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Link between cell area and efflux pump?
I conducted an experiment involving a fluorescent F-actin stain called sir-actin which is removed by an efflux pump. After increased time and removal of the medium containing sir-actin, the cell actively removed the sir-actin using the efflux pump but an increase in cell area was reported when the images were processed in matlab. I was wondering if anyone can propose a possible cause for the increase in cell area with the removal of sir-actin by the efflux pumps. The f-actin of the cytoskeleton was also found to have a reduced length with increased time. Thanks in advance. I also used MSCs and the cells were alive until fixed at each time point and then imaged.

When you added medium with sir-actin, were you also refreshing growth factors that caused the cells to grow?  Did you compare cells that effluxed your sir-actin with control cells that also received new media for the size you are concerned about?

@akaDrHouse Yes, growth factors were refreshed and it was compared to a control where the cells were fixed and then stained. All cells were passaged 8 times (P8).

It wasn't clear from your answer if the control cells also were given fresh media and allowed to incubate for the same amount of time as the sir-acting treated cells. I'm assuming yes.

@akaDrHouse the control cells were left to incubate for 5h and then fixed then stained and imaged. The test samples were incubated for 5h with sir actin and after the 5h period the sir actin containing medium was replaced with sir-actin free medium and incubated for additional hours (T0, T1, T3, T6) before being fixed and imaged.

So those controls don't actually mimic the treatment conditions. You may want to have controls that receive the media change again (same as the treated) for the different time points.  However, since you have a T0 time point where the treated cells actually do mimic the controls, does that set of cells still display the difference in cell area compared to controls?


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Why does snow not stick to the fur of wolves and some breeds of dogs?
This question made me wonder, why for example wolves don't suffer from these "paw snowballs"?

(...) but after a few miles on the trails in soft snow, he often develops snowballs between his paw pads - usually one big one right in the middle. (...) I have heard really bad snow buildup can lead to raw/bleeding paw pads.

they have very large paws so that prevents them going so deep, that would help.

I couldn't find scientific references, but regular web searches basically indicate that long fur as well as webbed toes promote formation of ice and snowballs in certain breeds.
From Hubpages:

The snow attaches to the dog's long hair, melts from the body heat, and forms ice balls that grow larger, stretching your dog's toes apart and causing cracking, bleeding, and hair pulling.  This is painful and distressing for the dog, who may then try to remove them by licking them, which then causes even more ice to build up.

And among the solutions:

Clip the fur between your dog's toes. [J]ust trim off the excess fluff.

A typical breed thriving in icy conditions is the Siberian husky. A comparison to to an airedale terrier breed shows the difference in fur length quite clearly, especially around the areas most suceptible to come in contact with snow (legs & chest areas):

And both breeds in the snow:

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Can bacteria, viruses, and cancer cells be destroyed by resonance?
Radiotherapy has been used to treat cancer.
Can the resonances by coordinated electromagnetic waves (and/or other forms of waves), of various frequencies, amplitudes and pulse rates, directed from various directions, be used to destroy harmful viruses, bacteria or cancer cells in a human body, without damaging the other parts of the human body?
(* NOTE * This question was posted here in Physics Stack Exchange too, but is possibly going to be closed in that forum as some claimed it is not so much about Physics.)

Welcome to Bio. This is definitely Bio and not a Physics question in this form. What do you mean with resonances?

By resonance I mean the molecules/structure of a, say, virus is made to vibrate with increasing amplitudes until the structure gets destroyed.

You cannot take things like that. Viruses/bacteria are made up of billions of atoms/molecules, all of which have their own resonance frequencies, and most of which may not coincide. To destroy a bacterium/virus, you will have to attack it with all of those billions of frequencies, millions of which will affect/destroy the neighboring cells too. It would be just like you make a man explode just by putting him on a speaker which produces that man's resonance frequencies. ;-)

Well, we don't have to explode something entirely to kill it.

...and we don't have to kill something to make it dysfunctional.

Your question included "other forms of waves" so I'm going to assume that the use of ultrasound to destroy cancer cells qualifies.
A paper published in the British Journal of Cancer in 2009: "[High-intensity-focused-ultrasound in the treatment of primary prostate cancer: the first UK series]"1 describes the use of a "Sonablate 500" device used to treat 172 men with prostate cancers at two hospitals in the UK, and its use is described as resulting in "acceptable short-term levels of cancer control."
However, the paper does lament the deficiencies of research in this area, the number of other treatments available, and the lack of longer-term follow-up to this research.
The answer to your question appears to be yes, with the qualification that this is an example using sound waves, rather than electromagnetic waves - isn't radiotherapy, mentioned in the first sentence of the question, electromagnetic waves?

Interesting. Yes, I am referring to all forms of waves, including perhaps magnetic fields, which have been used in MRI. I hope more research can be carried out in these fields.

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Can cell mediated immune response be transferred via blood transfusion
I read that human body can develop cell mediated immunity to viral infections and subsequently clear the virus. For example, people clear warts through cell mediated immune response against the wart virus. Is it then possible to transfer the blood from one person to another to transfer the type of immune cells that kill the virus?

May you consider to add some refferences to your conclusion?

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Is there a term for the entire system of moving oxygen around?

The respiratory system brings oxygen to the blood, and also can include stuff like nicotine from smoking.
The circulatory system brings oxygenated blood (and all its little friends) to wherever they're needed.

Both the respiratory system and circulatory system are extremely important in keeping hypoxia from happening, but I'd like to focus specifically on the system of oxygenation.  I don't want to include the systems of smoking, or moving around nutrients.
Is there are term for the "oxygenation" "stop hypoxia from happening" system?  Basically just the parts of the respiratory and circulatory systems that move oxygen?

Short answer
"Oxygen homeostasis" is the best I can think of.
Longer answer
Don't forget the other half of the oxygen equation: carbon dioxide is an important waste gas and failing to remove carbon dioxide is just as much a problem as failing to deliver enough oxygen.
You could refer to "oxygen homeostasis" if you wanted to just refer to keeping enough oxygen in distal tissues; as you describe, both respiratory and circulatory systems are relevant for oxygen homeostasis. However, it's hard to separate from the rest of the gas exchange system. Carbon dioxide is very important in determining the rate of respiration, for example, as well as the release of oxygen in peripheral capillaries. Therefore, even if you want to focus on just oxygen, carbon dioxide is going to come up no matter what! As is the function of the vasculature, heart, and lungs: even if these organs have roles outside of delivering oxygen, their functions apply to all gasses exchanged and everything that is transported in the circulatory system. Very little happens in these systems that will only affect oxygen delivery without affecting anything else.
The efficiency of oxygen delivery also depends on what exactly you're inhaling; I find it a bit bizarre to include "smoking" as seemingly part of ordinary biological function, but if you want to go there it's reasonable to consider the role of carbon monoxide and anything else that may interfere with oxygen binding to hemoglobin.

I'm writing a paper in which I'm trying to split the understanding of oxygens role into two distinct phases as systems, one which explains getting the oxygen and where it goes, and another that explains the CO2 release.  While they do use almost entirely the same systems, I still want to treat them as separate functionalities for the sake of the writing being more like a story.

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Where to find a list of genes coding for protein in human
I have raw read counts extracted by htseq from STAR alignment
I have both data with both Ensembl IDs and gene symbols, but I need only a latest list of protein coding genes in human; I googled but I did not find
Any suggestion please?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done (e.g., what search terms), what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Submit your ensembl IDs to biomart, and get the "gene biotype".  "protein-coding" is one of the options there.


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Auxin-what happens to the auxin chemicals if the Sun is just above the plant?
The Auxins goes to the shady side for the elongation of the cell. This moves depending on the direction of sunlight. But, what happens to the auxin chemicals if the Sun is just above the plant?

Have you attempted to answer this question yourself by scouring the internet? Basically this question is a 1-liner and we encourage a bit more background and leads in a question.

Nope, There is no answer to the question. I always search it in the Net before i ask it here!

What did you find?


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Why Fertilisation occurs only in Fallopian tube?
The Ova is released and stops in the fallopian tube for the sperm..The Fertilisation occurs at the Fallopian tube, but as the zygote divides and forms an embryo, it attaches to the lining of uterus.But why doesn’t the egg come to the uterus and the fertilisation occur in Uterus?? Simply,Why cannot the site of fertilisation be the Uterus?

Welcome to the site. What research have you done on your own to answer this question? 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 for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Hello Respected Sir! I’m a 14yr old Student..These subjects are out of my syllabus.But Still, I Would like to learn each topic, but to learn i have to ask questions. I Have gathered only this information regarding this.I Know you are helping me in a way to learn something myself.But I Would like to ask these questions so that i can self learn. I Don’t simply come to SE community and asks questions, i search the questions or info in google or youtube, when there is no help, i just ask here.
I’m Sorry, If I’m Hurting you! But I’m just a beginner and there are many other students in SE Like me!!

good for you for being curious! By previous research, I mean what did you learn when you took the title of your question and asked it on Google? What resources there helped? What are you still confused about? Essentially, the answer is that Fallopian tubes evolved to be the place where fertilization occurs in humans, and the uterus did not evolve to be very conducive to fertilization; rather, it is good for implantation and growth.


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What is human body's overhead when storing calories into fat, and when retrieving calories from previously stored fat?
Questions:

Suppose that someone ate an excess of 1000 kcal.  How much of this 1000 kcal will become fat?
Suppose that someone had a deficit of 1000 kcal.  How many grams of fat will be lost in order to generate the 1000 kcal?

What I've done so far
I found that each gram of fat contains 9 kcal. So, a naive solution would be:

An excess of 1000 kcal will become 1000/9 = 111.11... g of fat.
A deficit of 1000 kcal will cause the loss of 1000/9 = 111.11... g of fat.

This is naive, because it ignores that the body itself requires some calories for simply converting excess calories to fats, or for converting fats back to calories.
In Quora, I found someone claiming that such conversion has a 20% overhead for each direction.  So, if I understand his answer, the better answer is:

An excess of 1000 kcal will spend 1000*.2 = 200 kcal as calorie-to-fat conversion overhead, leaving us with 1000-200=800 kcal that is going to be stored as fat.  Since each fat gram contains 9 kcal, we will eventually store 800/9 = 88.88... g of fat from the 1000 kcal excess.
Likewise, a deficit of 1000 kcal will also have a 20% overhead.  So, to get 1000 kcal, the body will have to burn enough fat that gives 1000 * 1.2 = 1200 kcal, which is 1200 / 9 = 133.33... g of fat.

But, the problem with this answer is two folds:

It assumes that the overhead is 20%.  I couldn't find a study for this.
It assumes that the overhead is symmetrical so that calorie-to-fat's overhead equals fat-to-calorie's overhead.  I couldn't find a study to claim this symmetry.


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What is the effect of surfactant deficiency on dead space (of lung volumes)?
Surfactant deficiency in adults with acute respiratory distress syndrome has long been recognized. This deficiency causes decrease in lung volumes (tidal volume or redisual volume for example).
Dead space is the portion of each tidal volume that does not take part in gas exchange.
So this deficiency cannot cause decrease in the volume of dead space, right?
I am asking this question because our teacher told us that this deficiency causes decrease in all lung volumes, without exception.


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SARS-COV-2 replication speed
What is the speed of replication of SC2? Any information, including in vitro data would be appreciated.
I would be interested to know the length of SC2 eclipse period, latent period and something like burst size.
Alternatively, per day CT values of qtPCR of COVID+ subjects would be also helpful.

According to Amy Rosenfeld, it is about 8 hours eclipse and 18-24 hours until "its done". Not sure if it means until burst or until the latent period is over. These times are in vitro and are cell line dependent. In vivo might be different. Burst size also cell depndent. Source: https://youtu.be/NP56XjzyPfQ?t=1301
In this video https://youtu.be/4S3DXXtRZZg?t=152, it is said, that each cell can produce up to 600k viral particles of SC2, but I'm not sure, what is exactly meant by the number. Later in that video: https://youtu.be/4S3DXXtRZZg?t=187 it is said, that the virus seems not to kill cells for about 5-6 days.


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Why did whales end up larger than most sauropods and what is a whale's limits?
I understand that due to the square-cube law (when something grows 2 times but its volume grows 4 times and it goes on) sauropods were massive but not enough when compared to whales because whales got around the square-cube law by using the buoyant force to balance their bodies in the water. In addition, being mammals allowed them to breathe, oxygen-rich air while fish were limited to oxygen-poor water, this thenceforth allowed whales to grow many times more than the largest fish. So my question is what is the limit to whale size and if there is one what is their true potential?
A question presented by the scientific community and given to the public.

Food is pretty important. I wonder if the air oxygen argument actually holds since they need to hold their breath whereas fish get a continuous supply.

this would probably be better received on the biology stack since it is not about worldbuilding.

@DKNguyen nearly all the plankton is in the top 100m of the ocean, and a blue whale takes about 1-minute to each that depth because they can swim at 10 m/s and they only have to inhale every 30 / 90 minutes.

Re size, note that the whale shark (a fish) at up to 18.8 m in length is as large as some of the whales.  Some estimates put the extinct Megalodon shark even larger.

Basic error: "when something grows 2 times but its volume grows 4 times and it goes on" should be "when something grows 2 times but its volume grows EIGHT times and it goes on". Linear dimension cubed.

As best we can tell food availability is the relevant limits in whales.  its true that the bigger an animal gets the more energy efficient it is, it needs less food proportionally but still needs more total amounts of food. There is a limit to how much food you can find and eat, especially in the lean parts of the year. This is actually why we see dwarfism on islands lower food availability favors smaller size (less overall food needs). Finding food and even feeding itself takes energy and it reaches a point where the energy you expend is equal to or less than the energy you can extract from your food.
There are other limits like blood pressure, internal surface area, digestion time, heat buildup, but whales have not reached any of these.
https://science.sciencemag.org/content/366/6471/1367

So the depending factor here is mainly food like take for example the kiwi is a flightless bird that is in the same family as the ostrich and evolved to be smaller over time due to the lack of potential predators.

@ParinChitrada food is the limiting factor that determines maximum size. Food is NOT the only thing that determines size it is however what determines the limit on size.  there is a big difference between determining factor and limiting factor. there are plenty of small ratites. there are 40+ species of  tinamous for instance.


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Why is DNA replication not 100% accurate
I've been reading about DNA mismatch repair (MMR) and how this process improves DNA fidelity. However, I was wondering, what is stopping MMR from correcting all mistakes in the daughter DNA with 100% fidelity? Why is the error rate still around 1 in 10^9 base pairs? Is it because the MMR proteins aren't present in cells in a high enough concentration? What would you have to change about this process to achieve 100% fidelity?

Have you researched all the other questions on DNA repair and errors in DNA replication on this site? Please do, and then tell us why your question is not covered by them if you still need an answer.

Nothing is 100% precise - any measurement or process allow for some error, the only difference is how often such errors occur (i.e., the probability of an error). These wildely range in biology - e.g., it is about 1 per $10^4$ in HIV replication, but only 1 per $10^9$ for human DNA (due to the repair mechanisms).
Note that $1$ in $10^9$ for human DNA means pretty much that there is about 1 error per each copying of the genome (which has the size of about $3\times10^9$). One could therefore still pose a question of why the error rate is so high? E.g., Human body consists of about $15\times10^{12}$ cells. Thus, if the error rate were about 1 per $10^{22}$($\approx 3\times10^9$ by $15\times10^{12}$), we could have human organisms consisting of the cells with identical DNA.
The answer to this is that errors are not necessarily bad: the copying errors are the source of the mutations driving the evolution! Note also that many of the errors have no effect at all on the well-being of the organism. Thus, it is fair to say that the existing error rates were selected by the evolution for assuring the appropriate rate of the evolutionary change/adaptation, without causing immediate harm to the organism. (One could even speculate that 1 error per genome copy is the appropriate rate across the organisms, but for a moment I cannot support this assertion by references).

Just out of curiosity, what would be some ways to artificially decrease the error rate of DNA replication? Would increasing the concentration of MMR proteins do this?

I do not have sufficient background in biochemistry or molecular biology to answer this - my field is more population genetics. Exposure to toxic substances or radiation are certainly important factors increasing the mutation rate (hence the cancers).


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Could the use of genetically engineered crops result in the population decline of other organisms?
Population decline of other organisms has been an ongoing phenomenon since man learned how to domesticate corps. Many people, including me, is curious if the use of genetically engineered grops result in the population decline of other organism.

Why do you think genetically engineered crops would cause a decline in some organisms?

Pretty much any human activity will benefit some organisms and hurt others. What "use" of genetically engineered crops interests you? What type of genetic engineering are you thinking about? What population(s) of other organisms are you interested in? What time span are you interested in?

Do you have any specific example in mind?

Genetically engineered crops are more resistant to pathogens, harsh conditions, etc. As such they have advantage over other plants in competition for resources, and thus may lead to dicrease in biodiversity. On the one hand, this is not new - any crop or animal is cultivated by human to disadvantage of its natural competitors - just thinkn of the fate suffered by weeds, or by the natural population of the areas cleared for crops. On the other hand, if the genetically modified crops are able to reproduce (which is not always the case by design), they can take over other plants even beyond the areas where they were planted. Finally, the diversity of the organisms feeding or parasitizing on the genetically modified crops declines as well, for obvious reasons.
As far as my experience goes, the issue of genetically modified crops is somewhat of a controversial subject - public fears them, while the scientists forcefully push back against these fears. Thus discussing the issue seriously is hard. Still, I would be glad to correct/complete or remove my answer, if somebody more knowledgeable in the crop science chimes in.

I believe you are mistaken. There is no inherent reason a genetically engineered crop (whatever that means in a given example) would be more or less resistant to "pathogens, harsh conditions, etc", and no inherent reason for it to "have advantage over other plants in competition for resources".  As you point out, "any crop or animal is cultivated by human to disadvantage of its natural competitors " - but that is because it is disadvantaged relative to its natural competitors, and needs human help.

Could you expand on why "Finally, the diversity of the organisms feeding or parasitizing on the genetically modified crops declines as well, for obvious reasons"? Any such reasons are not obvious to me. Remember, we are comparing "genetically engineered" crops with "normal" crops.

@Armand my understanding is that crops are genetically engineered to make them more productive - that includes making them more resistant to disease and parasites.

@Armand Non-engineered crops are indeed disadvantaged - this is precisely what I was pointing at. So humans use pesticides or clear a forest to make place for a field - all of which literally means exterminating lots of specimen, sometimes on massive scale.

Re "crops are genetically engineered to make them more productive "  Some are and some aren't, but it is always in a context.  In one situation, that may result in increased productivity and in another lowered productivity. For example, "disease resistance" typically has a resource or metabolic cost, so in the absence of significant presence of the given disease, the plant will perform more poorly than an unmodified one. Productivity etc depends on the individual plant's genome and the environment it is raised in, not on how its genome was generated.

Re: "So humans use pesticides or clear a forest to make place for a field " This has nothing to do with genetic engineering; it is done for "normal" crops as well.  "Genetic engineering" only refers to how a genome is generated, not to farming practices.

@Armand this is precisely the point I was making in my answer - that affecting biodiversity didn't begin with genetic engineering. I will think how to rewrite it in more understandable fashion... this discussion seems to be based on a lot of misunderstanding.

Genetic engineering is a process, not a product or end result.  Thus, it has no direct effect on "other organisms".
Humans have been modifying organisms for tens of thousands of years. We've developed multiple techniques to do so, including selective breeding, mutagenesis, grafting, interspecies hybrids, multiploidy, "genetic engineering" and so forth. Just as with producing books, the resulting product is evaluated on its own, not by what process produced it.
What matters with a book is the words it contains, not whether they were handwritten, block printed or even carved in stone. Similarly, what matters in an ecosystem are the organisms present (and their function, much determined by their genes) and the conditions they live in, not how those organisms were created.


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If the IAVI G001 HIV vaccine proves itself, why would it work?
The IAVI G001 HIV vaccine trial looks promising.
If it works, will it work by preventing a single cell from being infected, or by allowing the body to attack infected cells?
What I'm trying to understand is if a person living with HIV for years can't develop immunity, why might the vaccine succeed?

There are a lot of sources of information about the vaccine that include information about how it works. Have you read those explanations, and if so, what are you not understanding?

Yes, I've read them but they either didn't answer my question or were too technical to be understood by a layman.

Can you please add more background to include specifics about what you've learned and how that doesn't answer your question?


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How do biologists infect cells with viruses within a lab setting?
I'm writing an experimental proposal as my final paper for my single molecule biophysics class. Part of the procedure I wrote involves intentionally infecting a culture of HeLa cells with SARS-CoV-2 in order to perform a series of tests on it. Are there any readings or articles that you guys can point me to which detail how biologists intentionally infect cells with viruses within a lab setting?

A good strategy when writing a proposal like this is to read the methods sections of papers in the literature. You can probably use searches that include terms like "in vitro" and members of the class of viruses you are interested in studying - both the original SARS virus and SARS-CoV-2 would be good places to start, MERS would also be reasonable. You might not find your answer in the first paper you look at, so expect to look at a few, and expect that you might need to go to a source that is cited by one of the papers you initially read. Note that your instructor likely wants you do to this.

I'm closing this question as Homework because I think getting a thorough answer here would interfere with the purpose of the assignment you were given. I'll let @MikeyC's answer remain because it is helpful but doesn't go so far as to complete your homework for you.

You'll probably want to consider whether HeLa cells are the optimal cell line for acheiving your objectives. This paper shows minimal change in cell viability of HeLa cells innoculated with SARS-CoV and SARS-CoV2, but it's probably a good resource for how cell-culture infections are performed. This paper claims that VeroE6 is the standard cell line for producing viral stocks of SARS CoV-2.
Best of luck with your proposal.


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What happens if ace2 from lungs is removed? Will there be any major impact on our body?
when ace2 receptors  are not present in the lungs will we experience any disturbance or suffer from any other problems

Yes, the  renin–angiotensin system is very important. Search about ACE2 knockout mice https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/expphysiol.2007.040014

According to my cursory and unprofessional assessment, the most prominent issue would be hypertension, flanked by excessive retention of water, sodium ions, and chloride ions, due to the boatloads of angiotensin II just sitting around. Potassium ions would be excreted gratuitously, however. The lack of the ACE2 receptors has been (ostensibly) linked to Hartnup disease as well, so make of that what you will.
Once again, I'm not a medical professional, so take my word with a bucketful of salt.

Welcome to Biology.SE! This looks like a could become a good answer if you provided more detail and included supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. A good example of how to format references. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thank you!

@tyersome My apologies, I’m new and I come from quora, so my standards are a tad low.


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What would happen if two different viruses penetrated one cell?
I want to know what would happen if two different kinds of viruses took over one cell.
Would nothing happen? Would the cell create both kinds of viruses? Would it make a fusion of the two viruses?

Are you thinking about viruses (which are "created" by cells)?

One infected cell may produce hundreds of new viruses. By the time the disease occurs, many thousands of cells may be infected and producing new viruses. These new viruses are released from the cell, often in bunches, and are almost identical. Sometimes the host cell makes mistakes in copying the virus nucleic acid, causing some genetic variation. However, the outsides of these new viruses tend to be pretty much all the same, and they will usually infect only some more of the same kind of cells that produce them ¯ either in the same host animal or, if they can get out, other animals. Viruses produced in the respiratory tract are usually shed in droplets from the mouth and nose; viruses produced in the digestive tract are usually shed in feces but sometimes also in vomitus.
One person or animal is usually infected with only one kind of virus at a time, so the bunches of virus they produce and shed are all the same. Then, if this virus infects another person, even if two of the same kind of virus bump into a single susceptible cell, the infection will still be all of one type. However (much less likely), if viruses from two different infections get mixed up in the air or in sewage and get into a single person, it is possible that two different viruses will attach to receptors on the same cell and infect that cell together. If the two viruses are closely related, their nucleic acids may "recombine" while they are being copied. When this happens, part of the genetic information from one virus is linked to the genetic information from another virus, and the new virus that is produced is a "hybrid."
If you read about influenza that is traveling about in populations you will see that the outside of the influenza virus has an H type and an N type. For example, you might read that this year's main influenza virus is type H3N2.A reason to get a new flu vaccination each year is that the vaccine has to be made to immunize us against this type. Somewhere out in the world, a double infection as described above may happen between two different types of influenza viruses and some of the new virus may be type H5N4. Once this new type is established, a new vaccine is needed, or people won't be protected. Development and production of vaccines are expensive, and distributing them and getting people to use them is difficult. So, here is at least one situation where your question about two viruses infecting one cell may have serious public health results. Of course, influenza viruses that develop in birds, and sometimes other animals, may also be transmitted to people. Not many other kinds of viruses can jump host species like this, but it is possible that Ebola was transmitted to people from apes, perhaps from eating "bush meat." Viruses and other infectious agents that are transmitted from animals to people are said to be "zoonotic"; once this happens, the virus can usually be transmitted from person to person after that. Obviously, this too is an important public health concern.
http://www.madsci.org/posts/archives/2007-12/1198562498.Vi.r.html

Well, it depends on the virus.
Assuming the virus were different strains of the same species, the viruses can swap their genetic material. Producing both parent strains and hybrid strains. Good example is the influenza virus.
If the virus are very different, and are not lytic in nature (ie they don't kill the host cell), the two viruses the can co-exist. And the poor host cell ends up producing viral particles of both virus.
It is possible that the two ended fighting each other. But I have not read anything like that before. Instead I have read, what happens in HIV, where infection with one strains of HIV prevent reinfection with a second strain.


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Where do the 2 hydrogen ions in glycolysis come from?
In the reaction for glycolysis, two hydrogen ions are produced as one of the end products. In all the ten steps, I am not able to figure out where exactly these two hydrogen ions are formed. Please elucidate
Glycolysis reaction:
Glucose + 2ADP+ 2NAD+ + 2Pi ----> 2Pyruvate + 2ATP + 2NADH + 2H2O + H+

Welcome to Biology StackExchange. Write the equation of glyolysis with glucose and pyruvate in molecular form. Then count the hydrogens, and they should match. Also, it should be $\ce{2H^+}$ in the products. You may help yourself also with Wikipedia page.


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PCR primer design for specific region
I want to amplify a specific region of my genome. I want the segment to be as precise as possible but the primers that would align to the start and end of the target fragment are not optimal in terms of qualities checked for primer design (GC content, melting temperature, etc).
Is there a way to amplify a specific segment of the genome as precisely as I want in this instance? Are there some tricks that one can use when primer pairs are not optimal?
Thank you!

Can you share the first 50 bases of the start and last 50 bases of the end? I find it hard to believe there is no primer length available you can use.

have you looked into primer design tools like primer3?


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Genes on the reverse strand of DNA indicated by (-) in GFF
In the transcription process, RNA is produced from the template strand of DNA (that is 3'-5') so the RNA molecule produced has the direction 5'-3'.
When working with genes in bioinformatics, there are many genes that we indicate with a (-) sign meaning they are from the reverse (coding strand).
I am really confused here. If RNA is only transcribed from the template strand, shouldn't all genes have the same direction?
I'd appreciate your input a lot!

There is a difference between the forward / reverse (also top / bottom) strand of DNA, and the template / coding strand during transcription. The designation of forward / reverse is rather arbitrary, one of the strands has to be forward (left (5') to right (3')), the other reverse, but it makes no practical difference which goes into which direction. DNA is double stranded and both strands go from 5' -> 3' in opposite directions.
The template and coding strand during transcription are a specific feature of transcribed DNA sequences, and typically relate to features of the 5' -> 3' sequence of the DNA, such as promoters and coding sequences.
For example this short double stranded DNA sequence:
 5' ATTTACGTATGTACAT 3'
 3' TAAATGCATACATGTA 5'

There is an ATG start codon in 5' -> 3' direction on the bottom strand, and this could serve as the start codon of a coding strand after RNA transcription of a protein coding sequence. In this case, the template strand would be the top strand, the bottom strand is the coding strand. Transcription would happen on the top strand from right to left, so in reverse (-).

Thank you! Wouldn't transcription occur on the top strand from 3' to 5', so from right to left? That is transcribing TAC....?

The new stand would be complementary to the top stand, so identical to the bottom stand (with the exception that in RNA T is replaced by U)


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Speed of reaction vs equilibrium
Does increasing the speed of a reaction (say by introducing a catalyst) shift the equilibrium of the reaction? I assume it does not, as Gibbs free energy is not changed, but I am not sure.

You are right in both the conclusion and the rationale. However, you pose the question in the wrong forum. You should pose it in phyics.stackexchange.com.

Welcome Ben. This is a chemistry question rather than a biology (or physics) question - I've flagged it for moving to chemistry.sx.

This is a physical-chemistry question but it is already answered in [chemistry.se].

The equilibrium constant $K$ is the quotient of the rate constants of forward ($k_1$) and backward reactions ($k_{-1}$) (for elementary reactions).
E.g., for an  equilibrium
$$\ce{A + B <=> C + D}$$
we get
$$\frac{[C][D]}{[A][B]} = K = \frac{k_1}{k_{-1}}$$
So,

If both rate constants are affected in the same way (multiplied by the same speed-up factor) so that the quotient doesn't change, then also the equilibrium constant does not change, no shifting, no change in Gibbs free energy.
That would be the case with your catalyst as that facilitates both forward and reverse reaction by lowering the energy of the transition state in the elementary reaction leading to just such a multiplicative increase in reaction rate - but no effect on the energy of educts or products (thus, no change in $\Delta G$).
This has an interesting link to the impossibility of constructing a "chemical" perpetuum mobile by use of a catalyst.
If the rate constant of either forward or reverse reaction (or both, but not by the same factor) change, the equilibrium shifts.
But, yes, that also means that Gibbs free energy has changed.
Thus, there must be a change in free energy of educts and/or products as the energy of the transition state does not affect $\Delta G$, it only affects the reaction rates.
Whether this is possible hinges on the question whether we consider it still the same reaction $\ce{A + B <=> C + D}$ or whether we say that now we have another equilibrium, say, $\ce{A' + B <=> C + D}$ or $\ce{A' + B' <=> C' + D'}$ which of course can have different equilibrium constants. An example where I think one may argue either way would be the dependency of equilibrium constants on solvent.
(And, btw, we still cannot build a perpetuum mobile: solvation energy makes the difference)


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How old is the oldest intact DNA?
DNA fragments are known from bone fragments from the Mesozoic, but these don't count. I'm guessing the oldest DNA is recovered from permafrost, but how old exactly?

This sounds like an interesting question, but I'm not sure why your example doesn't count. Can you expand on that?

Well, the oldest intact DNA found is actually 419 million years old, and it belongs to (not surprisingly) bacteria. Samples were extracted from surface-sterilized salt of different geological ages (23, 121, 419 million years of age, MYA).
But as you mentioned, these are fragments. Studies on the half-life of DNA suggest that even under ideal circumstances, DNA sequences older than 1.5 million years will be too short to be readable.
The oldest genome known to date, though, is 700,000 years old, and was recovered from samples from a horse leg bone. You were correct, the leg was in permafrost. That's a considerable jump from mastodon and polar bear fossils which were about 50,000 and 110,000 years old.


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toxin determination and treatment of wild water
I am writing an article on the treatment of wild water from a wilderness survival angle. I have come across the term "toxin" and am finding it hard to produce a determination and treatment strategy.
It is first difficult to advise if a water source contains toxins, other than the presence of algal blooms. For example, a lake had blue-green algae. I understand that the associated toxin is produced by the cyanobacteria, but not the bacteria itself.
Pathogen treatment would be boiling or if available, chemicals such as iodine, chlorine or chlorine dioxide. Chemically contaminated water would require distilling.
I don't know if I can treat water containing toxins at all without distilling it or if there are different strategies for different toxins.


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Where does DNA fit on the Chomsky hierarchy?
Since adenine pairs with thymine and guanine pairs with cytosine, this seems to imply that there's a trivial Regular Expression for DNA (i.e. it's trivially a Regular Language, which is Type 3 on the Chomsky hierarchy). With that said, is there a "less trivial" Regular Expression for DNA? Or, even better, is there a "deeper" grammatical structure for DNA, such as a Context-Free Grammar?

I'm voting to close this question as off-topic because it is about language hierarchies, and not biology per se.

@fileunderwater How is this not about biology? I'm asking a specific question about the overall structure of DNA - in particular, if we can find a structure of DNA on the Chomsky hierarchy.

Well, as a start, the theoretical background to your own question, and the only reference/link in it, goes to a wiki page on "formal languages of computer science and linguistics". Sure, you need knowlegde on DNA to answer it, but the question is dealing with language classes. That is my opinion though; others may disagree.

@fileunderwater The question's fundamentally about DNA.

In truth DNA doesn't fit in the Chomsky hierarchy at all. DNA isn't a language, it is a complex molecule in a complex chemical environment. The fact that in many situations we can usefully abstract the structure of DNA as a string of four symbols should not obscure the underlying complexity. There is a simple code that describes the aminos acids encoded by triples of nucleotides, and some elements of a "grammar" in the structure of genes if you squint (start codons, stop codons, introns, and exons). But much of the function of DNA is stochastic and driven by the biophysics of the binding of RNA and protein molecules to DNA.


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unsaturated fatty acids and hydrogenation
what is the need to hydrogenate unsaturated fats?
When we hydrogenate the unsaturated fatty acid, we eliminate double bonds by adding hydrogen atoms, and this straightens out the natural bent shape of the unsaturated fatty acids. But why would we choose to hydrogenate unsaturated fatty acids before consuming them?

It makes them (more) solid.


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How to determine which allele GRCh37 has?
is there a website where I can search GRCh37 by location or rs IDs, to determine which allele it has at a specific location?
I think http://grch37.ensembl.org/ might be the answer to my question, but I'm not sure if when it says the "ancestral" allele on the results page, if that allele is the one in GRCh37. Or if it'll tell me which one GRCh37 has somewhere else on the page.
Also as a side note: I assume GRCh37 only has one copy of each chromosome (i.e. it can't be heterozygous for something?).

Why are you using GRCh37/hg19? It's pretty out of date. If GRCh38 is ok, you might consider poking around the UCSC browser with the SNP track turned on: https://genome.ucsc.edu/cgi-bin/hgTracks?db=hg38&lastVirtModeType=default&lastVirtModeExtraState=&virtModeType=default&virtMode=0&nonVirtPosition=&position=chrX%3A15560138%2D15602945&hgsid=850023477_A5lwHGMEgIZ6APPQrAAOmPBJcTzT

(it does have GRCh37 data but it may not be convenient to access what you need)

I have data in terms of GRCh37, and haven't looked into translating it, but maybe I should. And thank you for the link! I will take a look.

Ok- UCSC browser has a tool to do the liftover from hg19 to hg38 if that is helpful: https://genome.ucsc.edu/cgi-bin/hgLiftOver

Oh that's great, thank you!


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What is the copy number of a given gene in GRCh37?
sorry for the naive question, but how do I determine what the copy number is in GRCh37 for a gene with multiple CNVs? (e.g. DRD4).

Can you give some indications of things that you've tried or what kind of data you have access to?

Thanks for the reply! I was poking around this page: http://grch37.ensembl.org/Homo_sapiens/Gene/StructuralVariation_Gene?db=core;g=ENSG00000069696;r=11:637293-640706
but I don't know enough to understand a lot of it. I also tried looking at DRD4 within GRCh37 in the NCBI variation viewer.

A very naive approach would be to simply ask how many copies of the sequence in question are in the hg38 sequence, at some level of homology. You could do this using a tool such as BLASTN (which has a web interface that you can use to search against a human genome) or, if you have the sequences downloaded somewhere where you can work with them, using a tool such as minimap2 (which will be faster) as long as you're comfortable using command-line tools.
If you choose to do this, you will have to be comfortable setting thresholds for what counts as a copy of the gene in question.
A more involved solution would be to obtain DNA sequencing reads for the sample you're interested in and use them to quantify the copy number of the gene based on the number that map to a given sequence of interest. An older approach would be to use microarrays.
I am guessing that since you are interested in the reference genome that you are not interested in going to that kind of trouble.
Is this a homework question? If so, you should add the "homework" tag.

Thank you so much for the detailed answer. Minimap2 looks great. (This isn't a homework question, just a question I am pursuing to try and learn more.)

Ok, gotcha. Minimap2 is an excellent tool by Heng Li, who is also the author of the ubiquitous short-read mapper bwa and a million other projects. I strongly recommend using him and his blog as a starting point if you're getting started in bioinformatics etc.: https://lh3.github.io/

Ah perfect, I've been looking for something like this. I definitely will!


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Assessing beta diversity variations with time
I'm just starting in the field of ecological statistical analysis and I have a few doubts regarding a dataset that I'm working on.
The dataset is composed of several samples collected at a single location during a few months multiple times per day.
From my data I have estimated the beta diversity (Bray-Curtis dissimilarity) and I'd like to know if there is a monotonic trend with time and how much of the diversity can be explained by the different sampling hours or days.
My questions are the following:
- Is the estimation of Mantel's Rho using Spearman correlation is a valid estimator for the linear temporal trend?
- To estimate the source of the diversity (days/hours) would it make sense to run a npmanova analysis (as I'm using R I'd run adonis in particular) using as explanatory variables the sampling hours and dates?

I think the Mantel test is a valid way to test for a correlation, but Spearman is a non-parametric measure of correlation, and will not necessarily test for or estimate a linear trend. A Pearson moment would be better, but you might need to look at your data distributions to see if they fit the assumptions.
In response to the first answer, I don't think Procrustes is the right test for this. It's used for comparing different ordinations, which are dimensionally reduced representations of your dissimilarity matrix data. You lose information when you ordinate a data set, and you want to include as much information as possible when testing hypotheses. Constrained ordination approaches like cannonical correspondance analysis (CCA), or distance-based redundancy analysis (dbRDA) might be more suitable. These are actually analagous to some of the functions performed in adonis.
You should be able to use adonis the way your described. You'll want to make sure you also run betadispersion, which can help assess how suitable your data are. You'll also want to consider how you code your time data. It's simplest if time values are considered as discrete (day 1, day 2, etc.) or categorical (morning, noon, night) variables. Since times of day are cyclical, there's a trick with treating them as a continuous linear variable. Unless you tell it otherwise, a model will treat 23:55 (11:55pm) and 00:05 (12:05am) as being parametrically more distant in time than say 06:00 and 08:00. Depending on your daily sampling window, this might not matter much, but if you want to treat time a continuous, there's a workaround that involves sin() and cos() transformations of the time collections were taken.
It sounds like you're already using Vegan, which is a great package. You might also consider looking into LabDSV, which has a fantastic tutorial page that's more in-depth than most R vignettes. It has good examples of some of the different approaches I mentioned, as well as some others that might be of interest to you.

Thanks for clarifying my doubts! I used Spearman as a more general approach to see if the correlation was monotonic. I used categorical data for both dates and hours, but I will give the sin/cos transformation a try!

Rather than Mantel, I would suggest doing a procrustes analysis. I didn't know much about it (and still I don't) but a reviewer required it for a paper I submitted, so I used the implementation in vegan package. You can also give a look at this nice tutorial
The idea of procrustes is similar to Mantel's but it should perform better for this case.
I don't what to say about the second question, sorry!


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What is the human species divergence time
How far back along the evolutionary tree do we have to go to find divergence to a completely different species to Hom. sapiens? I don't count Neanderthals because it seems that part of our genome contains fragments of Neanderthal DNA, and therefore, according to the species definition, Humans and Neanderthals could not have been an entirely different species. What about Denisovans? Is enough known about their DNA to consider them a completely different species? In fact, is it even possible to distinguish 'a species' from the DNA alone?

http://www.ncbi.nlm.nih.gov/pubmed/?term=%22Hominidae%2Fclassification%22%5BMAJR%5D This MeSH search should provide you with plenty of answer.

Our DNA contains fragments from many many many species, as a species doesn't get an entirely new DNA sequence when they split from another. While Homo sapiens and Homo neanderthalensis were able to interbreed, they are definitely considered separate species by the majority of biologists.

@MattDMo A majority is definitely a stretch, many consider them another sub-species.

Do you also consider tiger and lions as different species? (Limited) Gene flow between the two groups has occurred. (Due to female hybrids being fertile.)
There is evidence that gene flow between humans and neanderthals was also restricted. Neanderthal genes regulating fertility, speech, neural activity are absent in human (No Neanderthal Y chromosome has ever been found in human population either), although neanderthal genes for immunity, hair and skin and coagulation have been retained. This selective-ness is pretty much a sign that hybrid fertility was reduced and that there was selection pressure to remove Neanderthal genes that govern fertility from the human population. And this is the hall mark of different species.
If you still discount neanderthal as a separate species due to limited gene flow between the two groups. Then Denisovans are also not another species because there has been limited gene flow from Denisovans into humans (Melanesians and Aboriginal Australians)

In fact, is it even possible to distinguish 'a species' from the DNA
  alone?

It is possible if you have a pure nonhybrid sample of all three species. Which was obtained from human (africans do not have neanderthal DNA), neanderthal (from various samples),  Denisovans (from a single finger bone of a female from the Denisova Cave in the Altai Mountains in Siberia)
I guess the next homo species we are aware of and have no evidence of gene flow is homo erectus (mainly because we don't have DNA from Homo Erectus)... however there is some indication that Denisovans did interbreed with an older and still unknown population of homo...
And if true you start getting into a ring species problem.... both ends of the ring are infertile and by definition are different species... yet if all member populations of the ring are still alive... gene flow between the two species is possible. So are they different species or are they not.

The erectus line that gives rise to antecessor is your best bet, at about 1.2 MYA. http://www.nature.com/nature/journal/v485/n7396/full/485033a.html
part of the problem is you are hitting the limit of where the term species is useful, once you get really close to the speciation event the term breaks down becasue everything is a ring species once time is included. Erectus includes both our ancestors and populations wholly isolated from us. Its like trying to draw a line between yellow and orange on a spectrum.

That's something that's measured by generations.
If the neanderthals bred with humans after divergence times in a range of 631–789 KY, that's roughly 30,000 generations distance, at which stage their genetics converged again.
The notion of a species is so flexible, that Neanderthals and Sapiens are considered different species, and also Sapiens is a hybrid of both.
Horses and zebras can still nearly interbreed after 900,000 generations divergeance and 4.5 million years.
What counts is the number of chromosomes. If they have the same number of chromosomes, the species can mix genetically. If they have odd numbers, the species wouldn't have a chance to converge again.
Mammals mutate more diversely than other tetrapods and birds, i.e. bats and whales are more different than any two species of bird. Mammals have less protein diversity and gene diversity than species that can hybridize after longer speciations(some birds can be viable after 20mn years), and they have more gene control variations which regulate complex metabolism traits which have to be compatible in both parents.
https://en.wikipedia.org/w/index.php?title=Hybrid_inviability&action=edit&section=1


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Why does chlorination still work?
Chlorination has been used for over a century to disinfect water supplies. Why haven't microorganisms evolved immunity to this chlorine by now?

It's aspecific, like ethanol. A bit like humans can't evolve to sustain bullets.

Antibiotic resistance works because most antibiotics target specific sites on specific proteins. If these sites can be mutated to avoid antibiotic binding, while maintaining the proper protein function, they become resistant. Some resistance is mediated by enzymes that destroy the antibiotic, or by pumps that keep it out of the bacterial cell. Chlorination is a very harsh treatment that causes general damage to many biomolecules, it would be very difficult for any organism to develop a defense against it. TLDR, antibiotics is like picking a lock, chlorination is like breaking the door down.

@Dexter posted a nice answer on this: http://biology.stackexchange.com/questions/39931/why-is-70-ethanol-preferred-for-aseptic-techniques

It is possible for microbes to acquire resistance to non-specific agents.  Radiation resistant bacteria exist. Some bacteria can also tolerate high amount of oxidative stress (they can do that by upregulating enzymes like SOD). You may find this post useful.

@WYSIWYG You are right that there are organisms that can resist the effects of chlorine. It takes a little less than 11 days for Cryptosporidium to be killed in a chlorinated swimming pool, and given that water supplies likely use much lower concentrations of chlorine, there survival time in drinking water likely increases. http://www.cdc.gov/healthywater/swimming/pools/chlorine-disinfection-timetable.html

The reason chlorination still works is that it is aspecific, just as @AliceD mentioned.
The way chlorination works is mainly by oxidizing biological molecules. Chlorine, along with other halogens, is a strong oxidizing agent. It breaks down the phospholipid bilayer membrane, proteins and enzymes. There is no way organisms can overcome this, unless it uses none of the chemical molecules that react with chlorine, which is virtually none.
On the other hand, antibiotics inhibit particular enzymes and proteins in a particular way and by making one or two amino acids different in the protein, the microorganisms can easily overcome this.
Reference - http://www.sswm.info/sites/default/files/reference_attachments/TUE%202011%20The%20Chlorine%20Dilemma.pdf

@WYSIWYG But enzymes like SOD are mainly for tolerating oxygen radicals and reactive-oxygen species, not chlorine oxidation.

Chlorination refers to the addition of chlorate (ClO3-), not Cl2. Hence, it is not halogens being added to water - that would be bad :)

@AliceD Wikipedia doesn't back up your statement https://en.wikipedia.org/wiki/Water_chlorination

@MarchHo I'll look into it. Interesting. I must say I commented from memory. Thanks.

@AliceD technically you sre correct as the chlorine gas, when dissolved in water, forms thar ion... But I didn't include all the details. I just wanted to make it simplified.

Well, there are microorganisms that have adapted or were resistant in the first place... that is why cryptosporidium is such a problem in the potable water supply. While it is not much of an issue for healthy adults, it can be very bad for immunocompromised people. http://www.cdc.gov/healthywater/swimming/pools/chlorine-disinfection-timetable.html


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What causes fruit taste enhancement?
I'm not sure if this is a biology or chemistry question, maybe both? Some fruits, such as quince and quondong, taste of nothing when raw but have an extremely strong flavour when cooked. Why?

I am a little confused that does the word "cooked" means ripe？If yes, then the question will be easy to answer. Fruit has a kind of ripener, ethlyene. Ethlyene will help fructose break down and make up more glucose. That is why you may taste a strong flavour when fruit is cooked.

By cooking I mean literally heated with water in a saucepan. I'm not sure about glucose being the answer though. The 'flavour explosion' of cooked quince, in the mouth, seems to me to be far more than merely additional glucose.

So, when you cooked the quince (which means the quince got a higher temperature), the fructose would take a chemical reaction, polyreaction. And the fructose was transformed into amino acid. So you may taste sourer than before you cooked the quince. How do you think?


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How much genetic divergence must there be to yield two different species?
I read that humans are a few percent Neanderthal. So how much difference between egg and sperm is needed for there to be no offspring. That is, for there to be two different species? Is this a measurable quantity or just a random genetic mismatch?

The 'no offspring' barrier is a bit arbitrary, I'm afraid. Consider pizzly/grolar bears, who are perfectly fertile. And yet grizzly bears and polar bears are considered two different species.

Could you please add a reference to where you read something. It helps to give a frame of reference to people trying to answer your question. An article in the Daily Herald, is different than one that you read in Popular Science is different that one you read in Nature.

Try reading this first, Reproductive Isolation , and then if this still doesn't answer your question or if it raises other questions, please feel free to edit your question.

Besides "species" being an ill-defined term, the required genetic divergence isn't appropriately characterized by "how much" genetic change, but rather what precise genes have changed in what ways to prevent population mixing. A single gene or two might cause it, if it affects a critical function, say having to do with sperm/ovum compatibility.


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Why aren't more prostate glands just removed?
Some 80-90% of men have some problem with their prostate gland as they get older. Beyond about age 60 it is unlikely that men will need the prostate to contribute to seminal fluid, so there seems little point in keeping this troublesome organ - yet a huge proportion of older men end up with either benign prostate hyperplasia and/or prostate cancer. So why isn't the standard treatment just to remove the prostate altogether?

Are you saying men older then 60 don't need sexual lives?

Apart from the 0.4 to 3.0% of people who aren't interested in sex (depending upon who's survey you believe) sex is, of course, important. But the prostate only produces about 30% of seminal fluid, whilst at the age of 60 the chemical components generated by the prostate are unlikely to be needed to impregnate anybody.

Almost all men will experience erectile dysfunction for several months to a year after a radical prostatectomy - http://www.harvardprostateknowledge.org/achieving-orgasm-after-radical-prostatectomy

Your question is along the lines of "Many women will develop breast cancer, especially later in life. Why don't they just remove their breasts after menopause, because they won't need them for breast feeding?" There are a lot of disadvantages and only questionable advantages.
Chief among the effects of removing the prostate are urinary incontinence and erectile dysfunction. That area of the body is very highly innervated, and it is nearly impossible to just remove the prostate without damaging anything else. While it is true that many men will develop prostate problems as they get older, they can frequently be treated medically, or just observed for any dangerous changes. Benign prostate hyperplasia is just that - benign - so there's no need to undergo a major operation with significant side effects. Additionally, many prostate cancers are so slow-growing that they never metastasize or pose any threat, so they are simply monitored and treated medically as needed.


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How to determine the relationship of competition or cooperation?
I am currently studying the interaction of Twitter memes (two or many), such as competition and cooperation. Is there any model or method in biology that can identify the types of the relationship, such as competition or cooperation?
I have heard the Lotka–Volterra equations, but when I begin to dig deep, I found that it is still not suitable.

Welcome to Biology.SE. By identify, are you referring to methodologies of identification of to definition. In other words, are you asking for comonly accepted definitions or for methodologies to detect a concept that you have already defined (in which case, can you please your definitions).

@Remi.b Yes. I want to know the commonly accepted/acknowledged methods to define competition and cooperation between specifies.

I am not sure what you mean by "methods to define". Either just "definition" or "methods to detect"would make more sense to me. I wrote an answer to provide some info about the definitions of the different biological interactions (and not about the methods to detect them).

Species interactions
Generalities
Species interact. Species actually interact a lot. One can classify species interactions into categories based on the effect that the interaction has on their fitness (≈ reproductive success). Here is a table of possible biological interactions (comes from [wiki][1]), where a + indicates "beneficial", a - indicates "detrimental" and a 0 indicates it has no effect on fitness.

Different terms exist for a given relationship. Typically, antagonism is often called parasitism.
Note about symbiosis
Different authors use the word symbiosis differently. From wikipedia:

The definition of symbiosis is controversial among scientists. Some believe symbiosis should only refer to persistent mutualisms, while others believe it should apply to any type of persistent biological interaction (i.e. mutualistic, commensalistic, or parasitic).[6] After 130+ years of debate,[7] current biology and ecology textbooks now use the latter "de Bary" definition or an even broader definition (i.e. symbiosis = all species interactions), with the restrictive definition no longer used (i.e. symbiosis = mutualism)

Blurry limits
Generalities
It may seem pretty obvious that two species should have either one type or another type of interaction. However, the reality is often more complicated than that. An interaction might fall in one category under one set of environmental conditions and fall under another category under another set of environmental conditions. In addition to that, it is not uncommon that due to selection on the host genes due to the presence of a parasite, the host evolve so to tolerate the presence of the parasite up to the point of actually having a lower fitness in the absence of the parasite.
Example of environment-dependent interaction type
Consider an animal that is host to an algea. The host is providing shelter to the algea while the algea is providing sugar (produced through photosynthesis). If there is no light or if the enviroment is loaded with sugar, then the host has no gain of hosting the algea. In such case, the algea may even be parasitic. If, however, there plenty of light and there is few nutrients in the environment, then the algea and the host have a mutualist relationship.
Example of the evolution of a parasitic interaction
Consider for example a snail which is infected by a parasite. Let's assume (I think it is a real world example but I am too lazy to find out a reference) that the parasite need the snail to be eaten in order to reproduce in the body of the predator. In order to improve the chance of its host to be eaten the parasite is selected so to diminish the thickness of the snail's shell. In response to that, there is selection (which intensity depend also on the proportion of infected snails in the population) for having thicker shells. But now, snails that are not infected have shells that are so thick that the can't move as fast as they'd need to forage. So, by the end infected snails may have a higher fitness than non-infected snails. And therefore the interaction between the snail and its parasite is not a parasitic interaction anymore but a mutualistic interaction.

Is there a mathematical model or analysis that can determine the types of interaction based on the specifies' population growth curve?

Not that I am aware of. You might want to ask further questions on CrossValidated.SE and eventually use dummy data and ask how can one investigate this question knowing that there is a delay between the change in size of one population and its affect on the other population.


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Building microtubules
I have some questions regarding building microtubules:

Do alpha and beta monomers always exist as dimers when they are bonding to form tubulin?
When tubulin structure is destroyed, do alpha and beta monomers fall apart as dimers or monomers? and does it happen at the positive or negative end?

Microtubules polymerise from and depolymerise into alpha-beta-tubulin dimers.
Both happen on both ends, see this question: At which end does polymerization of microtubules occur?.

Thanks for your answer. Wouldn’t it be more favorable to connect monomers rather than dimers ? because then it wouldn’t matter how the dimers are oriented to get alpha on top of beta.

The orientation of each monomer would still need to be the same, regardless of the order in which the bonds are made, because none of the molecules involved are symmetric. I don't know though how it's better to have dimers around as building blocks rather than monomers.


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psbA-trnH intergeneteic spacer inversion
What kind of software tool would you recommend as best suited to detect psbA-trnH inverisons?
I have 1x coverage Sanger .fasta files and >2000 sequences, with 1 sequence per species.
Most tools I have found are only suitable for next generation seuqncing data or inversions that are larger than 50 bp.
Here is an example:

(dotted line)

Please [edit] your question and highlight the precise inversion you are looking for. I know you've shown us the relevant region but what is the "non-inversed" sequence and what is the inversed one? I don't see anything obvious in your alignment.

The inversion is where the dotted line is, for example. Non-inversed is TTCTAG and inversed is CTAGAA.
I don't know what I am looking for, that is what the question is about. I need to find the inversion. The pictures are just examples of what it could look like.

Yes, that much I understood :) However, since you've posted an image and not an actual alignment (not text that I can copy and investigate), we need more detail. I can't see what the inversion is and what the reference is. You also show two separate alignments with completely different regions marked. Your second seems to be referring to 5nt while your first to more than 20.

Yes exactly, I have 10000 sequences across all plant families and I don't know which length or which positons the inversions have, or if they exist at all. That's why I need help to find them. Maybe there is a tool that I am not aware of. Posting an alignment is not possible, because the standard alignment tools do not align this region, it gets spaced out, because it looks very diverse, however it's not. Alignments seen above are corrected by hand.


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Viruses and Transformation
Would the lysogenic cycle for the reproduction of viruses be considered a form of naturally occurring transformation since DNA from the virus is being incorporated into the DNA of the host cell?

The answer lies in the definition itself of transformation. See from here:

In molecular biology, transformation is the genetic alteration of a cell resulting from the direct uptake and incorporation of exogenous genetic material from its surroundings through the cell membrane(s). For transformation to take place, the recipient bacteria must be in a state of competence, which might occur in nature as a time-limited response to environmental conditions such as starvation and cell density, and may also be induced in a laboratory.

What is clear from this definition is that host cell needs to be competent for taking up extracellular DNA to call the process transformation. Also, the term direct uptake does not seem to fit here as, you know why, bacteria do not just go on collecting viral DNA from their surroundings.
Obviously, bacteria are not competent to take up viral DNA, nor the virus makes them so. The virus simply injects and joins its own DNA into baterial genome. Now, it would be some common sense to know that the host does not like it, so whether it is competent or not, is just a matter of debate (did anyone ask them?). In short, No, the process of lysogenic cycle would not be considered transformation as the bacteria are not made competent for this process.


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How much protein to add for complete binding
I have 7mg of a 74kDa protein $A$ bound to a column. I want to bind another protein $B$ which is 19kDa onto protein $A$ so that every protein $A$ is bound (or as close to 100% binding as possible). I also know the $K_D$ of protein $A$ to protein $B$ is $9\cdot 10^{-8} M$, I am not sure if this is even relevant. How much of protein $B$ to I need to flow through to try to get complete binding?
One protein $A$ binds to one protein $B$. Can I just convert the 7mg into the amount that would result in one to one binding, i.e., 1.8mg of protein $B$? Then does the dissociation constant even matter? I don't have a ton of protein $B$ so I need to be frugal and calculate how much to use.

I would strongly suggest starting with much smaller amounts (micrograms) and figuring out the conditions there before scaling up. Depending on what it is and how you're making it, 7 mg is a lot of protein. You don't want to waste it all (and however much Protein B you use) if you make a mistake.

@MattDMo The problem is the column is somewhat large, I may have to find a different way ultimately. However, I am still wondering about how to calculate the solution to this problem.

Can you figure it out from https://en.wikipedia.org/wiki/Dissociation_constant ? If not, where are you stuck?

One other thing to consider - will Protein B bind to the column itself, either specifically or non-specifically? Also, what kind of column is it - bead-based like a typical liquid chromatography column, solid-phase like a GC column, something else?

@BryanKrause It seems from the dissociation constant, if I were to want all of it to be in the bound state, I would need an infinite amount of the protein according to the equation?

@RuochanLiu That's correct; really, in biology and chemistry, complete anything is usually aspirational at best. Also as MattDMo points out, when you have other things to bind to the situation gets more complicated. So, you'll need to figure out what you really need based on what you're trying to do, which isn't particularly clear here so far.


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Electronic properties of neurons
This is about the electronic properties of neurons.
When a signal is sent from 1 part of the brain due to a stimulus,are neurons considered voltage or current sources?

Can you please provide context of what you already know and what you've read trying to answer your question? As written, it doesn't make much sense in the context of biology.

It is necessary to study the known substitution circuits of neurons - these are representations of neurons in the form of equivalent electrical circuits, where capacitances, inductances, or others imitate the potential-current properties of membranes and other conductive elements


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Are bacteria members of Kingdom Monera or a separate domain by themselves?
The openstax biology textbook by Rice University says: "For example, after the common beginning of all life, scientists divide organisms into three large categories called domains: Bacteria, Archaea, and Eukarya."
But the latest edition of the Indian biology textbook (grade 11) speaks of a Five Kingdom Classification: Monera, Protista, Fungi, Plantae, and Animalia. It also says: "Bacteria are the sole members of the Kingdom Monera."
Which of these is correct? Are bacteria members of Kingdom Monera or a separate domain by themselves?

A domain is a higher level of organization than a kingdom, so they do not necessarily conflict. Please see this lecture for more context. Wikipedia also describes this at some length. There are additionally other questions on this site that discuss the issue, though none directly seem to answer your question.
The domains were introduced instead of the 5-kingdom model due to molecular work establishing the very very large differences between bacteria, archaea, and all other forms of life to be more representative of the actual biological relationships, and particularly the large molecular differences between the otherwise very similar-seeming archaea and bacteria.
The 5 kingdom are an older, more qualitative and less precise grouping. There are now other models that have a larger number of kingdoms under the domains (which are sometimes called other names like superkingdoms). These kingdom models nest more or less naturally under the domain model.
Of course, all taxonomies are somewhat arbitrary. The domain model is an attempt to make the groupings resemble evolutionary history more, and outward organismal characteristics less.

So, which kingdoms are currently under the domain Eukarya?

@Thomas Did you bother to follow any of the links in Maximilian's answer?


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How do we know how long speciation occured?
Just as we use radiometric dating to age rocks, what is the method used to age how long ago speciation occurred in genetics?

https://en.wikipedia.org/wiki/Molecular_clock

Does this answer your question? Phylogenetics and the Tree of Life


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How do we logically infer large time scales using Molecular Clocks?
If molecular clocks are uses in genetics to determine the mutation rate of genes to estimate times speciation occurred between two or more life forms, are there genes that have mutation rates that we can observe that allows us to deduce mutation rates over hundreds of thousands to millions of years?
For example, Homo Sapien speciation occurred 300,000 years ago from Homo Erectus that existed 2 million years ago. How did we get those time scales? Are there mutation rates in simple bacteria or viruses that are constant that we can use to logically build up to those longer time scales?

There are a few different questions going on here.

Mutational clocks are not the only, or even the primary, means of dating specimens of these species. More common is to use carbon dating, for example as done here, to establish when certain species existed.
Mutational molecular clocks are calibrated based on observed mutation rates. It is fairly routine to measure mutation rates per generation using whole-genome DNA sequencing. We have a good vision of what substitution rates are on average throughout the genome.

For an intuition of why this works, consider that there are roughly $3*10^9$ bp in a haploid human genome. The human mutation rate is about $1*10^{-8}$ per generation. So every generation, we expect around ~30 new mutations on average per haploid genome. It's simply a matter of observing the whole genome to find them.
Mitochondrial genome mutation rates are quite a bit faster, and were some of the first genomic regions used to do this kind of dating, before whole genome sequencing became so routine.
Using that kind of information, we can make some statistical guesses about the relationships between Homo species (I'll let you look at some of those references to see how that is done).


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When purifying plasmid DNA after cloning, do you get endogenous plasmid in addition to your vector of interest?
Since bacteria naturally contain plasmids, when you do a cloning experiment and purify the plasmids at the end, do you get plasmid naturally present in that bacteria in addition to your vector? The standard plasmid purification kits (miniprep, maxiprep, etc.) aren't sequence specific in their purification (they just seem to isolate all plasmids in the cells). I would assume you want a constant purity of vector. Otherwise, for example, you could have 2 vials of plasmid at 1 ug/ uL plasmid while one has 0.4 ug/ mL vector and another 0.8 ug/ mL vector which wouldn't be good for reproducibility. Or is it that the bacteria used for cloning are devoid of naturally present plasmids which would fix this issue?

Very interesting question, Chris. What result do you see when you analyze a miniprep from non-transformed bacteria on an agarose gel?

I'm a bit newer to this area of biology techniques so I haven't looked at many plasmid preps yet. The plasmid prep that I have seen on a gel had one band (or 2 bands if cutting the insert out with a restriction digest). If this result is generalizable, it would suggest the vector was present in much greater quantity than any of the endogenous plasmid (if there was any endogenous plasmid at all). I can think of 2 reasons for this (if the result is generalizable):

Sorry I accidentally posted the previous comment before it was finished. I was going to say the 2 possible reasons that I could think of are (I don't know which reason is the primary reason though): 1) The strains used for cloning have less endogenous plasmid. 2) The bacteria had to express a lot of vector to get sufficient antibiotic resistance such that the vector was present in much greater quantity than you would normally see in endogenous plasmids.


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Crickets with live babies
From what I understand of Crickets, they lay their eggs in dirt and hop away and that is their parenthood.
But in the past month (since I moved into this apartment) I have found 1 adult cricket and half a dozen tiny baby crickets in my bathtub on THREE SEPARATE OCCASIONS.
There have been times I have found other adult crickets in the tub, I have never found a baby cricket in the tub alone.
Something is going on here that doesn't track, an adult cricket could easily get into the standard 18 inch-ish high bathtub, but these baby crickets are about 2mm long and can jump upwards of about 3 inches from my testing.
Why/How are they traveling together?  What is the gestation on crickets?  Is it short enough that she lays the eggs at night and they hatch by mid morning?   Are they coming up the drain?  Carrying their brood on their backs because this is Arizona and they learned it by watching scorpions?  I need answers! This is the weirdest mystery of quarantine, and it must be solved.


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Is there any animal database or website that classifies animals as wild / domestic?
Is there any animal database or website that classifies animals wild / domestic?
Or.. the site that I can get the wild / domestic information of animal list...

That’s a hard one. For many species, there are individuals that are wild/feral, and individuals that are domestic: cats, dogs, birds, snakes, lizards. iNaturalist has an option to indicate whether each observation is captive or cultivated, and that’s about it.

If we knew the purpose of the question we might be able to offer more help. There is a lot of grey area with domestication.

I need the list of wild animals for the project.. so I tried to get the database of the animal list which classifies wild / domestic.


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How do beavers learn how to build dams?
I was wondering whether all beavers, from all around the world, know how to build dams and lodges? Do they need to learn it from their parents? If you release a group of beavers in the wild that haven't been in contact with their parents, would they start to build stuff? or just hopelessly die/starve to death?

Question summary: is dam building learned or instinctive in beavers?
A blog post from 2011 references an article in the Juneau Empire titled Running water is sound of spring for beavers.  This article is no longer hosted on the Juneau Empire website, but archived versions are available.
Here's an excerpt (emphasis mine) --

Swedish biologist Lars Wilsson spent years studying captive and wild beavers, and he gained remarkable insights into their behavior. He raised beavers in an outdoor enclosure and in a large indoor terrarium ...
Wilsson initially captured four adult beavers and later he raised a number of beavers from infancy, some in small colonies with their parents and some completely isolated from adult beavers. He isolated the young beavers to see what beavers learn from their parents and what behaviors are instinctive.
He found that young beavers - who had never even seen a beaver dam - were able to build almost-perfect dams at the first opportunity.
The foundation of sticks and logs anchored to the stream bottom, the interwoven lattice of trimmed branches, the mud chinking, every aspect of dam building was hard-wired. Beavers do get more skilled at dam building as they gain experience, but the building behavior is instinctive.
Wilsson learned that the sound of running water is the cue for dam building and dam repair. In one experiment, he played a recording of running water, and the young beavers built a dam in a tank of still water in the terrarium. In another peculiar experiment, his captive beavers built a "dam" on a concrete floor against a loudspeaker that played the sound of running water.


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Umbrella term for agonist, antagonist, inverse antagonist, etc.
For most receptors there exist different ligands that induce different responses. Depending on the response these different ligands can be classified into different groups such as agonists, antagonists, inverse antagonist, etc.
My question: is there a term that summarizes all of these different concepts?
I'm looking to express something like the following: 'addition of a methyl group to the phenyl ring changed its X from agonist to antagonist.'

activity

"addition of a methyl group to the phenyl ring changed its activity from agonist to antagonist"

A technical word that encompasses agonists, antagonists etc. is effector, defined in the Wikipedia entry as follows:

Effector
In biochemistry, an effector molecule is usually a small molecule that selectively binds to a protein and regulates its biological activity.

However ‘effector’ does tend to be used more in regulation of enzyme activity than signal transduction. I suggest this is preferable to the term ‘activity’, suggested by  @DeNovo as it is the targets of agonists etc. that exhibit the biological activity that one may be considering, rather than the agonists themselves. Such effectors modulate the activity of other molecules, so one could even consider using the term ‘modulator’, described in a Wikipedia entry — for the particular case of allostery — as follows:

Allosteric Modulator
In biochemistry and pharmacology, an allosteric modulator (allo- from the Greek meaning "other") is a substance which indirectly influences (modulates) the effects of a primary ligand that directly activates or deactivates the function of a target protein.

However I would definitely not use a noun of this sort to convey the idea of your sentence.
I find that more complex and clumsy then necessary. Far better, in my opinion, to express yourself in simpler terms and more directly.

“Addition of a methyl group to the phenyl ring changed it from being
  an agonist to an antagonist.”

or

“Addition of a methyl group to the phenyl ring changed its action from that
  of an agonist to that of an antagonist.”

However ‘effector’ might be useful as a portmanteau description of agonists etc. in circumstances when you are listing things.

"Portmanteau - A word formed by merging the sounds and meanings of two different words" - American Heritage Dict.; "A word blending the sounds and combining the meanings of two others, for example motel (from ‘motor’ and ‘hotel’)" - Oxford Living Dictionaries

@mgkrebbs — Umbrellas at dawn! I referred to a portmanteau 'description'' not a 'word'. I use British English Dictionaries that include the definition in the sense I used it (and have used it all my life). Thus, Chambers on my iPhone has "Adjective: Combining or covering two or more things of the same kind". And Cambridge has the example "The Official Secrets Act was described as a piece of portmanteau legislation, covering everything from nuclear weapons to army boots" and also  has an example with the word "motivation".


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Why are precultures done in Luria-Delbruck fluctuation assays?
I looked at a variety of descriptions of the classic Luria-Delbruck fluctuation assay protocol for determining mutation rates in different organisms (e.g. 1, 2, 3) and noticed that they all start from a cryostock of an organism which is inoculated in medium and grown overnight.
Next, the preculture is split into parallel cultures. After another round of incubation the cultures are plated on selective medium and the number of colonies counted. With this count together with the number of generations the mutation rate can be estimated.
However, I'm wondering, why not start with parallel cultures directly from the cryostock?
It seems to me that the in between preculture might just introduce additional variability because mutants may arise during this period of time already. This appears especially relevant if the studied organism has a very high mutation rate.
Can someone explain why apparently having an additional preculture does not matter?

Perhaps you need a minimum population for the assay. The organism could be propagated either before or after freezing.

@PolypipeWrangler that's definitely correct, but could be achieved by directly inoculating a larger culture which at least standard lab work horses, E. coli, S. cerevisiae wouldn't be a  problem.


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Computational engineering of protein binding pocket
I have an X-ray structure of an enzyme with reported activity to a small molecule.
This activity is rather low since it is not the native substrate.
I can run molecular modeling simulations (e.g. using DOCK) to estimate the enzyme's binding behavior to different compounds. However, what I would like to be able to do is to mutate the binding pocket so that it better binds my small molecule of interest.
Exploring all possible amino acid substitutions is computationally too expensive, so I am wondering whether smarter ways of looking at this problem have been developed.
Can someone point me in the right direction? I've searched Google but can't really find a straight forward answer

Could you choose rational mutations that you think may facilitate binding and only study those? The results of one mutation may inform the next.

@canadianer There is probably a way. However, I would not want to have to reinvent the wheel if someone has done something like that before

You can try an evolutionary algorithm. If you can quickly evaluate the binding affinity you can initialize a set of copies of your protein but with random mutations. You can assign them a fitness score based on the affinity of the binding. The ones with highest affinity you replicate again with some probability of mutating each amino acid and you continue for as many generations as you need. If you find your parameters (mutation rate, population size, etc) correctly you can easily optimize the binding without knowing anything a priori about the different sites. There is a lot of literature on this, I suggest you do a quick Google scholar search on directed evolution or evolutionary algorithms to optimize binding affinity.
Paper on in silico evolution to optimize protein-protein binding

Thanks for the input. If I understand correctly they used in silico design and experimental optimization to get to the final result. They did not use an evolutionary algorithm. However, I think that this is generally a promising path to explore. I am just wondering whether so already developed such a tool.