because the fetus will develop the beginnings of its nervous system very early on and I'm not aware of the mother's CNS or PNS interacting with the fetus in any significant way.
Sperm cell
Can certainly pass on a mutation as long as the mutation is part of the sperm's DNA. Though the particular gene the mutation exists on may be inactivated, it would still be passed on to the offspring and potential future generations.
Cell from lining of the uterus
I'm not positive on this one. The fertilized egg cell must implant itself in the lining of the uterus, and the landing location eventually becomes the umbilical cord. I suppose it's possible, particularly if the mutation occurs closer to the child's end - like the obliterated artery.
Placenta cell
Probably not, though like Cell from lining of the uterus I'm not super positive on this one. Given that the placenta is detached from both the mother and child soon after birth, a mutation in a placental cell that hasn't metasticized won't affect either. However, there may be interactions I'm not aware of.
Stem cell
"Stem cell" is a little vague. The body has many specific types of stem cells, and the fertilized egg itself basically turns into all of the stem cells the developing fetus will ever have. If it's referring to the daughter cells of a fertilized egg, then only the child will have the cancer, as the genetic inheritance is unidirectional (the mother's genome is not modified to resemble the child's in any way).
If someone has better knowledge on the interaction between the fetus and the uterus/mother or can come up with some references, listen to them. It's been a while since I've studied development.


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What are the effects of caffeine on the mammalian circulatory system?
A friend of mine told me an anecdote about his mother, who drank too much caffeine, to the point she became hypotensive and would pass out. Because caffeine acts as a stimulant, I'm assuming the decreased blood pressure was some kind of tolerance effect.
How exactly would caffeine have disrupted her circulatory regulation and caused her normal pressure to decrease?

Caffeine's mechanism of action,, Hindawi journal (https://www.hindawi.com/journals/ijvm/2010/834060/)
Direct effects of caffeine:
On vascular smooth muscle:
Caffeine inhibits phosphodiesterase enzyme , which is responsible for degradation of cAMP to 5'AMP , so concentration of cAMP increases which activates protein kinase A which phosphorylates myosin light chain kinase (MLCK) . MLCK, on activation by calcium- calmodulin complex, phosphorylates light chain of myosin which then binds to actin and causes smooth muscle contraction. But MLCK in phosphorylated state is insensitive to calcium and hence can't be activated which results in relaxation of smooth muscles . So caffeine increases MLCK concentration in phosphorylated state which is insensitive to calcium hence cause vasodilation
Indirect effects:
On endothelium:
Caffeine inhibits phosphodiesterase, required for degradation of cGMP to 5'GMP.
It increases nitric oxide (NO) production in endothelium by activating nitric oxide synthase via increased cGMP .  NO then diffuses to vascular smooth muscles where it causes relaxation which results in vasodilation.
Hence caffeine causes vasodilation by both direct and indirect effects.

Welcome. Can you add your sources to this answer?

I added my reference now ,, it's form a journal on Hindawi : caffeine vascular mechanism of action


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Why did the urinary bladder evolve?
Sure it's convenient to decide when to urinate but not essential for survival or reproduction, as I understand. But just convenience is not a drive for evolution.
Does the bladder serve any essential purpose? If not why did bladders evolve?

The urinary bladder is not unique to mammals.

Well a Naïve answer for a Naïve question: It's not very "convenient" to leak urine constantly and create a beautiful path leading directly to you when you have lots of predators around looking for you. It's very "convenient" to be able to mark your territory if you're a predator.

The benefits of adaptations can be very small and still be widespread. It doesn't have to be life or death 100% of the time.

apparently mice urinate all the time/as they move

I've changed the question to be more general, without the mammal focus. @Paul A. Clayton's answer is more broadly applicable than just mammals.

@rg255: working with mice every day I can assure you they do not.

@shigeta: although I agree with you for the general case, this is probably a situation where the trait gives you a fairly strong "life or death" advantage...

@nico thanks, I thought that may be a bit of a myth

This is good explanation of a possible role of the bladder
https://link.springer.com/article/10.1007/s42452-019-1692-9

A few observations to add to Paul's:
Urinating on yourself in winter could be a fatal thermoregulatory mistake.
Urinating on your substrate could hinder locomotion.
Having a continual slick of high osmolarity fluid on your skin would be damaging to the epithelium and work at odds to the action of the kidneys.

perhaps this is better as a comment on the accepted answer? maybe ask @Paul-a-clayton to add them in if valid

@GriffinEvo Craig didn't have 50 rep.

I'll let you keep the rep and not delete your answer but please put well structured, referenced answers from now on.

Apparently, the urinary bladder is not unique to mammals, and is even found in fish, which one might presume can urinate at any time or even better - expel ammonia out of their gills, so why do they need a bladder?
I found the following article trying to understand what the bladder does in freshwater fish: https://jeb.biologists.org/content/155/1/567.
Apparently they concluded that the bladder is important because the kidneys let too much useful stuff (like Na and Cl ions) out, and letting it sit in the bladder for 30 minutes (as measured in the trouts in that research) allows some of these ions to be re-absorbed by the cells lining the bladder. I don't know if this is why the bladder evolved (which would have been easy - just as an enlarged cavity in front of the kidney holding some urine before it is expelled), or why couldn't a better kidney - absorbing more salts - have evolved instead. I also don't know if mammals still use the urinary bladder in this way. But once it has evolved, it is here to stay, unless it has a negative survival contribution. And as other answers suggested, it probably has positive contribution, if anything - such as avoiding leaving a strong trail of scent leading to you, or avoiding soiling your den with urine.


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Photosynthesis - Light Intensity
Say I was conducting an experiment for photosynthesis. If I moved light closer to the plant, what effect would this have on the process of photosynthesis?

Could you list a few ways that you've tried to research this question before asking here so we know that you've put effort into the question?

The rate of photosynthesis varies from plant to plant. Some plants require more light and some require less. If you move light closer to the plant, in most scenarios the rate of photosynthesis is likely to be increased. For some plants a minimal light is enough for their photosynthesis, so for those plants, moving light source closer or further will have less effect.

yes - Individual genetic composition often trumps the typical assumptions of physics in biology.


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How do lilies sense day and night and open and close their flowers?
We have lots of lily flowers inside our garden. Their flowers are open in day and closed in night. How do lilies sense day and night and open and close their flowers?

The three main cues for flower opening/closing used by plants are temperature, light and humidity (van Doorn & van Meteren 2003, freely available pdf), with the first two being most common. Plants with daily opening and closing of flowers can be divided into nocturnal (open at night) and diurnal (open at day). There exists several different mechanisms for how flowers open and close, and these include e.g. reversible expansion and contraction of cells by changes in water balance and differential growth of cells due to temperature (in either the petals themselves or cells at the base of flowers). See the previously referred paper for examples.
The evolutionary advantages and molecular mechanisms (along with the circadian clock of plants) behind opening and closing of flowers are open research fields. Several evolutionary hypothesis exists for explaining different flowering strategies, and these often deal with efficient pollination (close when good pollinators are absent), protection against frost, conservation of resources (e.g. water) or predator/pathogen defence.
I do not know what the specific mechanism in lilies is, and it can possibly/probably differ between different species.


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How can haired mammals synthesize vitamin D?
The human body can synthesize vitamin D in the skin from cholesterol, when sun exposure is adequate. But how can haired mammals do it? Do not they need it?

At least the vast majority of adult mammals have hair/fur (not sure if you are trying to make a distinction), possibly all (I will have to check on a hairless adult mammal or mammals that made to adulthood without hair).  Hair is actually one of the defining characteristics of mammals.  So what do you mean by "haired mammals" (humans have hair)?

@AtlLED, I think the OP means mammals whose skin is apparently inaccessible to the UV required for vitD synthesis, i.e. that don't have any exposed skin.

@AlanBoyd Right, I was trying to edit my comment and got distracted (and came back too slow).  OP: Would a polar bear and a dog be an ok example, then, for how different animals do it?


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Bioluminescence and photovoltaics
I work in the PV industry and was asked a question recently during a presentation. Could Bioluminescence provide enough light to power a PV array during off peak hours? I understand the PV portion and the light spectrums needed to power the photovoltaics, but I have no clue how the science of Bioluminescence works or what type of light is emitted. I have the suspicion that this may be theoretically possible, but would require too much raw material? Any insight would be appreciated.

Here is a report addressing this, I haven't read it in detail, but I've skimmed it and it looks like they've done a pretty good job, and address a number of key points, talk about the emission spectra of certain organisms, etc.
Bioluminescence – a source of marine energy?
From the conclusion: "The low light output of bioluminescent species relative to solar light may render the conversion of bioluminescent light into electrical energy uneconomic as a stand-alone option."
I agree with them that it would be possible to extract energy that way.  I also agree that its not even close to economical.  You lose energy at so many steps, you have chemical energy in whatever the cells eat to grow, then some small fraction of that chemical energy will be turned into light energy, most of that light will shoot out in the wrong direction and just get absorbed by other stuff in the culture.  If you want to use bugs, a better option would probably be a microbial fuel cell, where microbes sit on an electrode, oxidize some chemical, and take that electron and dump it straight onto the electrode.  This is still a pretty inefficient process as far as energy production technologies are concerned, but at least it skips the waste associated with conversion of the chemical energy into light energy and then back into electricity.


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Why to choose a grammar from a lot of grammars that can describe structure of proteins?
Why do we choose a grammar from a lot of grammars that can describe structure of proteins? Usually, there are a lot of (maybe infinite) grammars that can describe one language. Why do we choose a specific one? Especially the language of proteins of gene just has finite sentences or words.

Are you talking about protein nomenclature or what?

@MiguelÁngelNaranjoOrtiz,no,what I am talking about is the description of the protein structure by formal language,it is research that tries  to predict the structure by DNA or RNA

Actually when describing the 3D structure of a protein you only need the angles formed by the peptidic bond of every aminoacid, and the aminoacidic sequence. This is the kind of data yyou obtain when proteins are resolved by X-ray diffraction. Those are raw data thought, and they usually describe protein structure by different nomenclatures, such as domain organization or secondary structure prediction. In this case, you describe regions of the protein with a particular structure, often related with its function.

@MiguelÁngelNaranjoOrtiz You also need the sidechain orientations for a complete structure. The raw data for X-ray is the electron density, though in NMR torsion-angle space is often used for structure calculation.

I did not understand your question completely but this is what I guess you want to know:

Why genetic code evolved to be what it is ?
How the sequence of the protein coded by a mRNA give rise to a particular structure ?

Answer to first question cant be definitive. The textbook explanation for why a 3-letter code exists is because a 2-letter code cannot describe all the 22 amino acids, with all its permutations. But then comes another question: why only 22 amino acids. I can't even speculate the answer to this question; the simple amino acids are fine but for an example why lysine and not a similar amino acid with a shorter side chain - no idea.
So, given 22 amino acids, a 3-letter code and 4 nucleotides, the multiple codons for an amino acid are similar in sequence (usually the first two bases are conserved in accordance with the wobble hypothesis. The last base usually doesnt base pair strongly with the tRNA and is of minimal importance).

The answer to second question is somewhat straightforward. The sequence can give rise to infinitely many structures but in a given environment (consisting of the solvent, other solutes etc), the sequence adopts a particular structure in accordance with the free energy minimization principle. There is a possibility that given an environment a protein can have two different optimal structures and can switch between these two structures.

Good,thank you for your answer,but I don't know why somebody voted down my question.

,thank you,I know you did not.To tell the truth,I am not a biologist,and I am not familiar with bioinformation.

perhaps you can restate your question based on the comments and the answer. even if your query is answered it will be better for someone who looks up an existing answer.


text:
Can Naegleria fowleri enter through your ear?
Is it possible to get infected with the amoeba, Naegleria fowleri, through your ears, or is the nose the only way it can enter to cause infection? How commonly is it found in your stool as well?

@KyleCares - Naegleria fowleri eat myelin and neurons. The closest nerve bundle in the ears is in the Inner Ear (Vestibular Nerve) behind the Oval Window, Semicircular Ducts, and wedged between the Ducts and the Cochlea. Even if the Eardrum is compromised, it would still be almost impossible.

Ears? No. The tympanic membrane (eardrum) is a watertight barrier between the outer ear and middle ear.

Exposure to the organism is extremely common due to its wide distribution in nature, but thus far lacks the ability to infect the body through any method other than direct contact with the olfactory nerve, which is exposed only at the extreme vertical terminus of the paranasal sinuses; the contaminated water must be deeply insufflated into the sinus cavities for transmission to occur.

In short: Don't huff warm lake water too deeply through your nose, and you'll probably never get it.
You shouldn't find it in your stool. Other amoebic infections can be found in your stool, as they can attack the lining of your intestines, but Naegleria, specifically, will reside in your sinuses and brain until you die or receive treatment.


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Problems with analysis of small RNAseq data - Adapter trimming
I have always faced a problem while analyzing small RNAseq data, at the step of adapter trimming.
Overview of small RNAseq (Illumina)

RNA is size fractionated using columns or PAGE
3' and 5' adapter ligation
cDNA synthesis
PCR amplification
Sequencing

The length of the reads is dependent on the machine and recent ones like HiSeq can provide ~200bp.
The problem, however, is with reads smaller than the max read length of the machine and this is common with small RNAs such as miRNAs (especially if the concatemer of smallRNA and the complete 3'adapter is bigger than the max read length).
The first step of analysis is trimming of the 3' adapter (Illumina Truseq: TCGTATGCCGTCTTCTGCTTGT).
Several algorithms are available to do this job and what they precisely do is to check for overlaps between the adapter sequence and 3'end of the reads and then clip the aligned region.
Now the problem is this
You can't be really sure of very small alignments because they may not really be originating from the adapters, which means that you should specify a lower limit of alignment for clipping. I usually set it as 5 (intuitively).
But if a small piece of sequence really came from the adapter then it will remain and there is no way to clip it without any doubt.
The real problem comes during aligning the reads to the reference sequence. Aligners like bowtie (which i prefer to use), generally have user defined argument for number of allowed mismatches. Bowtie generally doesn't perform very well if you allow a lots of mismatches.
Subsequently, you might lose a really valuable read.
Alternative
To avoid this problem I sometimes trim the reads to around 25nt (for miRNA profiling). This creates a new problem:
You can't really distinguish whether the read came from a pre-miRNA (a longer RNA) or from mature-miRNA (smaller RNA that arises by processing of pre-miRNA)
Does anyone have an experience or an idea about how to solve this problem?

I would first recommend you ask this question biostar as the subject matter you are inquiring about is much more relevant there.
That having been said, you have another option which is to use an aligner that soft clips 3' ends of reads specifically to account for adapter (or polyA, or whatever) contamination that might have flew under your radar.
STAR is such an aligner. If you search their mailing list archives for "clip", you should find several posts related to your question.

Thanks Steve.. But I wonder why this forum is less suitable.. my purpose of joining here was to have all biology in a single forum without having to have multiple accounts.. i have an account in seqanswers and i shall ask this question there. but i am slightly disappointed by this concept of separate niches (especially when it all comes under same area of study)..

@WYSIWYG: I suggested biostar, not seqanswers ;-) Still, this forum is less suitable simply because your question is more of a bioinformatics nature than strictly biology one -- and you will find more expertise related to bioinformatics on biostar than here. I would imagine that there are likely many people on biostar who are strong bioinformaticians that do not have accounts on this site, and you would benefit from getting their input. Consider, for example, why there are different SE sites for math and stats :-)


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how to clone a gene fragment in two direction as sense and antisense in vector
I have a sequence ATG GGG CCC TTT AAA TAA and want to use it as antisense RNA in my vector. How should I clone it? I am confused with the direction of my clone. I looking for the direction and sequence of the clones.

Perhaps place a promoter or ori upstream in the antisense direction?

Tour sequence's complementary is TAC CCC GGG AAA TTT ATT. Together they form a DNA strand. Now replicate this and then, after transcription of both the DNA you get the RNA sequence you wanted. Use it as sense or antisense.

Is there something missing from "transcription of both the DNA"?


text:
Information Gene HBA2
Gene : HBA2? hemoglobin alpha 2 (Homo sapiens)
I don't find any tissues (or organs) in which the expression of this gene is strongest? What is the size of the gene (promoter off) encoding this sequence?

Hello, where have you tried to find information on HBA2?

On the NCBI site, but the site is rich in information and like I started in bioinformatics...

you could also use wikipedia as a starting point: http://en.wikipedia.org/wiki/Hemoglobin,_alpha_2 for many genes this will give you already a good overview and links to sources

GeneCards is also a decent site for these type of information.

Thank you for your answer but I don't find the size of the promoter, I know the size of the gene is 864 bases but with the promoter and i need is size without promoter

Gene size will not include the promoter. The main reason is that the exact location of the promoter is not defined (or defined arbitrarily).

not sure that I understand what is going on here, but the HBA2 gene product is 142 amino acids which corresponds to 426 nt plus a stop codon makes it 429 nt

You mention that you "started in bioinformatics", so perhaps you might feel more comfortable taking such an approach to better characterize where the promoter for HBA2 might be.
As @Bitwise mentioned in his comment, "the promoter" is not a well defined region. Often times "we" take the promoter of a gene to be some arbitrary (2-4) kilobytes upstream from the TSS. With more high throughput data coming online (especially from ENCODE), we are starting to get a better picture of where the functional regulatory elements of genes might be.
By combining data from several different high-throughput assays across a variety of cell types, the human genome has been segmented into broad regions of interest. You might start by looking for where the "Predicted promoter region including transcription start site" segment is for HBA2.
I'd also take a closer look at the DNase-seq data in this "promoter region" across as many cell lines as they have processed for you to look for regions that are differentially occupied in hopes of identifying more precisely which parts in the promoter region might be important for the gene's expression (this would, of course, require you to connect DNAseq data with gene expression (RNA-seq) data).

Thank you for your comprehensive answers that helps me a lot
I determined that the gene HBA2 had four SNPs but to find  how many allele phenotypically it is I do not know if I should take the column'' Allele origin " or the column dbSNP allele Thank you again


text:
What kind of tree could this be?
This may be a strange question, but does anyone know what kind of tree this could be?

I know, it's just a comic, but these trees, at “walking distance” within that comic are easily identifiable as Grandidier's Baobabs:

(That might indicate, of course, that the above tree also occurs on Madagascar, but it's a comic, so all bets are off.  And yes, we know, there are no squirrels on Madagascar.)

Is there any reason to believe that it is a real species at all?

@kmm it does look vaguely familiar, I'm pretty sure I've seen images of such trees.

I don't think this question can be answered, and it doesn't deal with real-world biology. The intent of the artist cannot be known and a silhouette can hardly be used for species determination.

I know, it's a cartoon tree, and might not be a real one, but the second one is clearly identifiable, which is why I believe the first one could be as well.

I noticed that in japanese animation, the fish are often identifiable, at least at the genus or family level. So the question makes sense to me.

Someone should just ask Randall Munroe, right?

I think these are two species.

Here's a link to the source: http://www.explainxkcd.com/wiki/index.php/1190:_Time/Pictures

It reminds me of the smooth-barked Australian gum trees / eucalyptus, like a salmon gum, ghost gum, etc.
Although there are no squirrels in Australia :)
This photo of a Salmon Gum is from http://www.fpc.wa.gov.au/content_migration/plantations/species/arid/salmon_gum.aspx

Of course, that's not a squirrel. It's clearly a brushtail possum. :)

As @fileunderwater suggested, this looks like an Acacia. Like many others with OSX, I have this incuded picture of an acacia as one of my screensaver rotations.
It looks very similar in bauplan to the illustration.

As Saxon Druce has pointed out it looks very much like a eucalypt. Specifically a desert or savanna species such as the ghost gum (Corymbia aparrerinja).

Other eucalypts (Eucalyptus and Corymbia spp.) have similar growth forms.

(source: masterfile.com)
The silhouette is obviously stylised and appears to have less foliage than a real eucalypt in order to make the profile neater. The branching pattern and the way the foliage is clustered in rounded clumps and textured in the image are representative of eucalypts. I would argue it is not an Acacia - they have very distinctive branching patterns and are more spreading with a flatter top than this.

It looks like a pine to me. Might be close to Pinus pinaster but take into account that
a) I'm not a botanist.
b) I'm only familiar with pines that grow in my area (Catalonia).

My guess (with an emphasis on guess) would rather be an Acacia species, since they are common on savanna/similar environments as Baobabs. They are fan/umbrella shaped (do a google image search). There are, however, more than 1300 species of Acacia worldwide.


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What is the relative power of GWAS studies in different species?
I would like to know of any publication studying the relative power of GWAS studies in different species. For example, I've seen reports that say genotyping and GWAS in dog breeds is much more powerful than in humans due to the extent of linkage disequilibrium and other population genetics considerations. Some claims say that many GWAS studies in dogs are 10-20x more powerful than many GWAS studies in humans. I have also heard from pigeons (pigeon-omics) to be a similar case. I would like to know if there are other comparisons for other species and the relative power of discovery for GWAS studies compared to human. For example, are there any numbers for yeast, Drosophila sp., C.elegans, zebrafish and then also for plants like maize, rice, etc.?

Part of the increase in power to detect a genetic association via GWAS-genotyping comes from long haplotypes. Many dog breeds went through selective breeding bottlenecks 100-200 years ago. Many lab model organisms, such as flies, worms and plants, have recombinant inbred lines that aid in GWAS discovery as well. The price one pays for this increased power, say for canine GWAS, is not being able to pinpoint the casual variant. The association SNP(s) found may be far, far away from the gene responsible for the phenotype, because of that long LD.
Another aspect not to neglect is the phenotype. In humans, there may be a 3-fold range in phenotype p, while in dog that value is just 35% (1.35x). That may mean that the phenotype is difficult to measure (accurately) and to assign to a given allele with statistical certainty.
A third aspect to consider is the effect size of the association, say on a per (risk) allele basis.
Thus, while I am not aware of any papers specifically taking such elements as haplotype length, phenotype range and effect size into an analysis of GWAS power across species, I feel that one versed in genetics of the organism of choice can readily accomplish this for the specific trait(s) of interest.

Does this mean that what one gains in increased power in canine GWAS is then partially lost in accuracy of fine mapping the causal SNP? See this piece I found: "The breed structure of dogs comes in particularly helpful here, as the very long haplotypes within breeds allowed the detection of the oncogene in a poodle-only dataset using only a 50,000 variant map, and the association could then be fine-mapped to a few tens of kilobases by looking at haplotypes across different susceptible breeds"

question looks like it's been dormant for a while, but i think there's some discussion to be had here-
I would argue that in many (most?) of the model organisms, power would be much greater than humans. Frequently (worms, mice, plants, yeast) you can work with basically isogenic inbred lines. I would argue this is much more important than long haplotypes:
a) less importantly, no heterozygosity.
b) more importantly, you can re-phenotype the same line repeatedly to directly estimate experimental/environmental variation, and get a very precise estimate of actual E(phenotype | genotype). this is opposed to humans, where you have the one individual, so you just have to pray that your experimental/environmental variation is low and your heritability is high in the sample population.
For example, for just 100 inbred lines of a plant, you get massive, beautiful GWAS peaks for many phenotypes: Atwell et al. 2010. Human GWAS sample sizes generally have to be in the 1000s before they are sufficiently powered (ref).
This subject is discussed a little further here.
In direct reference to the long haplotypes, note that power and mapping precision are different things. That is, your power to detect an association can be extremely high, but you might have a very broad chromosome interval that you will then have to go hunting in to find the causal locus. Note that this problem might actually be worse with large effects, which are probably under selection if they are interesting, and thus there is likely to be substantial linkage disequilibrium between the causal locus and surrounding regions. Of course, if the effect size is small (generally the case in humans though not in other orgs), this is less of an issue.


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Comparing BLAST and the Smith-Waterman algorithm
I've been asked: how does BLAST improve dynamic programming accuracy?
I do know that BLAST is based on heuristic approach that approximates the Smith-Waterman algorithm and that the Smith-Waterman is too slow for large databases but more accurate.
Can someone settle my conflict?

It doesn't improve DP, is less accurate but usable for large databases with excellent results

So I got this answer from my lecturer:
Since Smith-Waterman algorithm is based on DP, we will get the best performance on accuracy, but there is a change that the homologous sequence is not with the highest probability (so better matching sequences will be "hidden" behind worse ones).
Since blast is based on the heuristic approach, it overcomes the disadvantage described above, by adding biological information, and therefore make it more accurate from biologist's perspective.

BLAST uses a heuristic, but mainly to cut down the time spent looking for homologs, not to produce better alignment. So BLAST is not more accurate than S-W, but often times accurate enough.

ok another constraint I forgot to mention which I believe is crucial - the two sequences are not homologous

As Michael said, this answer is wrong; actually the question itself is wrong. BLAST uses heuristic for speed up, not for accuracy. It is less accurate than DP. BLAST does NOT "improve dynamic programming accuracy". With DP, we can also find suboptimal alignments. If we had an extremely fast computer, we would use DP, not BLAST.


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Differences between right and left handed people
Are there any articles reporting any significant differences in behavior, attitudes, intelligence, appearance, etc., between right and left handed people?


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Cat purring: What are some possible underlying mechanisms behind purring and bone remodeling and formation?
http://www.scientificamerican.com/article.cfm?id=why-do-cats-purr
The article above says that cats purr mostly when they're wounded or under duress. They hypothesis that cats purring leads to increases in bone density and bone healing. How is this possible? What are some physiological possibilities for something like this to occur?
I don't see any journal articles backing up any of these claims. Is it similar to how ultrasound in clinical trials works?
Is the cat purring affect formation of osteoblasts? What is possibly happening microscopically?

The author is likely referring to the mechanosensory behavior of bone (reviewed in Huang and Ogawa, 2010; lots of Google Scholar citations). Bone loading produces very tiny mechanical deflections (strain) which are translated into biochemical signals that promote bone growth through the action of osteoblasts. Burger and Klein-Nuland (1999) review possible mechanisms.
The low frequency soundwaves produced during purring overlap the frequencies that have been shown experimentally to induce bone formation (1-50Hz; e.g., Castillo et al., 2006; Xie at al. 2006). Although an interesting hypothesis, I don't think that osteogenesis in response to purring has ever been experimentally shown in cats.
Huang C, Ogawa R. 2010 FASEB J. 2010 Mechanotransduction in bone repair and regeneration. 24(10):3625-3632.
Burger EH, Klein-Nulend. 1999. Mechanotransduction in bone--role of the lacuno-canalicular network. FASEB J 13(Suppl):S101-S112.
Castillo AB, et al. 2006 Low-amplitude, broad-frequency vibration effects on cortical bone formation in mice. Bone 39:1087-1096.
Xie L, et al. 2006. Low-level mechanical vibrations can influence bone resorption and bone formation in the growing skeleton. Bone 39:1059-1066.


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Does an allergic reaction kill body cells?
I have wondered what actually happens in an allergic reaction that causes the symptoms such as pain, rash etc.
Is it possible that the human body actually kills its own cells in the process?

I would imagine that the complement system may trigger cell death.

@bobthejoe Do you have any paper or article regarding this topic?

Actually, the body often kills its own cells, look up apoptosis.

Is it possible that the human body actually kills its own cells in the
  process?

Yes it is. It is happens not only as a result of allergic reactions (see comment of @terdon). But in case of allergy our body have 3 methods for killing own cells.

Cytotoxic, antibody-dependent (Type 2 hypersensitivity) The antibodies produced by the immune response bind to antigens on the patient's own cell surfaces.These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen.
Immune complex (Type 3 hypersensitivity) Occurs when antigen-antibody complexes that are not adequately cleared by innate immune cells accumulate, giving rise to an inflammatory response and attraction of leukocytes
Cell-mediated immune memory response (Type 4 hypersensitivity) is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen.

See Wiki about types and diseases and about Hypersensitivity

Thanks a lot for the detailed answer, but in the wiki it says that only Type I Sensitivity is an allergy. So are your answers still relevant?

If you ask about Type 1 hypersensitivity - my answer is "No. Type 1 hypersensitivity didn't kill own body's cells directly". But if we talk about an allergic reaction that causes the symptoms such as pain, rash etc my answer still relevant

So basically you are saying that a Type 1 hypersensitivity could possibly trigger Type 2, 3 or 4 hypersensitivity? If so, how?


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Why do kefir grains stop growing in soy milk?
Kefir is a fermented milk drink made with kefir grains. It usually is prepared by inoculating cow, goat or sheep milk with kefir grains.
I would like to prepare the drink with soy milk, which worked fine for some months. Then the kefir grain stagnated in its growth. I use bottled soy milk from the supermarket. I do not produce the soy milk by myself.
In "real" milk the kefir grains never stop growing (and dividing), but in soy milk they apparently do.
Why do the kefir grains stop growing in soy milk? Are they lacking a specific nutrient that is only contained in milk from animals?

Animal Milk. The ideal environment for Kefir Grains is animal milk. Varieties include cow, goat, sheep, and other similar species. Kefir Grains thrive in animal milk due to the chemical makeup of the liquid. The lactose in animal milk provides the most efficient food source for the Kefir Grains and therefore the most efficient and effective culturing process.
Alternative Milks. While animal-based milks are the healthiest for the Kefir Grains, alternative types of “milk” (coconut, soy, rice, nut, etc.) can also be used under certain conditions. Generally speaking, Coconut Milk, Soy Milk, and Rice Milk can be cultured using Kefir Grains as long as a revitalization period is observed (see below). While some people report success culturing Kefir Grains in seed and nut milks (e.g. hemp milk, almond milk, etc.), these varieties tend to yield more inconsistent results.
Revitalization Period. When using a non-animal variety of milk, it is important to occasionally allow the Kefir Grains to revitalize in animal milk for 24 hours.
We recommend allowing the Kefir Grains a revitalization period at least once every few weeks and ideally more often. To revitalize the Kefir Grains, simply place the Kefir Grains in 1-2 cups of animal milk for 24 hours. Once the process is complete, the Kefir Grains can be returned to use with an alternative variety of milk.
This may be technically why...
''Kefiran produced by L. kefiranofaciens is a branched, water-soluble polysaccharide, containing equal amounts of D-glucose and D-galactose. The production of this polysaccharide is stimulated when L. kefiranofaciens grows in co-culture with S. cerevisiae (Cheirsilp et al., 2003).''
Without galactose, one of the monosaccharides present in lactose (a disaccharide glucose-galactose), the structural protein that forms the grains can not be done. When taking apart from the grain, the microorganism complex don't behave the same way and are not able to ferment the substrate properly.
I'm just starting and I will try with honey, which have a 10% galactose. Although not vegan, could work and try with other sources of galactose like beets... (Only they have little content but may be enough for a persistent growth and avoiding decay). Unless the lactose itself is needed in the process, it should work...
Source:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3833126/

While this answer does not explain in detail, which part of the chemical makeup of animal milk is missing in alternative milks, I tend to accept this answer because it simply confirms, that an entirely vegan Kefir is not possible (in the long run). But I am still curious why Kefir is more 'picky' than yeast – which grows well on different kinds of substrates.

@juantopo I'd say it's just the result of how Kefir was "husbanded" over time. Unlike simple yeast cultures, Kefir is a complex mix of many different lactic bacteria and yeast. Different parts of the culture thrive in different source fluids - it's probably quite enough for the Kefir as a whole to "die" when the cultures are no longer properly balanced. For example, lactic bacteria mostly thrive on lactose and in salty environments, while yeasts are more about simpler sugars like sucrose. Since soy milk has no lactose, I expect the yeasts outgrow the bacteria, and you lose the culture.

Yes, they are behaving differently because of the lack of nutrients, including lactose, and possibly because of the presence of other chemicals in soy milk that aren't in dairy.
Kefir grains are a complex community of different types of lactic acid bacteria and yeasts which metabolize (eat) various nutrients/chemicals in their environment. Because soy milk is a chemically different environment than dairy milk, these communities function in different ways. Over repeated propagations in soy milk, you probably have cultivated a very different community in regards to species diversity and the chemical products.
As Liu and Lin describe here
, the kefir community members in dairy milk are eating mainly lactose, whereas in soymilk they are eating sucrose, raffinose and stachyose. As a result, the reproduction of the bacteria and the yeasts differs, as did the alcohol and lactic-acid contents of the end-product.
Because your question is a practical one, you might be interested to know that in that paper, the authors found that adding 1% sucrose (table sugar) or 1% glucose to the soymilk produced an end-product that more closely mimicked that of dairy milk. You could give that a try and see if it improves your kefir growth.

 Liu JR, Lin CW. 2000. Production of kefir from soymilk with or without added glucose, lactose, or sucrose. Journal of Food Science 65: 716–719.

Thank you for your response and the link! I already tried sucrose (assuming that the kefir grains need a substitute for the energy providing lactose) but in the long term it does not seem to work: the growth stops. That is why I rather suppose the kefir grains are lacking some kind of trace element of the dairy milk than the need of a different type of carbohydrate. But I will give the glucose a try …

As you say, the added nutrients may just be a short term solution: when Liu and Lin added sucrose or glucose (or even lactose!) to the soy milk, they got alcohol and acid contents that were much closer to dairy milk kefir, but the community balance was still different: in soy kefir the bacteria:yeast ratio was much higher than in milk. I imagine that this community balance is what's affecting your long-term growth.


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What are the criteria for determining the origin and end of muscle anatomically?
For example the pectoralis muscle starts from sternum region and ends on the acromion or coracoid process. Why you can't say that it starts acromion process and ends on the sternum?

This is more of a convention.
The start point or origin is considered to be:

bone which is proximal
bone with higher mass
bone with higher stability during muscle contraction

The end point or insertion is:

the structure that tends to be moved by contraction
tendon
distal end of a bone

Reference: Wikipedia - Anatomical terms of muscle


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Excretion of small kangaroos while in the pouch
How is the excretion of small kangaroos done when they are in the pouch of their mother, fastened onto her teat? My question is what happens with the products; do they accumulate in the pouch?

Wow! What an interesting question!
I did a bit of searching around, and here's what I found. It looks like the baby kangaroos, or joeys, do in fact produce excrement while in their mothers pouch. The mother kangaroo uses her tongue to clean her joey and her pouch.
I found this information in a couple of differently places by doing a google search for "biology of marsupial reproduction pouch excrement."
One of the first sources I found was a New York Times article titled "Marsupail Maintenance." You can find this article at this link:
http://www.nytimes.com/2012/08/14/science/how-do-female-kangaroos-keep-their-pouches-clean.html?_r=0
The article was published in a reputable news paper, and used an interview with a curator of mammals from the Bronx Zoo as a source.
Another resource I found when researching this topic was an Australian wildlife sanctuary. This wildlife sanctuary has information web pages online to help visitors learn more about the animals that live in the sanctuary. You can find their entry on Eastern Grey Kangaroos at this link:
http://billabongsanctuary.com.au/native-animals/mammals/eastern-grey-kangaroo/
This web pages gives a pretty detailed overview of the Eastern Grey Kangaroo. The information on joeys and pouch cleaning can be found in the section called "Raising the Young."
I hope this fully answered your question!

i'm glad i'm not a marsupial

@shigeta: Koala's feed their faeces to their young so in Australia it goes both ways.

my desire not to be a marsupial remains one way...  :)


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Which is the best way to fix and preserve comet assay slides before staining with Ethidium Bromide?
I want to use the method of Single Cell Gel Electrophoresis (comet assay). I have many samples, but I don't have the appropriate microscope. So I have to preserve my slides until the time comes for staining and microscopic analysis. I've read many different protocols, and I can't decide which is the best. Also, after the staining and the analysis, I might need to reuse the same slide. Is that possible? and if yes, what should I do?

Can you give more information about what protocols you have looked into?

Most of them use either 100% or gradually increasing percentage of ethanol or methanol. Some suggest to hydrate before the staining and some of them don't. Also some use mounting media at the end and others just a coverslip. I suppose that most of these work but it would be very helpful if I had a specific protocol that I know that will work.

This could be of use: http://onlinelibrary.wiley.com/doi/10.1002/cyto.a.20071/full


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Genetic variation in humans and model organisms (measured by SNPs)
I was wondering what is the range of SNP density across species and model organisms.
I.e., what would be a reasonable estimate for the SNP density (i.e., x SNPs for each 1 Kb) in:

humans
humans with the highest variation (i.e., Africans)
flies
mouse
lab mice with highest variation (i.e., isogenic lab mouse 1 with isogenic lab mouse 2 with the highest variation)
model organism with the highest snp density (could be lab or naturally occurring)

SNP Density
Human = ~1.18 SNPs per kbases

Based on CgsSNP, the average numbers of SNPs per 10 kb was 8.33, 8.44,
  and 8.09 in the human genome, in intergenic regions, and in genic
  regions, respectively.

Source: Investigating single nucleotide polymorphism (SNP) density in the human genome and its implications for molecular evolution. by Zhao Z, Fu YX, Hewett-Emmett D, Boerwinkle E.
Drosophila melanogaster = ~0.02 SNP per kbases

FLYSNPdb provides high-resolution single nucleotide polymorphism (SNP)
  data of Drosophila melanogaster. The database currently contains 27
  367 polymorphisms, including >3700 indels (insertions/deletions),
  covering all major chromsomes. These SNPs are clustered into 2238
  markers, which are evenly distributed with an average density of one
  marker every 50.3 kb or 6.6 genes.

source: FLYSNPdb: a high-density SNP database of Drosophila melanogaster
Mouse(Mus musculus) = ~0.2 SNP per kbases
Source: Genome-wide single-nucleotide polymorphism
analysis defines haplotype patterns in mouse


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Cell state and cell function
I have read many papers that refer to cell type, cell state and cell function, but I haven't found an explicit definition for each of these terms.
For example this paper (Brown et al. 1994. J General Virology 75: 2367-2377) refers to cell type and cell state without providing an explicit definition of both terms.  I have a vague idea of what these terms mean but a more explicit definition would help me greatly in understanding them.

Mainly cell type refers to the differentiation degree to form a cell population whose characteristics are identifiable by using simple microscopy, stains or immunological methods. Examples of cell types would be T8 lymphocytes, peripheral astrocytes or hepatocytes. Cell types can be pathological too, like tumor cells.
Cell state makes references to the current physiological condition of a given cell. A given cell type can be found in different proliferation states, metabolic conditions (i.e: An adipocyte or a hepatocyte will have different metabolic profiles depending on the insulin and glucagon balance), electrophysiological state (The human oocyte rapidly changes its membrane potential once a spermatozoid has entered) or even degree of differentiation (The typical example are B lymphocytes, which can be in a "naïve" state if they haven't found an antigen, or into a mature state. Once they have matured, thay can be subdivided into cells that actively produce antibodies and cells that divide actively).
A cell function usually refers to a process that occurs inside a cell, or to the physiological function that cell type has in the whole organism. Cell functions could be metabolism, signaling, cell division, etc.; while also could be the likes of detoxification (hepatocytes), hormone production (Langerhans cells) or contraction (myocytes).

I'm busy writing a section on this topic for a dissertation and have run into the following useful definition, which I'll write here for posterity:

Cell type and state can be thought of as a location in "state space", a virtual landscape covering all possible cell states and types.
Each point in this space represents a combination of various configurations in the cell: its genomic arrangement (physically and chemically), its transcriptomic profile, its metabolic state, the arrangement of its organelles and cytoplasmic components.
Configurations which are similar will confer similar functions to cells (having gene expression skewed towards energy production and lysosome formation will probably be associated with phagocytosis, for example). Phagocytic cells thus might be near each other in this space.
Cell type and state can be thought of as snapshots of this cell space with different resolutions - cell type being a large zoomed out version, and cell state being a granular view. For example, the T lymphocyte cell type is a broad but useful classification of cell, but the cell states within that type could include naïve and activated T lymphocytes.

Some nice references here: an easy blog post by M Bernstein, and a more in-depth article referenced therein by C Trapnell.

As it’s currently written, your answer is unclear. Please [edit] to add additional details that will help others understand how this addresses the question asked. You can find more information on how to write good answers in the help center.


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Why are antibodies so expensive?
The amplification on vector transgenic microorganisms and the subsequent purification does not seem that complicated. Also, what are the processes that biotechnological industries follow, in detail, on their production?

Your question is not very clear - what exactly do you mean by the first sentence? I can answer your second sentence quite easily, as I used to work for a major antibody company, but I'd like to know what you'd like me to focus on, as the subject area is very broad.

Additionally, please read my answer to this question and let me know if you'd like more detail.

Making antibodies is mostly nothing you do with transgenic microorganisms. To make an antibody you first have to immunize an animal with the correct antigen. This includes have an animal facility where you can keep animals under clean conditions. If you are looking for polyclonal antibodies (meaning a whole bunch of different antibodies with different specificities) you will boost the animal before sacrificing them and isolating their blood to purify the antibodies.
If you are aiming for monoclonal antibodies then the animals will be boosted as well, then sacrificed and their spleens isolated. From the spleens you make single cell solutions from which antibody producing cells are isolated and plated one cell per well of 96 or 384 well plates and cultivate them to identify cells which produce antibodies. These cells are fused with immortal cells to produce immortal hybridoma cell lines which secrete a lot of antibodies into the cell media. These antibodies still need to be characterized to make sure the really bind the antigen of choice and not something else (in the spleen a lot a these reactions take place).
Just for estimations: Making one batch of a custom polyclonal antibody in rabbit with a given peptide sequence will cost you at least 5000\$ to 10.000\$ the last time we checked for it. Monoclonals are more expensive. So making an antibody is quite an investment on the first hand.

There are some pretty good articles on Wikipedia about antibody production here and here. My crude understanding is that, you will have to grow and animal and bleed or sacrifice it to extract antibodies. This process along with purification costs a bit of time + money. Additionally, antibodies for humans must be grown under more stringent conditions to avoid contaminants and reacting to human immune system.


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Does bleach destroy RNAse activity, and if so, how does it do it?
I am working with RNA samples, and I'm trying to be very careful about RNAse contamination.
I have some questions about bleach, though. Some people say that a solution of bleach is enough to destroy RNAse activity, but is it really? How does it do it?
I'm not sure if wiping the surface using a solution of bleach would be enough to kill RNAse activity, or if it is necessary to use products such as RNAseZap or RNAseAway.

RNAses are enzymes, and there are various ways to inactivate them. Unfortunately, RNAses are rather stable proteins and autoclaving doesn't completely kill their activity. The common methods to inactivate are unspecific methods that will destroy any enzymes, either through covalent modification or degradation.
The most common methods for RNAse inactivation are:

Treatment with DEPC. This covalently modifies histidine and a few other amino acids, which will inactivate RNAses.
Heating to 200-250 °C for at least an hour, this is most commonly used for metal and glass equipment
Incubation with 1M NaOH for an hour at 37 °C, which will hydrolyze proteins

Using bleach is not a method I've used, but it should work in principle as hypochlorite will react with proteins.

I think they are asking how to clean surfaces like benchtops.
Bleach might work. But a better solution would be to get a box of aluminum foil. The processes for making the foil are very harsh, so it's doubtful any protein would survive the process, not to mention that there are no proteins involved in aluminum manufacture to contaminate the process. Just be sure to always use gloves when handling the foil or you'll contaminate it.


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Why do obese people tire quickly?
Fat people have a large amount of calories (energy) stored, but I have noticed all time when they do physical activities they get tired fast in comparison to fit people - why does this happen?

This is a generalization based on stereotype and is not true for every person. -1. You also have to remember that based on the medical definition, your top rated Heavy Weight MMA fighters, many rugby and American football players, and some Olympic athletes in field events, wrestling, judo, weightlifting, etc. are obese, especially if you use BMI as a measure. Many of those people are endurance athletes who would outlast most all "fit" non-atheletes.

Fatigue on exercise is proportional to unmet demand for oxygen and glucose (sugar/fuel).
In people who are "fat":

They typically do less exercise. Therefore their cardiovascular system is not conditioned with the heart being able to cope with increased exercise i.e. it is unable to beat more efficiently and instead must beat A LOT more faster to cope consuming more oxygen and glucose. Even at rest, they will typically have a higher resting rate. They also have less efficient muscles (i.e. the muscles themselves can't breakdown energy as well, use it as well and the body isn't as great at picking the right set of muscles)
The fat itself can compress vessels carrying blood. This pressure increases blood pressure. This is worsened by a typical high diet of salt and again by typical lack of exercise. Higher blood pressure means the heart has to beat harder and faster to pump blood around the body
They weigh more so each movement requires A LOT more energy. Their resting metabolic rate is higher than a thinner person as is any exercise they do.
On exercise they do not lose heat fast enough. This impairs the breakdown of glucose and also more energy is required to lose the excess heat
They may be subclinically diabetic. Their body may have lots of glucose floating around in the blood but they can't use it because their muscles can't absorb it.
They have far increased rates of build up of fatty plaques on the blood vessel walls. This narrows the vessels and only multiplies with all the other problems
Then there's lots of other more minor but very important reasons like psychological (reduced capacity to brave through fatigue), reduced sleep meaning a higher baseline of tiredness (in the extreme side caused by obstructive sleep apnoea), increased rates of smoking (which does millions of things to reduce exercise capacity)

Firstly we must acknowledge there is a difference between being thin and being fit. An unfit thin person will also tire more quickly than a fit person, performance is not always directly related to weight. This is due to the "use it or lose it" nature of fitness.
In addition to the factors mentioned by Deepanjali Dwivedi it is often the case that overweight people are less active and so build up less of the muscle required for the particular task at hand. For example/comparison if you had to use one arm to lift a heavy bag it would be significantly harder than if you were to use both your arms and the muscles in that arm would fatigue more quickly.

Fat people have a large amount of body cells which need a large supply of oxygen from the blood.Heart beats at some constant rate and it has some upper limit to which it can supply blood. In fat people the same sized heart and same volume of blood needs to be circulated throughout the body and this becomes difficult during exercise or rather cells of the body of a fat person suffers from hypoxia faster than that of a thin person. thus he experiences fatigue faster.

Any references would be great!

"Fat people have a large amount of body cells" - I don't think this is true. The main difference is amount of ECM in adipose tissue.

I agree with Superbest. The amount of cells is not that massively different, instead it is the size of adipose cells. Also you don't explain WHY it is harder for the same amount of blood to be circulated. I've tried to answer this in my own answer.

The most popular method of getting fat in the first place involves exerting yourself as little as possible. This leads to the muscles and metabolism failing to become conditioned for strenuous activity, ie. remaining very untrained.
Therefore, a person who became fat in this manner is mentally and physically unprepared for intense activity, for the simple reason that they have seldom done it before and their body did not become adapted to it. It is not surprising that they are very bad at it compared to people of moderate fitness.
Thus the correlation between being fat and lacking endurance is not due to causality from the former towards the latter, but due to another factor causing both (also known as a confound). An added factor is that you over-simplify by focusing on calories: In the real world, the sort of diet and lifestyle that results in excessive weight also drastically impairs cardiovascular health, which then in turn impairs performance. However, this goes back to the question of being trained vs. untrained for strenuous activity, since exercise also influences cardiovascular health.
That said, fat is a good thermal insulator and most likely interferes with performance by making it difficult to evacuate heat. I don't think this effect is significant compared to the above reasoning, evidenced by the fact that even in extremely cold weather, a naked fat man will not suddenly become an effective athlete.
A further caveat is that an athlete who became very fit to begin with, could subsequently amass a large amount of fat without losing much muscle. This often does not impair performance all that much (and is a common practice in some bodybuilding circles).

most popular method i'd say bad eating habits not lack of general exercise than average non obese person.