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Trying to identify a beetle seen in Ontario, Canada...and its babies, or parasites?
I'm trying to identify a beetle I took video of in July (around 2010) in the Muskoka region of Ontario, Canada. Attached below is a still frame.
I've done some googling and was thinking this was a Milkweed Leaf Beetle because of the orange and black stripes. This beetle however has an interestingly marked green head, and Milkweed Leaf Beetles appear to only have a black head.
I'm especially curious to know if the smaller insects on this beetles back are its young, or some type of parasite.

I've just posted the original video to youtube. It's right here: Beetle Video....and a GIF below

Nice photo - could you give a bit more detail on where/when you found it? Thanks.

Thank-you. This is from about 10 years ago - and was shot sometime in July in the Muskoka region of Ontario, Canada.

In the future, please [edit] your original post. Comments are ephemeral and often overlooked, so they should not be used to convey information important to answering the question. Thanks!

@OrbitRob can I convince you to save a bi of your video as a gif and upload that directly to your post here? www.ezgif.com makes this process very easy. (you can upload your video, crop the length, and optimize to make the gif <2mb so SE lets you add it. Hope you consider it. thanks!

@theforestecologist - haven't logged in for awhile! I added a GIF like you suggested. Happy Holidays! :0)

Thanks to pascal's answer, I looked at the genus Nicrophorus and agree that this is some member of that genus. (The spelling Necrophorus has been used in the past but is now deprecated.)  The 60+ members of this genus are commonly known as burying beetles or sexton beetles from their behavior of burying dead small animals to serve as nourishment for their offspring.
However, instead of N. vespillo, I think the species might be N. tomentosus:
(Photo: Judy Gallagher via Wikimedia Commons)
The most distinguishing feature seems to be the green or gold hairs on the thorax as seen clearly in the large version of OP's photo. These hairs or setae Wikpedia mentions as separating N. tomentosus from other members of the genus.  A common name for the species is "gold-necked carrion beetle". Two other photos of this species are here and here.

Great picture. I like how the mites have placed themselves 'in colour-co-ordinated formation" on the beetle's back! Thanks for your help and FYI i've just added a link to the original video below the main photo in my question. Rob.

I compared what I could see in the OP photo with the identification key given in The Insects and Arachnids of Canada Part 13 (online here), and can confirm this specimen as Nicrophorus tomentosus.

I think I agree with mgkrebbs that this is N. tomentosus but the members of this genus are all very similar to one another. The part of your question that inquires about the "smaller insects on this beetles back" is of interest. They are not insects, they are mites.
The behavior of these mites is called "phoresis" and there is a good illustrated article here about it. The mites are simply using the beetle for transportation to food. The beetle is better than the mites at finding dead animals and is able to fly. This species of mite has evolved the lifestyle of a "hitchhiker" on the beetle. They have therefore become dependent on the beetle, but they are not a parasite, because the beetle is not harmed. In fact, there may be some benefit to the beetle, which would make this a mutualistic relationship.

Great info. Much appreciated! ...and FYI i've just added a link to the original video (it shows the mites moving around) below the main photo in my original question. Rob.

First clue that the mites are not the beetle's young are they've got 8 legs to the beetle's 6.

re: "there may be some benefit", from the linked article: "[the mites] feed on fly larvae and nematodes, which are competitors of the beetle"

This is a beetle of the species Necrophorus vespillo (or a relative), very common beetles. It is parasitized by some mites. A similar picture as yours can be found on this page. I like it very much! We can see on the external page, that those little creatures are mites.

(Picture from wikimedia commons)

Thanks for your help Pascal and FYI i've just added a link to the original video below the main photo in my original question. Rob.


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How many neurons are stimulated by electrodes in memory engram experiments?
Researchers have recently identified "engrams" in the mouse hippocampus, "sparse populations of neurons" or "small clusters of cells", stimulation of which elicits a specifically trained fear memory association. For example...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4874022/
http://www.nature.com/nature/journal/v484/n7394/full/nature11028.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331914/
http://www.smithsonianmag.com/innovation/meet-two-scientists-who-implanted-false-memory-mouse-180953045/
My question: Roughly how big -- how many neurons -- are the regions stimulated in these experiments? I looked through a number of papers and was unable to find this information.
10/18 -- Changing the title and wording to clarify that I am asking just about experimental procedures with electrode implants, not fMRI studies, and not about how engrams might actually work.

It's possible no one has measured accurately yet, but a more likely explanation is that it varies. I would assume that different memories take up a different amount of space - I have many detailed memories of my wedding day, for example, but not so many of the soccer game my child played in a month ago - it was very wet, that's all I remember :). So, it would make sense that, since the wedding memories are much more detailed, and there are many more of them, more neurons would be assigned to hold them.

I understand that there probably isn't a standard fixed size, though there probably are specific figures for the studies in question, but for some reason that is not published. I'm just looking for an order of magnitude to go with "sparse populations" and "small clusters". Is it 10, 100, 1000, whole fMRI voxels (100K-1M, which I doubt), etc.? IOW, how finely can implanted electrodes read and stimulate neurons?

edit: More directly answering the initial question, thank you, I misread what you wondered and was mislead a bit by a previous comment and your response to that comment.
In these experiments, they are using optical, not electrical techniques. Therefore it is a bit difficult to estimate exactly the number of cells activated directly, because light will scatter in the tissue but also fall off with distance. Based on the density of labeled and affected cells (to be stimulated, the cell has to be both a) labeled by a virus injection, and b) active in the engram) pictured in the second link you included, it seems like no more than a few to a couple dozen cells would have been activated directly.
In your comment, you said "IOW, how finely can implanted electrodes read and stimulate neurons?" - this is a different question. Implanted electrodes can read from and stimulate single neurons, or populations, depending on the electrode and experiment. It is difficult to target particular neurons with electrodes without an additional optical technique.
In the experiments you reference, optogenetic tools are used to selectively label cells that were active earlier in an experiment, and then reactivate those same cells with light. These sorts of experiments have only become possible recently with the development of those tools.
(original answer below)
Standard answer of biology applies here: "it varies", probably by species, type of memory, brain structure, etc.
But, to give you some ideas, one area that has been studied a lot in this field is the dentate gyrus of the hippocampus (the second and third links you sent, for example). One paper showed that a given memory activated something like 2-4% of the cells in that structure in a mouse http://www.sciencedirect.com/science/article/pii/S0166432811006462 with something like 1,000,000 dentate gyrus cells total in a mouse. So, that's a lot of cells, but those cells might be doing something special (pattern separation), so maybe it isn't right to think of them as the "engram" itself, or maybe we should be counting them PLUS all the cells activated in CA1, PLUS all the cells activated in cortex, etc. Whatever the case, one thing that is clear is that cells are involved in many many different engrams - if you are familiar with pop neuroscience you might recall the excitement about "grandmother cells" and "Jennifer Aniston" cells from a few years back. That's almost certainly not how engrams work, but that out of the subset of neurons and stimuli they examined, there was only limited overlap in those cases.
For fMRI studies, it's pretty hard to get a handle on the number of cells involved, but it isn't really possible to measure from "small clusters of cells" in fMRI on the same scale as in other measurement techniques. What is going to be more important for the fMRI decoding studies is "variation within a brain region" where the total number of neurons is many many millions, but the exact number involved in any one engram can't be measured with current technology.

Thanks @Bryan, but this does not address my question. I am not asking about fMRI images -- voxel cell counts vary but are well-known (for example -- link). I am asking about the reverse problem, stimulating cells directly and observing behavioral results. How many cells are stimulated in such experiments -- just roughly? So it's just about the experimental procedures, not about how big engrams are or how they are structured (which I agree is a tough question).

BTW, I am also interested in how many neurons are typically observed in experiments with implanted receptors. Again, this is just a question about experimental procedures, and not abut fMRI, but electrode implants in animals (and occasionally in humans as adjunct to medical procedures).

Hi David, hope the edits help a bit. To add more to your comment here, with a single electrode, one can either record action potentials/spikes from a single neuron, or a population of dozens (but not easily discriminate them from each other), or record "field potentials" which correspond to membrane currents in hundreds to thousands of cells (this would be like a "very local EEG").Electrodes with multiple recording sites (often "tetrodes") can record from a few cells at once. Many implants especially in larger animals may have dozens of electrodes.

yes that helps a lot -- thanks, and sorry for my sloppy wording and my neglect/ignorance of the role of optogenetics. And that's my clue -- searching it turns up this SciAm article by Diessseroth -- link which gives me the impression that it can stimulate a single neuron under some circumstances. But the figure you give -- up to a couple dozen -- is what I need. So you get the bonus.

Yep; if you either a) Shine light on only a single cell (most likely using 2-photon techniques or some other new tricks people are starting to use), or b) Express the gene in only a single cell in the light path, only that one cell would be affected. In the experiments you referenced, they shine light out of a 200um fiber optic cable placed into the brain area of interest. link has some information on how you can expect the light to travel out of the fiber and into brain tissue.

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Using egg whites as DNA destruction test possible?
My current theory to test for the destruction of any DNA that may be used as forensic evidence is to use an egg white. I would like to test various myths and methods for destroying DNA evidence and need a sure-fire method of testing whether or not the DNA is destroyed. The reasoning behind the egg white is because when you cook one or expose it to strong acids or bases, it turns white. Indicating the denaturing of the proteins within the whites. Would this work to test for the denaturing of DNA molecules to? Several experiments would be conducted with each method, using egg whites to determine whether or not the DNA would be destroyed. Would egg whites, with great accuracy, determine whether or not the sample can be identified. If not, could you please suggest another alternative?

just a side note: do you want to destroy DNA (e.g. remove traces of DNA presence) or damage it so that investigator won't be able to assign given DNA to particular person?

@aaaaaa First I'd try damaging DNA and then move on to removing any trace of it.

what is the end goal of this project? BTW this community does not support illegal activities

@aaaaaa Mabye create a youtube series and destroy the myltiple biohazardous samples ive collected from myself over the past month.

This isn't a valid test as egg white contains a lot of proteins and DNA is chemically completely different. For example you can heat DNA several times to 95°C and you will not damage it (in fact it renaturates when cooled down slow enough), but this is not possible with proteins. "Biohazard samples" (whatever this means in your case) are deactivated either by autoclaving or by incubating the cells/tubes/whatever with chlorine bleach. Both methods work well and are approved in labs.

Egg white would not destroy DNA. Egg white is composed primarily of proteins. How does denaturation of proteins upon heating in any way link with the proteins being able to destroy DNA? Since your hypothesis is not correct, the question is unclear.

@WYSIWYG I am not stating that the egg whites will be used to destroy DNA, instead I'm asking whether egg whites can be subjected to the same treatment and indicate if such treatment would have destroyed DNA. That is if I had enough DNA material and replaced the egg whites with DNA. I am trying to find a cheap solution to test whether or not the DNA would have been destroyed because I do not have the equipment to do so. Mabye try a bit more to comprehend the question next time.

@Chris Thank you. This should have been used as an answer, exactly what I was looking for. And the samples are mainly blood. Though I dont have an autoclave, I will use a NaOH and NaClO solution.

@TommyWoldt This was more a quick comment - but I can make it an answer later if you like.

@Chris I dont think that the question is going to be "unholded".

Cooking DNA will absolutely not destroy it. Few things will actually destroy DNA. Bleach is one of the only common substances that will do it.
To test for DNA quantity you need to perform qPCR. The equipment is $20,000+.

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How to get only perfect matches with blastn?
I have installed Blast locally and I've configured the nucleotide database to use. I want to search some sequences (from a .fastafile) in this genome. So I used blastn:
blastn -db NewDb -query input.fasta -out blast.txt

Then I added some options to require a 100% identity and no gaps:
blastn -db NewDb -query input.fasta -perc_identity 100 -ungapped -out blast.txt

But I still have some results where only a subpart of the string is matching the genome:
BLASTN 2.2.29+

[…]

Database: […].fasta
           20 sequences; N total letters

Query= Mutant M :

Length=226
                                                                      Score     E
Sequences producing significant alignments:                          (Bits)  Value

  chrom19                                                               435   3e-122
  chrom2                                                                429   1e-120

> chrom19
Length=W

 Score =   435 bits (226),  Expect = 3e-122
 Identities = 226/226 (100%), Gaps = 0/226 (0%)
 Strand=Plus/Plus

[…]

> chrom2
Length=Y

 Score =   429 bits (223),  Expect = 1e-120
 Identities = 223/223 (100%), Gaps = 0/223 (0%)
 Strand=Plus/Plus

[…]

Both results have an identity score of 100%, but the second result only use 223 of the 226 bases from the input sequence.
What parameters can I use with blastn to get only perfect matches, with 100% identity and all the nucleotide bases from the input sequence used?

From my experience, I don't think this is possible. BLAST was designed to find many distant hits, so it wasn't made for this very strong requirement of identical sequences. But you can probably filter it afterwards, no?

If you want perfect identity, won't a simple string comparison program (in any language) do the job?

Yeah I concur with @MarchHo. Just do a string search. You can use grep

this might be of help: http://seqanswers.com/forums/showthread.php?t=27735

@MarchHo in fact it was my first test, I used BioPython in order to read the genome and sequences. Nothing matched but now I realize it was due to the fact that the sequences can be backwards or complementary of the genome.

Agree with @MarchHo. Would rather use Perl =~ operator for matching (used as $template =~ /query/) than grep. And yes Blastn was not designed for that and will match smaller sequences that are 100% similar.

This is a grep question rather than a blast issue, and nothing much to do with biology. I'm voting to close it as off topic.


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Is evolution a fact?
Richard Dawkins in one of his videos says that Evolution is a fact and not just a theory.
He goes on to say that man and chimpanzees both evolve from apes.
Is this correct (Is evolution a fact and did humans & chimps evolve from apes)?

Yes. But Dawkins talks like this because of a cultural context, which is the struggle between science and some religions over the proper method for belief formation.  A minority of religious believers wish prescientific texts to have authority over scientific evidence.  Historically, when science has challenged religious authority, it has often been violently suppressed.  Nowadays, attempts to overrule science more often rely on bad methods, poor understanding, and misleading rhetoric.  Dawkins's statements of our scientific knowledge often lack nuance but help immunize the credulous masses.

@ShirgillFarhanAnsari: Lots of interesting and important things cannot be duplicated in a laboratory. However, you can extend laboratory-gained knowledge and apply it to things observed in the real world - e.g. dating objects using timings from decay of radioactive isotopes. Science is not limited to lab experiments, although knowledge from them can be considered more robust due to repeatability etc.

Don't confuse "evolution" with the "Theory of Evolution". "Evolution" is a fact. But the "Theory of Evolution" is an attempt to describe/explain how "evolution" happens in life. "Evolution" is fairly simple and it's easy to demonstrate its existence. But the details of how it works across all life forms in nature are many, complex and varied. Some of the details have possible variations, so some of the details are disputed. It is irrelevant to the fact of "evolution" that the complete "Theory of Evolution" is not finished. The theory is still a work-in-progress; the simple fact is not.

This question and its answers is mainly dealing with how you translate between scientific statements and common-language statements, and how the same words are used differently in the two domains. Therefore, this is mostly a question about semantics and the philosophy of science (at least until the words used by the OP is better defined), not about biology, and I vote to close. There is basically no hope of an Answer to this Q without clearer language, which the disagreements in the answers and comments show quite clearly.

The question has the default of improperly using the terms fact and theory and their definitions is a question of philosophy and not of biology. However, I think we should keep this question. The excitement it provoked probably shows the need for a declared position on our community. I also think that such post may come handy for future reference on Biology.SE even though the main answer is not trying to demonstrate a point but only to clearly explain the position of the scientific community.

Comments are not for extended discussion; this conversation has been moved to chat.

I've edited this to make it less about the is evolution a fact or theory? component (which will illicit opinionated answers) and focus more on the how do we show that humans and chimpanzees have a common ape ancestor? side of things (which should be able to get solid, fact based answers)

Minor point compared to the others, but you understand humans and chimpanzees are apes, right? Homo sapiens is literally the type species for the Hominoidea (apes). Saying we've evolved from apes implies we're not apes any more; it's a strange way to put it.

its the only origin of species that cannot be proven false, and is proven true in every test it has gone, geologically, DNA, physiology, berhaviouraly, and other tests all test know to man have confirmed evolution.

Humans and chimpanzees are both species of apes that evolved from another species of ape.

A tiny bit of terminology
Fact

In popular culture, the term fact means "something that is true". I would consider a theory as being the closest concept in science to what is called a fact in the population culture.
In natural sciences, the term fact is rarely used but would have the same meaning than the one in popular culture. The reason we are not often using this concept is that in science (nor in any other field of knowledge) one can never definitely know the truth. We can only have evidence that are congruent with a hypothesis or body of statements. In such case we talk about theory (see below).

Theory

In popular culture, "theory" is used to mean what the natural sciences call a "hypothesis."
In the natural sciences, a theory is a body of thoughts/statements that is very well supported by loads of evidence. In science, a theory is not a hypothesis. For example: Theory of evolution, Theory of general relativity, transition state theory, etc. Note by the way that various definitions of theory are in use (ref.). The below answer respects the definition that I gave above.

The scientific terminology presented above is actually a matter of philosophy and not science. If you need more information about the definitions of "theory", "fact" and other related terms, you may want to ask on Philosophy.SE. Stephen Jay Gould summarized the concepts of theory and facts nicely when saying

[..] facts and theories are different things, not rungs in a hierarchy of increasing certainty. Facts are the world's data. Theories are structures of ideas that explain and interpret facts.

In the answer below, I am using the scientific terminology.
Your questions

Is evolution true?

Evolution is what is called a theory in natural science (The Theory of Evolution a.k.a. modern evolutionary synthesis), and it is extremely well-supported. Evolution is NOT a hypothesis. In other words, we have a lot of supporting evidence that living beings have evolved and are evolving.

Did both humans and chimpanzees evolve from apes?

Humans and chimpanzees are apes (great apes to be more accurate). Both humans and chimpanzees evolved (and are still evolving) from a common ancestor who already was a great ape. We have a lot of evidence to support this common ancestry.
What does the theory of evolution say?
Understanding Evolution (by UC Berkeley) is a short and introductory course to evolutionary biology. Of course, there exist other good sources of information online such as Evolution and the tree of life by Khan Academy.
We have a number of posts providing book recommendations for

General biology (Books for beginners and Introductory biology text for an outsider)
Intro to evolutionary biology (Text Book Recommendation: Organic Evolution and Introductory books about evolution)
Intro to evolutionary genetics (Books on population or evolutionary genetics?)

You will also find a lot of introductory posts on biology.SE such as for examples:

Why do some bad traits evolve, and good ones don't?
Is there a biological mechanism for evolution encoded into our DNA?
Does it make sense to classify all humans in a single species?
Why is a heritability coefficient not an index of how “genetic” something is?
How could humans have interbred with Neanderthals if we're a different species?
If dinosaurs could have feathers, would they still be reptiles?
Why does evolution not make our life longer?
Why don't mammals have more than 4 limbs?
How to define “evolution”?
How did some humans evolve to be white?
Who are humans' closest relatives, after primates?
Did cats evolve from monkeys ? or vice versa?
Why do the ancestors of birds still exist?
How does Natural Selection shape Genetic Variation?

What are the evidence?
Demonstrable and repeatable examples of evolution lists sources that list evidence. There are probably thousands of pieces of evidence listed in total, all explained in lay terms with links to the original article. Of course, this is just a small sample of the evidence we have.
The post Is there any biological evidence that is not suggestive of or seems to disprove evolution? might be of interest too.

Thanks to @CortAmmon's comment for correcting a very poorly phrased sentence.

-1.  If you are going to answer the question of "is evolution true," you should use correct phrases.  We cannot say "We know for sure that populations of living beings evolve," but rather we must say "we have observed data consistent with the theory that populations of living beings evolve."  If we're going to answer one of the most contentious questions in science with "science is right," we are obliged to be very careful with our words.  Jumping from "evolution is well supported by evidence" to "evolution is true" is a tremendous faux pas.

Because my degree is in mathematics, and also by observation of how the word is used in science, I think this definition of "theory" in the natural sciences is completely incorrect. A theory is a description of some aspect of the world, complete with explanatory and predictive power. Whether it's correct or incorrect doesn't affect whether it is a theory. Newtonian mechanics remains a theory despite having been disproved. Superstring theories remain theories while awaiting experimental tests. In most cases (but to the dismay of logicians), "theory" could be replaced with "model".

Comments are not for extended discussion; this conversation has been moved to chat.

@WYSIWYG I am not pleased my comment has been removed. That was for others to see to place this answer into perspective. It was not a discussion, but a pointer for 'blind' upvoters only seeing the upvote score. Not appreciated to remove that. Biology.SE should pursue a high level of answering including citations to the scientific literature.

Thank you for your comments. Following your advice, I made a few edits to clarify my point. I think it is not desirable that I talk further about terminology as the question is not a question of philosophy about this terminology but a question about biology.

@AliceD comments are second class citizens on Stack Exchange by design. Expect them to be removed liberally.

@corsiKa- might be, but here at Bio comments are usually dealt with pretty seriously. They are not just removed. There are meta posts on it in fact. Answers with many upvotes on questions with >1k views draw more attention. The amount of comments should therefore be viewed at in terms of how many folks  are posting. A continued dialogue should be short cut. A series of comments by various posters should be left alone. But this discussion should be done at meta :-)

Evolution is considered a theory rather than a fact because to earn the label "fact" something must be reproducible.  Since evolution is a mechanism of action rather than a specific outcome it is inherently incapable of ever reaching this standard.

I see where you are coming from with this answer, but still think that it's  very misleading. In the middle of the answer you are indirectly implying that all scientific theories are "true", when scientific theories actually have different levels of support (Your argument: evolution = well-supported scientific theory --> evolution = true). You can very well have parallel scientific theories at the same moment in time (sensu Lakatos' Research programmes), and it is relatively meaningless to say that they would all be "true" on the merit of being scientific theories with some level of support.

A scientific theory is a structure of conjecture to explain an observed fact. The theory may be wrong, but that doesn't mean that the observed fact is untrue. Newton's theory of gravitation was a bit wrong, but gravity remained a fact. Darwin's theory of evolution might be a bit wrong, but evolution would remain true, we would just explain it slightly differently.

I don’t believe in deleting comments but the ones by J. C. Leitão and Cort Ammon, and the fact that they are so prolifically upvoted, reflects poorly on the community: They parrot an extremely naïve understanding of Popperian theory of science. People, please, don’t become so reflexively defensive of science that you put the meaning of words on their head. Of course science can prove things, and we can say that things are true. This isn’t “being careless” with words, but rather using words exactly the way everybody understands them. To say that “‘evolution is true’ is a faux pas” is inane.

@AliceD The comments are moved to chat and not really removed.

@Remi.b Please flag comments as obsolete if you have addressed the issues raised. As such I feel that this question shouldn't have been alive for so long +26 votes is infinitely more than what it deserves.

It is not the theory of evolution it is the theory of evolution via natural selection, we can directly observe evolution  the theory is the mechanisms behind it, this is why it is called the theory of general relativity not the theory of gravity.

@John It is actually called the modern evolutionary synthesis. Expressions like "theory of evolution via natural selection" would be very misleading given that natural selection is just one of several evolutionary processes.

@remi true, well depending on how you define natural selection, It just annoys me that people use theory of evolution as it it is a complete term, that organisms evolve is not a theory, why it happens is.

I understand your point. That's how theories are usually named though. The theory of gravity does exist. It is not the "theory of gravity by the concepts of inertia and other things, F=ma kind of things"

A scientific fact is something that is true. A fact cannot be proven false. This is no different from the common usage of the word. However, in science, we often do not definitively know what is true. Therefore, scientific facts tend to be observations based on specific evidence.
A scientific theory is a well-supported and rigorously tested explanation of a phenomenon.
These definitions are consistent with those given by the National Academy of Sciences.
In science, we use a body of facts to arrive at a theory. Science is a discipline of likelihoods, confidences, and uncertainties. We gather evidence to improve our confidence and minimize the uncertainty of a theory. This is how we arrive at a very likely explanation, such as the theory of evolution.
But we do not draw facts from theories - we draw theories from facts.

+1 for your answer, specifically the last sentence. Very well put and is one of the key principles we scientists hold sacrosanct (or should at least).

Re, We do not draw facts from theories.  Actually, the best theories predict new phenomena which, if tested, and found to be true, lead to new discoveries and advance our total body of knowledge.  I don't really keep up with evolutionary theories, so I'm sorry to say I can't cite any examples from that field.

@jameslarge precisely. Facts lead to theories which lead to predictions which can be confirmed as fact after experimentation and/or observation. Theories can lead to facts but do not produce them.

Can you give an example of a scientific fact?

@corsiKa An example would be: Say bacteria were experimentally treated with antibiotics. A fact is that 1% of those bacteria survived. Our theory is that those surviving bacteria are resistant to the antibiotics due to genetic mutations which confer a selective advantage. We can then validate and refine this theory by conducting another experiment to generate more facts. Certainly theories help us target further experiments, but the the facts that arise from those experiments are independent of the veracity of the theory.

That is not a fact. That is an observation. By your own definition, a fact cannot be proven false. That observation could indeed be proven false if better methods of detection and analysis are used on the data later. "Wow, before we observed 1% bacterial survival, but upon reexamination of the data collected, it looks like 3% survived!" I would go so far to say "There is no such thing as a scientific fact."

james, that is exactly my point - facts should not be possible to accept or reject. Thus, my statement "There is no such thing as a scientific fact." If we want to use the word fact as the common person does, that's fine. But we should not call it a scientific fact. Being precise with our language is important.

@corsiKa No, the 1% figure was and is true based on my methodology. Your methodology may produce a different number. Both observations are true; however, you may give one more precedence during interpretation, and in refining your theory. You may decide that my fact is inappropriate or irrelevant evidence for the theory, which is perfectly fine.

@corsiKa We can get even deeper than that and cay that 1% figure is a statement (about an observation, made by an observer supposedly using a methodology, ...) - this rabbit hole lead rather deep into philosophy with a sidetrack into psychology and sociology (e.g. if a figure is published there is no way to know if it's about a fact; you can only get your own figure or form a belief). So while you are certainly correct, you are considerably deeper in this hole than vervet seems to be. Probably the OP did not want it that deep or he'd ask on philosophy.se or something.

@EugeneRyabtsev I disagree. The entire discussion hinges on the definition of a fact. The word is used differently in different contexts. That said, I believe we're all saying the same basic things, but we simply have a different threshold for accepting common-usage versus precise scientific usage.

Tl/dr: No, evolution is not a fact (unless your definition of fact defines evolution to be a fact, in which case it is a fact...).  And if that phrase ruffles your feathers, it suggests you should read the rest of this answer.  I usually wouldn't put the Tl/Dr here on this particular topic, but apparently people have been unhappy with my answer being burred in it.
Richard Dawkins is a very loud personality who has demonstrated a consistent interest in silencing dissenting opinions.
Evolution is a theory which seeks to explain the world and predict future events.  It has entered a special class of theories where we have observed so much evidence to suggest that theory accurately models our world that people find that society operates smoother if we pretend that it is 100.00000% true.  In reality it is not.  It could be wrong.  However, we in society have a choice: we can pretend it is 100% true, or we can acknowledge that there is a tiny shred of doubt that must exist due to the nature of the scientific process.  In general, we have found the negative impact of pretending it is "true" is much smaller than the negative impact of people hearing that there's some doubt and presuming there is more doubt than there really is.
In my opinion, what has made evolution so tricky in the political world is that those who understand science well enough to actually understand what is meant by the statistical data captured to support evolution are generally happy "rounding up" evolution to 100% true, because they understand how to use the statistics, and there really hasn't been enough of an advantage to keeping track of the sliver of doubt.  Science always has a sliver of doubt, so they're always watching out for it anyways (no scientist is going to say "you can't be alive" to a new species because it didn't fit the model).  Those who find enough value in that doubt to take the time and energy to call it out by name typically do not have enough of a science and mathematics background to really comprehend what that level of doubt is, or how to manipulate it, so there is a trend of them doing so poorly and coming to very questionable conclusions. Probability is full of such cruel scenarios, such as the prisoner who runs at a wall repeatedly, once every second, and you may be asked to calculate how long it will take for him to have a 50% probability of quantum tunneling through the wall to escape.  Depending on the numbers, that timeframe may be more or less than the heat death of the universe, but the probability is absolutely there, and its never zero! (hint: if you get in prison, try to get out on good behavior... the running at the wall solution isn't the best approach)
In the end, it's all linguistics.  An interesting tangent is the use of "fact" in philosophy.  In philosophy, "fact" doesn't always mean exactly what you may intuitively think it does.  Many philosophers declare that an auditory or visual hallucination is a "fact" because it meets the philosophical definition of "a state of affairs," lending itself to strange phrasings such as "a fact about something which is not real" and other linguistic oddities.

EDIT
I pose a statistics question to you.  Your answer to this statistics question states how you approach the definition of some very key words, so the answer as to whether evolution is true or not will depend on them.

I flip a coin multiple times.  There's no reason to presume it's a fair coin, so no reason to presume P(heads) = 50% like in so many coin tossing problems.  I flip the coin a million times.  It lands heads every time.
I am about to flip the coin again.  Is the statement "The coin will land heads up" a true statement?

If you answer "no," because the coin flipping problem is in the domain of statistics, and statistically prior observations do not define the results of the next flip (though they obviously suggest at it), then your answer should be "evolution is not necessarily true," There's an extraordinary body of evidence supporting the claim statistically, so we can certainly make the claim "we are quite confident that evolution is true," but we cannot take the leap to declare it is "true" because we are basing our position in the statistics that form the foundation of modern science.
On the other hand, if you answered "yes," then you may state "evolution is true" to your hearts' content.  You have made the presumption that a bunch of evidence is the same as truth.  Of course, you make that statement without the backing of mathematics, so you don't actually have any proof to back your statement.  You are, in fact, making as religious of a statement as the claims that evolution is false made by creationists.  You are declaring something to be true, simply because you believe it to be true.
Why do I make such a big deal about this?  Because claims such as "evolution is true" are making it harder and harder for people who do not believe in science religiously to accept the results of science.  If I can talk to a creationist about evolution, I can get them to understand our POV in about 5 minutes... but it takes 30-50 minutes of battling them to get there.  Why?  Its because they have been told over and over a point of view about what science claims which is not technically accurate and conflicts with their beliefs.  The overstatement of the confidence in evolution from "very confident" to "100% proof positive without a doubt confident" actually gets in the way.
So please, decide which version of the word "true" you wish to use, the mathematical one or otherwise, and make your statements accordingly.  Just know that the mathematical rigor behind the study of evolution is only applicable if you're using mathematic's definition for key concepts like truth.

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Evolution is similar to gravity: we don't yet have complete explanation for either, but it would be pretty stupid to pretend that they are not real physical phenomenon ("fact") with all the supporting experiments humans have done over time.

@MikkoRantalainen The devil is in the details with such linguistic claims.  Gravity is an amusing example.  If I may use a slightly different phrasing than you did, consider the phrase "gravity is an attractive force between two masses." (recognizing that isn't your claim... work with me for a moment)  Such a statement might be deemed a fact until 1915, when General Relativity demonstrated that gravity is not a  force.  One can certainly add a few dozen additional words about phenomenology and human scales to clarify...

...but in the end, a "theory," as defined in science, is really awfully big to just boil it down to its name and say "X is a fact."

None of the answers so far have really provided much evidence, so here is a small sample of the peer-reviewed articles, based on genomic information that provides the facts that we know so far that provides us with the evidence to draw the conclusions that we do.
Morris Goodman, The Genomic Record of Humankind's Evolutionary Roots, The American Journal of Human Genetics, Volume 64, Issue 1, January 1999, Pages 31-39, ISSN 0002-9297, http://dx.doi.org/10.1086/302218.

Provides an overview of the sameness of the Human and Pan (chimpanzee and bonobo) genomes and also goes through other similarities such as extended gestational and postnatal upbringing for humans and Pan. Discusses similarities uncovered through observational studies that "chimpanzees are emotionally complex and intelligent."
It goes on to discuss phylogeny, different classifications and the history of some of the branching of species.

The Chimpanzee Sequencing and Analysis Consortium, Initial sequence of the chimpanzee genome and comparison with the human genome, Nature 437, 69-87 (1 September 2005) | doi:10.1038/nature04072; Received 21 March 2005; Accepted 20 July 2005 Here the abstract probably best defines the contents of the journal article.

Here we present a draft genome sequence of the common chimpanzee (Pan troglodytes). Through comparison with the human genome, we have generated a largely complete catalogue of the genetic differences that have accumulated since the human and chimpanzee species diverged from our common ancestor, constituting approximately thirty-five million single-nucleotide changes, five million insertion/deletion events, and various chromosomal rearrangements. We use this catalogue to explore the magnitude and regional variation of mutational forces shaping these two genomes, and the strength of positive and negative selection acting on their genes. In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles. We also use the chimpanzee genome as an outgroup to investigate human population genetics and identify signatures of selective sweeps in recent human evolution.

Feng-Chi Chen, Wen-Hsiung Li, Genomic Divergences between Humans and Other Hominoids and the Effective Population Size of the Common Ancestor of Humans and Chimpanzees, The American Journal of Human Genetics, Volume 68, Issue 2, February 2001, Pages 444-456, ISSN 0002-9297, http://dx.doi.org/10.1086/318206. From this paper we are given evidence of the following

To study the genomic divergences among hominoids and to estimate the effective population size of the common ancestor of humans and chimpanzees, we selected 53 autosomal intergenic nonrepetitive DNA segments from the human genome and sequenced them in a human, a chimpanzee, a gorilla, and an orangutan. The average sequence divergence was only 1.24% ± 0.07% for the human-chimpanzee pair, 1.62% ± 0.08% for the human-gorilla pair, and 1.63% ± 0.08% for the chimpanzee-gorilla pair.

The key to this evidence is this; "we selected 53 autosomal intergenic nonrepetitive DNA segments from the human genome and sequenced them in a human, a chimpanzee, a gorilla, and an orangutan."
The significance of this lies in the fact that intergenic non repetitive DNA has very little, if any, selective pressure on it to maintain its sequence. Assuming that random mutations do not significantly alter gene expression, then there is no reason that there should be such high rates of homology, unless we are closely related to these other species on an evolutionary time scale. That being said, if some of those changes do have modest effects on gene expression, whether they are timing of expression in development, levels of expression, or tissue specific expression, then those can result in the differences we witness in the modern versions of the species alive today.
It would not be too surprising to find this level of homology in coding regions of genes across mammals, especially if we looked at the amino acid homology of the proteins encoded by these genes, as mutations in these genes would be under evolutionarily selective pressure. But to see homology this close in DNA in between genes suggests a very close relationship.
Philipp Khaitovich, Wolfgang Enard, Michael Lachmann & Svante Pääbo, Evolution of primate gene expression, Nature Reviews Genetics 7, 693-702 (September 2006) | doi:10.1038/nrg1940
Finally this paper gives an explanation of how gene expression can account for the evolutionary differences seen between Humans and other primates. It is unfortunately behind a pay wall, but here is the abstract of the article to give a sense of what it has to say on the matter.

It has been suggested that evolutionary changes in gene expression account for most phenotypic differences between species, in particular between humans and apes. What general rules can be described governing expression evolution? We find that a neutral model where negative selection and divergence time are the major factors is a useful null hypothesis for both transcriptome and genome evolution. Two tissues that stand out with regard to gene expression are the testes, where positive selection has exerted a substantial influence in both humans and chimpanzees, and the brain, where gene expression has changed less than in other organs but acceleration might have occurred in human ancestors.

Zoonoses and Host / Viral Pathogen Interactions
I should also add that another way we can gauge evolutionary closeness is through host viral pathogen relationship. Viruses have evolved to have a high degree of specificity in their mode of infection, and what works for a virus in humans may be harmless to dogs or birds or mice because the cell surface proteins that viruses exploit to infect the cells of multicellular organisms have a greater degree of difference the further away species are evolutionarily from the last common ancestor. And while there are cases where there will be intraspecies differences that afford immunity, such as the CXCR4 mutation which provides some level of resistance to HIV-1, for the majority of the species, the virus will be able to infect hosts of that species.
Many zoonoses cannot be transmitted between distantly related species. With that in mind, Chimpanzees can catch most all diseases that humans carry and vice versa. Simian Virus 40 has been implicated in human cancers and research has shown that the Human Immunodeficiency Virus originated in Chimpanzees and is called the Simian Immunodeficiency Virus, though the virus proves to be harmless in Chimpanzees.
In contrast cats have the Feline Leukemia Virus, which is highly contagious and can be passed between cats and cause leukemia, but cannot infect humans. Dogs and cats can be infected with life threatening Parvovirus, but humans are not at risk of this infection.
So if you are skeptical of the genomic evidence, then trust the viruses, because they will tell you how closely related organisms are by how effective they are at infecting different species.

Finally a referenced answer +1

It is easily observed that populations of organisms change over time, both phenotypically and genetically.  With some organisms we can observe this over a few days of observation; with others we can use historical records.  Therefore, evolution is an observed fact.
However, most people, by "evolution", are actually thinking of "the theory of evolution through natural selection", which is a theory. In fact, there are a number of explanations for why and how populations change over time.  These include the theories of natural selection, of neutral and nearly-neutral drift, of sexual selection, and so on.  These are of course theories, albeit (for the ones I list here) enormously well-supported theories.
You can compare to gravity. If I drop an apple, it will fall to the ground; if I watch that, it is an observed fact that the apple fell, just as it is an observed fact that the population of viruses I looked at last week changed their genetic composition (that is, evolved) over that period. Newton's theory of gravity is a theoretical attempt to explain why the apple fell.  Like Darwin's theory of natural selection, Newton's theory was wrong, but useful, and like natural selection, other theories have come along to improve on Newton.  (Unlike Newton, Darwin seems to have been almost entirely right, so that the new theories have supplemented but not replaced his theory.)
So yes, evolution is a fact.

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I am not very happy with most of the answers here as they seem to be too ideologically motivated and not so much about scientific reasoning. So I decided to give it another try.
Is Evolution really a fact and not just a theory?
If this is too long for you, let me just say this:
Evolution is an existing phenomenon. There is variation, there is selection and inheritance of traits. This has been studied and there is no scientific doubt that evolution is a process that is happening now and all the time.
Note that I intentionally bolded the word scientific. The rest of may answer will be mostly about science.

In science just a theory is not meant in a pejorative way. Everything that can be disproved, but scientist have not been able to disprove is a theory. The important part is that it must be possible to disprove theories by scientific methods.
In a way you can think of the principle of gravity also as just a theory. If you happen to find mass that does not get attracted by other mass, you would be able to prove Newton wrong. But the evidence of the existence of gravity is so overwhelming that I would not spend too much energy on that :)
So - from a scientific view evolution is a theory with overwhelming scientific evidence. There is so much evidence that among scientist this debate is settled, just like the theory of gravity. The vast majority of the scientific community accepts the theory of evolution as the theory which is most probable to shape life here on earth.
But the attentive reader may have spotted a problem in the last sentence: There is an unlimited number of theories that can explain how the life shaped to a way that we can admire it today.

Long ago people realized that the most important part of a scientific theory is that it must be somehow possible to disprove it. Of course we can create a theory that contradicts gravity where a green-yellowish rectangular slime pushes objects together. Scientists will be able to disprove as long as it is falsifiable.
But if we now give the slime the sneaky attribute that it escapes human senses, we have a perfectly valid theory that cannot be disproved. So if someone would ask you if it is 100% sure that Newton's theory of gravity is correct, what would you answer? You cannot simply dismiss the theory of the green slime, can you?

Okay back to science. Science basically tells you: You can and you even have to dismiss any theory that is not falsifiable. Theories that cannot be disproved are not valid in a scientific sense. Back to your question:
He goes on to say that man and chimpanzees both evolve from apes. Is he 100 % correct?
Is he 100% correct? - Certainly not, we can make a slimy theory that works as well.
Okay, so let's put it in a different way: Is he 100% correct in a scientific sense - This we cannot answer. There may be many now unknown scientific theories that explain life in its current form equally well. But at the moment we only have evolution.

So why then are scientists so sure? Why does Richard Dawkins tell us all the time that evolution is real?
Well scientists are pretty convinced because of two things: Firstly, a lot of scientific evidence has been collected to support the theory of evolution. There are fossils, there is genetic information, there are experiments that validate certain aspects. But what is even more important: Until now nobody could come up with an experiment disproving the key aspects of the theory of evolution.
There is a second important point here: At the moment we don't have any competing scientific theory. The theory of evolution in science is a little like olympia with just one participant. If someone wants you to bet on the winner, what would you do?

I acknowledge that there are non-scientific theories that can explain all aspects of existence equally well, but I want to strongly emphasize that these are NOT scientific theories. You do not have to accept science as an important explanatory system. But if you do, I hope I could convince you that scientific reasoning of scientists regarding evolution makes sense and although there is no way to quantify this believe in 90%, 99%, 99.9% or 100%, there is overwhelming evidence that make people like Richard Dawkins such firm proponents of the theory of evolution.

Evolution is most real. Have a look at this Wicked Cool Phylogenetic Tree from wikipedia:

What it implies is that there is one common ancestor.
EDIT:
I remember my professor telling me that phylogenetic trees work like a cot mobile. During our lectures on phylogenetics he would on occasion pick up the chalk and make crude drawings of three fish of dissimilar sizes on the blackboard. Always three fish. He would then tell us about how the bigger fish eat the smaller fish. The way I interpreted this is that natural selection played a role in what we observe today as protein to protein or gene to gene similarities. That is what this phylogenetic tree represents. I think my professor made the analogy to mobiles not because they go in circles but rather because phylogenetic grouping can be monophyletic where an ancestor with all it's descendants are considered a group, paraphyletic where an ancestor but not all it's descendants are considered a group, or polypheltic where the common ancestor is not taken into account. I pasted this phylogenetic tree with a monophyletic view on the matter.

There are two other great sources to visualize the tree of life: onezoom.org and tolweb.org.

@MakotoKato: I don't think I have said this anywhere, 'Encyclopaedia Britannica is more reliable than Wikipedia'.

@ShirgillFarhanAnsari My point is that it's NOT full of lies and errors.

It is full of arcticles about Transformers toys, though.

This is a circular argument. You cannot use a phylogenetic tree which is created based on the assumption of the evolutionary process as evidence of said process. You could make a good argument if you explained how that tree was made, that it is a map of genomic similarity. As it stands, your answer is not really proving anything, I'm afraid.

@terdon you are right, I added some additional detail

Disproven: https://www.sciencedaily.com/releases/2015/08/150818153509.htm

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


text:
What is the probability of an XX female or XY male?
Homework question

In genetics the chance of having a male or female is 50% for male and 50% for female. Using factorial method and Punnett Square prove or disprove the claim.

My answer
Using the factorial method:
P        XY  * XX

F1     XX  XX  XY  XY

Punnett Square method:
+-----+----+
| XX  | XY |
+-----+----+
| XX  | XY |
+-----+----+

So yes, the claim is right 50% for male and 50% for female.
I want to make sure that I solved the problem correctly using the two methods (factorial and Punnett).

Looks fine to me

It is funny that some may see two different methods here. But yes, it looks good to me too.


text:
Evolution after the development of sexual reproduction
My understanding of evolution is that genetic mutation occurs in individual members of a species, and they become a new species.
Isn't a definition of species a group of genetically similar organisms that are pretty much exclusive in breeding ability?
Wouldn't there have to be a male and female with the same genetic divergence at the same time to make a new species?  What is the popularly accepted mechanism for the splitting into a new species in organisms that require sexual reproduction?

er, not all mutations "create" new species. also, as a side point, the definition of a species is still under debate. You might take a look here and here

My understanding of evolution is that genetic mutation occurs in individual members of a species, and they become a new species.
Isn't a definition of species a group of genetically similar organisms that are pretty much exclusive in breeding ability?

Well, no.
You are correct in that the origin for any new species lies in mutations which occur in individuals and are then passed down through DNA.
You are misunderstanding that simply because a mutation exists in an individual that they become a new species. Take Lactase Persistence as a widely studied example in humans. The majority of the world is lactose intolerant after they stop drinking their mother's milk, but a single point mutation results in the ability to consume dairy products into adulthood. It does not make people who are lactose tolerant a new species, but it does open up a potential new nutrient source, which benefits the people who have it and thus it was passed down successfully over other variations.
In addition to that example, the definition of "Species" is NOT exactly defined. There are many variations, including (but not limited to):
1) A group of organisms that cannot interbreed in the wild.
2) A group of organisms with significantly different phenotypes (appearances).
3) A group of organisms with sufficient* genetic divergence.
*There is absolutely no scientific consensus on how much genetic divergence is necessary to create a new species. We share >95% of our genetics with Chimpanzees, so it's not much - it could be as little as a few key genes out of the entire genome.
So where you define the boundaries of species is up for grabs to some extent, but the most common is what you delineated - when a member of one group cannot interbreed with another group.

Wouldn't there have to be a male and female with the same genetic divergence at the same time to make a new species?  What is the popularly accepted mechanism for the splitting into a new species in organisms that require sexual reproduction?

Nope. Assuming everything necessary for the gametes to produce fertile offspring is present (aka - the chromosomes aren't significantly altered and the gametes are compatible) then a new species emerges through successive generations.
One mother or father gives their mutation to their children, which pass it on to their children, which pass it on to their children, etc. If the mutation is significantly advantageous it will allow the children with the mutation to better survive in the environment, and over time it could become the dominant phenotype that could lead to the creation of a new species as further mutations build in the new group - further differing the generations of the mother/father from the original group the mother/father were born into. Good examples are the HAR - Human Accelerated Regions which are sets of genes that are pretty much the same throughout all other vertebrates, but startlingly different in humans. The HAR did not create humans, but it's thought the mutations contributed greatly to our intelligence - which allowed other mutations to be taken advantage of (like the humble opposable thumb) as our lifestyle changed due to the increased intelligence.
Not all mutations need to be advantageous, though. There's lots of fuzzy areas. If a mutation isn't beneficial, but also isn't that detrimental, it can also stick around in a population. These mutations might not lead to the creation of new species, but can certainly contribute to genetic divergence.

It should also be added that allopatric speciation is arguably the most common form of speciation (compared to sympatric speciation). This means that, often, the only thing needed for speciation is lack of gene flow, time and genetic drift. Add to that the different selection pressures at different locations. However, the different mechanisms of allopatric, sympatric and parapatric speciation are probably better seen as a continuum (Butlin et al. 2008). Generally, speciation is a gradual and incremental process, even though distinct mutations can sometimes surely be important. For a review on the genetics of speciation see Noor & Feder (2006)


text:
What's the longest intron in the human genome?
What's the longest intron in the human genome? Discarding isoforms were a long intron spans more than one exon, i.e. what's the longest distance between two exons without another exons in between.

Short answers: Based on gencode the longest intron for protein coding transcripts, is the intron 3-4 of the transcript ENST00000465127.1 with 1,240,120 bases.
Long answer:
Download the main annotation gff3 file from gencode first. Then run this script:
zcat gencode.v29.annotation.gff3.gz \
| awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}' \
| sort -k1,1V -k10,10 -k4,4g -k5,5g \
| awk -v FS="\t" -v OFS="\t" 'BEGIN {transcript=""; max_d=0; max_line=""} \
 $10 != transcript  {transcript = $10; end = $5; next;} \
 {d=$4-end-1; end=$5; if(d>max_d) {max_d=d; max_line=$0"\t"d;}} \
 END {print max_line}'

It will:

decompress the file
filter only lines that describes exons of protein coding transcripts
append the transcript id at the end of the line
sort by chromosome, transcript and position
calculate the distance between two exons of the same transcript
save the current maximum distance and the annotation line that belongs to it
print out the line of the exon which follows the longest intron. The last column contains the distance.

The output will be:
chrX    HAVANA  exon    38666121    38666309    .   +   .   ID=exon:ENST00000465127.1:4;Parent=ENST00000465127.1;gene_id=ENSG00000250349.3;transcript_id=ENST00000465127.1;gene_type=protein_coding;gene_name=AF241726.2;transcript_type=protein_coding;transcript_name=AF241726.2-201;exon_number=4;exon_id=ENSE00003644052.1;level=2;protein_id=ENSP00000417050.1;transcript_support_level=5;tag=basic,appris_principal_1,readthrough_transcript;havana_gene=OTTHUMG00000161009.1;havana_transcript=OTTHUMT00000363378.1  ENST00000465127.1   1240120

fin swimmer
EDIT:
gencode also includes transcripts that are only predicted, but never seen, or those where it is not sure that they exists. So you maybe want to just include transcripts having a certain transcript support level. For this you have to change the first awk line. E.g. to include only trasncripts with TSL1 change it to:
awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ && $9 ~ /transcript_support_level=1/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}'

You can also define a range, e.g 1-3:
awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ && $9 ~ /transcript_support_level=[1-3]/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}'

In both cases the result will change to intron 4-5 of ENST00000402655.6 with 1096453 bases.

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


text:
Can the protein extinction coefficient be calculated on a 3D structure pdb file?
I have so far only seen programs that work on monomeric amino acidic (1D) sequences, like ProtParam, but now that more 3D protein structure predictions can be trusted, I wonder if there is an implementation of the calculation of a "protein extinction coefficent" that works on a PDB file as input, which could be a multimer (more than one chain).

ProtParam estimates extinction coefficients solely by the number of tryptophan, tyrosine and cystine residues. It doesn’t matter whether your protein is oligomeric or not.
Or are you asking if there is a more accurate algorithm that considers the microenvironments of aromatic residues based on structure? That I don’t know.

Well, it might matter if your protein contained a prosthetic group that absorbs at the wavelength of interest: a haem group, for example (or a pyridoxal phosphate group)


text:
Open Source Variant Caller comparable to GATK Haplotype Caller?
Is there a Variant Caller comparable algorithmically and in performance to GATK Haplotype Caller but Open Source Compliant (non-restrictive use)?

You could also try asking on http://biostars.org.


text:
programmatic fast search of 100-1000 short reads to a public server and obtain list of nearby genes
What are the options for programmatic fast searching of 100-1000 short reads to a public server and obtain list of nearby genes where the reads map?
Input: ~100-1000 short reads
Output: GFF list of genes it maps to or nearby genes
Genome UCSC is restrictive to the number of searches and AFAICS it won't allow programmatic use.
Any ideas? I've asked this question to another forum without much luck:
https://www.biostars.org/p/114124/

i think if you have your script slow down and submit the searches over a longer amount of time this can work with blat/blast

This can be done offline and wont require too much of computational resource.
What you will need:

A fast short read aligner such as STAR or even bowtie (STAR is faster)
Genome sequence (you will have to build index for the genome for your aligner)
A GTF annotations file (get it from GENCODE or any other standard genome repository for your organism of interest)

Before you align remove redundant reads. Keep their counts if necessary.
Align the reads using any of these aligners and obtain the alignment co-ordinates. The default output is SAM format for STAR and a tabular format for bowtie (bowtie also gives SAM).

Column-3 of SAM shows the name of the reference sequence
where alignment happened (chromosome)
Column-4 is sequence start
Column-10 is read sequence. Add the length of this to column 4 value to get stop site.

The columns are tab separated
Now define a window that you define as proximal/nearby (lets say 500nt).
Now all you have to do is find genes that lie $\pm500nt$ from your start/stop sites. In your reference GTF parse for the lines that have the feature "gene".
I am giving an example using awk. You can use any programming language you are comfortable with. Check the GTF format also.
Assuming that you made a file (reads.txt) from your SAM output in this format:
Chromosome <tab> Orientation (+/-) <tab> Start <tab> Stop

I am giving an example awk script:
example.awk
#!/bin/gawk

BEGIN{FS=OFS="\t"}

NR==FNR{
    a[$1 FS $2][$3 FS $4] # store the co-ordinate information from your reads file
    next
}

$3=="gene" && ($4 FS $7) in a{ # quick parse for reference chromosome and orientation

    i=$4 FS $7
    for(j in a[i]){
        split(j,jj,FS)
        if(jj[1]>=$4 && jj[2]<=$5)
            print $0";contained"

        else if($4<=jj[2]+500 || $5>=jj[1]-500)
            print $0";partial overlap/proximal"
        }
}

call it like this:
awk -f example.awk reads.txt annotations.gtf

NOTE: In the above script I have not considered antisense proximity. If you want to allow that then don't parse for orientation. Also gawk version < 4.0 doesn't allow multidimensional arrays. So install gawk>=4.0
The output is by default a GTF because you are printing selected lines of the reference GTF.

If I am going to run this locally, which of the aligners will let me run the system as a client/server? I wouldn't want the aligner to take 5 minutes to load the reference in memory and 5 seconds to align my 1000 reads...

It wont take so much time to load the reference index. STAR uses a binary index and bowtie uses a compressed burrows-wheeler index. Both are quick to load. And if you see bowtie paper they say that one of the reasons bowtie is fast is because it loads the index fast. However, making index from fasta will take some time

These aligners were designed for reads in the order of ~50-200nt. However I don't think they would not work (or work subobtimally) with longer reads. In such a case you can split the longer reads.

I am doing alignment of ~1000 different reads of 50-250nt each, not "1000bp reads"

I am reading SSAHA documentation and it seems to be able to do client/server.

You can implement client/server kind of thing in this also. You just need to make a proper interface. I have used these tools and they work fine. If you want to save time on back to back multiple jobs then you can keep the index loaded in the RAM (for that you need to edit the source-code a bit)


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Why do we need two markers to measure a recombination rate?
In calculating recombination,
Why is it necessary to take into account pairs of loci where one marker is heterozygous?
Why is it necessary to take into account pairs of loci where both markers are heterozygous?

If at least one locus is homozygous
If a recombination event happens between two loci where at least one is homozygous, then you would not see anything. Consider for example the following strand sequences in a diploid individual
-----A-----B----
-----a-----B----

Whether a recombination event occurs or not, the two possible chromosomes passed down to an offspring are
-----A-----B----
-----a-----B----

Therefore, you cannot tell whether recombination has occurred.
If both loci are heterozygous
Now consider the following individual
-----A-----B----
-----a-----b----

If no recombination event has occurred between the two loci of interest then the two possible chromosomes that will be passed down are
-----A-----B----
-----a-----b----

If on the other hand a recombination event has occurred between the two loci of interest then the two possible chromosomes that will be passed down are
-----A-----b----
-----a-----B----

Therefore, you can tell whether a recombination has occurred or not.

You will be a beloved instructor someday (if you are not already).


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Why is the total length of Introns greater than the total length of exons?
I have just been reading that typically the total length of the Exons of a split gene is very much smaller than to total number of its Introns.
Could anyone please explain why this is the case if its correct, why are some genes composed of more non coding DNA(intron) than coding DNA.
Thanks

[..] if [it is] correct [..] Yes it is correct. Please note that a gene is made of other things than just introns and exons (see wiki > gene # structure_and_function).


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How are the words taxa and taxons used interchangeably? When are they different?
I am confused about the terms "taxa" and "taxon". In one video lecture it is said that

Dolphins represent taxa at a very low level, while fish has a litter higher level of taxa than dolphins and once again animals are at higher level of taxa.

Dolphins exist in forms of various sizes so it will represent taxa. I have considered taxa to be the taxonomic group when it combines together.
In the definition of taxonomy, why is this taxa a suitable word for this while not taxon in both the statements?

Welcome to Biology.SE. I did not read the whole post as I got bored midway through by the format. Can you please capitalize your "i" and use correct spacing (space after comas, dots and interrogation marks but not before). I don't get all your "Sir" in your question. Is it to be polite? It is likely that a woman would answer the question. Do not use all these please and sir. Don't beg for us to answer. Just ask your question straight. Also please use paragraphs. You can have a look at other posts in this website to take example for the format.

It is indeed very off-putting to see sir so many times. Ultimately though, I have no idea what the question is (and I did read it to the end)! This is beyond editorial help.

Do thorough google search or read an introductory Zoology book to form a clear concept of taxonomy.

@GH05T seems to have made a very good effort at editing the question! Well done, but it seems that the question is merely about semantics, and would still be considered off topic in most cases.

Taxa is the plural form of taxon.

From wikipedia

In biology, a taxon (plural taxa; back-formation from taxonomy) is a group of one or more populations of an organism or organisms seen by taxonomists to form a unit

So, in short

Taxon is a synonym of taxonomic group
Taxa is the plural of taxon. Therefore, taxa is a synonym of taxonomic groups

You say one taxon but two taxa. While most words in english takes an s in plural, some have an irregular plural. Here are some examples drawn form the field of biology (and data science in general):
Regular plural

adaptation / adaptations
finger / fingers
cell / cells
flower / flowers

Irregular plural

nucleus / nuclei
cactus / cacti
stimulus / stimuli
fungus / fungi
analysis / analyses
diagnosis / diagnoses
hypothesis / hypotheses
louse / lice
mouse / mice
bacterium / bacteria
genus / genera
offspring / offspring
tooth / teeth
gouse / geese
vertebra / vertebrae
taxon / taxa

The video you linked
I had a very quick look at the video and I understand you are getting confused.
From 1:50 to 3:30 the author of the video repeatedly makes the false statement that dolphins are fish! No, dolphins are not fishes!! Also, the author of the video seems to be very confused about the difference between the terms taxon and clade. It is probably the worst educative video I have ever seen! Please don't trust them.
For more information about related terms, please have a look at What is the difference between these terms: clade, monophyletic group and taxon?.

Besides I would like to add that Original Poster should look up wikipedia when stuck with anything instead of watching youtube lectures with are seldom faultless. @RKhan


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Why does a broad-leaved evergreen (Mahonia aquifolium) has red leaves?
To my knowledge, oregon grape (Mahonia aquifolium) is purportedly an evergreen shrub? Deciduous broadleaf plants lose their leaves in autumn usually and before that as the leaves die they oxidize and turn shades of yellow and red as carotenoids and anthocyanins are expressed.
For what reason does M. aquifolium turns red in the fall given that they DON'T drop their leaves? Does it somehow benefit the plant? Is it because oregon grape's ancestor used to drop leaves?

@user17343 I edited your post to try to improve the format. Feel free to roll back if you don't like the edit. +1 btw

Thanks to all the helpful answers!! I'm a little put off by the condescension on here, particularly in the scientific topics. It's an app, not a journal. We're coming to YOU for YOUR expertise, so talking down to people about their grammar or use of Latin here seems exceeding condescending and priggish.  Either way I appreciate all the input and time spent

Not directed at you @Remi.b

@JaguarDomingo It is sometimes hard not to be considered pedantic when you are trying to (1) explain things and (2) improve the quality of posts so that it gets more view and motivate people to answer the question. As you agreed, we all appreciated AlwaysConfused's contribution to this post.

No @JimYoung, I meant Always Confused --they've dogged other posts of mine with useless grammar suggestions and no actual answers or ideas. Yours was the most useful comment offered.


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Is it possible for an organism that is polypoloid with an odd number of sets of chromosomes (e.g. 5 sets) to be fertile?
Is this possible, since there is five sets, there would be an unequal separation of homologous chromosomes during anaphase I of meiosis?

what do you think? have you thought through this question? have you looked somewhere for the answer? is this homework?

I think it is a good question +1

Yes, it is possible. There seems however to always come up with a cost in fertility eventually of the order of 2/3!
You should have a look at Ramsey and Schemske 1998. I don't remember it well enough to make a good summary (maybe someone else could do that?!) but it is a classical article. Here is a sentence from their abstract

In contrast to the common claim that triploids are sterile, our results indicate that the triploid bridge pathway can contribute significantly to autopolyploid formation regardless of the mating system, and to allopolyploid formation in outcrossing taxa.

The question was about odd numbers of sets, and talks about unequal separation, therefore I assume the question uses the word "odd" in the mathematical sense of having a remainder when divided by 2, rather than "unusual" - can you edit your answer?

@BryanKrause Ooops, I wrote 'tetra' instead of 'tri' by mistake (fixed now, thanks). I suppose this is what made you think I misunderstood the question. I understood the question correctly I think.

Indeed that was it; thanks for updating and for the additional quote from the article. Any other details you could add to your answer on how this mechanistically works out would improve your answer even more (e.g., the ploidy of the gametes and resulting offspring).

Triploid and pentaploid Rhododendron and deciduous azalea are sometimes fertile.
In our flow cytometry testing of seedlings from triploid Rhododendrons, the offspring can be diploid, triploid, tetraploid, pentaploid or aneuploids normally between triploid and tetraploid.  The seedlings of pentaploids tend to be aneuploids between tetraploid and pentaploid.
One can think of a fertile triploids as producing 1x to 2x gametes centered around 1.5x. Fertile pentaploid seem to produce gametes between 2x to 3x centered around 2.5x.
In general the question is not whether gametes are produced from odd ploidy but instead whether the gametes are successful in combining to create a viable seed.
We have many seedlings growing in our yard where the parents were triploid and pentaploid deciduous azaleas.
See the early work of C D Darlington on the meiosis of triploids.
Note: In our yard is a very fertile triploid deciduous azalea called 'Anna's Smile' bred by Ed Mezitt of Weston Nursery. This year we successfully crossed onto this azalea using pollen from diploids, triploids, tetraploids, hexaploids, and octaploids. 40 of the attempted 45 crosses produced seed. This triploid produces open pollinated seed. Another triploid deciduous azalea produced by Ed Mezitt called 'Deep Rose' also appears to be fertile.
Note: We crossed Rhododendron flammeum (diploid) X Rhododendron atlanticum (tetraploid) to produce triploid seedlings. One of triploid seedlings from this cross is semi-fertile. We have a dozen or so seedlings from this semi-fertile triploid.
Note: A pentaploid seedling from a fertile triploid seems to also be very fertile. We have 50 or so seedlings from this fertile pentaploid.
Note: The tetraploid Rhododendron cultivar 'Countess of Derby' is documented to have 2 triploid parents, namely 'Pink Pearl' and Cynthia'. The pentaploid Rhododendron 'White Ginger' is documented to have a triploid seed parent and a tetraploid pollen parent, namely 'Phyllis Korn' and 'Trude Webster' where 'Trude Webster' is documented to be 'Countess of Derby' selfed. So 'White Ginger' has triploids in the background of both parents.


text:
Why Milky serum in diet rich with Triglycerides?
When we eat the meal rich with triglyceride our muscle or blood after seperation of the serum the color of the serum will be milky. What is causing to happen in our serum ? Milky serum (lipemic serum)

Can you quote from your source?

I read this information in the some medical cases and also an A&Q website link . I know these are not suitable sources but i didn't understand so i wanted to ask .

Tyndall effect makes a sense but still not clear. Cause according to these informations that milky color occurs in lacteals that is a part of lymphatic system and we dont get the serum from lymphatic vessels actually we obtain the serum from the blood.


text:
Source of blood glucose during starvation
During starvation there is many source for glucose such as pyruvate, lactate, amino acids (except leucine and lysine) and glycerol from triglycerides but what is the major source of blood glucose ?

Welcome to the Biology SE site. Please take the tour and carefully read through the help to learn more about the site, including what is on-topic and what is not, and how to ask a good question. Please ensure your post is formatted correctly as well.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

It is not my homework its my question i am a medical student and we dont have homework ok?

@AhmetÖz you should at least show some attempt in order to answer your own question. This community is not a QandA forum.

I dont undetstand this rules i have a question about a subject and i want an answer . look my profile i asked a question about ldh reversiblity and it was my own question too . there is not any difference this two question for me .

@AhmetÖz there are some answers below, you should take a look at them, and then either comment with any clarification or elaboration that is necessary, or select one of them as an answer.

@AhmetÖz "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning. Just because you're a med student doesn't excuse you from doing some research before you ask here. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked, what you do know about the topic, and where exactly you still have questions.

I have been researching this question for 6 hours. Even I still cannot understand the mechanism of starvation.

@Ahmet Öz - if you want to be a good doctor, asking questions when you don't know something is important. But if you want to be a really good doctor, reading and researching are critical, as is good communication skills. People on this site gave you site guidelines and you responded very bluntly if not quite rudely. As a doc, I think I know a bit about this. Starvation is not a mystery by any means.

The (very) short answer is gluconeogenesis. When glucagon levels are high in response low glucose or low Insulin (perceived in the case of Insulin resistant DM Type II) key enzymes will be inhibited to prevent glycolysis and other enzymes will be activated to produce glucose from various substrates.
There are a few sources that can feed into the gluconeogensis machine. Two that are commonly used in short term fasting are lactate via the Cori Cycle and Alanine via the aptly named Alanine Cycle. Now when we get into long term fasting (i.e. starvation) things start to change a bit.
In starvation, glucose is conserved as much as possible and many tissues start using ketones (which are derived from Acetyl-CoA which are in turn usually derived from fatty acids) for energy. But even then, there is still a demand for at least a minimal level of glucose. This can be synthesized from a few sources. The backbone for triglycerides, glycerol, can be fed into gluconeogenesis. But that is not the main source for glucose during starvation. The main source is from gluogenic amino acids. These amino acids can be metabolized into pyruvate which can then enter into gluconeogensis.
This is one of the reasons you get muscle wasting during starvation but not in calorie restricted diets. During calorie restriction you have enough glucose to maintain adquete blood sugar between meals, and any energy deficits can be met through β-oxidation of fat. Thus you lose fat. However, when you enter starvation, the glycerol obtained from lipolysis (breaking down fat) isn't sufficient to maintain adequate blood glucose and you have to turn to muscle breakdown. This breakdown of muscle tissue is mediated by high levels of Cortisol, a hallmark of starvation that is not seen in calorie restricted diets. If you want to see the effects of starvation levels of Cortisol in a non-starving person, look into Cushing's Disease. You see similar breakdown in muscle that you would normally see in a starving person.

There are a couple of different levels of starvation, from fasting to malnourishment to long-term starvation.
Let's start from consumption of a carbohydrate-heavy meal. The carbs in this meal are readily converted into glucose, and blood sugar levels will increase. Assuming you're not diabetic, this will lead to increases in insulin production, which will lead to among other things, uptake of glucose by hepatocytes (liver cells) and conversion into glycogen for short-term storage. At some level, excess energy is also converted into fatty acids for more long-term storage. Other cells (like muscle, brain etc) will continue to use glucose for energy.
Say this was an evening meal, and you don't eat again until the morning. Over time, blood sugar levels will drop. This leads to decreased production of insulin and increased production of glucagon. As a result, hepatocytes reverse course, breaking down glycogen, turning it into glucose and secreting it from cells to raise blood sugar.
But let's say you miss the morning meal. Eventually, the liver's stores of glycogen will run low. At this point, the body can turn to stores of fat for energy. But most fatty acids cannot be converted into sugars. As a result, blood sugar levels do not rise. Instead, they are converted to molecules called ketone bodies, which can be released in the blood and used by most cells for energy.
However, some amount of sugar is still required to construct certain biological molecules. Also, certain cell types (particularly red blood cells) cannot use ketone bodies for energy. Even with abundant fat reserves, if no additional carbs are consumed, those sugars have to come from somewhere, and they can't come from fat. Instead, the body will begin to degrade cellular protein - some amino acids can be broken down to generate sugars. During long-term starvation, muscles, including those in the heart, begin to be consumed, and anemia is often an early symptom of starvation (since RBC's don't have sufficient energy).

Some of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted.


text:
Calculation of NADPH molecules number needed to reduce a substrate in enzymatic reaction
I am inquiring if it is just simply possible - as it seems to be - to calculate the number of NADPH molecules needed by an enzyme (let say for example Dihydrofolate Reductase DHFR) to reduce the substrate (FH2 or BH2 for DHFR) to (FH4 or BH4) directly from the apparent enzyme reaction?
In DHFR case, can I simply figure it out that I need two NADPH molecules to reduce (FH2) to (FH4)?
Here is the reaction of reducing FH2 to FH4:
https://upload.wikimedia.org/wikipedia/commons/2/29/DHFRmechanism.png
Or is there anything else to keep in mind?
In the figure in the link, the NADPH transferd Hydride, but where did the positive hydrogen come from?

But then where does the other hydrogen come from? one of them comes from NADP(H), which is in hydride form, but what about the second one? it comes in proton form (H+), but from where?


text:
What are the structural factors affect enzyme's Km?
Is there any rules (should not be exact), to estimate the kinetic changes in an enzyme if I did any mutation on it?
If I cannot estimate the new kinetic values, is it possible at least to clarify or suggest any explanation for the new kinetic after mutating an enzyme depending on the point mutation I did on it?
So I want to explain the changes in the kinetic parameters (Km / Vmax) in my enzyme after mutating it, maybe depending on the 3D structure? or the charge/size of the new amino acids? Or any other factors I may use to suggest anything logical how and why those changes happened to my enzyme after mutating it?
I need that for my dissertation and I am still totally lost, any ideas (with the proper references) will be great. I really appreciate any help.

Any mutation affecting the interactions between the enzyme and the substrates, intermediates and products will change the enzymes behavior.
I suggest reading some structural biology books and papers... Also please don't call it structural factors, that term is already used in crystallography. Finally you may want to add structural biology as a tag and possibly also ask the question at the chemistry stackexchange.

What you are asking is not completely clear: do you want to predict the effect of mutations? Or do you want to make sense of experimental kinetics data comparing the wild-type enzyme to point mutants?
To predict the effects of mutations, ideally you need a three-dimensional structure of the enzyme in complex with a substrate analogue. Is there such a structure in the PDB for your enzyme? This would help you reason about the potential effects of point mutations. If there is no such structure, you can only rely on sequence alignments (and possibly structures of homologous enzymes, if they have been solved) to figure out which residues are important for substrate binding and catalysis.
KM is related to the binding affinity of the enzyme for its substrate. So, any mutation that for example disrupts an H-bond between the enzyme and its substrate would increase KM.
Any mutation that targets a catalytic residue (say, an amino-acid side chain acting as an acid-base catalyst) would affect kcat (and therefore Vmax as well), and could make it larger or smaller depending on the mutation.
If you are trying to make sense of experimental kinetics data, then ask yourself why you chose these mutations in the first place. One usually mutates residues to test an hypothesis. Or are you trying to understand the effects of naturally occurring mutations?

do you want to predict the effect of mutations yes. Is there such a structure in the PDB yes. any mutation that for example disrupts an H-bond between the enzyme and its substrate would increase KM. why? that does not make sense for me. Without referencing any study which proves that I cannot rely on it.

Km is different than Kd (see textbooks for the precise definitions and meanings of both), but close enough so we can approximately consider Km as the binding affinity for the substrate. What causes binding? Well, any interaction between the enzyme and the substrate, including H-bonds, salt bridges, hydrophobic pocket on the enzyme that can accommodate the hydrophobic part of the substrate, etc. Disrupting any of these interactions will give a weaker binding affinity, therefore higher Kd and Km values.

Regarding the available 3D structure of your enzyme: have you tried using it to figure out the potential effects of mutations? If so, how did you proceed, and what difficulties did you run into? Helping you would be easier if you told that.

My problem is understanding how these factors you mentioned (H-bonds, hydrophobic pockets, etc.) may effect Vmax and Km differently? tighter binding (more bonds) between enzyme and substrate stabilizes the transition state, and that increases the Vmax, but I cannot get how Km will be impacted differently. In other words, I cannot distinguish which changes in the structure may change the Vmax, and which may change Km.

To the best of my knowledge (I am not an enzymologist), this is really hard to predict. Ultimately, the predictions you make from a structure need to be tested experimentally. The structure is a useful guide to narrow down the potential interesting mutations to only a few residues, because it clearly shows which ones have nothing to do with the catalytic site (i.e. most of them).

Here actually comes the problem of energetically coupled residues (distal amino acids, may play a role in the catalytic activity, even they appears to be far and not important on the 3D structure). In my PhD. dissertation I discussed that, but that was really not so simply, and they are still somehow not very clear.