text:
Do all sources supply all sinks on a plant?

Sources include any exporting organs, typically mature leaves, that
  are capable of producing photosynthete in excess of their own needs.
Sinks include any nonphotosynthetic organs of the plant and organs
  that do not produce enough photosynthetic products to support their
  own growth or storage needs. Roots, tubers, developing fruits, and
  immature leaves, which must import carbohydrate for normal
  development, are all examples of sink tissues.

Sinks are always supplied by sources. Now, I want to know do all sources transport their photosythetic to all parts of plant or some sources just supply some especial sinks.
This is a question for me:
Do all sources supply all sinks on a plant?

I really can't understand your question.

@WYSYWYG let me describe i this way. there are some sources and sinks in a plant. sources supply sinks. Now, I want to know do all sources transport their photosythetic to all parts or some sources just supply some especial sinks.


text:
How does Darwinian Evolution work?
Let me explain... A friend and I read some articles, part of a Biology book, and watched a video on evolution. We then tried to explain what Evolution is to each other.
My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.
I told him that DNA from male and female recombines and randomly mutates making a new "recipe" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature "selects" who survives and reproduces a lot.
So is the DNA mutation process random or is mutation directed to make an organism that is suited to survive its environment?
None of my friends are Biology students, so I can't ask then which explanation is correct (or at least more valid).
I'd prefer you don't answer: "None of these explanations are correct," but to say which one is more valid and correct misconceptions or add more that is missing (of course these are only summaries of our discussion). But of course, you can answer that neither of our explanations is correct...

Mutations and evolution are both complete random processes which are undirected.

Well evolution as i understand is not random because of natural selection but mutation is.But even if evolution is not random i think is undirected too .What do you think ?

@Chris It's not really accurate to call evolution 'random' (depending in part on how you define 'random'), but either way, the randomness in mutation and evolution are very different. Mutation is (mostly) a random process while evolution can be driven by different processes (natural selection, sexual selection, genetic drift etc). Evolution by natural selection is certainly stochastic but natural selection is also injecting alot of information into that process, and it cannot be seen as "undirected" (rather the opposite).

@chris mutation is (mostly) random but evolution is NOT random, Natural selection is a non-randomizing process. evolution is the coupling of a random and non-random process.

I accidentally wrote a lot!
I first discuss the term Darwinian evolution. I then describe the main evolutionary processes insisting on the two elements of interest in your question, that is mutations and natural selection. In the end, I directly address your two statements and bring a few more complications into the subjects.
Did you say Darwinian evolution?
Evolution is more than Darwinian evolution
The expression "Darwinian evolution" easily yield to misunderstandings. Darwin was probably the most important scientist and one of the first (if not the first) to develop the theory of evolution but evolutionary biology today is so much more than Darwin's theory of evolution.
Examples of very basic things Darwin did not know

We discovered the structure of DNA in the 1950s-1960s only with Miesher, Chargaff and most renowned Watson and Crick (history of the discovery). Darwin had no idea of the existence of DNA and had not even hypothesized about the existence of such a molecule (which came first by Erwin Schrödinger).
Darwin was not aware either that inheritance was through the transmission of "particles/atomic" and not through the inheritance of some kind of "fluid/continuum". In other words, Darwin did not know the Law of Segregation by Gregor Mendel (even if they lived in the same epoch).
Darwin had no idea about Evo-Devo, that is he had no idea about the similitudes in developmental processes among related (even distantly related) organisms.
Globally speaking, while Darwin managed to touch a little bit about many of the subjects of modern evolutionary biology (which is very impressive), he only manages to mention them and failed to provide any prediction. This is a large part because no one had no concept in genetics at that time.

Evolution is more than natural selection and mutations
Evolution is not only about natural selection. Even C. Darwin knew that evolution is way more than natural selection. It is for example very important to consider random events. One of them is mutation, another is genetic drift (I am not trying to list every process that influence evolution but only to give you a sense of why natural selection is different than evolution with a goal of explaining why a trait that is needed do not necessarily appear). Both mutations and genetic drift explain why a species will not necessarily be perfectly adapted to its environment. Evolutionary biology is a big field of knowledge and there is a lot to know about evolutionary processes.
Natural Selection and Mutations explained by the Lewontin Recipe
The Lewontin's recipe is a good way in order to understand what is natural selection and when it occurs. The Lewontin's recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

In such a situation, natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.
Natural Selection
Natural Selection is the process by which variants of genes called alleles are selected and therefore increase in frequency. This selection result from a differential reproductive success.
Mutations
In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen than other but in any case, the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, a phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of "if a trait would be beneficial"), then a mutation will occur to make this trait existing is wrong. Note that most mutations are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to rise in frequency in the population.
Genetic drift
If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency deterministically. An intuitive explanation of what is genetic drift can be found on this post. It will also allow you to understand why small population undergo a more random change in frequency of their genes than are big population.

Considering your opposing statements
Hopefully, the following is clear from the above discussion but I would like to directly address your statements.

My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.

You are right that your friend is wrong!
It indeed sounds more or less Lamarkian. In any case, it is very wrong, as you said. Mutations are not caused deterministically under the pressure of natural selection to do specific things.
Are mutations completely random?
See Are mutations random?.
I do not want to go into too many complications. The sentence "mutations are random" is unclear. Does it mean that the mutation rate is random? Does it mean that the effect of a new mutation is random? And also the concept of randomness only make sense if we consider a set of a priori knowledge. So it is a little hard to fully answer this question and the easy, close-enough approximation for a starter in evolutionary biology is just to say that mutations are random (whatever that means). A slightly better approximation of reality is that mutation rate is an adaptive trait and can vary depending on the environment where the individual is found (adaptively or not). However, the effect of new mutations is really not deterministic.
The mutation rate varies with the type of sequence considered. For example, a microsatellite sequence is a sequence or repeated DNA. For example AATAATAATAATAATAATAAT etc.. (note that the genetic code is written with 4 letters, A, T, C and G). Such sequences are highly mutable. So a mutation is more likely to occur in this region than in the middle of a coding region. And it is more likely for a mutation occurring in a coding region to affect fitness than for a mutation occurring in a microsatellite (it is possible that a mutation occurring in a microsatellite will affect fitness).
Depending on the level of stress some organisms (plants mostly to my knowledge) can change their mutation rate. Consider for example an individual that is maladapted to its environment. If it mutates little, then the offspring will likely be as maladapted and in the long run, the lineage will disappear. If the individual is mutating a lot then, most offspring will have a very low fitness but eventually one will receive a beneficial mutation that will make it very strong and by itself, this offspring may save the lineage. This is what is called a bet-hedging strategy. The concept of bet-hedging can be summarized with the expression "Don't put all your eggs in the same basket".
You will note that the mutation rate is an evolving feature of an organism. This yield observation such as what is now called Drake's rule (original paper). Drake's rule indicates that the genome-wide mutation rate is always at the order of 1 (there is quite a bit of variation but it is a good approximation).

I told him that DNA from male and female recombines and randomly mutates making a new "recipe" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature "selects" who survives and reproduces a lot.

Sounds quite right!
You pretty much nailed it. Mutation adds genetic variation and natural selection selects from the available genetic variation. Your wording is a little uncommon though :). For example, an individual, it is incorrect to say that an individual has fitness or not. Each individual has a fitness, that is some value that encompasses both its fertility and survival probability. In a simple model, fitness is simply the expected number of offspring.
Note also, that the majority of mutations that affect the fitness of the individuals are not so much dependent on the details of the environment. Many mutations are just bad wherever you are. Think about a mutation that would reduce the efficiency of energy production (ATP in mitochondria). Such a mutation will be deleterious regardless of whether the weather is hot or cold for example.

Introductory course to evolutionary biology
You probably want to have a look at an introductory course to evolutionary biology such as Understanding Evolution.

Wow :) 'Accidentally' :P

"the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, phenotype is how an individual looks like) and on the reproductive success."
The following paper seems to have shown that this claim is false.
Non-Random Directed Mutations Confirmed
http://www.i-sis.org.uk/Nonrandom_directed_mutations_confirmed.php

@MakotoKato I am not going to be able to address all the unclear questions and bad claims that you are making in comments of my various answers on this website. As I already said, if you have a (well defined and concise) question, just open a new post and ask it.

Your link is not a scientific paper and is not showing any evidence. Also, the author (Mae-Wan_Ho is criticized as doing pseudo-science and not science). You should read it before claiming what they did. However, from the text you link, Ho cite a paper (Cairns et al. 1988) that seems (from reading the abstract) that cells may have mechanism for choosing which mutations will occur (which contradict what I said indeed).

You might want to ask a question specific to Cairns et al. 1988. But before you do so, I recommend 1) following an introductory course to evolutionary biology so that you are are to ask a clear question, 2) reading this article who seem to be a direct response to the previous paper and 3) consider the generality and potential importance of the mechanism described by Cairns et al. 1988 (I haven't read the paper).

@Remi.b "As I already said, if you have a (well defined and concise) question, just open a new post and ask it."
Unfortunately I cannot do so because all the previous questions of mine were closed as being too broad while they were specific enough. It seems that questioning the tenet of the theory of evolution is kind of taboo in this site, which I think is a pretty unscientific attitude.

No, it is not taboo! If you have further questions about why your questions have been closed, ask them on meta.biology.SE.

Please just accept learning about evolutionary biology a little bit and you will be able to ask better question. I promise that I am doing my best to help (i.e. right above I have suggested a question and have described steps on how to best ask this question). I will not react to any further comments below, we already wrote too many useless comments here.

@Remi.b "No, it is not taboo!"
I asked for some evidences(e.g. papers) for the following claim of yours in my comment in another thread, but not only did you refuse to answer it, but it was deleted by a moderator.
"the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, phenotype is how an individual looks like) and on the reproductive success."

@Remi.b "Your link is not a scientific paper and is not showing any evidence."
How about this?
Predictable Evolution Trumps Randomness of Mutations
http://www.scientificamerican.com/article/predictable-evolution-trumps-randomness-of-mutations/
The following brand new paper(published on August 25, 2015) has confirmed the directed(or adaptive) mutation.
Evidence for Retromutagenesis as a Mechanism for Adaptive Mutation in Escherichia coli
http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1005477

That looks like an eventually interesting paper (the second link). I never heard of such process. I would love to hear more on this subject. I'll include your paper in my answer and might modify the answer later once I read the paper. Thank you.

@Remi.b. Don't. I read the paper. It is bad science, whether or not it was published on Plos. In their methods, they mention that their strain is AmpR, but they then make no mention of using antibiotics. That is a recipe for contamination. They also do not check to see whether or not any of their strains were LacZ diploids with an F Plasmid. Their controls are bad, their analysis is bad, and their conclusions are based on incorrect assumptions. No one ever said that you cannot have revertants within a species, gene conversion is well documented, but they aren't reverting to an ancestor.

The article was published more than 3 months ago, and does not have a single citation in a peer-reviewed paper.

@Remi.b I wasn't telling you to not read it, just that I didn't think that you should edit. The paper is troubling me, because it could be one of those papers that could be pure crap or could actually have something profound to say, but would require several read throughs and needs to be debated many times. I still am heavily leaning towards it being pure crap, but... I still maintain, however that MK is vandalizing posts, even if the paper has something interesting to say.

Mutation is a random process that mainly happens when a cell's DNA is replicated (= copied) before the cell's division, because the enzyme responsible for this replication sometimes makes mistakes. It's a rare process, as for eukaryotic cells (the ones with a nucleus, so animals and plant cells), it happens once every $10^9$ nucleotide.
Now, let's say we consider an organism that has sexual reproduction.
To be transmitted to the descendants of the organism, the mutation must appear in a cell of the germline (spermatozoid or ovule for example).
If transmitted, this mutation can have several effects :

It can be lethal, the organism cannot survive because the mutation makes a vital protein inoperative
It can give the organism a disadvantage in his environment (e.g. living in a snowy environment, the pigmentation of the organism's skin becomes glowing red)
It can be neutral, something is modified, but it keeps working (e.g. a certain protein has a different amino acid sequence but keeps working)
It can give the organism an evolutive advantage, the protein works better, in a way that favorises the organism vs. its fellows' organisms in surviving in their environment (e.g. in the snowy environment, the pigmentation of the organism's skin becomes perfectly white, whereas one of its fellows is greyish)

In the fourth case, this organism has more chances to reproduce (because he is less likely to be killed, or more likely to access a resource), and hence, to transmit this mutation. This is where natural selection applies: the "fitness" of the organism in his environment is greater than the one of the other organisms of his species.
Now, it's important to note that the evolution (= the change in a specie) is driven by the natural selection (= the process of selection), and that those changes, in nature, are random and take a long time and aren't easily noticeable at the scale of a human life.

Your description of Evolution seems more accurate than your friends. DNA cannot mutate with a particular goal in mind, mutations are random. Most mutations have no effect on an organism's survival, but some will be detrimental, and a few will helpful. Helpful mutations will improve an organisms odds of surviving and passing on its DNA, so those traits will eventually spread through a population.
However, if we wanted to talk about "goals" for evolution, then the goal of every piece of DNA is to be copied and passed on. (of course it cannot think about achieving that goal, it's just a chemical.) DNA mutations that make an organism more suited for a particular environment will be selected for, and those that are detrimental will be selected against. This competition between different copies of DNA eventually optimizes the species for that environment.
So at the molecular level, mutation is a totally random process, but if we zoom out to the ecosystem and population levels, then evolution "designs" a species to better survive in its environment. But this design is a result of random mutations and trial and error.

Great answers have been given already. But one phenomenon that is mostly not explicitly mentioned that can and should be regarded a part of the process of Evolution is symbiosis.
symbiosis
The probably most fundamental example for symbiosis is endosymbiotic theory. This theory in strongly simplified terms says that eukaryotic cells are the result of a symbiotic relationship between prokaryotes and early bacteria: both evolved separately with the prokaryotes probably being predators of some bacterial species. These species then are proposed to have evolved towards mutually beneficial, symbiotic relationship which essentially created a new form of life, eukaryotes.
From a more abstract point of view, symbiosis can be regarded a further mechanism of evolution: while mutation and recombination act on a molecular level, symbiosis acts on a similar level to selection. It is basically a macro-level recombination of not just genes, but whole or partial organisms into new life forms.
Some random examples:

eukaryotes: mitochondria from proteobacteria, chloroplasts from cyanobacteria.
bioluminescence in "fireflies" by vibrio bacteria
microbiome inside "guts" of more complex organisms
mycorrhizae (phosphor fixing) at the roots of some plants

Short Answer: As far as we know, it doesn't.
Mutations at Conception
The mutations you describe as occurring during conception which generate new information have never been observed to take place. Instead, we have observed mutations which reduce existing information. In humans, approximately 100 such mutations take place every generation.
Necessarily if information-additive mutations existed, they'd need to produce a lot more information to make up for the loss. Necessarily, descendants would have a larger and more complex genome than their ancestors. The opposite has been observed, where descendants have smaller genomes than their ancestors.
Abiogenesis
Before Darwin had written On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life, Pasteur was disproving the idea of abiogenesis, as the theory had gone around that germs could spontaneously appear. Despite this, Darwin took abiogenesis as part of the theory of evolution, which has consistently proved impossible in tests with no observable data to the contrary.
Genetic information is fragile and is quickly destroyed over time if it doesn't have enzymes to continually maintain it. There is no gradual process of accumulated information that can result in life able to reproduce, as far as we have found from study and observation. The very difficult process of creating amino acids to bond and form the nucleotides (necessary to form DNA chains) is complicated by the chirality problem, where artificial tests have resulted in both left-handed (L) and right-handed (D) optical isomers were created in a racemic mixture. In biological systems, almost all of the compounds are non-racemic, or homochiral, and biological creatures only use left-handed amino acids in the construction of DNA and RNA. All subsequent have tests run into the same problem.
Theory
As for the theory itself, you and Remi.b have described it accurately. As genetics was an unknown field at that time, it was the mistaken idea that natural selection changed a creature through the creation of information, rather than the reformation, sharing, and loss of existing information.
Sources: Genetic Entropy and the Mystery of the Genome by John Sanford. The Miller–Urey experiment.

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Does DHA increase the effects of clarithromycin?
I've read on this publication that every drug that induces CYP3A can reduce the effectiveness of clarithromycin. Clarithromycin inhibits CYP3A.
But it does not say anything about the opposite situation: does a low concentration of CYP3A increase the effect of clarithromycin?
This research shows how DHA can inhibit CYP3A.
Now the final question is: does a high concentration of DHA increase the effect of clarithromycin?

What is DHA? Please define abbreviations other than the most generally accepted ones.

You've misread the paper. Clarithromycin is metabolized in part by CYP3A, but to an active metabolite. A significant proportion of clarithromycin and its active metabolites are excreted unchanged in the kidney. Clarithromycin, and other macrolide antibiotics do inhibit CYP3A enzymes, as you noted in your answer. You can read about this in chapter 55 of Goodman & Gilman's the Pharmacological Basis of Therapeutics.
We certainly worry about clarithromycin and other macrolides increasing the half-life of drugs that are primarily metabolized by CYP3A4 (again, see Goodman and Gilman). Midazolam is an example, and is what the paper you cite was about. If you give clarithromycin together with midazolam, expect the effects of midazolam to last longer. The important relationship between CYP3A induction and clarithromycin discussed in the paper is not that it reduces the effectiveness of clarithromycin, but that CYP3A induction does not overcome clarithromycin mediated CYP3A inhibition.

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How come all my family have brown eyes and I have blue eyes?
My whole family tree up to my grandparents have brown eyes,
I have blue eyes, how come?
I don't know if it matters but I have not received enough oxygen at birth, doctors said it's probably the reason I'm left handed while my most of my family is right handed

let's say my grand-grand-grand parent had a blue eye genes, what is the statistic for me to have blue eyes?

How many (genetically related) aunts and uncles do you have, and are any of them blue-eyed? How many siblings do you have?

about 14 aunts and uncles, many more cousins, all have brown eyes. what is the statistic for me to have blue eyes?

While I don't know much about the inheritance of eye color, I suppose that a perfect answer would compare 1) the probability of such thing to occur assuming the alleles that make you eyes blue are inherited by some family member, 2) the probability that you carry a new mutation that make you eyes blue and that your recent ancestors did not carry and 3) the probability that your father is not your real father (my apologies for saying that this might be a possibility).

After wiki missatributed paternity is around 5% (with large standard error). It is important however, when talking about the misattributed paternity hypothesis, to not forget that there is a multiple comparison issue here. Eye color is not just a randomly chosen phenotypic trait but is one that you notice make make you different from the rest of the family.

Since blue eyes are mainly related to recessive alleles (so brown eyed parents can carry the alleles that cause blue eyes) at two different loci this is perfectly normal, even if all your grandparents have brown eyes. This link provides a nice overview of the basics of eye color inheritance: http://genetics.thetech.org/how-blue-eyed-parents-can-have-brown-eyed-children
However, even more genes are related to eye color besides the two main ones, so besides these main modes of inheritance, there are also other possible combinations and cases.

An age-old problem with a fairly obvious solution: "My mother certainly says I am Odysseus' son; but for myself I cannot tell. It's a wise child that knows its own father." - Homer, "The Odyssey. ca 1100 BCE.  (I write this as the only green-eyed blonde in a family with dark hair & brown eyes.)

The eye color follow quite well mendelian inheritance rules...
Probably your parents are heterozygote recessive for the blue color, hence the children have 25% of probability of having blue eyes.
Let's say color of the eyes has 2 alleles "BLACK" for the dark eyes and "blue" for the light eyes. Your parents are probably both BLACK-blue, BLACK-blue. They show the dark eyes because that allele is dominant over the blue one.
During recombination all the possible combination can come out:

BLACK x BLACK=25% resulting color=dark
BLACK x blue=25% resulting color=dark
blue x BLACK=25% resulting color=dark
blue x blue=25% resulting color=light

Check out the wiki page about mendelian rules of inheritance if you wanna know more!!
Of course in realty the situation is much more complicated, however you can still approximate the results to mendelian rules...
have fun!!


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Are bacteria necessary for an individual's life, or, how long could a person live without bacteria?
Bacteria are essential to life in that they are responsible for breakdown of organic substances, etc. but are bacteria necessary for an individual's life?
In other words, how long would a human survive if they took a super-antibiotic which killed all the bacteria in their body, with the current state of medical technology? If they died what would be the most likely cause of death?
Assume bacteria don't recolonize your body.
Background: I call bacteria the "Lords of the Earth" both to remind myself to be humble and (rather more) as a conversation-starter. I'd like to be able to underline their importance in the ensuing discussions.

I grant that the "Background" sentence is opinion-based but it was just intended as a light-hearted introduction. The "How long" sentence was my real question and is IMHO factual. In any case anongoodnurse has answered to my satisfaction (and surprise). Thanks!

Related: Do animal experiments really mean anything when it comes to extrapolating findings to humans?

You might need to demote your single-celled 'lords' to 'squires'. They're not essential to an individual's life. You wouldn't die (dispensing with the "how" right off the bat.) You'd be just fine if no bacteria reentered your body. Your fecal output would be greater; you would derive somewhat less nutrition from your food, you would need to take vitamin K, and there would be an adjustment period, but theoretically, you'd be just fine. You might even be healthier.
Your hypothetical is impossible, of course, because experimentation on humans is unethical. However, it might surprise you to learn that there are colonies of germ-free animals (also called gnotobiotic) used to study the effect of certain bacteria on animals.
The derivation of such subjects was initially fairly gruesome.

The process of engineering biology and machine began by removing intact uteruses from near- to full-term pregnant animals within a purpose-built germ-free "surgical isolator." The uterus was subsequently passed through various disinfection procedures, involving total immersion in germicide-filled "dunk tanks," before the progeny were surgically released and hand reared within a second microbially sterile isolator.

These animals are costly to keep, as you can imagine. The originals must be delivered by Cesarean section, and housed and raised in sterile conditions. But once you can do that, they can multiply.

To start a germ-free colony, one must remove a young animal from its mother’s womb through a careful surgical procedure to avoid exposing it to the microorganisms in the mother’s vagina and skin. Then, the animal is raised in a sterile cage and only exposed to food, water, and other equipment that has also been sterilized. On a weekly basis—or more often—a technician swabs cages and animal feces to ensure that no bacteria have contaminated the sterile housing. Once the colony has been created, it becomes easier to rear new germ-free animals; a germ-free mother can give birth naturally without exposing her newborns to any bacteria.

By the 1950s, researchers were rearing germ-free mice, rats, guinea pigs, and chicks inside sterile stainless steel (and later, plastic) housings. Germ-free animals are especially useful in researching, among other things, diabetes, auto-immune diseases, obesity, genetic engineering, cancer, immunology, nutrition, and the effects of normal intestinal flora on health.
Vitamin K must be added to their diets, and it is important to sterilize their food without destroying nutrients, but otherwise they do well in their environments. Their feces, of course, are sterile. Everything is microbe-free. They also have no "normal" antibodies.
Since generations of germ-free animals can exist and multiply, it is not only possible but quite likely that germ-free humans can exist as well.
Which is not to say that gut (and skin, etc.) microbiomes are unimportant. If you release a germ-free animal into a normal environment, it can die if it picks up pathogenic bacteria before more normal gut flora. To do this safely, a germ-free animal is first given a cocktail of bacteria to colonize the gut. After a while, they can be in a normal environment without problems. But your hypothetical human wouldn't even have this problem.
Germ-Free Mice
Gnotobiotics
Technology Highlights：ESTABLISHMENT OF THE FIRST GERMFREE MOUSE AND RAT COLONIES IN TAIWAN
"Life in a Germ-Free World":
Isolating Life from the Laboratory Animal to the Bubble Boy

I am rather confused how you cited the 4th source, but didn't use its case study of the bubble boy.

@MarchHo - answered in Meta.

So finally, how long can humans live without bacteria? Is there any data on the longivity of such animals? Please include it in your answer. Do they live longer? Is the lifespan normal? Or is it short?

@CRags The life is definitely not NORMAL if normal means what is most common. Such a person may need to take a lot of dietary supplements. However, it is possible to keep that person alive as long as there are no other problems (independent of the said problem). It is same as: can a AIDS patient survive as long as their replica without AIDS -  yes, as long as they are kept in sterile environment

@WYSIWYG - their lives are "normal" compared to the controls, who also don't live a "normal" life. A better question is, What is the average lifespan of a patient with HIV on all the proper medications compared to one without HIV. Normal here applies to health, lifespan, etc., not activities in the wild.

Now it begins to sound as if bacteria-free humans would suffer from vitamin K deficiency (hemorrhaging?). After all, a question like "how long could you survive in a vacuum" would hardly be acceptably answered by "indefinitely, if you had an adequate spacesuit"

I am not asking about normalcy of life but lifespan. (That is the question?) Does the bacterial flora affect the lifespan? Many physiological processes are altered, due to sterile environment. So will this alteration increase / decrease or have no effect on lifespan? How do you relate HIV with this question? Patients with HIV have bacterial flora. And having HIV is not a part of normalcy.  HIV would actively work against host immunity, while absence of bacterial flora would result in a situation where no immunity reactions need occur. Please explain more @WYSIWYG. As the OP pointed out,

contd... let's say that all nutrients that are known as needed as of today are provided resulting in no deficiency of "known micro and macronutrients" for simplifying the answer.

@NL_Derek - Vitamin K is actually a group of compounds. The most important of these compounds appears to be vitamin K1 and vitamin K2. Vitamin K1 is obtained from leafy greens and some other vegetables. Vitamin K2 is a group of compounds largely obtained from meats, cheeses, and eggs, and synthesized by bacteria. No deficiency would necessarily occur.

@CRags I don't think loss of microflora would have any direct effect on lifespan. We don't even have enough cases to document the problems that may manifest because of living in sterile environment for a long time. Recent studies suggest the role of microflora on cancer (both positive and negative): this is mostly related to the biochemical reactions they carry out but we have insufficient data to say if their absence would make a great impact on the body except in case of nutrition. Low immunity on the other hand can also lead to cancer even in sterile environment


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Different flowers have same colour
I notice that certain (wild) flowers have the same colour, although they are not closely related. For example, the yellows of the dandelion (Taraxacum) and the buttercup (Ranunculus) are, at least to my eyes, identical (my observations are in the Netherlands).

I know that the colour is intended to attract insects; is this parallel evolution or are there certain biochemicals which provide colour and are easy for the plant to synthesize? Or something else?
Edit: I used the buttercup and dandelion because that was the first pair I found physically close enough for a photo; the cowslip, celandine and charlock mustard are all (to my eyes) the same yellow. I have also seen similar blues, reds and violets, and shall try to collect examples next time I go cycling on the dyke.
When I look at colour tables like https://en.wikipedia.org/wiki/Web_colors#Extended_colors I see numerous colours which I do not recall ever seeing in wild flowers.
Edit2: I retract my remarks about blues, reds and violets; it's hard to judge colours when cycling past and when I pluck the flowers and compare directly there's a definite difference, for example:

However I still find the yellows very similar; here the charlock (left) is lighter but the buttercup, celandine and dandelion look identical to my eyes.

Comments seem to suggest a biochemical cause; can anyone confirm (or disprove) it?

I don't have an answer, but note that many insects see a different spectrum that we do — for example bees can see into the ultraviolet, but IIRC don't see reds. Consequently, what we see isn't necessarily a good representation of what an insect pollinator sees — in fact the UV pattern on a dandelion may be very different from that on a buttercup. Search for "UV" images of buttercups and dandelions to see example images.

Antheraxanthin, is the pigment that is causing the yellow colour in dandelions. It is built from a basic carotene molecule. Carotene is a another basic pigment that is found in many plants specifically to produce colour. Antheraxanthin in dandelions, is associated with photoprotection from the sun. Possible topics you should explore to understand your questions are: carotenoids, flavonoids, and anthocyanins, all of these molecules groups are associated with flower pigmentations.

link Here is a article about buttercups, apparently the the pigment molecule in buttercup is also a derivative of  carotenoids, just like dandelions. Though the purpose for the presence of the pigment is totally different. As mentioned by @tyersome, the pigment in buttercup produces different UV colour, which some animals see and this feature brings about different physical properties such as reflectivity that is seen in buttercups and not dandelions.

Wow! You guys are fast! tyersome's link seems to exclude parallel evolution, and Sentma's data suggests a biochemical explanation. Is anyone confident enough to make an answer?

@NL_Derek, could you make your question a bit more clear, at its current state it is a bit vague.

You might consider that there are many fewer colors (at least to human perception) than there are species of plants with showy flowers.

@Sentma is this an improvement?

WRT those color tables, note that there are many more colors there than can be distinguished by the average human.  Honestly,  can you tell the difference between LawnGreen, Chartreuse, and GreenYellow,  or between Firebrick and IndianRed?

@jamesqf valid observation, but my point is that I don't recall ever seeing a flower with, for example, LightSlateGray or RosyBrown.

@NL_Derek: Perhaps you haven't looked hard enough?  Here's a local wildflower that approaches RosyBrown: https://en.wikipedia.org/wiki/Paeonia_brownii  You could probably find grays in for instance Aril & Arilbred irises.  Like this one: https://garden.org/plants/view/527214/Arilbred-Iris-Iris-Eyes-on-You/  (I really can only approximate the particular shades myself.)

@jamesqf your remarks led me to check further and I have now restricted the question to yellow. Also I suspect Dutch dykeside wild flowers are less varied than in your locality, alongside yellow and white I see mostly shades of blue, pink and purple/violet.

@NL_Derek: Perhaps - I've never been to the Netherlands.  (And the Aril Irises are definitely not wildflowers hereabouts, being native to the Middle East.)  But even within some species, there are considerable color variations.  For instance, the common wild California poppy (Eschscholzia californica) is usually a bright orange, but it's not that uncommon to see plants with bright yellow flowers, or intermediate shades: https://en.wikipedia.org/wiki/Eschscholzia_californica

I think parallel evolution is likely due to the cost to produce the pigments in plants.
Xanthophylls and carotenes are made from only carbon, oxygen and hydrogen. This provides most of the yellow colours without using up nutrients.
Anthocyanins and betalains also need nitrogen, which can be a limiting nutrient for plants.
Wikipedia has a section on plant pigments at:
http://en.wikipedia.org/wiki/Biological_pigment

+1 for the Wikipedia link


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Nail polish toxicity studies?
Are there any well-founded studies that authoritatively demonstrate negative effects from the use of nail polish, particularly in children?
I've been brought into the fray of a couple of folks who are having a rather serious debate of whether or not a child of 6 or 7 years of age should be allowed or discouraged from wearing traditional (not the "safe brands") nail polish.  It was my opinion that it is better err on the side of caution and that one should rather be safe than sorry, opting for safer non-toxic alternatives if fingernail paint must be worn by such a young child.
The debate has boiled over into allegations of quack science and over-caution.  Seems absurd to me, but I wanted to do some more research into the biology of the matter.
A recent report appears to urge on the side of caution, but could someone help to point me in the right direction with regards to substantiating valid scientific claims and studies that fingernail polish can, has and/or does contain harmful material that should not warrant careless usage, especially by younger children who may be more hormonally susceptible to adverse effects?
I'm really looking to button up the "quack" or kooky science arguments if possible and to put this debate to proverbial rest.

I seriously doubt you will find any peer-reviewed data on this as no one would be willing to fund the research. You may get a public health department looking into the claims of health issues, but there you will tend to have politics tainting the answers. If you look at the controversy that was generated this year with the NY Times exposé on Nail Salons, there was a response at the state level, so maybe the New York City or State health departments issued reports on the chemicals involved. That may be your best bet to finding a source that is even remotely scientific.

You may want to start by Googling Material Safety Data Sheets for Nail Products. Here is one of the links that came up. http://www.nsinails.com/nail-lab/science-of-beauty/material-safety-data-sheets.html#.Vl6LQ4T41NE . Also OSHA has issued safety guidelines for salon workers https://www.osha.gov/Publications/3542nail-salon-workers-guide.pdf

I wouldn't have thought that the nail polish is a problem. What might be a better reason for caution from a dermatological point of view is the nail polish remover, which is a known allergen. "In addition to blister formation, polish removers may cause irritant and allergic contact dermatitis, onycholysis, paronychia, and brittleness. They represent a fire hazard and may cause systemic toxicity following excessive inhalation."

That website looks like it is about scare-mongering.  I can't read beyond the abstract of the study, but people are exposed to trace amounts of all kinds of chemicals all the time.  You can't avoid them all, and you don't need to, if there is no evidence of harm.  Honestly, the kids are far more likely to suffer harm swimming or bike riding than from wearing nail polish.


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How would i describe a Cladogram as paragraph?
I have this paragraph that i have halfway finished, but i do not know what to put in the spaces.

A Cladogram is a branching diagram that represents the proposed phylogeny or evolution of a species or a group. The groups used in Cladograms are called clades.. To construct a cladogram, two characters are defined. Then the outgroup of various species are identified based on the sequencing or closeness of the derived characters in the clades. In making a cladogram, ______ assume that groups that _____ more derived characters have a more close common ancestor.

The letters that are italicized are words that i think are correct. This paragraph is needed for part of a recite that i have to do in front of my class. The prof. gave me a page like this. And  I don't know what those spaces are. Can someone help me.. please?

Maybe: construct=infer, two=homologous, outgroup=ancestors, sequencing=presence, closeness=absence, clades=clades, _____(1)=always, ______(2)=share, close=recent. The last sentence assumes you are only considering maximum parsimony.

ok, this is to all the people that put this on hold HAVE shown an attempt to answer.my answers are the ones in ITALIC. So, can you please explain to me why you put it on hold? Because clearly, you can see the italic words.

@mcg256 thanks. and thank you for the explanation, you are very kind.

I provided some edits in my comment -- hope the following clarifies things for you a little bit.

To construct a cladogram, two characters are defined.

You may be confusing character and character state. It's valid to have a cladogram with a single character (e.g. the single character, "warm-blooded"), but you will need at least two character states to infer a non-trivial cladogram. The states for the character warm-blooded would be Yes or No.
A molecular example would be a cladogram inferred from a column of a sequence alignment. That column is the character, and for, say, DNA, the character states are the set {A,C,G,T}.

Then the outgroup of various species are identified based on the sequencing or closeness of the derived characters in the clades.

The outgroup is specified by you, the investigator. It's typically a hypothesis (viz. model parameter), which is either a guess or is based on some external evidence.
In short, the analysis starts from character-state data for some number of taxa ("species" in your paragraph). From this data you are selecting (constructing) a tree-topology that best fits this data.
E.g. for four taxa, labeled A,B,C,D, with D the outgroup, the process is like:
 start  --> cladogram
 ABC(D)     A  B C (D)
             \/ / /
              \/ /
               \/

There are many different methods to construct the cladogram. One popular method is  maximum parsimony, but the assumptions of that model are severe. However, any method is effectively selecting a tree topology out of all the finitely-many possible tree topologies over N leaves, where N is the number of taxa (species) in your investigation.

In making a cladogram, ______ assume that groups that _____ more derived characters have a more close common ancestor.

In this sentence, you seem to be expressing a relationship between the number of shared derived characters (synapomorphies) for a given clade, and the common ancestor of that clade.
This can be very confusing, maybe an example will help. Let me annotate the above tree with a binary character, having states + and -.
            +   +  -   -
            A   B  C  (D)
             \ /  /   /
              +  /   /
               \/   /
                -  /
                 \/
                  -

The idea is that the ancestral state for the entire group is -, as was the state for the ancestor of {A,B,C}. However, the + state was derived after the ancestor of {A,B,C} but before (or "in") the ancestor of {A,B}. Then it was passed to the terminal units, A and B. (Note: typically you don't have this ancestral-state information, only the information at the tips of the tree. You're actually inferring the ancestral states and topology from the data at the tips.)
I would claim that, in general, taxa that share more derived character (states) have a more recent common ancestor than taxa that do not. Although, this can be confounded by homoplasy.

thanks for the in-depth explanation. you deserve more than one upvote! Not enough thanks to be given.


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Sequence compression method / format
As someone working with sequencing data and sequence files I was wondering whether is there a compression method / format for sequence / read files? Of course one can use general compressors like rar or zip to compress a fasta file, which is suitable for transferring data, but reading the sequence out of it is infeasible. Also I'm aware of BAM file format which is a block copressed gzip file of a SAM file, but as far as I know it is mainly used in alignments. But is there a compression for plain fastq(-like) files for storing millions of reads or a collection of sequences while being able to get sequence and quality info directly from the file?

Normally one gzips such things. Do you actually need random access and, if so, how many reads/sequences are we talking about? BTW, BAM isn't a bunch of block gzipped SAM files, it's its own binary format that's block gzipped.

Yes, I know I just didn't express myself well I'll edit my question, thx for pointing that out

Ohh I forgot to answer your question in my previous comment. I'm talking about millions of reads or tens of gigabytes of data.

Sequence files can be compressed after Burrows-Wheeler transformation; but you cannot read them directly. See here. Bowtie indices are burrows wheeler compressed; you can use bowtie-build to transform your fasta file.

Note that block compression can be applied to any type of file, including fastq or fasta, using the bgzip utility that comes with samtools. That said, I don't know to what point this makes the file more easy to deal with than just using plain gzip. Biopython has some degree of support for bgzip.

I can conceive of two scenarios when block compression of fastq files would be useful. Firstly, if for some reason one wanted to search for a specific read, then sorting the file by xy read position would make the search quick. Secondly, in theory a super super fast aligner could have multiple decompression threads. In the first case, I really doubt anyone would want to do that. In the second case, I hope the files are in memory or on a solid state drive (and I would LOVE to use an aligner fast enough to care about this scenario!).

BAM is the current standard for sequence alignments, and can be used to store unaligned reads/sequences, but when used for unaligned sequences also contains unused alignment data that would bloat the file.
An alternative way to compress a DNA sequence file is via 2-bit (or 4-bit encoding) which can compress the sequence content by 75% (in 2-bit encoding, each nucleotide can be represented by 2-bits in the file eg A: 00, G: 01, C: 10, T: 11). I do not know of a generalizable tool that will compress/decompress aside from rolling your own. Further, the data must be de-compressed prior to streaming it into any alignment/sequence software. For general purpose compression algorithms, bzip2 can outperform (at least in compression) other algorithms (eg zip, gzip)

Hi, thx for the answer. I was thinking about the 2 bit compression myself but as you pointed out it needs to be decompressed for currents softwares. My 'problem" with BAM file is the as you said it contains many extra data that is useful for alignment but not otherwise.

With a 2-bit encoding you cannot have Ns, right?

You can, the format isn't exactly 2 bits per base. Instead it's actually 4, with the additional 2 bits being a mask that can convey information like, "it's an N", or "it's soft-masked". What this can't do is store quality information (or IUPAC ambiguity codes, as sometimes appear in fasta files). In fact, the space savings of a 2-bit variant format over straight fastq are 0.5 bytes per base in the sequence plus 3 bytes per read. Standard compression has better compression than that (you can, of course, compress 2-bit data).

BFQ = binary fastq
Described here:
http://ngsutils.org/modules/fastqutils/
I have not used it myself, but I gather that the maq aligner package can use (or generate) these files.
Even though the bam format already incorporates the block compression (described by yourself and others), we routinely deal with gripped bam files and my sense is that there is some additional compression that takes place (I haven't calculated a percentage)

It should be noted that bfq can't store quality scores above 61 (it says it can go up to 62, but a T with a phred score of 62 is an N...). Anyway, a compressed bfq file is about 90% the size of a gzipped fastq file, so space savings are marginal (particularly given the added overhead of processing bfq). An uncompressed bfq file is about half the size of an uncompressed fastq file.


text:
What does it mean to use DMSO as a dissolvant in biology experiemnts?
In many biology publications, I saw that dimethyl sulfoxide (DMSO) is used to dissolve drugs. However, the cell-based assays are still performed in water-based medium such as RPMI or PBS.
My question is: If a compound is not soluble in water, what is the purpose of using DMSO? Although the drug can be dissolved in pure DMSO, won't it precipitate after putting the DMSO-dissolved compound into culture medium?

Usually such compounds are dissolved in DMSO to make a concentrated stock solution (e.g. 1000x), which is then diluted into the culture medium. Often, the compound is soluble in water at this lower dilution, but not at the higher concentration required to make a stock. Sometimes the compound has low solubility in water and much of it precipitates. This still lets us test the effect of the fraction that remains soluble.


text:
Is spliceosomal RNA called snRNP or snRNA?
I have been reading articles by various sources, and they seem to interchangeably call the U1/U2/U4/U6 compounds involved in RNA splicing snRNPs as well as snRNAs.
This confuses me deeply. They must only be one or the other, no?
Thank you in advance!

Another post with no reference supporting your assertion and no evidence of an attempt to solve a trivial question of nomenclature that an internet search would have answered. Please discontinue this practice.

I'm voting to close this question as off-topic because it is a trivial question about nomenclature that is easily solved by an internet search.

snRNA: small nuclear ribonucleic acid
snRNP: small nuclear ribonucleoprotein
snRNA refers to the RNA itself. snRNP refers to snRNA complexed with some protein(s). You could call spliceosomal RNA either depending on the context.

Most small and large RNAs typically exist and function in complex with proteins as ribonucleoprotein particles so the second denomination is more appropriate.


text:
Reason for name "Motile sperm domain-containing protein 2" if it has nothing to do with sperm
I am interested in a gene with the name "motile sperm domain-containing protein 2".
The entry for the human gene in uniprot suggests that it does not have any relation to sperm or spermatogenesis.
If this is so, why does the name make reference to sperm?

Please read the Tour as a new user to this site and especially how to ask good questions. Then, do some research yourself. Have you looked up the original papers on this protein or any reviews. They may be able to clarify a question of terminology. If you have to post, give a reference to the gene (Uniprot number and link) and tell us what organism it is in. Otherwise your question is unlikely to receive responses and is likely to be closed as off-topic.

Hi, I have checked many references and no chance!

Organism? Reference? Please read comments carefully before replying.

Hi David and thank you for your helps. There is not any organism or references that I can mention and there is no difference that this gene is expressing in which organism! we have a sequence of nucleotides that its annotation is refering to "motile sperm ...", So it is not important that this gene is expressing where in the animal kingdom. about the reference, it is not important to mention (I have mentioned one). many annotation database share same names, uniprot, trembl, NCBI. please attention that my question is this"why we use sperm in a gene name that is not working in sperm?"thats all.

Also asked on biostars

But eventually you are someone else did provide a link and I edited your question to indicate the species and take into account the content of the link. @DevonRyan has provided you with an answer. I suggest you accept it.

@FarbodEmami Note that you don't have to accept an answer if you don't believe it adequately answers your question (or if you believe the way in which it answers the question is unsatisfactory).

As you can tell from the gene name, it contains a domain (a "major sperm protein domain)") that happens to have "sperm" in its name. That doesn't mean that the protein itself have anything to do with sperm. There are a lot of examples of gene names like this, where they're named after some random domain they contain until later their names are changed. MSOPD2 has only had a known function for a few months.
As an aside, if you actually work on this gene then one would hope that you would have taken the whopping 5 minutes required to figure this out in pubmed.

Downvoted for the belittling snark of the "aside". If you think this question is too simple to be worth a Q&A on this StackExchange, then don't write an answer - downvote or vote-to-close and move on.


text:
How is a very small quantity of poison able to kill a large organism?
Take cyanide for example: it prevents mitochondria from producing energy in form of ATP but, in the process, it binds with it and hence it's spent.
It's theorized that half a gram of cyanide can kill an average adult human. How is this possible? There surely is more than half a gram of mitochondria in an adult human. So, if cyanide molecules bind and hence get spent so fast, how are they able to kill so many cells so fast and continuously?
Is it something to do with the amount of molecules in half a gram of cyanide being several times higher than the amount of cells in one gram of human tissue?

I'm pretty sure cyanide deaths are due to high levels of oxygen in the blood vessels, rather than loss of energy to the individual cells.

@TwistedGenes Based on what?

"Cyanide" doesn't refer to just one compound, but given the lethal dose you mention of "half a gram" you are probably referring to potassium cyanide, with a molecular weight of about 65g/mol, so 0.5 gram is about $10^{22}$ molecules. Potassium cyanide becomes hydrogen cyanide in the stomach, and hydrogen cyanide is the gas (at body temperature) that causes toxic effects.
The toxicity of cyanide containing compounds is because they bind with high affinity to cytochrome c oxidase, an enzyme that is part of the mitochondrial electron transport chain. The result is that electrons cannot be efficiently transferred to oxygen molecules. The effect is roughly the same as if oxygen was not present in the inspired air.
$10^{22}$ is a huge number. That's about 250 million molecules per human cell in an adult (taking # of human cells from Bianconi et al). Even so, it isn't likely that cyanide molecules be perfectly bound at every molecule of cytochrome c oxidase, just that there is enough to cause massive brain damage or stop the heart.
By comparison, cyanide is not even close to the most toxic substance. Toxins that target neurotransmission can be much more potent. For example, the IV LD50 for botulinum toxin is about 2 ng/kg, so something like 125 ng for an average adult, equaling only $5\times10^{11}$ molecules.


text:
Quantity of genetic material in humans vs nonhuman animals
I am using a simple, rigorous definition of genetic material- the total number of base pairs in all of the coding regions of a species' genome.
For example, take human genome H and snake genome S. H has some genetic sequence of 5 bp. S has an identical sequence followed by a different sequence of length 2. Thus H and S have 5 bp of genetic material shared with humans, and 2 bp of genetic material not shared with humans.
We can take the set of genetic material in all studied animal species, and count the number of unique sequences in this set. Call this variable A.
What percent of A consists of sequences shared with humans?
Certainly not all species' genomes are documented, so this number will be biased toward a high value. It would also be too much work for anyone here to compute such a value, even though the data is well cataloged. But I am interested in knowing if anyone has performed a similar calculation and what the results were.

There have been plenty of calculations of genetic similarity between all sorts of organisms. Are you unaware of those, or does your question and the description of what you want calculated specifically exclude them ?

Nevermind, I understand your question now. There is still an issue with it though: when you describe your calculations it's clearly a difference in raw base pair sequences, however you then ask "what percentage of A consists of genes"; differences in genes and in nucleotide sequences are two very different things. Did you mean that switch, and if not is it sequences or genes you're asking about ?

I've edited your question slightly to make it clearer, hopefully the meaning of your question wasn't lost.

@DapperLad Please do not spam! This comes in reaction to your, now rather obvious, recent spam where you make the question and the answer and then delete both once I highlighted the spam. Such behaviour is a bit of an insult to the user of this site and could result in your account being blocked.

OK, that's a very confusing question but I think I've figured it out (uncertainty about "genes" vs "genetic material" notwithstanding).
I am almost certain that this calculation has not been made, for these reasons: as you say we don't have nearly enough information to make the calculations, even a partial calculations would be an enormous amount of work, which raises the question of what the purpose of this work would be, and I don't really see a use biologists might have for this number.
The reason it is an enormous amount of work is that most comparative genomic studies are done between a few species; to put all that information together you'd have to trawl through all those different studies. This is more feasible now with huge genomic databases, but it leads to the big issue: you can't just add all the genes in the different organisms, because most of those genes are shared between them. The closest thing I've found to a calculation of your "A" number is this paper:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4466264/
If that were the total number of distinct genes in the biosphere then you could approximate the percentage you're looking for by dividing the total number of genes humans have by the total number of genes in the biosphere. Or you could get a better approximation by substracting from the total number of human genes the number of genes humans don't share with chimpanzees; I doubt it would change the number much though.
However that paper has an estimation of the total amount of DNA in the biosphere, a completely different issue from the number of genes, which is itself completely different from the number of distinct genes, which would itself rely on completely arbitrary distinctions because almost all genes vary between species, but if we count those small variations as "different genes" then obviously none of them are shared with humans at all, but there isn't a sharp line between "genes with different sequences that code for the same protein", "genes with different sequences that code for basically the same protein", and "genes with different sequences that code for similar but different proteins". The question is a bit easier with genetic material, but it's still clear that cross-comparing ALL genomes we have to list ALL of the distinct sequences is a computationally monumental task. And we're already using those computers for more immediately useful genomics analyses.
As for the issue of biologists having no use for the number, I simply don't see how knowing that number can increase our understanding about life, animals or humans compared to things we already know or are investigating, such as what genes humans have, what genes exist out there in the world, what relationship any specific human gene has to the genes of other relevant animals, etc.
I would like to know more about why you're interested in this number. You must certainly have a question in mind that having this number would help answer, and if we know that question it might be that there are other numbers, that have actually been calculated, that could inform it.
EDIT: Having said that it occurred to me you could still find things like the total number of distinct genes that have been identified by biologists in all living things, since that's more about counting the entries in various gene databases (this could also make a gene-based calculation actually easier than a sequence-based one). This would give at least bounds on the number you're looking for. In that spirit I found this paper about the total number of distinct genes in human gut bacteria:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0006074
Which appears to be 9,000,000, which would put an upper bound for the percentage human genes make up out of the total number of genes at 0.00025 or so. (you said nonhuman ANIMALS though, I don't know how strict you were about that factor)
REDIT - The number might be very different in animals actually, given these two papers :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3130542/
http://www.nature.com/nature/journal/v476/n7360/full/nature10249.html
Looking at the sequenced genome of a sponge and a coral respectively. The latter in particular has a convenient phylogenetic tree that illustrates how the sponge is the furthest branch away from us (i.e. our common ancestor with that sponge is pretty close to the common ancestor of all animals) and the corals branch off soon later. The former was estimated to have 30000 genes, of which 20000 were homologous to genes in other animals. The latter they found 25000 genes, of which 93% matched the genes of other metazoans. So we have something like 10000 genes that sponges don't share with us; 2000 genes that corals don't share with us; the numbers get smaller as we get groups that are closer to us, and presumably most of the genes, say, sponges have that are different from us are common between sponges, so you could get a ratio of genes in humans/genes in all animals that's as high as one half.

It would be interesting to know the distributions of differences as well. For example, how many of those nonshared genes are completely identical except for a single base pair, two base pairs, three base pairs, etc. Would further describe how similar the DNA of all animals is.

Again, I would really like to know why you think those things would be interesting, because I don't really know why you want to know those completely non-standard things as opposed to the things the field of genomics measures as a matter of course ? I feel like I would better know how to answer the question if I knew. (...)

As for "how many of those nonshared genes are completely identical except for a single base pair", the answer is none, because genes that differ only by a single base pair would be considered "the same gene", or more specifically homologues. To quote the paper on the sponge : "18,693 (63%) have identifiable homologues in other organisms in the Swiss-Prot database". Emphasis added by me: if the standard for "same gene" were "identical sequence" you wouldn't need to use the word "identifiable" which suggests a bit more effort and judgement than "checking if they're identical or not".

For more detail on how biologists identify gene homologues : https://en.wikipedia.org/wiki/Sequence_homology and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820096/. While the Wikipedia page leaves some ambiguity as to whether "similarity" usually means "identity" or not, the paper clearly gives the standard for "similarity" as being statistical significance, i.e. being more similar than you would expect from chance.

@rozzen Because they provide genetiticists have no idea

@DapperLad ????


text:
Does the oxygen concentration equilibrate between red blood cells in the liver sinusoids?
In the sinusoids of the liver, venous blood from the hepatic portal system mixes with arterial blood from the hepatic arteries.
Do oxygen molecules move between oxygenated RBCs and non-oxygenated RBCs, so that the partial oxygen saturation of the blood in the sinusoids reflect partial saturation of the RBCs? Or do RBCs retain their initial oxygen saturation, so that the partial saturation of the blood in the sinusoids reflects a mixture of saturated and unsaturated RBCs?

I am not sure if these are the best tags, feel free to adjust them is they can be improved.

The oxygen saturation (in lungs) and desaturation (in target organs) takes place via diffusion along the concentration gradient (i.e. partial pressure for gases). Therefore as long as RBCs from two different sources and having different partial pressure of oxygen mix up, the oxygen level starts to equilibrate between these cells.
But diffusion as a passive mechanism is not very fast and can take some time. So the only possibility for the second variant (there is a mixture of two types of RBCs) is if the mixture exists for very short time in liver sinusoids, so that the blood leaves them without really mixing completely up.
This is not true, at least in some animal models the blood within the liver seems to reach equilibrium very quickly and its resulting partial pressure can be influenced by adjusting the blood flow from different sources (using vasoactive substances injected directly, as in the referenced paper).

I don't understand why you think that diffusion wouldn't be fast enough, since it is the same mechanism that ensures that blood becomes oxygenated in the pulmonary circulation, and deoxygenated in the peripheral tissues.

@AlanBoyd is right to be confused. This answer is unsourced and based on statements that are generalizations and, when applied to this question, false (diffusion of oxygen is is not fast enough to equilibrate within a blood vessel).

I'm not aware of any studies that investigate the equilibration of oxygen saturation between two individual cells in hepatic sinusoids, but I will answer based on what we know about these issues in the general context.
See West, Pulmonary Pathophysiology, Ch 2, oxygen loading in a healthy lung occurs to full saturation in about 0.25 seconds, one-third of the available contact time:

This involves diffusion through surfactant, the alveolar membrane of an alveolar cell, the cytoplasm of an alveolar cell, the basal membrane of an alveolar cell, the basal lamina, the basal membrane of an endothelial cell, the cytoplasm of an endothelial cell, the luminal membrane of an endothelial cell, plasma, and the membrane of an RBC. (see this illustration from Ross Histology)

In the liver, oxygen rich blood arrives from the hepatic artery, nutrient rich blood arrives from the portal vein. Blood from these different sources mix directly in the same vessel in the same hepatic sinusoid. There is no alveolar cell, basement membrane, or endothelial cell in the way. Oxygen just has to diffuse across one plasma membrane, in blood, and across another plasma membrane, all in a fluid moving together.

Diffusion of a small molecule like oxygen is quite fast, and RBCs are made for rapid diffusion, even of a large globular protein like hemoglobin.

Good answer overall; I think it might be worthwhile to quantify the speed/distance of oxygen diffusion, though. Oxygen does indeed diffuse quickly over short distances, but in tissue the oxygen concentration falls off quite rapidly with distance. RBCs are simply quite small, and I think this is at least if not more important than the rate of diffusion.


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Is this bear excreta on trees?
We were hiking lately in Canadian Rockies (the Kananaskis country) and kept encountering branches of conifers near ground covered in brown substance similar to mud or excreta.

It didn't have any strong smell but it also was mostly dry and looked quite old. There were many occurrences mostly, but not only, along trails.
One of the hiking books we have here calls this a "rarely seen bear toilet paper".

However, for us this definitely wasn't "rarely seen" and I also doubt it to be bear's poo as there was just so much of it everywhere. What is this? And if it's a bear's poo why do bears do this?
EDIT: After asking on Facebook some people suggested it's a kind of fungal infection. Though they weren't able point out the species. What kind of fungi may this be?

In your photograph, it looks like the crown of a small conifer. Unless a bear reached up to swing the top down to assist in the force applied to its behind, it's unlikely that a bear's poop would be on the top of a tree. So, not bear poop.
The saying is, "Trees grow from the top up and die from the top down." That deterioration is called crown decline or crown dieback and happens to branches sometimes as well. Seeing this in multiple trees, not rarely, and near the trail, indicates that these trees are experiencing significant stress. That it's happening along hiking trails may be because there is compacting of soil or some other human activity affecting the tree's roots, and therefore its vigor.
When we were in the planning stages of building our house on wooded land, the builder warned us that heavy equipment compacting the soil would kill trees as far as 15 feet away or more from the tree (it was a fairly mature forest.) He wisely told us to pick the trees most important to us in planning our driveway and building site. These trees were marked, and tape was put up along the route of the future driveway and the house. It saved us from the nasty surprise many homebuilders face a few years after their home is finished. God bless conscientious builders!

Thanks for your thoughts. I'm still seeking an exact answer to what that substance is. It's definitely not the tree "just dying" as there is this brown thing on top of the branches. After asking on facebook some people suggested it's some kind of fungal infection. Though they weren't able point out the species.

Also, although the photo depicts a crown of the three the three was still small enough for a bear to reach up there with his bum. .)

@Jen - You'd need a lab analysis to determine the exact nature of the substance. Most likely it's composed of multiple communities of microorganisms present on dead organic matter. When the organic matter no longer nourishes these communities, the whole thing tends to dry up like dry gangrene. So you won't get a definitive answer here. :)


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What do ants do with human finger nails?
There is place in my house where I cut my nails. Here, there is an ant hole where an ant colony is seen.
Whenever I cut my nails from here, they take my nails inside their hole. I was wondering what they do with them.
Do they protect their houses with them or feed them to their young ones?

How fast are your nails growing that you cut them daily? (I cut my finger nails about weekly, the toe nails even less often.)

Me too cut weekly. I was just kidding in comment to MattDMo's answer. :)

If nothing else, they can probably make  a throne for their queen out of this flexible material!

That is gross....

Based on the confliction of the two answers, can you take a photo of the ant closely so we can identify which ant it is?

Can't see the image..!

But please leave out the nails on the macro. If you do close-up those nails I will close-vote and bribe the moderators ;-)

@AliceD Gross for you, food for them. :D

My pet ant found this page by googling what can we ants do with all these fingernails we've collected.

@Imprisoned It's not gross. It's called curiosity to know science behind. :)

There are a number of papers studying the ability of fungi to metabolize keratin, the primary structural component of nails (as well as skin and hair). Ants are also known to cultivate fungi for nutrients, so this may simply be a case where the ants are bringing food for their "farm animals."

Nice explanation. Thanks :) Now, I will feed the hungry ants daily :D

It's true that some fungi can break down keratin, and that some ants cultivate fungi, but these two facts do not imply that this is what is going on here.

Do you have any evidence at all to support this? I agree that it makes sense as a possibility but that's not enough for accepting it as fact.

@terdon I never claimed to represent it as fact. The OP didn't state what part of the world s/he was in, and it's impossible to identify the ants in the picture. I stated "this may simply be a case ...", not "this is exactly what's going on, and no other explanation is possible." The other answer is just as much of a guess as this one. One couldn't know for certain unless they were on location, excavated the anthole, and studied the whole situation in situ.

Fair enough, I only posted that comment because your answer has been accepted. It is a very intriguing suggestion if true but it's not really all that likely. I was just hoping you might have a reference to support it is all.

I believe that MattDMo's hypothesis is incorrect.  Only one group of ants, the Attini tribe, cultivates fungus as a food source.  This group is exclusively a New World group, thought to have originated in the Amazon rainforest and spread out from there.  I see from your profile that you are located in India, which is outside the range of the fungus-cultivating ants.
So if the ants aren't using your fingernails for fungus cultivation, what are they doing with them?  Fingernails are primarily composed of keratin, a very tough protein which ants cannot digest.  However, it is likely that the clippings also contain materials like dead skin, nail fungus, or other organic substances that the ants can eat, making them worthwhile for the ants to collect.
References:

U.G. Mueller, T.R. Schultz, C.R. Currie, R.M.M. Adams, & D. Malloch (2001). "The origin of the attine ant-fungus mutualism". Quarterly Review of Biology 76 (2): 169–197. doi:10.1086/393867

Maybe fungi are on the nail digesting keratin partially on the ground so that ants can eat partially digested nail.

Maybe the ants are stupid and don't realise fingernails are useless to them. They could smell delicious to an ant but not be usable.

Maybe the ants are really smart and need the fingernails to complete the human they are building.

Do you have any evidence that the only cultivating ants are in the New World?

@MattDMo, 10 second Google search found this.

@MattDMo Added a source, can be read for free on JSTOR but requires registration.

@JasonC  This hypothesis and several others have been proposed here.


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Which mass spectrometry database search algorithms include the fragment mass accuracy in the calculation of protein scores?
E.g. in a MASCOT search, the accuracy of the fragment ions in a ms/ms spectrum does not have any influence on the scores of identified proteins (unless the fragment ions are out of the set ms/ms tolerance of course).
I want to know other search algorithms that do include the fragment mass accuracy in the protein identification scores.
Also, if the protein scores are not influenced, i would like to know in which way other evaluation values of MASCOT or SEQUEST results are influenced.
Thanks for your time.


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Is there an example in evolution where a huge jump in evolution happened due to a dramatic mutation?
Here is a chicken that due to a mutation got 4 legs:

I wonder, are there examples, where such one-time dramatic mutational chages gave rise to a new species?
Are there species that appeared not due to gradual mutations, but something like this?
For instance:

A new instance or pair of organs appear, such as an extra pair of limbs.

An organ reverts to its function in distant acestors (like wings to legs or legs to fins), using already existing genetic code (e.g, not like in penguins or dolphins, gradually but abruptly).

A long-lost organ re-appears (like tail)

Why do you think this is a "dramatic mutation"? Seems to me like a quite basic, simple one, and possibly not a mutation at all.

This chick will most likely not be able to reproduce (having raised chickens and roosters, it doesn't look like fertilization will be possible.) Not reproducing will mean the end of that 'mutation' (agree it's not a genetic mutation.) "Dramatic mutations" have costly consequences and usually die in utero or before reproducing. Re: organ duplication; without surgery, the only survivable one I've encountered was extra kidneys. Polydactyly is fairly common, though. The answer to your question is "No." Finally, a surviving example is not a new species; the chick is still a chick, but with 4 legs.

FYI: polymelia is the name for a congenital disorder resulting in extra limbs. Often (though not always), this is a result of a partially degenerated twin.  Your image would not be the first identified case in chickens:  in fact, in 2006, many news outlets ran an AP story about an older chicken with this condition [photo here].

@theforestecologist interestingly, in the both cases the front legs are functional but the back legs are not.

@Anixx also, how are you wishing to define "species" here? (i.e.,by which "species concept" are you binning?). E.g , morphological concept may suggest you already have a new species, whereas both an ecological concept and a phylogenetic concept would not... Additionally, "extreme" morphological changes due to a single genre mutation are not that common, especially since such mutations often have deleterious effects. Also, as I mentioned, your specific chicken case is likely due to a failed twin separation and not a mutation, so no opportunity for evolution (allele freq change) has occurred...

Tangentially, this is closely related to "The Mutation Theory" by De Vries (1901), which was an early hypothesis of how evolution happened (that was later largely debunked). See also punctuated equilibrium.


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Hand-eye coordination in 3D space
A simple daily event has amazed me and triggered this question. I have read and heard about hand-eye coordination. It quite straightforward when you e.g. want to open a door or play Xbox. In this case either your hand is in your view or your hand will feel the buttons of your Xbox.
But when it comes to catching a ball or try to catch a falling object, our hand is totally out of our view since we are closely following the trajectory of the moving object. But meanwhile our hands moves in a 3D space and align it self perfectly in the path of trajectory correctly. This is what amazed me.
If you can see your hand and the object/ball simultaneously, its just a matter of moving our hand in the path of that ball/object. But having hands totally out of sight but catching the ball/object perfectly every time is amazing piece of nature's engineering.
How humans have achieved such a amazing piece of coordination in a 3D space without seeing where the hands are located?

Body self-awareness?

sight is not the only sense that tell us how our limbs are moving - otherwise blind people wouldn't be able to move

Short answer
Proprioceptic receptors provide a feedback mechanism from the body to the brain, telling the brain what our limbs are doing and where they are with respect to the body without visual feedback being needed.
Background
Muscles, skin and joints contain proprioceptic receptors. They sense position and movement of our limbs and trunk, they register force as well as heaviness. Examples of such receptors are limb tendon organs and possibly also muscle spindles, which contribute to the senses of force and heaviness.
Proprioceptive sensations are influenced by visual input, but operate without it. The proprioceptive system is responsible for the ability to touch your nose with your eyes closed and the examples you have given related to catching a ball while not paying visual attention to the position of your hands.
Afferent signals from these receptors are combined and processed in the brain. Together they form information about limb position and movement. This information is mapped relative to a central body map to determine the location of the limbs in space.  The proprioceptive senses, particularly of limb position and movement, deteriorate with age and are associated with an increased risk of falls in the elderly.
Reference
Proske & Gandevia, Phys Rev 2012; 92:1651-97


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Is it possible to grow brain tissue in vitro? Can we make a super-brain this way?
I wonder whether such experiments were conducted? Is it possible to create a "biological super-computer" this way?

Hi, this is John from the ethics committee at your local university. Please meet me tomorrow at 9 PM at my office so that we can further discuss the details of your oncoming experiment.

can you specify what you mean by "brain tissue"? it is possible to culture stem cells to neurons. It is possible to create organoids (artificial collection of several tissues).

More importantly, you currently asking two questions: is it possible to create artificial brain, and is it possible to use such brain as super computer. COnsider asking two separate questions instead

This is actually not an unheard of idea among neuroscientists and is an aspect of much research.  Brains in general have amazing computational powers and abilities that allow them to circumvent the limitations of computation which is usually based on a Turing Machine. Neurons pursue highly parallel architectures and exhibit cognition or even emotions or do highly sensitive signal processing, which has heretofore been unapproachable with computational methods such as Machine Learning.
As such many researchers are focused on understanding the brain or at least the brain's structure to augment or produce computation.  Here are a couple of examples of neuron arrays flying virtual or real drones....
The ethical issues aren't great concerns because neural cell networks can be encouraged to grow differentiating from easy to grow cell lines like fibroblasts.
Another approach to augmented computing is to interface directly into a living brain. Model brain organoids are a popular topic of interest and could one day be used to interface to other computational systems.  There are of course many devices that try to interface to the brain via electrical fields in the same way EEGs work.
there are connectome projects that are trying to understand the neural connections between cells that are so important to brain development, with the theory that the topology of these networks might enable even computers to perform like brains.

Moore's Law of computation (which was in no way a law) was an observation of a trend in the fabrication of computor memory). Unless your brain is receiving upgrades from Intel every two years, your statement would seem difficult to understand.

fixed this in edit


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Are there any plants that parasitize on animals?
It seems, fungi often infect animals, while plants it seems, never. Is it because the cellulose cell walls make them incompatible with animal tissue?

The question in the title differs from the one in the post. Can you please pick one of the two questions only?

The threshold between parasite and predator is somewhat blurry. Would carnivorous plants be a good example? The only true good example coming to my mind are plants that get insects to carry their pollen but don't give them any nectar as reward. There are also plants that lure insects in but imitating a potential mate and then just use these insects for pollen transportation again. Are these good examples or did you mean endo-parasites only?

Why would they? They evolved to become phototropic.Although carnivorous and protocarnivorous plants exist for survival advantages.Can you be a bit more specific so that it's easy to relate?

Boundaries between parasite and symbiotic are also fuzzy. What about the algae that are symbiotic with sloths? Molecular evidence for a diverse green algal community growing in the hair of sloths and a specific association with Trichophilus welckeri(Chlorophyta, Ulvophyceae)

Well...there is the Venus Fly Trap.

I am voting to close as unclear as long as the OP has not address the difficulties of definitions of ecological interactions and has not addresses whether the presented examples would answer the question or not.

Helicosporidium https://doi.org/10.1371/journal.pgen.1004355

Yes
Acrochaetium spiculiphilum is an marine endozoic parasite on sponges.
It is a Biliphyte algae and thus a plant.
https://www.cambridge.org/core/journals/journal-of-the-marine-biological-association-of-the-united-kingdom/article/abs/observations-on-an-endozoic-red-alga/A2486145D3811B18BCC65A81B24ADA56

Yes! Here's a paper published August 2018
https://www.sciencedirect.com/science/article/pii/S0960982218308157

No, ans the abstract says, the parasitic plant attacks the insect-induced tumors of the other plants. In other words, plant tissue.

Link-only answers are generally not acceptable on Stack Exchange sites. The link may change or become unreachable in the future, and without a summary of what the link contains this answer would be useless. Please summarize what is in the link (don't just copy and paste) and use the link solely for reference. If you remove the link and the answer cannot stand on its own, it is not a good answer.

Could you please summarise the relevant content of that paper? Posts should be self-contained and not rely on a link only, because the link might get broken.


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Is the deep ocean fish look ugly because due to darkness there is no visual sexual selection?
Is the deep ocean fish look ugly because due to darkness there is no visual sexual selection? If so, is there a common notion of beauty between humans and animals?

Probably your query will be unresolved, but in researching deep water fish courting you will find info like:
they engage in parasitic mating, they digest their own face and whatever part of the female they’re latched on to via teeth so that they can become fused at a tissue level ... https://www.youtube.com/watch?v=XhsyZnVx2rQ perhaps best rephrase like: why do deep water fish have completely different and ugly facial proportions compared to most other vertebrates? Is it because they can't see each other.

I suspect the deep ocean fish look ugly to you because they are unfamiliar.  The iconic fish species with which humans have coexisted forever are all surface fish, with common adaptations for surface living in the light.  When one thinks of a fish the salmon or cod is what we think of.
The deep fish have different selection pressures.  They do not need to be streamlined or svelte.  A deep fish might think a surface fish is ugly because it cannot make its own light - how plain and dull.  How can the surface worlders find a good mate if everyone is dark?

The peacocks are also unfamiliar to me, yet their looks seems festive nevertheless. http://mirplaneta.ru/images/2/412.jpg

good info, they often swim slowly and have low energy so they are less streamlined. The goblin shark swims quite fast though and it is also one of the most strange of all sharks.  https://www.youtube.com/watch?v=fYpn2u2Wag4 .... https://www.google.com/search?q=goblin+shark&source=lnms&tbm=isch&sa=X&ved=0ahUKEwib47mA0-bgAhWQERQKHZ1bAGIQ_AUIDigB&biw=1431&bih=734#imgrc=AdlcEl7MK3cpcM:

@Anixx: Perhaps peacocks look beautiful to you, but how about vultures?  Yet both must be attractive to the opposite sex of their species, no?

@jamesqf perhaps in vultures looks plays less role in sexual attraction than obtaining resources?


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Example of code with pypgen (python)
I have a VCF file and wish to calculate a few indices of population divergence over a sliding window.
I consider using pypgen but the documentation is currently very limited. Can you please give me an example (for Jost'D for example) of a code that would work?

vcftools can compute a few things in sliding windows (Tajima's D, Pi, Fst, LD at least), but that's probably not enough, is it?

Nope it is not indeed. It cannot calculate Jost's D or Dxy for example. There is also EggLib (for which I am currently reading the documentation).