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What is the viability of Intelligent Design as a supplement to chemical abiogenesis and Darwinian Evolution?
First of all I am not endorsing Intelligent Design (Wikipedia link); I'm asking this because I (someone who does not have a background in biology, organic chemistry, or philosophy) got into a conversation with someone who does endorse it, and I'm trying to see his point of view as far as rationality can allow. Second of all, I apologize for any vagueness; Intelligent Design isn't well enough defined as a theory for me to help that. I also apologize if this is rehashing content already plentiful on the Internet, but for my purposes I can't simply depend on the likes of Wikipedia or Talk Origins, so what I'm looking for here instead is to take the opposite approach and see, based on your informed minds, if there could possibly be any reasonable likelihood of an ideal ID theory being adopted.

I'm looking for the most favorable consideration for what ID might be
  if it were best developed as a viable hypothesis or theory to get an
  idea of how far such a discussion is worth taking. An unbiased,
  informed Devil's advocate, if you will.

My cursory investigation of what Stephen Meyers (video link) and Michael Behe (video link) say (correct me if I'm wrong) seems to be that either the first cell was likely designed intelligently judging by the complex code of DNA and that evolution took course from there, or that the first cells were made and many instances of evolution were from some kind of intelligently guided mutations as was needed to make "irreducibly complex" cells or body functions (whether the guidance stops after the Cambrian or continued even to the point of making different types of new bacteria and different types of apes/humans or whether every single mutation and adaptive ability is being guided, I'm not sure if they're at any consensus, and that's why I don't know if I should stop my question at abiogenesis or include evolution). The person I spoke with also brought up some specific claims (everything looks designed, DNA has ordered, complex information, blood clotting is irreducibly complex, ID can and has make predictions like decades ago that "Junk DNA" wasn't junk) that I don't need you to debunk (I have Google).
But if there could be any possible support or truth to any of the above, I would appreciate knowing about that. (Again, Devil's advocate so I can be informed and understand where the points come from.) Reading an ID book alone, it would be in places hard to know where they differ from actual scientific conclusions. After all, when someone who seems to know what they're talking about and can explain something in technical detail says that something is impossible or extremely unlikely, it's hard for me to know why they would be wrong (are they ignoring other possibilities? misrepresenting facts? are they really right and just getting the cold shoulder from an atheistic scientific community because it implies a deity?). So I focus on mainstream sources, even if they don't bother entertaining ID and leave me ignorant of its possible virtues. And thus I'm hoping someone from this informed community might enlighten me to what those possible virtues might be.

Regarding "junk DNA": The claim of 80% functional DNA is using a very very broad definition of "functional". The claim is strongly debated - for a non-scientific piece see http://www.guardian.co.uk/science/2013/feb/24/scientists-attacked-over-junk-dna-claim . Even if it were true, I do not see how this supports ID.

I'm not certain that this is suitable for a Q&A since you have a large number of questions bundled into one. As it reads now it deals with an entire "theory", and this cannot be explained in a single answer. Would it be possible to narrow down to the aspects that you are most interested in (and you could ask follow-up questions afterwards)?

Oh boy. @Bitwise, that’s a pretty bad article, even the title gets it wrong – ENCODE does not claim that junk DNA is “vital to life”. The “80% is functional” claim says nothing about necessity of that function. If ENCODE had made this claim (and if it were correct) then it’s true that the ID proponents in the 60s would have made a correct prediction (albeit for the wrong reasons). As it happens, this claim is a strawman.

If you look at any actual biological systems, its pretty clear they are too complicated to have been designed! Who would design a system with so much waste, multiple receptors and multiple ligands in each system, only a handful of which seem to actually do anything. The more you look at biology, the more absurd the idea it was designed!

@KonradRudolph I completely agree, and this is the exactly my point. I am not saying that the "80% functional" claim is incorrect, just that it means something very different than what the ID people think it means, and it doesn't support ID in any case. Sorry if that was not clear.

@Nick that just disproves the idea of intelligent design :).

You may want to have a read through this wonderful post. Specifically, point 19.

@fileunderwater I suppose I may need to do that, but if there could be any support from any point, that would be fine in my book as an answer here. Everyone else, thanks for the links and insights, keep it coming.

@terdon Thanks. Point 10 was also relevant (though I'm going to have to read the thread he linked to because there he dismissed the probability argument tersely). As was point 22. Regarding point 19, this may also be explained to me as I read through the thread from point 10, but correct me if I'm wrong, but Meyers might have, at least weakly, met his first two criteria of point 19 (Criteria: Ordered information; Methodology: Sequence DNA).

@fileunderwater I was thinking more about your suggestion, and upon further consideration I think this is indeed the one question I want answered. I have found talkorigins.org to have suitable arguments against the individual points above, but the question I indeed am looking to have answered is is there any (non-specific or specific) way that Intelligent Design could be imagined to be refined and viably fit in with Evolution or Abiogenesis (short, of course, of far-fetched speculated data like God appearing to everyone).

@AL You can always go the philosophical route and claim that an omniscient god would know that by creating a universe in a certain way how the randomness would produce human life through random processes. But there would be no testable predictions from this, since its indistinguishable from a situation without the omniscient god. That's a question for philosophy.stackexchange though!

I think the issue with Intelligent Design is not so much that its patently proven wrong.  On the contrary, the problem is that it not a scientific hypothesis and so it really isn't a scientific question.
If I may, the basis of the scientific method, as formulated by Karl Popper, but commonly in use today, is that science is the putting forth of theories of cause and effect which are testable (or if we are being precise, falsifiable).
That is to say, you put forth a theory such as 'God/some diety figure made all living things' and then you perform an experiment which can differentiate whether the hypothesis or its null version (i.e. 'no intelligence is the source of life / biology is the result of accidents') is more likely true.
This question will not be testable in a way to answer enough of the reasonable skeptical questions ( or at least so far it has not).  Experiments have been tried, but they are often not acceptable to everyone.  For instance the idea that some biological structures such as the eye or the flagellar motor are too complex to have evolved through a typical Darwinian process which involves a series of small changes are almost biological theology - one can always hypothesize a more inhuman God (probably appropriate) who acts and 'thinks' in such an inhuman manner that anything you see could be created/inspired.  While I think you should feel free to believe either way, I also believe that this is not an argument that can be won or lost.  The tendency for any experiment to confirm both the hypothesis and its inverse seem inescapable.
That is to say, that biology and physics will ultimately fail where philosophy and logic also did in proving the existence of God, besides the less interesting truism that if God does exist, the deity is consistently elusive to proof.
On the other side of the coin, the proof that life has emerged from naturally occurring phenomena such as lighting strikes in a prebiotic environment are interesting since it shows that nucleotides and amino acids might have been available without metabolic pathways to synthesize them.  In its way, the molecular origins of life on earth is a question which is really testable only in theory.
Anyone who thinks they are going to re-create the event of the beginning of life itself is scientifically on thin ice - the prebiotic environment may have extended to the entire surface and atmosphere of the earth as well as down into mud and bodies of water and sat incubating for maybe hundreds of millions of years.  The idea that the fundamental moment of life generation is just going to show up on a well chosen set of conditions in a 500 ml flasks with some electrodes attached is an idea that workers in the field don't even entertain.
Until such an experiment produces life, the work will have to rely upon the idea that there was a moment in time where the necessary elements came together.
This being said, cosmology, biogenesis work has approached the moment of the genesis of life asymptotically with amazing clarity.
The RNAWorld hypothesis strongly supports the idea that an early biotic system might have been very simple - maybe only RNA and its four nucleotides.  Clearly after what Dawkins calls a replicator exists, then the pathway to living things as we know them is pretty easy to envision.
I should add that I'm not one of those people who think that science is everything - the trend that is impoverishing some humanities program is alarming to me.  Its just that some things are not science.

I totally agree on testability. Another way to put it: ID makes no predictions, so it's useless - besides being untestable, ergo unscientific.

thanks -  Its a common problem even with scientists really - I know I never got this stuff in a class. It also comes up in general with 'new' theories of evolution, relativity, and cosmology - the new theory tries to just make the same prediction as the textbook examples, but doesn't bother to look at the sometimes thousands of other experiments which confirm the established theory but might not confirm theirs.

The problem with Intelligent Design is that it doesn't appreciate that the forces that shape species (and individual organism) have to be constant and ongoing or the species disappears. The past matters little, it's what happens right here, right now that keeps species in any particular form.
Biological system are not static structures like a building. You put energy into a building when you move and shape it material during construction. Immediately though, the energy in the structure begins to flow out into the ambient environment, causing the building to loose it's structure and decay. Eventually it will fall to dust.
Biological systems are dynamic, not static. A living organism is like a whirlpool.  A whirlpool is a complex ordered structure that dissipates energy caused by friction between streams moving at different velocities next to each other.  It is never composed of the same molecules of water from moment to moment and once water has passed through the whirlpool it never returns. The whirlpool is the structure, not the transitory water.
Changing the rate of flow, depth of the water, temperature etc changes the exact structure of the whirlpool instantly.
Biological systems are non-material structures like whirlpools. Matter and energy constantly flows into and out of bodies. We stop stop breathing, we die. Your body, even scars and bones are continuously begin torn down and regenerated. The average half life of atoms in your body is seven years. Even atoms that do remain in the body are moved from molecule to molecule and from tissue to tissue. Only the pattern remains semi-constant. Species and individuals organisms are the structures, not the transitory matter.
Changing the flow of matter and energy into an organism, changes it's structure instantly. Changing the flow over long periods, changes entire species.
If I show a picture of a whirlpool in water but crop it so you can't see whether it's occurring in a natural stream or a flow tank in a lab, how could tell whether the whirlpool was artificial or not?  You couldn't, because there is no structural difference between an artificial whirlpool and natural whirlpool. They look the same because the same forces and laws create them and do so continuously
The same is true of life.
You can't look at living things and determine whether they are natural or artificial because just like a whirlpool, it is the flow of matter and energy through life, at any particular moment, that defines it's structure.
Even if some intelligence, divine or material, did alter or even start life, it would have to fit into the material environment exactly like one that arose naturally. It would be indistinguishable from a natural one because the same forces would give it shape and maintain it.
So the best argument against intelligent design is that we don't need to evoke it explain how life exist now, moment to moment. If natural forces continuously create and maintain life continuously today, then they had to be able to do so yesterday and the day before, all the back.

ID addresses an obvious question which nearly everyone considers very strongly at some time. Those who don't choose to believe in God will often argue that it is a non-issue. But is it a non-issue because they are so obviously right that others have no right to voice their opinion, or because it doesn't matter? The former is a very childish view, and certainly isn't very helpful if the goal is to convince others of the "correct" view. And if it simply doesn't matter to Atheists, then surely we can all recognize that it matters quite a lot to others. I'm not suggesting that theists simply be allowed to rewrite the curriculum (which some have attempted), but this is a question which costs more time and energy to ignore than to address. And we have a lot to learn from each other in the process.
Many people, as they study evolution, very naturally begin to conclude that life could have, and therefore must have, emerged entirely by accident. This is not so different from observing that autism diagnosis has been on the rise since about the same time a certain vaccine came into widespread use, and the fact that symptoms often set in shortly after said vaccine has been given, and concluding that increased cases of autism could have been, and therefore must have been, caused by the vaccine. There is an appearance of a causal relationship, but the conclusion does not exactly follow from the evidence. In the case of the vaccine suspicions, I'm grateful that they have been solidly proved false now.
As for the true origin of life, many of us think we know the answer. Be that as it may be, this answer is not delivered to us through the study of evolutionary biology. Anyone who tells you that science has proved that we did in fact evolve without any external manipulation into what we are today, or that life emerged completely by chance, is misinterpreting the facts (or more likely, believing a rumor they heard). Anyone who tells you that science has proved the opposite, that life could not have emerged by chance, is likewise not following the logic correctly (or more likely, favors different rumors). I think that it would be a healthy exercise of critical thinking to open up this kind of discussion in a high school biology classroom, consistently reinforcing the fact that none of it on either side of the argument offers any conclusive evidence on the actual true origin of life. People who feel passionately either way on this must cringe a little at this suggestion, perhaps comparing it to the way Fox News feigns a "fair and balanced" presentation by presenting the plain and obvious truth on equal footing with an extremist view. But which is the extremist view on this issue? It depends on where you stand.
The biggest problem I foresee is that most of the instructors are so strongly biased one way or another, that they would have a hard time honestly mediating such a discussion. But, frankly, this is already the case, so I would argue that it is better to formalize this as a critical thinking exercise in the curriculum. It probably won't open anyone to new thinking on the origins of life, but hopefully, it will help them resist the next vaccine scare. And it will help them to distinguish scientific proof from speculation or belief. For many religious students, this will allow them to digest the rest of the material without feeling like it is an attack on their sacred beliefs.

If anyone down-votes for actual problems with the quality of my answer to the specific question that was asked, please educate me on my failure with a comment.

Nothing in modern science asserts that life arises by chance or accident. It arises from natural forces. You might has well say that rocks roll down hill, by "accident" and not gravity. Evolution is driven by energy from light and heat finding the maximal entropy path through organic molecules. The molecules accelerate entropy by forming complex structures dissipative structures. It's just like water turns from chaotic liquid into organized ice to shed heat or currents forming complex whirlpools to shed energy from friction of current against current. Nothing random at or chance at all.

@TechZen - Interesting conjecture, but I'm not sure how it is meant to relate to the question or to my answer.

The problem is that most curricula on evolution already point out very clearly a large amount (although encompassing only a small fraction of the total) of experimental evidence, while creationism tries to justify its assertation by pointing out the few gaps of evidence within evolutionary biology. One must also remember that the Catholic Church itself does not reject evolution as "an attack on their sacred beliefs".

@MarchHo The problem with this discussion is that too many people on both sides would rather dismiss other ways of thinking as invalid. The core of a Creationist view is not the fallacies they seek in the case for evolutionary biology, but the record of prophets. As you point out, there is not necessarily any contradiction between what is written in scripture and what science has discovered. But when you approach a person who is already certain of the truth of scripture, and begin to belittle what they know to be true, YOU CREATE opposition, and begin to convince them that evolution is a lie.

"The core of a Creationist view is not the fallacies" Yes it is. The fallacies are: circularity (codes/complexity/information/amazement necessarily implies design, while science says what design requires: brains, organs, cells, and [DNA] codes, which are complex and have information), faith (faith in in intelligence without certain parts like brains, cells, etc.), scope violations and/or faulty generalization (using biology-based intelligence as a universal truth, without bothering to explain/describe/demonstrate how non-biological intelligence can exist and function.

"science has proved that we did in fact evolve" What science has demonstrated is what intelligence needs: brains, cells, and DNA. ID totally ignores this, while hypocritically using the same cause/effect reasoning to say what codes/complexity/information needs. ID is self refuting because it inconsistently applies the same rule of cause/effect, and fails to do the same for the hypothesized cause.
"I think that it would be a healthy exercise of critical thinking" to apply the same rule you used for codes, to intelligence.

There's really two components to ID:

A No-Go Theorem (http://en.wikipedia.org/wiki/No-go_theorem) on the likelihood of spontaneously arising life, or of it reaching some threshold in evolutionary development naturally.
...which leads to "the design inference", which posits that the characteristic of intelligence is able to overcome the problem established by the no-go: that life exist, but could not allegedly have arisen from a random process.

Now certain no-go theorems claim something is physically impossible, like transmitting information faster than the speed of light, some are about the provability in mathematics like Godel Incompleteness theorem, but the ID no-go theorem is about being statistically imprlausible- but what is implausible in a Big, Old Universe? Something like 1/Number of atoms in the universe is sufficiently low (2^82), and you can demonstrate this easily by thinking of DNA code 1/4^N where N = min num of base pairs for self-replication, where N~100,000 M genitalium. This is a very naive model, but it's a start: see George Chaitan's work for better maths: http://www.youtube.com/watch?v=RlYS_GiAnK8
The design inference is really Stephen Meyer's domain, and I'll refer you to him, this is much more a philosophic argument. One thing that's important to note for people who are dismissive of ID is that this is about reasoning about intelligence in the abstract, not the manifestation in physical form, not "some being".
What's my opinion? Could I get back to you in 300 years? We'll finally have data on thousands of other planets and whether any of them have ever harbored life, and that I think would be the falsification of ID if other life was found. But I think both a barren universe, and one with other life are both plausible given what we know now. That's why I don't get why people are so staunch on this issue: it's impossible to know the one key thing we need to know in this debate in our lifetime. But in a few generations we in fact will have this answer. We get to live in some interesting times.

Stephen Meyer's explanation: http://www.discovery.org/scripts/viewDB/filesDB-download.php?command=download&id=1491

Why would finding independent extraterrestrial life disprove ID? If we find ET, it might be vastly different, perhaps not even DNA or RNA based, or based on right-handed amino acids. Or perhaps we could discover something so hauntingly similar that we could almost have expected to find it here on Earth. In either case, I don't see that it offers any evidence against ID, or even against one single Intelligence. If I discover Mona Lisa and postulate that paintings must be created by humans, later discovering The Last Supper or The Persistence of Memory proves nothing to me either way.

If we find life arose independently somewhere else (or even twice on Earth), it would substantially change the range of probability that life could arise by random process. That's the first component I described, which can be answered thru data. I think it's the second component, the inference - which you have a problem with.

No. You're already presupposing that life arises by random process; ergo finding another instance of emergence proves that such random emergence is more likely than previously assumed. But this is circular logic. If instead, you presupposed that all life was created by Intelligence, finding another independent creation of life would lead you to conclude that this same Intelligence, or perhaps some entirely other Intelligence, has created this new world full of life. If you presuppose nothing, you know nothing new about the Go/No-Go probability, nor the inference.

The key to the Go/No-Go idea is to somehow prove INDEPENDENTLY that the probably either is or is not within reach of reasonably happening by chance, without Intelligent manipulation. If we knew that it was astronomically improbable even in this vast ocean of galaxies, then the more times we find life, it would only be more evidence that this Intelligence must be out there creating it.

You can't calculate the probability of some pattern occurring without understanding mechanism that creates the pattern. Calculating the odds that molecules would form into certain patterns, without known the electron dynamics that force atom into specific configurations under specific conditions, would show that every clump of matter in the universe was fantastically improbable. But once you know the rules of chemistry, it looks deterministic,not improbable. The same applies to evolution. Once you understand the thermodynamics, improbability disappears.

@TechZen ...and then someone asks how the mechanisms came to be that way, why the universal constants are so tuned to allow the universe to work this way. It's the scientists place to persistently explore and discover more. And it's the philosopher's place to humble the scientist by reminding him how much he still doesn't know, none of which has anything at all to say about what Gods may be. Science is magnificent, but must be careful not to overreach beyond what it can prove. Good science states what we have learned precisely, and leaves the mystery to the mystics.

@MarkBailey -  I don't see the relevance of your comments to my argument. You seem to be making a "God of the Gaps" argument, which is tedious. By that reasoning, since we will never know everything, we never know anything. My comment merely focused on what is known about the formation of organic molecules and the thermodynamics of their evolution into living structures. It's not a random process at any level or stage so calculations based on the premise it's entirely random are automatically false.

@TechZen Evolution is a heavily stochastic process. Don't ruin your credibility. Your previous comment however, was great. I'm not arguing against it, but hoping to complete it. Your understanding of thermodynamics will never be complete enough to conclude with any confidence that life emerged by itself. If you disagree, then "God of the Gaps" is indeed an appropriate concept to consider. If anyone thinks they can jump from a solid understanding of organic thermodynamics to a claim that Life emerged without any Architect or Director, then they are inserting quite a lot into those Gaps.


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DIY extraction and long term storage of human DNA sample?
What is the recommended DIY way of extracting and long term storing of human DNA samples to store at home and send for sequencing in years time? Considerations:

Sample material: cheek swab, hair, blood?
Extraction: which detergent, alcohol?
Storage: freezer? what temperature?

Any ideas?

I'm not sure the source of the DNA (buccal swab, peripheral blood) matters since it will need to be extracted and purified for sequencing applications. Storage is probably best in -80 C for long-term storage (years, maybe decades?).

sorry for not understand your question before

If you have access to a centrifuge, either spin columns or phenol:chloroform will give very pure, high-quality DNA. Even with dirty methods, you can re-extract the product several times, to sacrifice yield for purity. Just be very clean. Whatever method you use should remove salts and proteins, which are the major contaminants. I won't go too much into how to extract DNA, as that's a whole separate question - but the most important thing is that purer is better.
You should resuspend in Tris-EDTA. Tris buffer maintains pH at slightly acidic (best for DNA) and EDTA chelates metal ions which can catalyze oxidative damage of DNA. Very pure distilled water works too, but if you get contaminants they will do more damage.
Afterwards you can store the DNA for quite some time provided it's frozen. At -20C you can store DNA for years. It may not be perfect quality when you pull it out a decade later, but most of it will be good, and I'm sure it will be okay if you use a good sequencing method (and I'm sure sequencing technology will advance more in 10 years than the degradation of your DNA). The good news is that you can simply store it in your freezer, and it will be okay. -20C particularly is not hugely important, you can probably get away with -10C or so - the crucial thing is for it to be frozen, not liquid (this vastly reduces diffusion).
If you want to do it like a pro, you would put it under -80C. This is considered very safe for multiple years. You can do even better by precipitating it with ethanol, and then storing at -80C. In my opinion, this -80C is overkill - DNA is fine, for the most part, stored at -20C and even 4C, especially if you work reasonably clean and contamination-free. If you had some extremely valuable, very sensitive DNA, sure, do the -80. But just personal sequencing/genotyping? Just extract a bit extra DNA  (a couple micrograms).
The really safe method is liquid nitrogen, which stops practically all chemical activity. Higher temperatures are too cold for most DNA-damaging reactions to proceed at a significant rate, but the molecules still move around. At -200C, they stop dead. But, once again, overkill unless you are saving very critical DNA for centuries later.
Source.
Three simple things I can recommend that are less obvious: First, do not handle your sample with hands, even gloved. Use some kind of plastic tweezers. Hands are warm and will locally warm up the sample. I would go as far as to put the sample tube in another box so that there is no direct contact. Second, avoid freeze/thawing. Whatever your storage system is, make sure it is very reliable. Third, wrap it in something opaque, to minimize light exposure.
Note as per Chris's comments: Always consult the MSDS of the substances you work with and take appropriate safety precautions! Always make sure to receive proper training before working with hazardous materials, and never purchase illegal contraband without appropriate authorization!

Please do not use Phenol/Chloroform outside of safe cabinets. This is nothing you want to do at home as especially Phenol is highly dangerous.

@Chris Always consult the MSDS of the substances you work with and take appropriate safety precautions!

That's right, but you need proper training as well. Reading about safety precautions alone won't help. Additionally I don't think private persons will be able to order phenol.

Would a safe organic solvent like a vegetable oil be hydrophobic enough to remove the proteins and cell debris from a DNA prep?

@user137 Doubt it. Phenol is needed to denature the proteins.

@Superbest In this procedure for getting DNA from an onion, they just use shampoo or laundry detergent to lyse the cells and free the DNA. I suppose that could denature and remove proteins, but I don't think this protocol is designed for high quality DNA extraction.

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Difference between Bioscience and Lifescience
Are bioscience and lifescience the same things? I am a little bit confused about it. If not, then what is the difference between the two?

they're pretty much the same thing in my mind - bio means "life" and biology is the study of life.

I agree with @MattDMo, they're the same thing.

I agree with everyone. Also, you originally tagged this question bioinformatics - that is not the same.

I agree with the comments and largely see them as the same thing, and many dictionaries would probably agree with this. However, in practical use (from my experience) Life science is used somewhat more broadly (everything from ecology and agricultural science to genomics and biochemisty), while Bioscience is more often applied to "whiter" lab-based biology and more technical applications (biotechnology, genetics, etc.). Personally, I would feel comfortable to label my research as life science but a bit more uneasy with bioscience. However, the terms are so vague that I wouldn't pass judgement on the content of research just based on these labels.

Whiter? What do you mean by whiter?

Lab coat (white) vs. field clothes (green), not caucasian ;).

hah. I've only seen one person wearing a lab coat lately, and it was an undergrad. No one here does field work, either. :P

@dd3 Wearing a lab coat in a lab is a sensible, if minimal, way of protecting your clothes and body against chemicals, radioactivity and biological agents. Not wearing one is neither clever, professional, nor, in some countries, legal. Certainly in my University students are not allowed into teaching laboratories without one. The same probably applies to research laboratories under British Health and Safety regulations. Your comment does you no credit.

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Do thymine and uracil ever appear in the same strand of RNA?
Wikipedia says that "in RNA, thymine is replaced with uracil in most cases."  I'm curious what are the cases when this does not happen?  Does this ever occur in normal functioning, or is it an error?  Do T and U ever appear in the same strands of RNA together, or does a single strand just use T or just use U?

tRNA molecules contain a T in the T arm. I believe that this results from post-transcriptional modification of a U by uridine methylase.

just curious:  can RNA polymerase incorporate thymine from TTP against Adenine ?

Do cells make TTP? (or 5-methyl UTP, as it is usually referred to)

I am not sure.. UMP is the first product of de-novo pyrimidine synthesis. The ribose is reduced and uracil is methylated to produce dTTP.  I dont know if the order of the reactions is unchangeable ?
I guess if artificially provided, Thymine can be incorported in RNA. (Sorry, i should have looked it up instead of commenting)


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Mitochondrial DNA and recombination
Firstly I could do with a brief description of mitochondrial DNA. How does the structure of DNA in mitochondria compare to animal DNA (for the sake of simplicity let's say human - some animals might have unusual DNA structure) and what living organism is the mitochondrial genome most akin to? (Circular like bacteria maybe?) and are the mitochondria within a single human homogenous?
Secondly, and most importantly to my aim, does the mitochondrial genome recombine in anyway? Is the process of recombination affected by its structure? Are there any patterns/rules in mitochondrial recombination? Is there DNA transfer between mitochondria which could have a similar effect?
I am trying to think about how male deleterious alleles can spread differently in diverged populations given potential recombination to female beneficial (or recombination away from female deleterious mutations).

Working at the NIH Institute on Ageing in 1990, i found PCR generated evidence of resolved Holiday junctions in purified mtDNA from rat. mtDNA is non-randomly enriched in inverted repeats, which generate intra- and inter- molecular homologous recombination. I know mtDNA is recombinatorial in plants and lower life forms, such as molluscs. If anyone has any more info on recombnation in higher life forms, i would like to hear it. Wade Edris
Penn State College of Medicine

Mitochondrial DNA is circular, like bacterial DNA, and around 16.6 Kb long. It codes for 37 genes in total but the majority of these are simply the machinery for gene expression (curiously, mitochondria have a slightly different codon->amino acid translation 'table' to nuclear DNA) and so just 13 code for proteins. Single mitochondria usually have multiple copies of the DNA.
Mitochondria are thought to be most closely related to the bacteria Rickettsia, an obligate intracellular parasite that causes typhus. Mitochondria are so degenerate, however, that they've lost nearly all the genes that normal bacteria have.
While there is some small level of heterogeneity in mitochondria in a single person because mitochondria are exclusively transmitted down the female line most people typically only start with a single clonal population of mitochondria. Because of this, there is no other mitochondrial population present that the mitochondrial DNA could undergo recombination with.
Mitochondrial DNA does undergo recombination with nuclear DNA, however, in that genes can be transfered from the mitochondria to the nuclear DNA and because of this the majority of genes necessary for mitochondrial function are now coded not on the mitochondrial DNA but on the nuclear DNA and their protein products transported into the mitochondria after translation.

Thanks @JackAidley - I have a couple of follow up questions now having read your answer, I'll give them some thought and put them to you later.

Addition to Jack Adley's answer:
Evolutionarily, mitochondria are thought to be descended from α-proteobacterium (Rickettsia are also descendants of this bacterium).
There are evidences that nuclear genes have also been imported to organellar minigenome. This can also happen because of recombination. I am not sure about the case of mitochondria, though. Since the current hypothesis is that organeller DNA that got leaked because of organeller damage, got incorporated in the nuclear genome, there not much of a likelihood that active recombination takes place between the two. However inter-mitochondrial recombinations have been reported, which perhaps happen during mitochondrial fusions.

Mitochondrial chromosomes do not undergo recombination. They replicate their DNA in an asexual manner, producing identical copies (except for the occasional mutation).  Mitochondria do not exchange or transfer DNA between themselves as they have no mechanism for that.
Very rarely a piece of DNA might get out of a mitochondrion and into another or into the cell's nucleus.  The latter type of transfer is believed have happened multiple times in the more than a billion years eukaryotic cells have existed.  Most of the genes needed for  mitochondrial functioning are located in the nucleus, not in the mitochondria, and many of those genes probably had such a mitochondrial source. Having mitochondrial genes in the nuclear genome is advantageous, exactly because it allows them to undergo recombination and thereby allows improvements to spread through a population of organisms.

Any references to add?

Recombination of mitochondrial DNA does seem to be possible, but it doesn't seem anywhere near as common as nuclear recombination. This is important because mtDNA is subject to much higher mutation rates, and so would be subject to the same kind of degeneration you see in the Y chromosome - i.e. Muller's Ratchet, if it wasn't so small. Nevertheless mtDNA does generate considerably over a multicellular organisms life span and this is one possible mechanism for aging.


text:
Does photosynthesis occur on cloudy days or does it require direct sunlight?
In my basic science classes in high school, I have learned that during photosynthesis, plants absorb sunlight and produce food by converting carbon dioxide and water into sugar and starch.
To me, this seems similar to the analogy of solar cells that convert sunlight into electricity. When sunlight falls directly on the solar cell, it produces electricity, but even when it is cloudy with no direct sunlight available, electricity is produced, but with less efficiency.
So can photosynthesis occur in plants only when they are in direct sunlight or does photosynthesis also occur during cloudy weather when the light is diffuse or indirect?

I recently took a trip to a nearby abandoned ore mine. Deep in there, I was surprised to see plenty of mosses around the installed neon tubes. So, photosynthesis does not even need actual sunlight to occur. I also agree with WYSIWYG's answer regarding the performance of leaves under diffuse light conditions.

Yes, photosynthesis does occur on cloudy days where the light exposure is diffuse - but the overall picture is not as simple as your solar cell analogy.
Consider one of the findings of the following article: "Impact of clear and cloudy sky conditions on the vertical distribution of photosynthetic CO₂ uptake within a spruce canopy" (Urban et al. 2011), where one of the findings is that

that shoots from deep within the canopy contribute substantially to the overall carbon balance during cloudy days. But, although shade-adapted shoots had a markedly positive carbon balance over a 24-h period on cloudy days, their performance was impaired on sunny days contributing only a marginal or even negative carbon balance from the middle and shaded parts of the canopy.

So, while leaves at the top of the canopy have a reduced rate of photosynthesis on cloudy days, leaves within the canopy and those that are shade-adapted, still photosynthesised.
I hope this helps a bit.

Moreover, chlorophylls don't absorb all wavelengths equally. See here


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Hearing and neurons- do ears have a sampling period?
From what I have read, outer hair cells in the human ear amplify incoming signals and inner hair cells "pick-up" the signals and generate action potential. However, neurons have refractory periods during which they cannot fire again. Does this mean that the human ear has a "sampling period" within which it cannot "pick-up" sounds?

Inner hair cells (IHC) do not fire action potentials themselves. It's the auditory-nerve that synapses with IHC that generates action potentials. The firing rate of the auditory nerve can be as high as few hundred Hz with a refractory period as short as 1 ms or so (depends on the animal).
However, it is important to note that the signal is not sampled at this rate. As you may know, the auditory signal is first transformed to the "frequency" domain through the physical structure of cochlea. Each inner hair cell therefore is roughly only encoding the relative strength of a frequency band. There are presumably inner hair cells in the human cochlea that correspond to a range centered around 18 kHz for example, but neither the neurotransmitters of the corresponding IHC nor the auditory nerve can fire at 18 kHz. Nevertheless, the amplitude modulation at this high frequency is what is transmitted.
Also, thinking of neural firing as a "sampling period" is not always a good analogy. There are debates about this, but it could be that precise timing of action potential carries large amount of information about the stimulus (perhaps not so much so in early auditory system.)
If you want to see some computational modeling work for inner ear, IHC, and auditory nerve, I recommend the Meddis IHC model:

C. J. Sumner, E. A. Lopez-Poveda, L. P. O'Mard, R. Meddis. A revised model of the inner-hair cell and auditory-nerve complex, J. Acoust. Soc. Am. 111 (5) 2002

I agree with your explanation. I think cochlea can be modeled as a bank of band-pass filters giving a spectrogram-like analysis of the audio. Lets consider the 18KHz IHC for example. If the auditory nerve connected to this IHC fires(sensing a strong 18KHz band), it cannot fire for another 1ms. Does this mean that I can hear the 18KHz signal only after 1ms again?

@user1155386 No. Signal is ENCODED by the train of action potentials. The information is there and can be DECODED if needed. This is more so because the amplitude envelope of the 18kHz signal will not change very fast. The brain is capable of interpolating through time, and it has many mechanisms for short-term memory. Things do not have to be represented instantaneously.

It probably bears mentioning that there is an extensive feedback stream from the auditory cortex to the thalamus that serves as a sifting mechanism for the incoming signal.


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What is the limit of time resolution in fMRI?
I was reading about a few studies on estimating functional connectivity between brain areas using fMRI signals. However, as far as I know that fMRI has a very poor time resolution, roughly in the order of 1 second. Individual neurons communicate with delay less than 100 ms, and many brain functions happen within a second, in which case fMRI wouldn't have enough time resolution to determine if things happened simultaneously, or in a sequence at all. This problem would be even greater for causality analysis such as Granger causality framework.
So my question is, what is the theoretical, and practical limit of time resolution in fMRI on human?

The quick and dirty answer is: fMRI doesn't perform well in the temporal domain, but excels in the spatial domain among non-invasive imaging methods. If you need an answer as to where the action is, use fMRI. If you need answers to temporal questions, I recommend using electrophysiology such as EEG, which excels in the temporal domain, or MEG for a combination of good temporal and spatial resolution.
As to what the limit exactly is, I would say a few seconds. fMRI measures blood oxygentaion responses, (See the answer on the question: "What does fMRI measure exactly"), which are inherently slow. Neural processes in local neural networks occur in milliseconds, in larger networks in the order of hundreds of milliseconds. Blood flow differences, in contrast, occur in the order of seconds.

I don't think it excels in spatial domain either. Though there has been a recent report about correlations at a single neuron level. See Schulz, K., Sydekum, E., Krueppel, R., Engelbrecht, C. J., Schlegel, F., Schroter, A., Rudin, M., and Helmchen, F. (2012). Simultaneous BOLD fMRI and fiber-optic calcium recording in rat neocortex. Nat Meth, 9(6):597-602. http://dx.doi.org/10.1038/nmeth.2013

I say excel because there is no non-invasive imaging method that matches that accuracy as far as I am aware

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Suitable introductory book on Bioinformatics for a computer scientist?
Do you have any suggestions on a suitable introductory text on bioinformatics for a computer scientist? Any recommendations with pros and cons of different books would be appreciated. I'm mainly looking for a brief introduction since I'm a novice to this field.
I found some books like

Systems Biology by Edda Klipp,
Introduction to Bioinformatics  by Arthur Lesk
Bioinformatics For Dummies
Bioinformatics and Functional Genomics by Jonathan Pevsner
An Introduction to Bioinformatics Algorithms by Neil C. Jones and Pavel A. Pevzner

I would like to develop software related to sequencing applications, so any suggestions should ideally aid in this goal.

Can you narrow down your requirements any, as I think this is too broad to get a reasonable answer.

I was looking for something related to sequencing, Since looking for developing software for it

I would put as much information as possible into the question itself.  Asking for the "best" book is going to get a host of opinion-based answers.

With a slightly reformulated Q I do not see a big problem - BioSE has many open questions about book suggestions. Adding specifics about future software development and therefore need for technical aspects of sequencing would probably be useful though.

@fileunderwater why did you remove one of the books from the OP's list?

@terdon Mistake on my part or the Q was updated while I edited. Maybe a mod can put it back in.

@fileunderwater no worries, I put it back. I was just asking in case there was a valid reason.

I added the bit from your comment - I think it's an important point that actually narrows the books under consideration.  Please edit it as you would like, but I'd encourage you to put specific information into the question directly as @jonsca suggested, since few people are going to read this long comments section.

"Biological Sequence Analysis" by Durbin et al. is the classic bioinformatics text for people with a CS background. If you are interested in a more quantitative approach to biology without necessarily focusing on algorithms, you will also probably find "An Introduction to Systems Biology" by Uri Alon and "Physical Biology of the Cell" by Phillips et al. interesting (depending on your area of interest). Additionally, any Machine Learning text will be relevant and some often have examples from biology/bioinformatics.

@Bitwise I've reopened the question now, could you please create an answer from your comment.

Systems biology and bioinformatics are quite diverse subjects, but here are some options:

Biological Sequence Analysis by Durbin et al.: the classic bioinformatics text for people with a CS background. Does not deal with networks.
An Introduction to Systems Biology by Uri Alon: A physicist's view of systems biology, focusing on design principles and networks. Interesting concepts and some math (no algorithms). Doesn't really deal with methodology.
Physical Biology of the Cell by Phillips et al.: Nice introduction to biophysics and quantitative biology (no algorithms). Many parts are relevant for systems biology.
Any diverse Machine Learning text will be relevant and many have examples from biology/bioinformatics.
Probabilistic Graphical Models are also quite popular in bioinformatics (e.g. Hidden Markov Models, Expectation-Maximization, Bayesian Networks). Probabilistic Graphical Models by Koller et al. is a very comprehensive CS book on the subject.

Another suggestion is to look for primers/reviews in relevant journals. This is important because the field is new, so once a new technology is developed, it takes time until the appropriate computational methodology is developed enough to make it into a text book. Also, they can point you to relevant research papers. For example, PLoS Computational Biology has an Education Collection which features a large variety of such reviews.

I second these two I used both and liked them overall:

Bioinformatics and Functional Genomics by Jonathan Pevsner
An Introduction to Bioinformatics Algorithms by Neil C. Jones and Pavel A. Pevzner

For my bioinformatics class a few years ago, we used these:

Fundamental Concepts of Bioinformatics - Krane and Raymer

Was excellent as an intro text. Explained a lot of the biological concepts while it was teaching you the methods. Useful either for biologists or computer scientists bridging into bioinformatics.

Statistical Methods in Bioinformatics - Ewens and Grant

The go to book for more comprehensive coverage of algorithms and applications. Did a good job covering the details of a method, like dynamic programming, from start to finish.  Much more computer science oriented.

For a really brief introduction, I recommend the 37 page paper
Bioinformatics - An Introduction for Computer Scientists by Jacques Cohen.
It is a well written text, assuming some knowledge about algorithms, computing and maths, but not about biology. It helped me a lot getting comfortable with the field.
Afterwards, I'd stick to Durbin's "Biological Sequnce Analysis" (as already mentioned by Bitwise) as a book that provides you with the theoretical foundations of the models used in bioinformatics. It focuses on Sequence processing, which is what you want as far as I understood your question. It is also quite accessible from a computer scientist's or mathematician's point of view.

There several popular books for bioinformatic

A First Course In Computers 2003 Edition (With Cd)
Foundations of Computing (English, Paperback, Sinhs Pradeep K.)
Introduction to Bioinformatics
Bioinformatics: Methods and Applications: Genomics, Proteomics and Drug Discovery by S. C. Rastogi
Bioinformatics: Concepts, Skills & Applications
Principles of Genome Analysis and Genomics

You can find the list of bioinformatic books here 6 Best Books for Bioinformatics

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Good poly-A filtering rules or tools
I am aligning a large number of ESTs. It seems poly-A tails show in many different ways. In addition to occurring at the very end, they can be flanked by the cloning sequence one one end, or have mismatches/errors. What is a good rule or available tools that will handle the usual cases?
A few examples of the non-trivial cases I found, with their Genbank Accs:
>EE409337
... AAAAAAAAAAAAAAAAAAAAAAAAAGGAAAAAAAAAAAAAAAAAAAAAAAAAAAACCTTGTC
>EE409340
... TTTCTACAAAAAAAAAAAAAAAAAAAAAAAAAAAAAACTTGTC
>EE409361
... TTGTTAAACTGAAAAAAAAAAAAAAAAAAAAAAAAAAAACCATGTCGGC
TTACTGAATTGAA
>EE420306
.... AAAAAAAGTTATGTTAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAGGGAAAAAAA
AAAAAAAAAAAAAAAAA

Cross-posted on SeqAnswers,Biostars.

Did the answer on Biostars not work for you? (If so, what is it that it doesn't do that you would like it to do?)

@dd3: trimest has an option for trimming the poly-A regions, but we have to specify the rules. I have already done the basic filtering, but what are the "good" rules? Is there something better than min-length and max-mismatches that will handle real sequences I have given examples of?

You could try the empirical approach. Take a random sample of N ESTs and calculate the distributions for min-length and max-mismatches. Use the distributions to pick appropriate cutoffs (some sort of statistics thing).

@dd3, that definitely makes sense and seems like a good idea. (although there's some judgement to be made for things like ...GAGAACTGGGCAAAA: where does the tail start?). Since EST processing is well established, shouldn't something like this already exist in the tools or the literature? How does everyone else do it?

I'm still a little unclear as to what you are trying to achieve that min length was failing (as you seem to be fine with trimming.  Are you wanting to trim from ACA... on 409340 and AAACTGA... on 409361 but don't want to set min-length less than 7?

@highBandWidth: that, I have no idea. I'm just getting into bioinformatics myself. sorry.

@AtlLED, I don't know what the right answer is. Min-length of 7 may be too high for some cases and low for others. Seems like max-mismatches should be high if there's a cloning palindrome at the end and low otherwise. Are there well-known settings everyone uses? Has anyone done empirical studies to see what the right conditions are?

@dd3: no, your ideas certainly help. I'm just curious as to what people have usually done.

Can you give the search criteria for the ESTs?  I have an idea for this I'd like to try.

@AtlLED, well for my purpose I am just using all the EST's for one organism from NCBI. You can just search EST's with an organism and download the results in FASTA, eg.,: http://www.ncbi.nlm.nih.gov/nucest?term=Brassica%20napus%5BOrganism%5D

Use dust and remove all low complexity sequences.. Or simply use a regex search to filter out poly-As


text:
What causes autism?
What causes autism?
By this I don't mean what is to blame i.e. Vaccines, Gluten or Pharmaceuticals etc.. I mean what exactly is happening in the brain to cause the autistic behaviors such as little to no communication skills, regression of skills around age 3, hand flapping etc..
I see a lot of research looking for something to blame however I see little to no research on identifying the physical causes or links (maybe I'm not using the correct search terms).

There's a significant body of anatomical research that is going on, both in neuropathology and neuroimaging, see http://www.ncbi.nlm.nih.gov/pubmed/21360830 for example.

Fragile X syndrome is a genetic disorder which is highly related to autism and is considered to be the most common single gene association with autism.
Establishing what actually happens in autistic people is difficult because it is hard to quantify someone as being autistic or not - it is common for some people to show some signs of autistic type behaviour and some people are more extreme than others - plus the symptoms are numerous:

Clinically, autism is defined by a “triad” of deficits comprising
  impaired social interaction, impaired communication, restricted
  interests, and repetitive behaviors.

Wikipedia splits the mechanisms in to two key groups, pathophysiology and neuropsychology. The pathophysiological aspects are perhaps better documented and some known correlates to autism are listed:

Excess of neurons in key brain regions
Disturbed neuronal migration during early gestation
Unbalanced excitatory–inhibitory networks
Abnormal formation of synapses and dendritic spines

Our understanding of the mechanisms causing autistic behaviours does not go much beyond this. This paper is a review of the neuroanatomic associations with autism which could, at least in part, help you to identify the physical differences linked to autism.

Here is a brand new article on autism http://www.the-scientist.com/?articles.view/articleNo/36379/title/Maternal-Antibodies-Linked-to-Autism/

It's also worth noting that conditions aren't always due to single gene mutations and their aetiology can be more complex. Autism could easily be the result of 10 different gene mutations affecting different processes during brain development (e.g. receptor trafficking, spine growth and all sorts of stuff). The same is true for loads of psychiatric conditions

I would like to asnwer this question. I will try to avoid repeating any information about possible causes of autism, which was mention here. Anyway there is new interesting information.

Autism spectrum disease (ASD) is typically diagnose from the psychological point of view. Such thing like repetitive behavior, echolilia, stimming and stuff like that. True reason why does we still diagnose ASD in this way is because we still dont know causes of this disorder.

Sleep inconsistency
Kids with ASD are well know for theirs sleep disturbance.

Polysomnography studies of ASD children showed most of their abnormalities related to rapid eye movement (REM) sleep which included decreased quantity, increased undifferentiated sleep, immature organization of eye movements into discrete bursts, decreased time in bed, total sleep time, REM sleep latency, and increased proportion of stage 1 sleep.

REM sleep is one of the two types of sleep in general. By the ontological point of view the REM sleep might provide neural stimulation. In this way good sumury provide us at wikipedia page on REM:

REM sleep prevails most after birth, and diminishes with age. According to the "ontogenetic hypothesis", REM (also known in neonates as active sleep) aids the developing brain by providing the neural stimulation that newborns need to form mature neural connections.Sleep deprivation have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, and decreased brain mass,and can result in an abnormal amount of neuronal cell death.unreliable medical source? The strongest evidence for the ontogenetic hypothesis comes from experiments on REM deprivation and the development of the visual system in the lateral geniculate nucleus and primary visual cortex.

So lack of REM sleep can be one of the many important factor to autism brain development.
Autistic microbiom
Microbiome is an ecological community of commensal, symbiotic and pathogenic microorganisms found in and on all multicellular organisms studied to date from plants to animals.

Recent studies suggest that autism is often associated with dysregulated immune responses and altered microbiota composition. This has led to growing speculation about potential roles for hyperactive immune responses and the microbiome in autism. Yet how microbiome–immune cross-talk contributes to neurodevelopmental disorders currently remains poorly understood. In this study, we report critical roles for prenatal microbiota composition in the development of behavioral abnormalities in a murine maternal immune activation (MIA) model of autism that is driven by the viral mimetic polyinosinic-polycytidylic acid. We show that preconception microbiota transplantation can transfer susceptibility to MIA-associated neurodevelopmental disease and that this is associated with modulation of the maternal immune response. Furthermore, we find that ablation of IL-17a signaling provides protection against the development of neurodevelopmental abnormalities in MIA offspring. Our findings suggest that microbiota landscape can influence MIA-induced neurodevelopmental disease pathogenesis and that this occurs as a result of microflora-associated calibration of gestational IL-17a responses.

It may not sound like something related to the neural system but now study lift up mircobiome importance.

EECs play an important role in gut chemosensing to orchestrate appropriate functional responses to a variety of stimuli ranging from nutrients, food degradation products, toxic chemicals, microorganisms and bacteria products. This complex balance between maximizing nutrient assimilation and minimizing danger to maintain optimal homeostasis is the result of the interplay of different detection systems including the distinct types of sensory receptors expressed by EECs, the variety of signaling molecules released by EECs and the targets that are activated directly and indirectly such as neighboring cells, distant targets reached via the bloodstream and neuronal pathways. Considerable progress has been made in understanding EECs relationship with neurons of the ENS and CNS and EEC bidirectional communication with the brain. There is now strong evidence that EECs can directly participate in the brain-gut axis bidirectional communication through axon-like processes or basal cytoplasmic processes. The basal processes connect EECs and neurons innervating the gut forming neuroepithelial circuits, which allow sensory transmission from the gut lumen and feedback from the brain to the gut EECs. The activation of afferent and efferent nerve pathways may be explored for the management of diseases related to feeding disorders and GI dysfunction. Alterations in the bidirectional communication between the brain and the gut are likely associated with an impairment of gut functions (e.g. intestinal secretion, motility, blood flow and afferent sensitivity). The modification of the homeostatic reflex might lead to a chronic perturbation of the gut such as visceral hypersensitivity. Therefore, a better understanding of the EEC roles and their relationship with the brain and sensory nerves is an important research target. Future studies are required to fully decipher this complex network. The direct EEC to nerve connection opens a new horizon of research and provides new tools to understand the mechanisms underlying EEC control of food intake and GI dysfunction as well as potential new therapeutic targets.

I think there more and more clues that the biggest role in development may be complexes imune reactions on brain development such as recent relation was found in homosexual brain development
Source
Devnani, P. A., & Hegde, A. U. (2015). Autism and sleep disorders. Journal of pediatric neurosciences, 10(4), 304-7.
Why We Sleep: Unlocking the Power of Sleep and Dreams book by Matthew Walker
Cutting Edge: Critical Roles for Microbiota-Mediated Regulation of the Immune System in a Prenatal Immune Activation Model of Autism
Latorre, R., Sternini, C., De Giorgio, R., & Greenwood-Van Meerveld, B. (2015). Enteroendocrine cells: a review of their role in brain-gut communication. Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 28(5), 620-30.

While still not entirely clear as to what causes autism, there is a growing body of research (as jonsca said), and a model is being developed.
A suggested explanation from "Causes of Autism Spectrum Disorders", that the disorder may begin in utero, with the interaction of genes and nutrients. However,

recent research suggests that Autism may result when a child with a genetic susceptibility and/ or abnormal Omega-3 fatty acid profile in cell membranes is exposed to one or more environmental insults (heavy metal exposure, virus or bacteria) resulting in malfunctioning cells (often in the gut and brain). This can happen “in utero” (during pregnancy) or after birth (post-partum).
  (from the first link).

Genes seem to certainly play a role, as in the article "Support for the homeobox transcription factor gene ENGRAILED 2 as an autism spectrum disorder susceptibility locus." (Benayed et al. 2005), the homeodomain transcription gene EN2 are associated with Autism, associated with about 40% of the people they tested.
Disorders in the serotonergic system have also been found to be a mechanism of autism, according to "Serotonin transporter genotype and neuroanatomy in autism spectrum disorders" (Raznahan et al. 2009).
I hope this goes part of the way in answering your question.

Cerebral folate deficiency (CFD) has been found to be the cause of autism in as many as 75% of autism patients. Specifically, the folate uptake into the brain occurs primarily through folate receptors in the choroid plexus.
Folate receptor alpha antibodies (FRAA) in autism patients, bind to these folate receptors and block folate uptake. Folate is of course an essential nutrient for various brain functions. So one can expect numerous brain functions to be impacted by CFD.
Cerebral folate receptor autoantibodies in autism spectrum disorder
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578948/
Folinic acid (not to be confused with folic acid) has been used to treat CFD induced autism. Basically, it is a method of getting folate to the brain by an alternate pathway, that bypasses the primary path that is blocked by FRAA.
Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial
https://www.nature.com/articles/mp2016168

I know it's been about a year since you posted this but, I'm just now seeing this one... thank you!


text:
Can antimicrobial peptides be called antibiotics?
Antibiotic peptides are present in almost all multicellular eukaryotes. So can they be called antibiotics ? ( which are usually defined only for fungi and bacteria )

Antibiotic peptides are definitely antibiotics.  They are often referred to more specifically as peptides because the fact implies that they are less toxic and conveys some important understanding of how they work.  Not sure if they all form pores in the target cell, but that's how magainins work.


text:
DNA Replication
I just wanted to understand the basic steps behind the replication of the lagging strand of DNA:

Have helicase unwind it first
DNA Primase lays down RNA primers in fragments, called Okazaki fragments
DNA polymerase III goes through and corrects all the mistakes (essentially replace the Uracil with Thymine)
DNA polymerase I goes through and removes RNA primer
DNA ligase hooks up each of the 5' to 3' end fragments

Is this the correct order of steps? If so, does the leading strand need any RNA primer or does the DNA polymerase just start and go to the end without any help?
Thanks

I think that you have a couple of points wrong. Since your question is asked using bacterial terminology, I'll stick to that.
The leading strand, the one that is initiated at the origin of replication, is synthesised by pol III which is a highly processive polymerase, i.e. it keeps on going for long periods, making very long products. In principle a single pol III molecule could produce the entire leading strand copy of the template.
The lagging strand is, as you say, initiated at multiple RNA primers. The enzyme that extends these primers is pol I. As polI  extends a primer it creates an Okazaki fragment (i.e. this is not an alternative name for the primer itself). Eventually the pol I will encounter the 5' end of another RNA primer. At this point the 5'>3' exonuclease activity of the pol I comes into play and removes the primer, replacing it with DNA. The pol I will probably also degrade some of the DNA that has been added to that primer by another pol I, resynthesising it as it goes. This is so-called "nick tranlation" since as the pol I moves along the template it moves a nick in the new strand as it goes. pol I is not a very processive enzyme however and will fall off, leaving the nick to be sealed by DNA  ligase.
The leading strand does require a primer, and in most cases this is an RNA laid down by the initiation complex at the origin of replication. In some cases, a protein provides an -OH  group for DNA polymerase to initiate at.


text:
Are chromosomes from each parent split between gametes with equal probability (esp. in humans)?
I've recently read a little on Wikipedia about genetics, but I can't find a direct answer to this question.
My rough understanding is this:

Both males and females have pairs of chromosomes, one copy from each parent
Both produce gametes (eggs in females, sperm in males)
The gamete is produced during something called 'meiosis' to take only one set of genes

What I can't find an answer to though is whether that selection is completely random, such that every chromosome in a gamete has an equally likely chance of being taken from the male parent set and the female parent set.
Another way of putting it, perhaps: Would the range of 100% male parent to 100% female parent chromosome selection in the gamete be a binomial distribution?
My background is computing, so please assume very little knowledge of biology.

To clarify on your question: Imagine a species with two pairs of chromosomes, with one member of each pair coming from each parent. So there is one copy of chromosome 1 from the father (1F) and one from the mother (1M) and the same for chromosome 2 (2M and 2F) with one member of each pair going in to a gamete. Do you want to know whether the 1M+2M or 1F+2F combinations would be more common in the gametes than the 1M+2F or 1F+2M combinations?

Not quite - what I want to know is whether nM is just as likely to be in the gamete as nF. Another way of putting it (maybe): Is it correct to say (in a human for instance) that a gamete has a 1 in 2^23 (~1 in 8 million) chance of having entirely the nM or nF set of chromosomes? Also, in that extreme case, would such a gamete be indistinguishable from a gamete from the parent? Say, a male producing a sperm with 23 chromosomes all from the male parent.

I have heard of some research being done in to whether the chromosomes associate in such a way but can't remember who was doing it, also you might want to look at meiotic drive elements. However recombination occurs between chromosomes so the chromosome in a gamete is also likely to be a cocktail of the parental ones - here is a wiki section that should help, I might write an answer this weekend for you http://en.wikipedia.org/wiki/Intragenomic_conflict#Nuclear_genes

Other answers are correct in their own terms, but because of homologous recombination during meiosis, the idea of maternal and paternal chromosomes becomes meaningless. Any chromosome in a gamete will be a mosaic of the maternal and paternal versions. In this sense the chromosome is not the unit of inheritance.

Ah.... that's really helpful, I didn't realise the chromosomes themselves were mixed up like that.

Excellent point. I can't believe I forgot to mention that.

Have marked as the answer - but one other question in relation to this, if I may. This 'mosaic', what would be the 'unit' of this? Is it at the gene level? So a resulting chromosome would be a mixture of genes from each parent chromosome pair?

@MarcosScriven no it is not at the gene level, it is usually in a much larger scale than that, resulting in the mix of groups of genes. This is a process that has nothing to do with genes really, if genes are the paragraphs in a book, meiotic recombination consists of mixing up the pages. This means that genes can be split as well.

Yes, for all intents and purposes, the assorting of chromosomes during meiosis is random. In fact, it's difficult to imagine a mechanism by which the chromosomes would assort in any non-random manner (i.e., how would the maternal chromosomes "identify" each other so as to assort together during meiosis?)

That was indeed my intuition, but I wanted to comfirm it. My only thought was perhaps there could be a case where a chromosome from one parent may have some characteristic (however minor) that made it more likely to 'follow' another chromosome from the same parent. Another way to put it - I recall reading about how during development symmetry is even possible (it was above me, but something to do with ion flow). I wondered if there was some similarly subtle mechanism possible in this case.

As far as we know, chromosomes tend to be equally distributed across normal gameteogenesis, following Mendel's second law of independent assortment. However some versions of DNA repair and chromosomal condensation can malfunction and result in more versions of one parents genes in a cell than another. Two phenomena which are exceptions to the equal parental ratio are Gene Conversion and Chromosomal Fusions.
Although a much smaller scale than chromosome segregation, Gene Conversion is a case of unequal allele transmission. While repairing double strand breaks during meiosis, one parent's DNA may be used as the repair template instead of the original version. This phenomena distorts the 1:1 allele ratio on the scale of hundreds of base pairs.
Robertson translocations are when two nonhomologous chromosomes fuse into one. Chromosomes which were once separate, segregate together into the same gamete. These cases can serve as exceptions to Mendel's second law of independent assortment.
There are also several cases of transmission distortion, while these cases may not affect the segregation of chromosomes during meiosis, they do cause unequal fertilization. The t-haplotype in male house mice, is passed on to up to 95% of offspring! The mechanism is still under investigation, but it appears that this gene when expressed in sperm, kills all other sperm without the t gene. The Sd gene is a similar element in Drosophila.
A great book on selfish genetic elements and intragenomic conflict is Genes in Conflict by Burt and Trivers.

Yes, every chromosome in gamete has an equal probability of being taken from the male parent set and the female set.

Thanks for answer. While I'm here is there a technical term for 'male parent chromosome set'?


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In DNA repair, how is it determined which strand contains the error?
DNA replication is more accurate than transcription (or RNA replication) because mechanisms exist for proof-reading and repair of DNA, but not for RNA.
Consider a segment of a DNA strand, AGTC. Its complement is GACT. Now suppose its complement is mutated to TACT — the DNA repair system will replace the wrong T by G. Why isn’t A in the original strand replaced by C? How does the system determine that the first strand is correct and its complement is incorrect?

I've edited this question, removing anthropomorphic "know" and the implication that the DNA, rather than enzymes, did the repair. Although the question was answered some time ago, this makes it more useful for indexing and reference.

The reason the fact it isn't realistic is important. DNA repair machinery works by repairing common errors that occur due to common mutational pathways. The enzymes are specific for this, for example one particular enzyme targets mutations caused by UV and itself is activated by sunlight thus it's specificity makes it repair the correct chain. Also during replication, newly synthesised DNA lacks methylation. The repair enzymes thus know which chain is correct.

There are many types of DNA repair. Let us limit to the following three different types to answer this condition.
1. UV damage
Exposure of a cell to UV light can result in the covalent joining of two adjacent pyrimidines (usually thymines), producing a dimer. These thymine dimers prevent DNA polymerase from replicating the DNA strand beyond the site of dimer formation.
In such cases, UV-damage specific endonucleases cleave both the 5' and the 3' end of the lesion. Along, with the lesion some normal DNA is also lost as an oligonucleotide. Here modifications are being made only on one strand, the other is taken as a template (correct) and the DNA in the lost part is replaced.
The UV-damage may occur on both the strands but locally, one is affected and the other is the template (since you can't have thymine both sides)
2. Base Excision
Normal DNA bases can get deaminated spontaneously or on insult to an abnormal base (not on DNA).The abnormal base is excised by glycosylases and gap is later filled by considering the other strand the template.
3. Mismatch repair
What you are talking of in your example is not a case of deamination or UV damage but a mismatch repair. There can be errors in replication too where such a case could set in. There are specific enzymes for this repair, but discrimination is based on the degree of methylation. GATC sequences, which are found approximately once every thousand nucleotides, are methylated on the adenine residue. This methylation is not done immediately after synthesis, so the newly synthesized DNA is hemimethylated (that is, the parental strand is methylated but the daughter strand is not). The methylated parental strand is assumed to be correct, and it is the daughter strand that gets repaired.
The above said mechanism of discrimination is only in the gram negative bacteria. To quote Wikipedia,

However, in other prokaryotes and eukaryotes, the exact mechanism is not clear. It is suspected that, in eukaryotes, newly synthesized lagging-strand DNA transiently contains nicks (before being sealed by DNA ligase) and provides a signal that directs mismatch proofreading systems to the appropriate strand. This implies that these nicks must be present in the leading strand, and evidence for this has recently been found.

There are other cases where there is damage occuring to both strands that I'd suggest for further reading.
References

Lehninger's Principles of Biochemistry, Ed. 6
Lippincott's Illustrated Reviews, Biochemistry, Ed. 5
Wikipedia. DNA mismatchrepair

Your specific scenario is not realistic, thymine is a pyrimidine base while guanine is a purine base. They are very different chemically and can't spontaneously convert into each other. So this is a type of damage that only occurs during the replication of DNA.
The typical damage that occurs and can be repaired is oxidation, methylation and hydrolysis of DNA. This kind of damage results in modified or missing bases and can be detected due to that.
You might also be interested in why thymine is used in DNA instead of uracil, as uracil can be easily damaged in a way that would not be detectable.

Perhaps it is not realistic, but talk theoretically, if this kind of error happened, can it get auto repaired?

This kind of error can totally happen in a laboratory setting - true, it's maybe not a natural context, but it's not unimportant

To solve the problem of which strand is edited to correct mistakes, immediately after DNA replication, the original strand is methylated to prevent correction on this strand.Thus only the newly synthesized strand is searched for errors for correction. In short methylation prevents the template strand from being edited error and correction.

Could you add some references to this, please?


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Improving transformation efficiencies- induce supercoiling?
From my limited knowledge of science, I know transformation can be one of the hardest step in cloning, and that a large amount of research/trial and error has been done to improve on this step. I've heard electroporation is the most efficient technique, though I have no reference, and of course the cell, media and duration all have vital parts to play in the process.
However, I've never heard of supercoiling as an important factor. Size of the plasmid plays a large part in transformation, so intuitively it makes me think supercoiling the plasmid prior to transformation would improve the efficiency. I thought transformation was simply DNA diffusing through holes, but are parts of the plasmid required to bind/interact with the host?
Why aren't we suggested we supercoil prior to transformation? I have several thoughts but I'm just guessing:

Is it because gyrase can disrupt the integrity of DNA?
Or is it that it's just an expensive enzyme and the gain isn't worth it?
Or perhaps supercoiling reduces efficiency of subsequent plasmid preps/transcription (though wouldn't the host's natural enzymes supercoil anyway?)

Two comments on this from my lab experience with transforming bacteria: Making cells competent (I usually use chemical competent cells since we have no electroporator in our lab) is not a hard thing to do. Transformation effeciency isn't usually a problem either (with good competent cells you easily get 5x10^8 transformants (and more) per ug of DNA. So my guess, why nobody bothers to use an additional step (besides the time and money it costs for the enzyme), is that the methods we have are simply good enough.

Here is a report that shows significant increase in transformation efficiency for large plasmids (transformation was by electroporation. However the paper has been cited fewer than ten times so clearly the technique did not catch on.

Zhixing, Y and Nahon, J-L (1995) DNA gyrase improves DNA transformation of E.coli cells with large recombinant plasmids. Nucleic Acids Res. 23:3353-3354

Thank you, interesting to know in case of any problems with transformations that this might actually work!

The paper predates bluelight and sybr safe, which improve the efficiency by several orders of magnitude, so they were definitely ahead of their times.
The reason why nobody does it is that from what I can tell they use Micrococcus luteus gyrase because they had it. Sigma sells Eco gyrase but at £500 I am not sure who would try it —I myself am working with epPCR libraries with a big plasmid yet I wouldn't spend that much.

Correction. (NEB)[https://www.neb.com/products/m0306-dna-gyrase-e-coli] sells it for USD70 —for 100 0.5 µg rxns. That makes it worth a shot...


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Can ant colonies have two "branches"?
Could an ant colony have 2 or more "branches" located far from each other (i.e. physically separated but interconnected nests) ? If so, how far is the limit?

Yes, sub- or satellite colonies are common in many species (see e.g. Hölldobler & Wilson, 1990; Debout et al. 2007), and these are then labelled as polydomous species. Subcolonies can either contain extra queens, but sometimes only contain foraging workers. The purpose can be both to expand foraging grounds or as a pre-stage for colony budding. The distance between colonies can differ dramatically between species, but there are cases of supercolonies (especially in the Argentine ant) streching over hundreds of square kilometers (Moffett 2012).
Satellite colonies are also common in e.g. Carpenter ants (Camponotus) and wood ants (e.g. Formica rufa), and when colonies are found inside a house there is often a primary colony somewhere outside the building (see e.g. Ants in the home).


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Living organisms with properties similar to both plants and animals?
Is there any example of currently living organisms that shows close resemblance to both being a plant and an animal?
What is the plant with the closest possible resemblance to animals, and
What is the animal with the closest possible resemblance to plants?

It should be stressed that any resemblence found would be due to convergent evolution: natural selection leading to similar solutions from  diverged evolutionary histories.

I have added important new information in a new answer to the proposed duplicate question.


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What is this beetle and what are the strange antennae for?
I found this wonderful creature in my yard (I live in the south of France) last night:

It was about 2-3cm long, with a hard carapace and wings. It also made loud hissing noises when agitated. I am curious as to what species this is, I'm quite surprised I'd never seen it before cause the beastie is quite large and last night I found it because of the noise it was making. It was upside down and hissing like a kettle.
More than the specific species' name, I am curious as to what the large antennae are for. Does their shape and size somehow increase the beetle's sensitivity to whatever stimuli these are atuned to?

Alan Boyd's comment below helped me along a bit. I seem to have found a close relative of the ten-lined June beetle (Polyphylla decemlineata) pictured below (image source)

My guess is some kind of chafer. The elaborate antennae are probably an adaptation for detection of mating pheromones during nocturnal mating flights.

From the pattern on the elytra (hard upper wings), it looks like you might have a beautiful male Polyphylla fullo. Compare your photos with the P. fullo in this illustration, or photos on the Wikipedia page.
edit to fully respond to the comments:
I suspect you're right that the antennae plates in your picture are just tightly closed up, giving a different appearance. Here's a photo I took of a related species where you can see both appearances of the antennae.
And I think that Alan Boyd is correct about the antennae being used as chemoreceptors to locate females. The wikipedia page on the Ten-Lined June Bug also mentions both of these points.

It is indeed a beautiful specimen.

Ah yes, I think you nailed it. That does indeed seem to be it. However, whereas the specimen I saw seems to have solid antennae, other photographs (e.g. here) show a kind of brush or duster like arrangement of what looks like separate filaments. Is that the same antenna that can be fanned out at will, is this is male/female thing or perhaps an adult/juvenile difference? Also, could you shed some light on why the antennae are shaped as they are?

Thank you! The second photograph is just what I needed. So these little buggers can expand their antennae at will? I guess they do so in response to pheromones, cool!

Polyphylla = 'many leaves'. This may refer to the structure of the antennae, when fully deployed.

@AlanBoyd argh! Yes, that makes perfect sense and should have been obvious to a native Greek speaker like myself.

It's likely the this structure (the 'many leaves') is adaptive because of increased surface area / volume ratio. The more the 'frilly' your antennae are, the greater the surface area, which means more contact between the pheromones in the air and your chemosensory bits.

@Wajurgmitr yup, that makes perfect sense. Also, conversely, you would want to be able to compact them into a less fragile form.

Are we sure about this? To me the elytra look pretty different; in the OP's photo there is yellow patterning but it's relatively smooth, whereas this one is very 'ribbed' but lacks the yellow colour.


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What species is this large-ish spider?
Last night I came across this spider outside my house (costal Southern California). It was bigger than any I'd seen before, about 2.5 or maybe 3 inch legspan, maybe just under an inch for the body length. It is a brown-gray color, the cephalothorax has two dark brown stripes, and some mean looking fangs. Can anyone identify it?

Looking at this reference "Frequently synanthropic spiders of Southern California", I would have to say that it is possibly a grass spider. (Please someone correct me if I am wrong).
Beautiful looking specimen!

Ah, it does look like a grass spider. Or possibly a wolf spider? Any chance of narrowing male/female or which particular species?

I've found some species of wolf spiders and grass spiders to look and behave almost identically, though typically wolf spiders are larger.

Yes, it's definitely an adult male Agelenid - one of the funnelweavers.  More specifically, one of the outdoor species known collectively as Grass Spiders.  The nice long exhaust-pipe spinnerets at the back tell you that, and the racing-stripe pattern on the body.  The big boxing-glove palps hanging in front of the face tell you it's an adult male, which is why it was wandering around looking for love.  I'm not familiar with the California species, but this is probably one of the western Agelenopsis species.
https://bugguide.net/node/view/2001


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Preventing Diabetes by preventing stress?
I have came to know that taking a lot of stress increases the risk of Diabetes, and patients of Diabetes are adviced not to take too much stress, am i correct? if yes then I am unable to understand that how stress affects the level of glucose in our blood?

Prolonged stress leads to elevated levels of cortisol. Cortisol interacts with insulin action and blood glucose levels in various ways, essentially promoting hyperglycaemia.


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Realtime PCR plate cleaning
Have anyone used realtime PCR, is that the plate for realtime PCR is one-time using or not ? Otherwise how to clean the plate after reaction to prevent wrong result in next time using ?

ahh... it is usually used only for one round.. but if your experiment is not very sensitive then you can wash it in hot water and autoclave it. (I think they are autoclavable)

@WYSIWYG thank you so much, can you describe more what matter occur to DNA when they being autoclave ? Are they denatured ?

nothing happens to the DNA.. it might get damaged but we cant rely on that. autoclaving is just for making it sterile. hot water wash should remove the DNA.. you may use a mild soap/detergent too but make sure that none remains.

Ok, thank you so much, i hope it will work. Otherwise i will try another way to reuse the tube.

A possible solution is to use the DNA ZAP solution, which I know many people used in adjacent labs and were happy with for cleaning their DNA free workbench. The product sheet states

When 500 ng of template DNA is dried down in a PCR tube, it is rendered unamplifiable upon treatment with DNA ZAP solutions. Additional experiments demonstrate that the DNA is degraded down to free nucleotides.

Please note that I'm not promoting any specific product here and you can purchase any similar product/technology for your particular application. Obviously the best recommendation is to use new plates for each reaction but this/or a similar product can be an option too although the risk of DNA contamination in a PCR based reaction should be carefully balanced against simply using fresh plates considering the product itself is not free either.
The product sheet provides instruction for cleaning/treating PCR tubes hence I assume you use the same protocol for plates if you have the plate centrifuges available in your lab. You can get rid of the solutions by tapping the plates on a tissue to get the liquid out of the wells.

Honestly spoken I would never think about re-using the PCR plates. Sure, they are not for free, but the reagents of the assay aren't either. If you blow up one experiment because of a contamination (and you will likely use the same genes in an assay more than once), this is more expensive (plate, reagents, sample preparation) than what you save. Besides that, these commercial solutions aren't free either.

@Chris I 100% agree! I would personally never re-use anything for any reaction and its just best to use new consumables but just though I provide a possible solution to the OP question, which might also be of interest to others but again I agree with you and I would personally never re-use any consumables specially for reactions such as PCR!

@Chris I changed the language used in the response to highlight it as a possible solution and not a suggestion and clarified that the best thing to do is to use a new plate.

One of the claimed virtues of RT-PCR plates is their inability to bind DNA. (See for example the assortment at http://www.fisher.co.uk/product/brand_listing.php/T/Thermo%20Scientific%20ABgene/PCR%20plate ). As such, all you need to do to remove the DNA (genomic, amplified, or primers) is to rinse them. This suggests that rinsing may also work for dNTP.
On the other, many types of RT-PCR plates are made of polycarbonate, which is able to bind protein. I would be concerned about an uneven amount of polymerase sticking to the well. To go around that, you should re-use, in any PCR plate, only those wells that saw polymerase before.
I have no idea whether other molecules bind to the wells, but presumably they fall on the DNA or protein paradigm.
It will cost you only one plates and regents for as little as four reactions to test whether these plates are reusable. In the first run, measure two samples, A and B, for some transcript. Rinse the wells, and measure samples A and B again. If the transcript ratio A/B is the wildly different between first and second attempt, you know you can't reuse them. I would also be concerned if it will take many more cycles to reach the plateau stage at the second attempt. Passing these tests, you may be all set. Failing these tests, you may still be able to use the remaining wells. Let us know.

Welcome to Biology SE! Can you clarify what you are asking?


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Do non-green flower colors have any functional interactions with the sun?
I always hear the pseudo-evolutionary claim "plants are green because they need to use red and blue light".  If this premise to my question is true,
What (if any) other functional relationship occur between the color of the blossom of the flower or the color of the leaves in the fall, and the spectrum of the sun.  Could it be said that plants are actively absorbing a particular spectrum for a particular purpose by expressing particular colors other than green?

FYI, "optogenetics" refers to a very different field from what you're describing here.

I was thinking someone with experience with proteins like opsins would have a better chance of answering the question.

Some functions of non-green flower colors:
#1: plant-animal interaction. Flower colors act as signals received by animals with eyes (e.g., pollinators, which many plants need to attract in order to reproduce).
However, it sounds from your question as if you're looking for other physiological effects. Two that come to mind are:
#2: heat. Flower color and opacity have a great effect on flower temperature.
This can be especially important for arctic and alpine flowers. Many of these are not only shaped like satellite dishes, but even pivot to follow the sun. This creates a warmer micro-environment which can be important to attracting pollinators and to increasing/speeding seed production. (See, e.g. Mølgaard 1989)
#3: UV protection. Certain pigments can be more effective at filtering UV.
I work in the alpine and occasionally encounter "glasshouse" plants, which have translucent floral parts that act to create warmer microenvironments, with the same effects as above. In addition, these floral parts have been shown to be more effective at UV filtering than green floral parts (Tsukaya 2002)
*edit: as these papers are behind paywalls, I'll also point out that the Wikipedia pages on Heliotropism and Rheum nobile contain similar information.

 Mølgaard P. 1989. Temperature Relations of Yellow and White Flowered Papaver radicatum in North Greenland. Arctic and Alpine Research 21: 83–90.
 Tsukaya H. 2002. Optical and anatomical characteristics of bracts from the Chinese “glasshouse” plant, Rheum alexandrae Batalin (Polygonaceae), in Yunnan, China. J Plant Res 115: 59–63.


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Antigen Antibody reactions during blood donation
A person wih blood group O is called a Universal Donor. Well, his plasma contains antibodies A and B. During blood donation, if blood group O is given to a person with blood group A (since blood group O can be donated to all the blood groups) then wouldn't the antibodies of the donor with blood group O harm the recipient?
Although nowadays doctors prefer giving blood having 100 percent compatibility...

The key feature of type O blood as "universal donor" is that the incoming red blood cells have neither A nor B antigens and so the resident antibodies (anti-A , anti-B) will not react with them. Since transfusions are carried out with packed red blood cells the plasma antibodies of the donor don't matter - they will not be introduced into the recipient.

For plasma donation the reverse is true, O is the universal acceptor and AB is the universal donor.

@AndroidPenguin What if the entire blood is donated instead of just RBC's would that affect the receiver?? Well i would also like to know why the reverse is true in case of plasma donation??

That would cause the cross reaction effects you'd imagine, and so hence neither is done

ok, it really cleared my confusion thanks....

This is because the Group A or Group B recipient's plasma contain soluble A or soluble B (antigen not bound to red cell surface). These free antigens will bind to the antibodies from the donors and prevent it to react on the red cell surface antigen A or B. The other thing is usually universal O should be low titer Anti-A or Anti-B.

Welcome to Biology.SE. Please add one or more references to support and strengthen your answer.

If red blood cells have no A or B antigen on its surface it means it O blood group.it is said Universal donor bcz no antigen antibody reaction take place the reason is that it has no antigen for any antibody

Since a person with blood group O does not express the A and B antigens, his blood does not contain antibodies to A and B. Therefore, it is safe to transfuse into someone with type A, B, AB, or O blood.

(http: // anthro.palomer.edu/blood/ABO_system.htm) well the table given here states the presence of both the antibodies anti a and anti b in a person with blood group O.