What would happen if there were no more spiders? In an office conversation about arachnophobia, one colleague declared "they're hoorrible and they should all be killed". He doesn't like spiders.

I've heard of the scenario where bees die out quite a lot, sounds like that would be pretty catastrophic.

So what would happen if suddenly there were no more spiders?

Spiders are extremely important predators, both in "natural" ecosystems and in agriculture. They therefore function as biocontrol agents, and without them we would suffer larger crop damage from pest insects (or would require much higher levels of pesticide use). Loosing them from all natural ecosystems would also cause enormous effects, due to cascading effects through the foodwebs. The effects would differ between different ecosystems though (with the largest effects probably in forests and grasslands, see links 3 and 4 below), and nobody can really overview or predict the full implications.

  A new study reveals some stunning estimates about just how much the world’s spiders eat annually: between 400 and 800 million tons of insects, springtails, and other invertebrates. In the process, these eight-legged carnivores play an important role to keep countless insect pests, especially in forests and grassland areas, in check.

(from third link below)

For more, see e.g.:

Rusch & Bommarco. 2016. Agricultural landscape simplification reduces natural pest control: A quantitative synthesis. Agriculture, Ecosystems & Environment
Öberg & Ekbom. 2006. Recolonisation and distribution of spiders and carabids in cereal fields after spring sowing. Annals of applied biology. DOI: 10.1016/j.agee.2016.01.039
Spiders eat astronomical numbers of Insects (popular overview of paper below)
Nyffeler, M. & Birkhofer, K. (2017). An estimated 400-800 million tons of prey are annually killed by the global spider community. The Science of Nature


Is wiping with RNAse Zap enough to destroy RNAse activity? From the RNAseZap MSDS, it is an SDS at some unknown concentration, maybe with some NaOH?

Some other links suggest there is some NaOH as well.

The Ambion site states that RNAseZap destroys RNAse activity on contact, but they also instruct to rinse with water twice after wiping RNAseZap on the surface being cleaned.

So, does RNAseZap actually destroy RNAse activity, or is it simply a "good detergent" to pick them up and rinse them away?

Thanks!
Carmen

It's hard to know what RNaseZap does since the ingredients list is a trade secret.  However, I expect it is a lot more than just detergent.  RNaseA is extremely hard to destroy; moreover it can easily renature once the denaturant is removed. Therefore, very minute quantities are sufficient to annihilate RNA experiments.  The historical method of purification was to boil solutions of it until all other proteins denatured and could be easily separated. I can personally attest that you can precipitate it in pure alcohols and it will spontaneously refold as soon as it is rehydrated.

I would not trust a simple detergent to get rid of it; you'll need something more volatile to be reliable.  A lot of "home made RNaseZap" recipes on the internet include hydrogen peroxide, which causes a variety of covalent modifications to the protein.  It also has the advantage of cleaning itself up (eventually turning into H2O).  The detergent is useful because you typically don't want any protein residue floating around your experiments, denatured or not.  If you have some dried RNaseA aggregates, it will also help break those up.

I work with RNaseA itself, so I can't personally vouch for the recipe below (since I'm not interested in destroying my sample), but it seems sound.  But if you have the cash to blow, just get the RNaseZap.  It's very widely used by RNA labs and you really don't want to chance a potentially expensive experiment on it.  Especially since you're constantly shedding tons of RNaseA from your skin, being sloppy will probably bite you eventually.

Mechanism of action for H2O2
plausible recipe


How to compare models of evolution to make assumptions about selection? I'm having trouble understanding the concept of comparing models of evolution with LRT. I have following models: M0 (neutrality), M1A (negative selection) and M2a (positive selection) with following results from Maximum Likelihood:

M0: w=0.81; lnL=-5702.55
M1a: wo=0.50, po=0.65; w1=1.0, p1=0.35; lnL=-5650.21
M2a: wo=0.46, po=0.64; w1=1.0, p1=0.25; w2=2.38, p2=0.11; lnL=-5632.10.

I want to do the Likelihood Ratio Test to compare the models and make assumptions about the selective pressures on the analyzed sequences. So, first I compare M0 and M1a and calculate LRT=2(lnL1-lnL0)=104.68.

Now I want to take a look at a Chi table, but what am I using there? Am I supposed to used the po value for the M1a model? And if that value exceeds the value of the p-value in the table then the simpler model is chosen?

The answer to this question depends strongly on how you are formulating the different models. Are you for example computing this from dN/dS from a sequence alignment? Or based on explicit phylogenetic models? Those can have quite different formulations. The model names you are using out sound like they might come from PAML, but it's not clear. There are some exercises for this specific case elsewhere.

I am assuming that what you are really asking is how many degrees of freedom to use when e.g. computing a p value.

For this question, you have to think about the LRT a little. What it is really asking is "do I explain the data better by adding parameters to a model (while accounting for the fact that likelihood will by definition increase with more parameters)?"

So what you need to first establish is what the parameters of your models are. Assuming that the models are "nested", you can just use the difference in the number of parameters as the degrees of freedom. "nested" in this context means that the base model (e.g. H0, probably M0 for you) doesn't have parameters that are missing for the alternative model (which is assumed to have more parameters).

More flexible than the LRT are things like the AIC, which gets rid of Chi square and just computes a value from likelihood and model parameter number. This works well in practice and is nice because it's more flexible and a little less convoluted model comparison technique than the LRT. You can additionally use the AIC to compare non-nested models, which doesn't really work for the LRT.

I hope that this helps.


Fibonacci sequence in nature, truth or just wishful thinking? I'm reading a bit on the Fibonacci sequence in nature, be it the golden ratio or the golden spiral forming over and over again in biological structures, and then I came across this online article by Donald E. Simanek, refuting a lot of these observations as merely optimistic 'flim flam'.

So which is true?

Does the Fibonacci sequence have a place in nature or is it all just a case of vigorously looking for anything that resembles a correlation?

As far as I remember, Fibonacci patterns emerge in plants from hormone gradients. I.e. an apical meristem forms a leaf where the auxin concentration is highest, and already existing leafs lower auxin concentration, leading to some negative feedback.

See e.g.
http://www.sciencedirect.com/science/article/pii/S1360138507000581

or http://en.wikipedia.org/wiki/Phyllotaxis


Maximum loading volume for agarose gel with 10 well comb I want to load my agarose gel with my PCR products, which are 50 µL reactions.

I am wondering how much of those reaction I can load into one well if I use a standard agarose mini gel (10 well comb, ~8 mm thickness, 1.2%).

Should I try loading the entire 50 µL into one well or should I split it into two?

Thanks in advance

Phil

How many samples have you got? You can tape neighbouring teeth of the comb together to create double- or triple-wide wells to load more sample.

I don't normally load more that about 20 µL.

You could also make the gel thicker potentially.


Why can't two different genetically species reproduce to give a viable offspring? What is the reason that only organisms belong to same species can produce a viable and reproductively healthy offspring but organisms of two different species cannot?

The short answer is that "different species" are defined as "not being able to produce viable offspring".  So the answer to your question is that it's a tautology; it's that way because that's how it's defined.  You're asking a question about words, not about biology.  If you were able to persuade people that a "species" was "anything living in the same area", then "different species" would be perfectly able to reproduce.

More specifically, there are many different definitions of "species", and you're asking a question about one particular definition, the "biological species" concept that was first presented by Ernst Mayr in 1942 in his book Systematics and the Origin of Species.  Mayr's definition is a useful one, but it's far from the only one; there are literally dozens of other definitions of "species".  See Wikipedia's The Species Problem for more information.

Still, it's worth asking why there biology does (to some extent) have "species" that don't interbreed; Mayr's definition has stuck because it is useful.  The first thing to consider is how remarkable it is that any two individuals (of the same species) can interbreed at all.  It's not the default option! There are thousands of highly specialized quirks that allow fertilization to happen at all. Males and females have to be incredibly fine-tuned to recognize each other, to have sperm and egg meet each other, to have the sperm identify the egg, to enter and mix genetic material ... the cascade is tremendously unlikely and has to be rigorously maintained.

So when it's not maintained -- when there's no selection pressure on two populations -- inevitably there will be genetic drift that will randomly disrupt this fine-tuned system. If a population of, say, voles is isolated on an island, they will continue to have pressure to be able to interbreed with other voles on the island, but if they can't interbreed with those on the mainland there won't be any consequences, and so over long enough time they'll drift and lose that ability -- just as many apes, not suffering any consequences from not synthesizing vitamin C, gradually lost that ability from random drift.

There's another side to it. Two populations in the same location may be positively selected to not be able to interbreed. Think about two groups of finches, one with small fine beaks that eat tiny seeds deep inside pine cones, and one with heavy beaks that crush and eat thick-shelled nuts. They each do fine, but they can interbreed and produce offspring that have intermediate beaks -- too thick to reach the fine seeds that one parent eats, but too delicate to crush the nuts that the other parent eats. Those intermediate offspring will die off, and both parents will have wasted their resources raising them.  Both parents would be better off not breeding with each other,  but only breeding with their own kind to produce specialized and efficient offspring. There is now selection pressure on the birds to recognize their own kind (perhaps through songs or mating displays) and ultimately to be inter-sterile, so they never waste resources on the un-fit offspring. There's a gradation of separation over time, in which the different populations become more and more distinct. Eventually, at some arbitrary point, humans start calling them "species", but that's just us, not biology.

"Species" is an important concept, but it's not special in evolution; speciation is just one aspect of natural selection, there's nothing magical about it.


Why do anaerobic bacteria require a low redox potential for their culture media? I'm reading Clostridium ,which is an anaerobic bacteria in my microbiology text and it says,

  of more importance than the absence of oxygen is the provision of a sufficiently low redox potential in the medium. Third can be achieved by adding unsaturated fatty acids, ascorbic acid, glutathione, cysteine, etc.

Why? Do they reduce oxygen free radicals or something? Well, are these present in Clostridium's natural habitat?

The higher the redox potential is, the higher the oxygen dissolved in the media will be. Lowering this potential insure that the oxygen concentration is lower and that the anaerobe will be able to grow easily.

Several steps can be done while preparing the media such as boiling to remove oxygen and adding chemical which reduces this redox potential to dissolve oxygen back into the medium.

As for the natural habitat, they naturally have no or really really low amounts of oxygen. If the habitats containing little oxygen have other molecules able to reduce redox potential is a good question.

Lowering the redox potential is mainly important for the medium since there is oxygen involved (hard to remove 100% while preparing media).

I hope my answer helps.


Concentration of a specific promoter in a cell? I want to simulate transcription activation by a given transcription factor (TF) with known kinetics. The binding rate $k_{on}$ is given in $\mu M^{-1} s^{-1} $, describing a bimolecular reaction mechanism (second order reaction kinetics). However, what is the concentration of a specific promoter in a cell?

In a diploid organism there are two copies of DNA which means two copies or "molecules" of promoter in the entire cell. The volume of a typical eukaryotic cell (HeLa) would be 2.25×10-12 litres (Zhao et al. 2007, BioNumbers).

$$\text{Concentration }(M)=\frac{\text{Molecules per cell}}{\text{Avogadro No.} \times \text{Volume of the cell }(l)}$$

This comes to around 1.4758×10-12 M for 2 molecules of promoter. Accordingly, you can calculate for a haploid cell, multiple alleles or prokaryotic cell.

You can also assume a 2-compartment model with nucleus and cytoplasm as two different compartments. In this case, the DNA would be localized in the nucleus and therefore its effective concentration would be higher in the nucleus. You can look up nuclear volume in BioNumbers and plug that in the above formula to obtain the effective concentration.

Zhao, L., et al. "Intracellular water‐specific MR of microbead‐adherent cells: the HeLa cell intracellular water exchange lifetime." NMR in Biomedicine 21.2 (2008): 159-164.


Is the "freeze response" really a remain of our reptilian past? I'm looking for any reliable sources relating the common-known human reaction on a stressful situation, humans sometimes freeze and can not move. From some materials found on the internet I got that it is supposed to be a remain from the bugs' playing dead. But it doesn't seem to be an advantageous reaction from the point of view of big mammals.

My explanation is that the brain just can't process the new complex signals. Are there any studies about this topic?

Freeze response is also a part of the fight or flight response. See this paragraph below from Wikipedia:

The fight-or-flight response (also called the fight, flight, freeze, or fawn response in post-traumatic stress disorder, hyperarousal, or the acute stress response) is a physiological reaction that occurs in response to a perceived harmful event, attack, or threat to survival.

This, being enough of a definitiin, does not explain the point in your question i.e. how could the freeze response help our ancestors in some dangerous situation (and thus become evolutionarily helpful)? Its actually quite simple. Let me first explain how the fight and flight responses would've helped us.

For the fight response, imagine a simple situation: a small animal (say, cat) runs towards you to attack you. Now, fight response immediately turns on. Hormones in your body tend to make you feel more powerful and aggressive, so that you easily fight off the cat and make it run away. This would be helpful for someone who would've otherwise done nothing and simply get a couple of injuries from a notorious cat.

In flight response, imagine a simlar situation: you are being attacked by a larger animal (say, bear). You know that you just can't fight with it, but if you run fast enough, you can outrun that bear. Now, flight response rapidly takes over. Hormones, like adrenaline and nor-adrenaline, tend to get more blood to your legs (so that you can run faster), dilate your pupils (so that you can see everything more clearly), etc., everything required for a faster sprint. This would be beneficial for someone who would otherwise not run away and reach a near-death situation.

So, how does the freeze response help? Consider another (last one) situation: you're being attacked by a lion. In this case, you know that you can neither fight with an angry lion nor outrun it. What should you do? One immediate idea would be to play a dead man's role in front of the lion so that (maybe) it will leave you. Of course, it doesn't pay off everytime, but surely it does, sometimes. And in such a case, this would be better for someone who would otherwise either try to fight with the lion or to outrun it. And, obviously, it is a better option for many other organisms too. So it indeed seems that this response developed much earlier in time, maybe even long before first chordates appeared.
With the above part explaining why it is beneficial, one part still remains i.e. how does it work? For this, see the paragraph below:

Studies show that particular connections from the periaqueductal grey (brain region located along the spine) to the pyramis at the base of your skull are integral to the freeze response. When these connections are activated, it causes the body to freeze. They can be activated by things that are actually dangerous and by things that aren’t, so even irrational fears can cause us to freeze. While giving a presentation, you might not actually be in danger, but your body responds like it is and causes you to clam up.

Below are images of the periaqueductal grey in spinal cord and pyramids in brainstem to help you understand their locations.

To conclude, freeze response is not a mere "remain" of our reptilian past, it is still beneficial for us.
References:

https://en.wikipedia.org/wiki/Fight-or-flight_response
https://www.psychologytoday.com/blog/evolution-the-self/201507/trauma-and-the-freeze-response-good-bad-or-both
https://joyable.com/blog/fight-flight-freeze/
https://www.slideshare.net/mobile/dr_ansari2000/the-brain-stem-ii
http://slideplayer.com/slide/4637165/


Why do neurons die so fast without oxygen and nutrients? Some human tissue can survive without oxygen a couple of minutes, even hours.

Why are the neurons are so "weak" and depends so much on oxygen and other nutrients and cannot live without them for more than a few seconds or 1 or 2 minutes?

Are they missing some parts of their cells which can store nutrients for worse times in favor of their function or what is the case?

Neurons use lot of energy to maintain their polarized state, this is not required to other cells [1,2].

When O2 or blood flow (which is carrying the nutrients) is reduced, the neuronal ATP levels breaks down very fast, with 90% ATP depleted in less than 5 minutes. Without ATP, the neuron can not maintain the correct ion flux, so depolarization occurs causing glutamate excitotoxicity, cell swelling and finally cell death.

1] http://www.acnp.org/g4/gn401000064/ch064.html

2] http://www.scientificamerican.com/article.cfm?id=why-does-the-brain-need-s


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

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


What is the mechanism of oxygen uptake in E. coli? How does E. coli uptake oxygen? Most of the literature I found is concerned with response to oxygen level supplied in the medium, as opposed to how much is actually transported inside. Can they shut down the oxygen uptake if required? For example, to avoid damaging effects of reactive oxygen species.

There exist bacteria which die in presence of oxygen (strict anaerobe), while some use oxygen when available but also can survive in absence of it (facultative anaerobes, like E. coli). Are there bacteria which cannot consume oxygen for metabolism, but when exposed to oxygen they don't die, rather simply discard the oxygen and carry out fermentation? In a sense, they are strict anaerobe (their mode of metabolism is anaerobic), but they can still survive in presence of oxygen in environment.

This question got me thinking about what are the metabolic enzymes that take oxygen up in E.coli. I searched the metacyc database for reactions that consume molecular oxygen and there are only 3 that take in oxygen and one that produces oxygen.

All three consumers of oxygen in E.coli are the oxidation of ubiquinone by at two sites in cytochrome-bcl or by cytochrome-bo.  All of these export protons to create the gradient that drives ATP formation by F₀F₁ ATPase in the periplasm (the region between E.coli 's inner and outer membrane).

On the production side, superoxide dismutase reduces superoxide to oxygen to control oxidation damage.  Apparently the innards of E.coli are somewhat oxygen tolerant.


Would current-day human-initiated panspermia be effective? With current technology, we are able to easily send a probe to the Alpha Centauri star system at a speed of about 20 km/s (velocity of voyager probe), which means it would take about 65000 years to get there.

In light of this, suppose we sent a probe capable of delivering 100g of biological material to an Earth-like planet in α-Centauri.

  Are there organisms that:

  1) Could survive the journey, perhaps frozen or in a dormant state;

  2) Would have a fair probability of surviving in the barren oceans (or land if preferred);

  3) Eventually have a change of evolving to more complex lifeforms?

If possible, give a rough estimate of how likely you think that would be -- would we need to send 10 probes for a good chance, or billions of probes?

The lifeless environment seems to necessitate either photosynthesis or chemosynthesis to survive. But what about the necessary food (organic matter)? Would any of those restriction make it virtually impossible to achieve long term life with current goals?

Okay, there are technically four questions here, but I'm willing to have a stab anyway.

  [Are there organisms that c]ould survive [65,000 years], perhaps
  frozen or in a dormant state;

Probably/possibly (prossibly?). There are claims of the recovery of viable bacteria from samples that have been frozen for millions of years, and viable green algae have been growth from permafrost samples at least 5,000-7,000 years old. Dormant bacteria have also been  reportedly recovered from 25-40 million year-old amber and salt crystals formed 250 million years ago. Several of these results are controversial, since in some cases the organisms's genomes are suspiciously modern, and it's not clear whether they could represent sample contamination, but confidence in several of the ones in the range of 10-100,000 years seems to be fairly high (for example, this Carnobacterium recovered from 32,000-year-old permafrost . Using freezing methods optimised for viability, it should be possible to achieve better viability levels than occur naturally (but you'd have to test your samples after 65,000 years to make sure!).

It's also (with a fairly high degree of confidence) probably possible to create micro-environments containing viable bacterial communities that can survive for thousands of years without light or nutrients, but this looks like it would require liquid water, and the maximum lifespan of most radioisotope thermal generators (RTGs), which would be the lowest-maintenance form of heat generation, is only a few thousand years (I am not a physicist though - you might want to post this on Space.SE).

  [are there organisms that w]ould have a fair probability of surviving
  in the barren oceans (or land if preferred)

Yes, if you have liquid water and CO2. If you don't, you might need to engineer something. There are various currently-available technologies for inferring the atmosphere of exoplanets.

I'd recommend sending as many species as possible to encourage the formation of a complex ecosystem (and increasing the chance that one of them survives!). The gypsum-crystal samples mentioned above contained around 40 strains of bacteria plus several viruses, so that's a start. Maybe try freeze-thawing that first. Happily (pretty much by definition) any crystals proven to contain bacteria are water-soluble, so if the planet has an ocean of water then they'll eventually dissolve, releasing their (hopefully) highly invasive payload.

  [Are there organisms that would e]ventually have a change of evolving
  to more complex lifeforms?

This is the easiest one to answer: an unqualified yes. Any organism relying on error-prone information storage (so DNA, RNA, or pretty much anything else) is capable of evolution.

  If possible, give a rough estimate of how likely you think that would
  be -- would we need to send 10 probes for a good chance, or billions
  of probes?

This is the problem. The reasons go rather beyond this SE (again, maybe try Space.SE) but literally any machine you can conceive based on anything more complex than chemistry or melting points is going to fail after 65,000 years in space. Forget computers, moving parts, rockets, etc. So how do you do it? You really want something that starts to melt as it approaches the other star and releases tens of thousands of packets, each containing copies of everything you're trying to seed the planet with and capable of surviving re-entry (for this, you should post another question on Space.SE - those guys are going to love you). Even so, I don't have the figures for this (again, Space.SE) but I have a very, very strong suspicion that since you're basically throwing darts at a pinhead millions of miles away you'd need to build a moon-based factory or something and fire synthetic comets/meteors containing your payload every few minutes for thousands of years. But since that's trivial compared to the travel time, and that in turn is miniscule compared to the time it'd take for the arrivals to evolve into anything worth visiting, I imagine that's fine. Launch early, launch often.

(I have posted a related question on Space.SE)


CAM Photosynthesis Oxygen Generation? I've been looking into CAM plants - notably the snake plant which is native to West Africa.
Upon researching the CAM photosynthesis cycle, I've found it fascinating that the plant stores CO2 at night and photosynthesizes during the day. But I'm a little confused as to how oxygen is a byproduct of this reaction. There seems to be no images of the cycle where oxygen is involved in any of the diagrams I've seen.
There was one question somewhere online that explained it, but I was nowhere near smart enough to understand their technical language and so I didn't really get an answer.
So here's my question.
Does a CAM plant release oxygen during the day? If so, is there a specific ppm value or some other value that that is applicable to a snake plant or another similar plant that I can use to calculate the approximate amount of oxygen released?
Your help is  much appreciated.
Thanks!

In the process of photosynthesis light is used as as a source of energy to generate sugar from carbon and water. A by-product is oxygen.

This process can be broken into two cycles: light reaction and Calvin cycle. In the light reaction energy from photons is transformed into usable energy and reducing agents (ATP, NADPH) and water is used as a source of electron, this results in the release of oxygen. In the Calvin cycle this energy coins are used to produce the actual carbohydrates.
There are three known wide-spread mechanisms of photosynthesis: C3, C4 & CAM
One can think of C3 as the "common" system and C4 & CAM as adaptations.
The CAM adaptation is a way to overcome dry, hot climates. The problem is that photosynthesis requires CO2 but opening the stomata allows water to escape. This is not acceptable. CAM plants separate the time of acquisition of CO2 and the actual fixation. They open the stomata at night, allowing oxygen to get out and CO2 to get in but fix the carbon, and thus create the oxygen, during the day.
Although the Calvin cycle is not light dependent it needs substrates created in light conditions so it will not work in the dark under normal conditions.
This article has assimilation curves depending on temperature in different CO2 concentrations. You can use the above equation to estimate grosso modo the amount of oxygen released. They also supply graphs of oxygen change inside a bag following several hours.

Please remember that the amount of oxygen is less important that the concentration, especially compared with CO2


Is a walnut a nut or a drupe? We've been learning about fruits (and the various categories thereof) in class; among them we have the nut and the drupe.
My textbook differentiates between those terms as:

Nut: It is a single-seeded indehiscent, dry fruit.

Drupe: A fleshy fruit with a stony endocarp.

How here's the problem.
My textbook lists the walnut (fruit) as a nut. But Wikipedia disagrees on this point, calling it a drupe instead.

I'd like a second opinion, since both my book and Wikipedia have had reliability "issues" in the past.
Q- Is a walnut (fruit) a (botanical) nut or a drupe?

Short answer
Walnuts are classified both as nuts and drupes ('stone fruits').

background
According to University of Wisconsin - Madison, Department of Botany , hickory and walnut can be classified both as drupes and nuts, but are best classified as nuts.

Nuts fall into the class of indehiscent fruits: dry fruits that do not open when mature to shed their seeds. Many of this group are one-seeded fruits, such as the nuts. In addition, nuts have a thickened and hardened wall. Examples are beech, chestnut, oak, hazel, walnut and hickory. Because of extrafloral bracts, or "husk", the latter two fruits are sometimes called "drupes").

As opposed to indehiscent fruits, the fleshy fruits have a wall that becomes soft and fleshy as it matures. Drupes ('stone fruits') fall into this class. Drupes one-seeded, simple fruits developed from a superior ovary in which the innermost portion of the wall (endocarp) becomes hard and stony, the outermost part (exocarp) becomes a relatively thin skin, and the middle portion between the skin and the stone (mesocarp) becomes either fleshy or fibrous. Examples are cherry, coconut (the endocarp is the thick wood shell that surrounds the fleshy and liquid-filled seed), but also walnut and hickory. The latter two are, however, best called "nuts".

Indeed, according to a popular scientific article in the Guardian, many tree nuts are also drupes, including walnuts and pecans.


Beginning with centrifuge experiment This is the first time I do a centrifuge experiment with my own centrifuge machine, it's just simple made by a rotor that can rotate the tube at high speed. As I know a centrifuge machine can be using for separate biology samples like bacteria, cells, molecules ... But I need some advice to understanding more how to working with it.

As the suggestion from Alan Boyd, I'm planning to separate Lactobacillus from diluted yogurt. How do I know where the bacteria will be located in the tube after centrifugation (is it usually in bottom ?) and how do I  calculate the RPM that is suitable ? And any other interesting diy experiment to do with it ?

It would be interesting to see a picture of your centrifuge, which you appear to have built in a few days.
Centrifugation simply accentuates the effects of gravity, and since bacteria are denser than aqueous solutions they will move to the bottom of the sample to form a fairly tight pellet.
The conditions for your centrifugation will depend very much on the design of the centrifuge since as well as the rotational velocity, the radius of rotation is also important.
I found a suggestion on the internet to use a relative centrifugal force (RCF) of 12000 g for 2 minutes (I must admit that from memory I always spun slower and for longer than this suggests). Anyway...

using RCF = 1.12 * 10-5 * r *N2
r = radius of rotation
N is revolutions per minute
and plugging 12000 g into that, for a rotational radius of 10 cm, I get 3300 rpm.

Don't know if you can manage that with your machine, but as I say, a lower RCF with a longer spin will probably be ok as long as you can dilute the yoghurt sufficiently to reduce viscous drag. Of course if you have access to any microbiological growth media you could grow a standard liquid culture by inoculating some sort of broth with a small amount of yoghurt.
Try a Google image search for hand powered centrifuge to get an idea of what has been used in the past.
after comment from Mad Scientist
see here for a typical large table top centrifuge maximum RCF is 3120 g at 4600 rpm. You can certainly pellet bacteria in something like this in tens of minutes.


Is setting high mismatch and gap penalties sufficient to distinguish perfectly mapping reads? I have a fat pile of 125bp whole genome shotgun reads that have undergone quality control, and I would like to pull out just those reads that do not map perfectly to the genome. When I set extremely high penalties for mismatches and gap opens/extensions (with bwa mem -B 1000 -O [1000,1000] -E [1000,1000]), it looks like the alignments for perfectly mapping reads are shown, and the rest of the reads are reported as unmapped. If this is true, I could then pull out the unmapped reads with samtools -f 4.

Are there any holes in my reasoning here, or will it work to discard all of the reads that map perfectly to the genome?

The short answer: No, setting extremely high penalties (100 or 1000) does not seem to work. I'm not sure why.

The medium answer: Since I posted the question, I did a bit of exploring, and it looks like the reads that perfectly match are the reads that are not soft clipped and that have an edit distance of zero, as indicated by the CIGAR string and NM tag, respectively.

The long answer: See https://standage.github.io/how-to-distinguish-perfectly-mapped-reads-from-a-sambam-file.html.


Are the social-distancing measures implemented against SARS-CoV-2 also suppressing the spread of other viruses? With social-distancing measures being implemented in many countries I would expect other viruses, like the ones that cause seasonal flus, to have also a hard time propagating in these circumstances. Are there any estimates or research (epidemiological models) I can check, about the possibility we are winning by accident a war against many other less alarming viruses?

Yes, this helps as well with other infectious diseases. A good example is the flu, which season was measurably shorter this year than in other years on record. See the figure from the reference 1 for comparision:

Reference 2 shows that this is also true for other respiratory diseases (figure 2):

This shows very well that the isolation measures and the social distancing work very well to control such transmissable diseases.

References:

How coronavirus lockdowns stopped flu in its tracks
Monitoring respiratory infections in covid-19 epidemics


Why is it always Sodium that we talk of in blood pressure? Why is that we emphasize so much on sodium in blood pressure? I understand that it is a major extracellular ion, but, it also is tightly regulated. So when something is that tightly regulated, won't small concentrations of the potassium matter? And what about the chloride and bicarb? They are all there in the blood in comparable quantities but we never talk of their osmotic importance. Sodium retention and blood pressure - why not chloride retention?

Is it not required (like calculating sodium includes them too)?
or is it that they actually don't matter?
Also aldosterone, we conserve the sodium but aren't we pushing out potassium? Potassium also is an ion with oncotic activity right? Why is Natriuresis so important why not say, Chloriuresis?

So all in all, why does sodium steal the limelight?

The key is in fluid compartments and osmotic activity. For the purposes of this discussion, let us say that there are two fluid compartments the ExtraCellular Fluid (ECF) and IntraCellular Fluid (ICF). Only the ECF contributes to blood volume and blood pressure.

Na is not only the major ECF ion, but it is also confined there. The ICF concentration of Na is much lower than in the ECF, and it is continuously, invariably and actively kept out of the ICF. In other words, the vast majority of ingested Na ends up in the ECF, and drag the associated amount of water (ie volume, thereby increasing blood pressure). It is the opposite for K, which is mainly in the ICF. As for Cl, it is more or less equal in the ICF and ECF, and is allowed to move freely between them, meaning that you need to ingest twice as much as a given amount of Na for a similar effect on volume distribution. Bicarb is a minor ion, and moves freely between compartments. These are the reasons why, clinically, if someone is hypovolemic (ie dehydrated, losing blood) they are given a sodium based fluid or a protein based fluid (colloid), because both will drag volume and stay in the ECF.

As for the other part of your question, isn't it tightly regulated? Yes, but extra sodium takes some time to get excreted (much less than 1% of sodium that goes through the kidneys is excreted). In other words, any extra sodium (i.e. extra volume as we have established) will stay there for some time, and if you are continually having high sodium meals, every day, you will walk around with extra sodium most of the time. Therefore, your blood pressure will be higher than it would be, if your diet was lower in sodium.

So, no, sodium is not stealing the spotlight from anyone when it comes to ECF. But the other ions have their glory under other spotlights.


Why is it better to drink room temperature water instead of cold water? My teacher told me that drinking water that is room temperature is better for you then drinking cold water, but she did not tell me why that is. I want to know because I often drink cold water (with ice), because I can't stand water that is room temperature or warm.

Your teacher was passing on a myth.

This false belief might be related to the equally false belief that hot exerted horses should not be fed cold water. It could also be down to someone downing a big glass of ice-cold water in one go as a child, get a brief stomach ache and spin a health-advice on it.


What are pseudoknots? I'm trying to get my head around what a pseudoknot is and how I can identify them given some RNA string. For example, suppose I have a string s = CGUUGUGUACACGAUAGUACAU. Suppose the two longest substring inversions are identified in bold CGUUGUGUACACGAUAGUACAU, which form the stack of the hairpin and everything after the first substring and before the start of the last substring make up the hairpin as illustrated below.

                                  U G U
                                G       A
                                 U     C
                                  C - A
                                  G - C
                                  U - G A U A G U A C A U

By definition, a pseudoknot is defined as a secondary structure formed by pairing between a loop and a region located outside of the stem flanking the loop. In this example, we would start the pairing using some substring of the outer tail and start matching bases around the hairpin. My question: is the pseduoknot the alignment of these base pairs, and what is the significance of this alignment?

is the pseduoknot the alignment of these base pairs

I'm not exactly sure what is meant by alignment, but if you mean base pairing from the flanking RNA to the loop of the hairpin you have depicted, then you would have an H-type pseudoknot.

Since you are interested in predicting these structures, it's important to note that a nucleic acid sequence capable of forming the necessary base-pairs for a pseudoknot structure does not imply that the sequence indeed forms a pseudoknot. It's likely that the sequence has a minimum free energy (MFE) structure that is not pseudoknotted. So the base-pairing capability is necessary but not sufficient for predicting these structures.

Take a look at the following (full-text) articles on pseudoknot prediction for additional information:

Computational Analysis of Noncoding RNAs
DotKnot: pseudoknot prediction using the probability dot plot under a refined energy model
A fast and robust iterative algorithm for prediction of RNA pseudoknotted secondary structures
KnotSeeker: Heuristic pseudoknot detection in long RNA sequences


Can nosebleeds cause death? Can epistaxis or nosebleeds be a cause of death?

Yes, it can, but it is extremely rare.

  ... nosebleeds are rarely fatal, accounting for only 4 of the 2.4 million deaths in the U.S. in 1999 [1].

The main issue is that epistaxis can be a sign of potentially fatal diseases:

  The instances in which nosebleed is potentially fatal are those in which there is a history of recent head injury, severe arteriosclerotic cardiovascular disease or an underlying vascular tumor in the nasal chambers. Fatal nasal bleeding has not been reported in children [2].

Here are some causes which can lead to fatal complications if left untreated [3]:

  Leukaemia
  Hypertension
  Coagulation disorders
  Hepatitis
  Head injury
  Myelodysplastic syndromes - Epistaxis

Death by massive hemorrhage can occur when epistaxis is the result of a ruptured aneurysm [4, 5, 6]:

  An instance of fatal epistaxis is reported in a patient with an unsuspected aneurysm of the infraclinoid portion of the internal carotid artery. There was no known history of trauma. The aneurysm was subsequently detected on an old X-ray film. Epistaxis from an aneurysm at this site is nearly always preceded by significant head trauma and is associated with cranial nerve palsies, a syndrome with a high mortality. Epistaxis from rupture of a non-traumatic aneurysm is very rare [4].

References:

Work Table I. Deaths from each cause by 5-year age groups, race and sex: US, 1999 Page 1922. U.S. Centers for Disease Control Published 2001-05-11. Via Wikipedia contributors, "Nosebleed," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nosebleed&oldid=617613780 (accessed July 21, 2014).
QUINN FB. Fatal epistaxis. Calif Med. 1961 Feb;94:88-92. PubMed PMID: 13738727.
Right Diagnosis (tm). Epistaxis Deaths. Available from http://www.rightdiagnosis.com/symptoms/epistaxis/deaths.htm (accessed 21.07.2014)
HORNIBROOK, J. and RHODE, J. C. (1981), FATAL EPISTAXIS FROM AN ANEURYSM OF THE INTRACRANIAL INTERNAL CAROTID ARTERY. Aust. N.Z. J. Surg., 51: 206–208. doi: 10.1111/j.1445-2197.1981.tb05942.x
P. N. Pathak (1972). Epistaxis - due to ruptured aneurysm of the internal carotid artery. The Journal of Laryngology & Otology, 86, pp 395-397. doi:10.1017/S0022215100075423.
Urso-Baiarda F, Saravanappa N, Courteney-Harris R. An unusual cause of massive fatal epistaxis. Emerg Med J. 2004 Mar;21(2):266. PubMed PMID: 14988378.


Why would a single celled organism evolve to be multi-celled? I read a story this week on Richard Lenski who has been 'evolving' E. coli for more than 50,000 generations now.  One comment I read was from someone who doesn't accept Evolution who pointed out that we haven't seen a single celled organism 'evolve' into a multi-celled organism.  Another person responded and said that a bacteria is not going to evolve into something that isn't a bacteria.

So, if Evolution created single celled organisms and then multi-celled organisms how might that change have happened?  And is it possible to recreate that set of driving forces to make a bacteria something other than a bacteria?

To that end, what advantage does being multi-cellular have over being unicellular (if that's even a word)?

How did multicellularity evolved?

It is an ongoing field of research - Some insights about the origin of multicellularity

This is a big ongoing field of research. To start with an example, there was relatively recently (2012) an important article by Ratcliff et al. that shows that yeast can quickly evolve multicellularity under selection on the speed they sink to lower water layers. This article is one among many others and is far from being able to explain everything we would like to understand about the evolution of multicellularity. Typically, I think that this yeast species had a multicellular ancestor and we might think that this species would already have fixed alleles (=variants of genes that is fixed meaning that the whole population is carrying this variant today) in the population predisposing this species to easily (re-)evolve multicellularity. Also, they may have kept some standing additive genetic variance in their genome from their past and they would therefore very quickly respond to selection as they don't need de novo mutations. (Sorry if this last sentence was slightly technical).

One of the first traits that we usually refer to when talking about the evolution of multicellularity is the presence of sticky proteins allowing individual cells to paste to each other.

Some insights about the evolution from simple multicellular to more complex multicellular

Then, we could talk about more complex multicellular and argue how do these simple multicellular evolve into some more complex organisms. A common argument is that multicellular can have specialized cells are very could at doing what they're doing as they are specialized. Also, some level of complexity is thought to have raised due to the fact that multicellular organisms tend to have smaller population size than unicellular (see Lynch and Conery, 2003). It is important not to confuse evolution of complexity with the evolution of multicellularity although these two notions are somehow related.

What do you mean by multicellularity?

The evolution of multicellularity can be discussed in the context where sister cells form an organism together or when unrelated cells (among the same species or even cells from different species) come together to form an organism. Also, the multicellularity can be discussed at a different level depending on how we want to define multicellularity. Is a stack of cells reproducing individually, working for their own benefit a multicellular? Do we need a division of labor? Do we need a division between germline (reproductive caste) and soma line (non-reproductive case)?

How many times did multicellularity evolve independently?

Some people consider that there are multicellular bacteria (biofilms) but we will avoid discussions that are based on limit-case definitions. Let's talk about eukaryotes. Most Eukaryotes are unicellular and multicellularity evolved many times independently in eukaryotes. To my knowledge, complex multicellularity however evolved only (only?) 6 times independently in eukaryotes.

Metazoa (animals)
Ascomyceta (fungi)
Basidiomyceta (fungi)
Viridiplantae (green plants)
Florideophyceae (red algae)
Laminariales (brown algae)

Model organisms and interesting cases to study multicellularity

There are a bunch of specific clades that are particularly interested in studying multicellularity because they present transition states. For example Volvox is a chlorophyte genus and the species in this clade present different stages of multicellularity; Some species are exclusively multicellular, some form small groups, some create big colonies, some have some division of labor and some even have separation between the germline and the soma (Some castes don't reproduce). (ref1, ref2, ref3, ref4, ref5, ref6). Yeasts are also a good model organism for studying the evolution of multicellularity.


Mammal vs Placental Mammal So for Google Earth Day's quiz I ended up being a "Pangolin." Turns out I had no idea what it was so I looked into it and honestly it reminded me a lot of an Armadillo. So I decided to find out the difference between the two, and I stumbled across this site.

It was all making sense until I got to the "bullet points" at the bottom where I saw this

  Pangolin is a mammal while armadillo is a placental mammal.

And I'm now very confused. I thought placental mammal was just a subset of mammals. And I look up Pangolin's taxonomy and now I'm seeing all kinds of stuff I have no idea how to interpret. Back in my day, it was "Kings Play Cards On Fat Green Stools" for "Kingdom Phylum Class Order Family Genus Species". And now I'm seeing things like clade, infraclass, subcohort, superorder and all kinds of things I just don't get.

So I guess I have many questions, but I'm going to boil it down to "If the Pangolin isn't considered a placental mammal, then what kind of mammal is it, and where does it diverge in taxonomy from the Armadillo?"

Oh, and if someone could point me to a primer on the changes to taxonomy in the last 20 years, that'd be cool too.

From the Tree of Life page for Mammalia:

All of these groups of animals are mammals, including extinct triconodonts and multituberculates. Among living mammals are monotremes (most notably the platypus), marsupials (kangaroos and opossums), and eutherians. Eutherians are placental mammals, so all eutherians are placental mammals, but not all mammals are eutherians.

Both armadillos and pangolins are eutherian mammals, so both are mammals and both are placentals. "Difference Between" is quite incorrect.


Can a protein go outside of nucleus after go inside with nuclear localization signal (NLS) To make a protein (for example Cas9, GFP...) able to enter the nucleus, we need to add a NLS tag for it. So will it able to go outside the nucleus after get inside ?

It seems that I need to add a NES (nuclear export signal) if I would like to make it able to export the nucleus : https://en.wikipedia.org/wiki/Nuclear_export_signal  .


What evolutionary advantages are provided by ovoviviparity? I read that some sharks are ovoviviparous.  What advantages and disadvantages are provided by this type of reproduction as opposed to egg laying and live birth?

Reading this website (www.sharks-world.com/shark_reproduction) it seems that for most sharks the eggs develop inside the mother (ovoviviparity), and the young sharks ("pups") are born fully functional, but this is not true for all sharks (as you mention in your question).

This persons blog (morgana249/modern reptiles give birth to live young) discusses evolution of ovoviviparity in some reptiles, but not others. In some species this seems to have gone back and forth in their evolutionary history, which suggests that changing conditions favour one then the other at different times, possibly influenced by temperature, among other things.

  The researchers stated, "These results suggest that parity mode is a labile trait that shifts frequently in response to ecological conditions."

This could be similar for sharks, although I could not find an article postulating this.

Alternatively, this could be because the mother does no "parenting"; the pups are immediately independent. Because sharks do not have many eggs at a time (according to the sharks-world website) each individual egg/pup has a higher "value" than each individual offspring in other fish species, which often lay many hundreds of eggs at once outside their body (oviparity). Therefore sharks that evolved this trait may have been selected because the offspring are more likely to survive if they are protected until fully functional within the parent.

No doubt there are other possible explanations, but as with all these questions along the lines of "What are the evolutionary reasons..." we cannot ever actually know, only suggest.


Are there any organisms with larva more advanced than adult form? Usually adult organisms are more sophisticated than corresponding larva, i. e. frogs, mosquitoes, fish. Are there species where the opposite is true?

First let me agree with the commenters that your question doesn't really make sense.  Nonetheless here's an example that you may find interesting. Arachnocampa are insects that spend almost their entire lives as larva. These larva spin silk trap lines which capture and poison prey. They can only live in windless places (wind will mix up the lines) so to lure insects into caves they glow. By contrast their imago forms are short-lived poor fliers which are unable to eat.


What is Chronic immobilization stress (CIS)? I am trying to self study BNDF a little bit when I found this article:

  Abstract Stress impacts multiple systems within the CNS, including the
  hippocampus. A key molecular mediator in hippocampal functions,
  including learning and memory, is brain-derived neurotrophic factor
  (BDNF). BDNF mRNA is reported to be decreased following chronic (every
  day) immobilization stress (CIS) in the rat, however the effect on
  protein is unknown. Utilizing a mouse model of CIS, the hypothesis
  that total hippocampal BDNF protein, in addition to BDNF mRNA, would
  be decreased was tested. The effects of intermittent (alternating day)
  immobilization and cold stress on hippocampal BDNF protein levels was
  also examined.

  In this study it was demonstrated that CIS results in a small (8 per
  cent decrease relative to non-stressed controls), but significant (p =
  0.0013) decrease in the exon coding for mature BDNF (exon VI). In addition, there was a significant (34 per cent, p = 0.005) decrease in
  the mRNA coding for exon I in the stressed animals. Contrary to
  expectations, however, CIS resulted in a significant (116 per cent, p
  = 0.0087) increase in hippocampal BDNF protein levels. Furthermore, both intermittent immobilization and chronic cold stress both
  increased BDNF protein levels. Chronic stress, therefore,
  differentially regulates BDNF mRNA and protein levels in the
  hippocampus. Copyright © 2004 John Wiley & Sons, Ltd.

I'm really curious what they mean with CIS: Chronic immobilization stress.
I can't find anything on the internet that actually explains what this is.

There are >1200 articles tagged "chronic immobilization stress" on pubmed.

From Hennebelle et al. (2012):

  Half of the 6-month old male rats from each dietary group were subjected to a validated chronic stress procedure (Buyntsky and Mostosky, 2009) based on a restraint stress procedure adapted from Veena et al, [32]. Rats were placed in wire mesh restrainers for 6 h a day (fom 10 am to 16 pm) for 21 days (5 days a week) over a period of 4 weeks. Unstressed rats were handled weekly. The unstressed and stressed animals were housed in different rooms.

Hennebelle, H., et al. 2012. Influence of Omega-3 Fatty Acid Status on the Way Rats Adapt to Chronic Restraint Stress. PLoSOne 7: e42142.


Where is coagulation factor v produced? My textbook (Physiology 9th edition, People's Medical Publishing House, Beijing) tells me that coagulation factor V is produced in endothelial cells and platelets, which is different from some other books (saying in liver). So where exactly is it produced? Or is it just not quite clear?

Factor V is indeed mainly produced in liver (Wikipedia), which releases it into blood plasma.
But platelets are also an important source of factor V and "may account for "~25% of the circulating factor V" (ref 1)
Platelet factor V is synthesized in megakaryocytes (ref 1), which of course are the bone marrow cells responsible for the production of platelets.
The following reference gives a much more detailed explanation of factor V
Reference (available as free pdf)
Factor V Is Complexed with Multimerin in Resting Platelet Lysates and Colocalizes
with Multimerin in Platelet α-Granules *

Catherine P.M. Hayward
Emilia Furmaniak-Kazmierczak
Anne-Marie Cieutat
Michael E. Nesheim
John G. Kelton **
Graham Côté

Journal of Biological Chemistry (1995) Vol 270, pp19217-19224


Could there be any effects from low powered infrared being used to track eye movements long term? Basically,  looking  into infrared LED's and a camera with an infrared bandpass filter for tracking eye movements; my concerns are whether there would be any potential negative long term effects from constantly illuminating the eye with low power infrared?
TIA
A

I would have said that IR is safe, but some studies have suggested otherwise.

This is a vague study on rabbit eyes:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116568/

https://academic.oup.com/annweh/article-abstract/35/1/1/170395

So there may be a dosimetric exposure limit of some kind that you have to aim for. LED's are very controllable. I'm amazed that they talk about cataracts with a chemically soft, non -ionizing wavelength like IR, because we get IR all day from the sun. If you control the levels to be less than a sunny day, you may find that you can use equivalent of 1hr of sun exposure to run many hours of eye tracking. the figures are a matter of research.


How does a protein reach its substrate within the cell? After a protein has been synthesized and its the final tertiary/quartenary adopted, how does it reach its substrate within the cell and what causes it to interact with it?

The transcription factors for a particular gene are proteins which are translated from genes on some other portion of the DNA. (That happens in the cytoplasm) But how do the transcription factors know that it has to diffuse into DNA region of the nucleus.

The protein doesn't move towards anything. It just randomly diffuses (bounces around) in the cell until it sticks to something. The particular chemical structure (the shape) of the protein and whatever it hits will determine how tightly they stick together and whether or not a chemical reaction occurs.

A way to imagine this is to think of a jar filled with a lot of glass marbles (water), 1 marble shaped magnet (the protein), and 1 metal marble (the substrate). Put the magnet at the bottom, fill the jar most of the way full with glass marbles, and then put the metal marble on top. Then close the jar and shake it. Eventually, after colliding with a lot of glass marbles, the magnet and the metal marble will collide and stick to each other. That's how it works in cells also. In cells, the speed at which the molecules move is proportional to temperature.

Here's a cool video that shows how proteins with a very specific shape bouncing around randomly can assemble into a complex structure.

To get a sense of just how quickly molecules move in a cell, think of a bacterial cell. An E. coli cell is about 1 micrometer in diameter. In a cell of that size with no sub-cellular compartments, every molecule will collide with every other molecule in the cell about once every second (if we make some assumptions such as no binding to other molecules). So if the cell contains just one unit of a certain enzyme, and just one molecule of its substrate, they will still collide fairly frequently (about once every second).

This rate decreases dramatically as radius of the cell increases. For example a cell with double the diameter (2 micrometers) has a volume eight times larger, so collisions between any two molecules take 8 times ($2^3$) as long to occur (in other words, it takes molecules 8 times longer to "find" each other). This is one reason why there is a kind of upper limit on the size of an individual cell. Bigger organisms are bigger because they have more cells, not because they have larger cells.

The field of biology concerned with how likely it is for a reaction to occur is called enzyme kinetics. A related field, which deals with how frequently molecules collide is called statistical mechanics.


How do traits with no negative effects get "weeded out" via evolution? If only those who are most fit to reproduce are the ones reproducing the most, it makes sense that traits that prevent one from reproducing would eventually disappear from a population.

But what about traits that have no effect on reproduction, like the presence of wisdom teeth? Humans don't need them, but they don't inhibit us from reproducing either. So how do humans evolve past the point of having wisdom teeth or other similar traits with no negative effects?

Oops I wrote a lot! This is almost a very brief introduction to some concepts of population genetics.

A little bit of terminology first

Locus

A locus (plur. loci) is a position on a chromosome.

Allele

At a specific locus, different individuals may have different variants. One individual might be ATTCTA while another might be ATTCAA for example. These variants are called "allele". The whole goal of evolutionary genetics is to understand the creation (mutation) and change in frequency of the different alleles in the population.

Heterozygosity

You probably know that in many species, we carry two copies of each chromosome. One individual can therefore carry twice the same allele at a given locus or can carry different alleles. Expected heterozygosity ($H$) at a given locus is the fraction of the population that carries two different alleles at this single locus.

Fixation

When an allele reaches a freuqency of 1 (100%), that is only this allele exists in the population (and therefore the other alleles have been wiped out), we say that it has reach fixation.

Natural Selection

The process you describe in your first paragraph is called natural selection.

Natural selection is a fitness (=a function of both reproductive success and survival) difference between different genotypes. As you said (but with other words), deleterious alleles will decrease in frequency through time and will eventually end up being weeded out from the population through natural selection.

Genetic Drift

There are other evolutionary processes than natural selection. Typically, the one we will be interested in to address your question is genetic drift.

What is genetic drift?

Genetic drift refers to the random sampling of a population in order to build up the next generation population. There are different ways to model genetic drift (Wright-Fisher model, Moran model, coalescence model) but without having to talk about the details of these mathematical models, it is important that you can conceive the role of random sampling in the change in allele frequency through time. For this, I invite you to first read Why is the strength of genetic drift inversely proportional to the population size? and when you have finished, come back to this post.

One the below figure, you can see the effect of drift through time. The below graph consider a bi-allelic locus (a locus where 2 and only 2 different alleles exist in the population) starting with an initial frequency of 0.5 (=50%). Each line is a separate simulation and shows the frequency of only one of the two alleles.

The above graph considered a population of size $N=100$ individuals. Below, the same types of simulation with a population size of $N=25$ individuals. As you can see that the genetic drift is stronger

Every single locus is subject to genetic drift whether it is under selection or not. However, if a locus is under strong selection, then genetic drift with have little power to explain what allele will get fixed in comparison to when the locus is neutral.

Genetic drift and loss of alleles

It is clear from the graph above that genetic drift also wipe variant out of the population. We just don't know for sure which variant will be wiped out. To be more accurate, the expected heterozygosity due to genetic drift is reduced by a factor $\frac{1}{2N}$ each generation. One can make plenty of calculations from basic models of genetic drift. For example the expected time to being wiped out is $\bar t(p_0)=-4N\left(\frac{p_0}{1-p_0}\right)\ln(p_0)$, where $p_0$ is the starting frequency of the allele of interest.

A interesting result is that the probability of an allele to reach fixation is equal to its frequency. If there are $N$ individuals in the populations, there are $2N$ alleles (but not $2N$ different alleles). If there are, say 235 alleles A in the population and $2n - 235$ alleles B in the population, then over the long run (so that one will necessarily fix) the probability of fixation of the allele A is $\frac{235}{2N}$ and the probability of fixation of the allele B is $\frac{2N-235}{2N}=1-\frac{235}{2N}$.

Wisdom teeth

In your question, you are interested about a supposedly purely neutral locus. You talked about wisdom teeth I suspect more as an example rather than because you are interested to this trait.

Let's assume that the presence of wisdom teeth is completely neutral. Note by the way that as a rule of thumb if $2 N s << 1$, (where $s$ is the selection coefficient on a given allele) then the allele will behave essentially as if it was a neutral allele. So, if wisdom teeth is neutral, then the probability of this trait to disappear over the long run depends on the frequency of the allele causing this trait. So far, I have assumed that we were interested in a single locus only. In reality, variation in many traits are caused by variation at several loci. In such case calculations are a little less straight forward (but still feasible). I do not know the genetic basis of wisdom teeth, so I cannot make good predictions for the evolution of this particular trait.

Other evolutionary processes

Here are a few example of interest

Gene flow

Note of course that there are other processes to consider when trying to predict the fate of a given allele or trait. For example, in a given population you might have a flux of migrants that come from a population where one allele is fixed therefore affecting the allele freuqency in the focal population. This is called Gene flow.

Hill-Robertson effects

Never forget that a locus is not alone on its chromosome. It is physically linked to other loci and selective pressures at other loci will affect the allele frequency at the focal locus. This is called Hill-Robertson effects.

Mutations

Of course, when a locus is not polymorphic (has only one allele), mutations is the ultime source of variation. When a locus is polymorphic, then it is likely the mutations will have a minor effect on the allele frequency (although it depends on the size and type of locus and depends on whether mutations can make up new functional alleles).

Pleiotropy and covariance between phenotypic traits

Phenotypic trait do not evolve independently. If wisdom teeth is a consequence of the activation of the molecular pathway for resistance to HIV (which it very probably is not), then wisdom teeth will not evolve as a neutral trait. A locus that affects several traits is said to have pleiotropic effects.


Colchicine addition to cells When is colchicine added to dividing cells for karyotype studies?

I know that colchicine inhibits polymerization of microtubules.

2 So, why should it stop the cell cycle at metaphase when microtubules have already assembled and the next step(anaphase) requires depolymerization rather than polymerization ?

Colchicine inhibits the formation of the microtubules by binding to tubilin and rendering it unavailable for the polymerization. Thats why the cells get arrested in the metaphase and can not go on further in the cell cycle and divide. For chromosome studies this is very useful since this is the phase where the chromatin is most condensed and can be viewed best. It inhibits the positive side producing the microtubules to prevent it from moving to the negative side, in cell division.


Is there any evidence of animals wanting to die? Is there any evidence of animals wanting to die? Specifically, animal communication which says "come and eat me".

Is it possible that an individual would benefit form being eaten?

In theory it is possible that such behaviour would evolve. An individual may improve the probability of its genes to be passed on by letting a related individual (which carries similar gene variants) to feed on it. When counting the fitness of an individual as being the sum of the fitness of all related individuals weighted by their coefficient of relatedness as inclusive fitness. We refer to the selection pressure that is due to a differential in inclusive fitness as kin selection. The field that study the evolution of altruistic behaviours is called social evolution and is an active field of research.

Example

For example, a male could much enhance the probability of survival of its offspring by being eaten by the mother. The type of cannibalism where one mate eat the other is called sexual cannibalism. A famous example of sexual cannibalism is the mantis prey. Note that it has been suggested that in natural conditions sexual cannibalism could be rarer than expected previously thought. Note also that the question of whether the male benefits from being eaten by the female in prey mantis is still controversial and could result from a sexual conflict.


Age-Dependent STD Infection It seems that young females (comparing age 15 vs age 24) are 20x more likely to get chlamydia
from a single unprotected sexual encounter with an infected male.  What are the reasons for
this?  Are there other diseases with such extreme age-dependence?

Reference:

Estimating age-dependent per-encounter chlamydia trachomatis acquisition
risk via a Markov-based state-transition model.

The "Description of the analyzed data set" section seems suspicious to me:

In a nutshell, young women between the ages of 14 and 17 years old
were identified and recruited by the project.
...
At each follow-up visit during the study period, enrolled participants
underwent STI testing and treatment. Also at each follow-up visit, the
participants received follow-up interviews, in which they were queried
about the number of unprotected coital events since previous visit.
Most of the participations did not visit the clinic every quarter and left the project before its completion.
For our analysis, we collected 1173 quarterly test results from the
first 200 participants who were never infected and have completed at
least two follow-up visits. Their average enrollment age was 15 years
with standard deviation of 1.1 years.

It means that data is biased as for some reason most of girls were not able to participate in the study.
And I'm not sure about the correctness of your interpretation. I'd interpret it as "females are 20x less likely get chlamydia infection after being treated and warned about STD" as there were relatively continuous followed-up 15-17 y/o females and no older females. And I guess it was one of the goals of this "Young Women’s Project".


Transformation of E.coli cells As a team of undergraduate researchers we are looking to transform two genes of interest into our competent E.coli cells. Both of these genes are in separate plasmids and we would like to put them into one E.coli cell. Is it possible for a cell to uptake two plasmids in one transformation process? If the last question is impossible, is it possible to transform a cell and then transform the colonies produced by that transformation? Thank you very much.

The two plasmids have to have different origins of replication. Two plasmids from the same incompatibility group cannot survive together in the same cell.

This quote is from the Wikipedia entry on plasmids:

  Plasmids can also be classified into incompatibility group. A microbe can harbour different types of plasmids, however, different plasmids can only exist in a single bacterial cell if they are compatible. If two plasmids are not compatible, one or the other will be rapidly lost from the cell. Different plasmids may therefore be assigned to different incompatibility group depending on whether they can coexist together. Incompatible plasmids normally share the same replication or partition mechanisms.

This is a nice definition/explanation from an OpenAccess article:

  A formal scheme of plasmid classification is based on incompatibility (Inc) groups (Novick, 1987). The procedure for incompatibility grouping is based on the introduction, by conjugation or transformation, of a plasmid of an "unknown" Inc group into a strain carrying a plasmid of a known Inc group. If the resident plasmid is eliminated in the progeny, the incoming plasmid is assigned to its same Inc group (Datta and Hedges, 1971). Plasmids with the same replication control are "incompatible", whereas plasmids with different replication controls are "compatible". On this basis two plasmids belonging to the same Inc group cannot be propagated in the same cell line (Datta and Hughes, 1983; Couturier et al., 1988). Inc group identification has been frequently used to classify plasmids. The method has been an important tool to trace the diffusion of plasmids conferring antimicrobial resistance and also to follow the evolution and spread of emerging plasmids (Anderson et al., 1977).

A synopsis of the Datta & Hedges article sited above:

  Classification
  In 1971, Hedges and Datta proposed a plasmid classification scheme based on the stability of plasmids during conjugation (incompatibility). The first incompatibility (Inc) groups were IncI, IncN, IncF, and IncP. Currently, 26 Inc groups are recognized in Enterobacteriaceae including six IncF (FII to VII) and three IncI (I1, Iγ, I2) variants. Major plasmid families occurring in Enterobacteriaceae are HI2, HI1, I1-γ, X, L/M, N, FIA, FIB, FIC, W, Y, P, A/C, T, K, B/O, FII, FIII, FIV. IncF plasmids are low- copy-number plasmids, often carrying more than one replicon with at least one replicon strongly conserved.

One way to think about it is: if one prepares a plasmid cloning vector to accept foreign inserts, and ligates in a "shotgun" collection of fragments from some DNA of interest. After transformation, selection and growth on plates, none of the colonies whose plasmids carry inserts ever contain more than one unique plasmid.  In other words, it may be possible for two different inserts to be inserted during ligation into the same vector backbone, but it is not possible to find a single pure colony that contains cells harbouring two different plasmids, each carrying a different insert.

If a cell gets transformed by two different plasmids from the same inc group only one plasmid will "win."

Examples of compatible ori's commonly encountered:

pMB9 (pBR322, pUC, etc., etc.,)
F (fosmids)
bacteriophage lambda (some cosmids)
bacteriophage M13 and relatives (also yields ssDNA phage useful for Sanger sequencing)
bacteriophage P1
pSC101

Here is a nice table, but I cannot vouch for its accuracy.


Why do some cells like myofibrils have multiple nuclei? I see that myofibrils (muscle cells) contain not one, but multiple nuclei.

Why is this so?
Do all the nuclei participate in cell division?

In the case of myofibrils this is the case because of the syncytial nature of that given structure. It means that in developing muscle tissue after a certain stage the cell divisions become somewhat different in that the final step, being separation of the daughter cells via invagination of cell membranes, does not happen. The nuclei though keep dividing after that. In the end what we have is a big membrane coated structure (basically a cell), with lots of nuclei in it.


Human somatic cells have 22 pairs of homologous chromosomes? I am studying for my Bio class and I am stuck with questions that I came up with during this chapter of Meiosis. I understand that human somatic cell is made up of 22 pairs of autosomes and 1 pair of sex chromosome. I am confused about what made up each pair of autosomes? is that 1 chromosome from the father and 1 chromosome from mother made up 1 pair of autosomes in somatic cells? and therefore, since each pair of autosomes consisted of 1 chromosome from dad and 1 from mom, we can say human somatic cells consisted of 22 pairs of homologous chromosomes (not to mention the sex of the human), right?

Answer: *Yes  , human somatic cells have 22 pairs of homologous chromosomes

The human genome consists of 46 (2n*(22+1) ) chromosomes.

Most of our cells are somatic and diploid (2n), they have two homolgous chromosoms (called homologs, one "father" & "mother") these cells multiply by mitosis.

Reproductiv cells or gonosomal cells, (gametes; Sperm and eggcell(ovum)) are the product of meiosis ( a part of gametogenesis ) . These cells are haploid (1n), they only have one set of chromosomes (1n * (22+1)) which is a combination of "fater&mother". When 2 gametes  combine a diploid zygote is formed.

In both cases (Mei- and Mitosis) chromosome (pair (2n)oder single(1n)) number 1 -22 are called autosome , while

Chormosome number 23 is an allosome (sex chromosome), either Y (male) or X (female).

Since the gametes are haploid (1n) they have only 1 single allosome, egg cell always X , and  sperm cell either X or Y.

If the allosome (the 23 chormosome pair) of an human is hemizygot ( X–Y ), he is genetically male. Is the allosome pair X-X
,homozygot the person is genetically female.

Somatic cells can have therefore 22  pairs of homologous chromosomes the 22 autosomes. The allosome pair of chromosomes is not considert homologous but either "homozygot / homogametic"[XX] or "hemizygot/ hemigametic"[XY].


How is the concept of species defined in asexual organisms? In asexual organisms such as bacteria, archea and some fungi, as well as in some plants where asexual reproduction is the only reproductive strategy, how can we be unambiguous in defining if an organism belong to a different species from another or not?

There is no taxonomic category called "asexual organism". It is rather a phenotypic trait of scattered occurrence.

However the absence of sexual-reproduction in a group of organisms sometimes causes problems in scientific classification. This caused development of the artificial-group fungi-imperfecti (or deuteromycota) at one time, for fungal strains which lack sexual reproduction.

Bacteria and archaea (prokaryotes) are not known to show sexual reproduction. However  they  show  some gene transfer processes like conjugation and transformation; but this is not the same as sexual reproduction because cell fusion does not take place.


Can epigenetic structures carry a trait? Can epigenetic structures cause a trait to manifest in a person if the trait is not already in the DNA? In all my readings I have yet to find a definitive statement that it is impossible.

Yes, epigenetic changes does affect the phenotype. This is here the whole interest behind epigenetic. Environmental variation (incl. parental care) affect epigenetics which in turn affect the phenotype (incl. behaviour) of an individual. It is pretty much clear from the wikipedia definition of epigenetics

  Epigenetics studies stably heritable traits (or "phenotypes") that cannot be explained by changes in DNA sequence.

The term "phenotype" (or "phenotypic") is actually present 3 times is the first small paragraph of the wikipedia article.

For example, you can read here on wikipedia an example of a study showing that maternal care affect epigenetic variations which in turn affects stress level later in life as measured by HPA.


How do biologists infer correct ORF of a DNA sequence? Each DNA (RNA) sequence has 6 possible Open Reading Frames(ORF). My question is: What are the theoretical bases of in vitro or in silico tries to find correct reading frame of a sequence?

Is it just distance between Start and Stop codons, or are there some other factors with more important impacts in this subject?

TransDecoder is a commonly used program for extracting likely coding regions from transcriptome assemblies, which does the following to make a call:

  TransDecoder identifies likely coding sequences based on the following
  criteria:

  a minimum length open reading frame (ORF) is found in a transcript
  sequence
  a log-likelihood score similar to what is computed by the GeneID
  software is > 0.
  the above coding score is greatest when the ORF is scored in the 1st
  reading frame as compared to scores in the other 5 reading frames.
  if a candidate ORF is found fully encapsulated by the coordinates of
  another candidate ORF, the longer one is reported. However, a single
  transcript can report multiple ORFs (allowing for operons, chimeras,
  etc).
  optional the putative peptide has a match to a Pfam domain above the
  noise cutoff score.

So in essence, look for the longest ORF, and then use some secondary metric (hidden Markov model, position weight array, database query, etc) to refine your prediction.


What is this insect that has invaded my home in Texas? After the recent floods in central Texas this past weekend I noticed my that bedroom has suddenly been infested with these small insects that have climbed in through the window. Previously, the hole in the window was used by ladybugs who hatched larvae in the room (they didn't survive long).

However, these insects have been here for 3 days now. They seem to disappear at odd times during the day (haven't nailed down a pattern yet) and return a bit later. There are roughly 20-30 of them in my room at a given time. They don't do much and seem very uninterested and passive, mostly just flying around or meandering across the walls on and off. Some of them have wings and others do not (that or the wings are hidden and they just aren't using them).

I would like to identify what this insect is so I can find a way to get rid of them. A picture is linked below. Note in the picture that the white-ish segments on the leg are actually closer to yellow in color.

Myodocha serripes

http://www.americaninsects.net/ht/myodocha-serripes.html

Nice picture! Generally, the body plan of this guy indicates Hemiptera (the 'true' bugs), but the long neck is a bit strange, so a google image search for "Hemiptera + long neck' brought up this strong candidate. It looks like it's distributed in Texas, and is in fact, named for that distinctive neck: "The Long-Necked Seed Bug".

See also the BugGuide.net page for Myodocha


Myelination and time constant In textbooks, it says that myelination doesn't really affect the time constant as tau=RC where R is the membrane resistance and C is the membrane capacitance. Myelin increases membrane resistance while decreasing membrane capacitance so there isn't really an overall effect on the time constant. However, during active regeneration of the action potential, the current only goes the path with least resistance i.e. the nodes of Ranvier, so wouldn't the R be the resistance of the node of Ranvier instead of the resistance of the entire membrane as stated in the textbooks? If this argument is correct then wouldn't myelination increases decreases time constant? Thanks!

No. When a signal is sent through a myelinated axon, the Nodes of Ranvier act as repeaters in electronics. The signal/action potential will disperse down the axon, the Node of Ranvier will pick up the signal, amplify it, and send it to the subsequent Node of Ranvier. I think you're thinking of the Nodes of Ranvier as cracks in the myelin/axon rather than as mini re-amplification sites.


What do these novel splicing sites mean? I'm sure that the anwser is obvious for some of you but I just endend my internship where we found novel splice junctions (junctionseq; RNAseq data) (see the attached file) and I have some difficulties with splice junctions.
I understand that reads can map in the junction of 2 exons (which can be linked to quality assesment) and that comparing 2 conditions, we can find groups of exons more "associated" but I dont understand :

How a novel junction can be discovered in a previous junction (sub1), or behind the last exon of a gene (sub2) and thus, what can be the consequence(s)

A splice junction is formed from a pre-mRNA (or primary transcript) whenever an intron is removed, or spliced out.  Two segments of RNA that used to be separated in the pre-mRNA are now ligated to each other, forming a junction of two exons.

RNA-Seq reads that span such a splice junction site would not align very well to the genomic sequence, however if you create a file of all the potential simulated splice junctions there may be some RNA-Seq reads that now align perfectly.

The distinction between what constitutes an intron, and what constitutes an exon is purely empirical.  While it is true that the spliceosomal complex preferentially recognizes and binds to properly juxtaposed splice donor and splice acceptor sites, a variety of different processed, mature, transcripts can result from a single primary transcript.  This differential parsing of the cis-acting sequences at the boundaries of potential introns and exons is called alternative splicing.


What current evidence supports the use of hydroxycloroquine used as a prophylactic for (corona)-viral infections? I've also read comments from doctors suggesting that hydroxychloroquine has been studied in the past as a potential prophylactic for viral infections.  A search through US clinical trials yields many results which mention this drug in connection to lupus, arthritis, and cancer.  But I have yet to find completed clinical trials which revolve around viral infections - does this exist somewhere or has this never been studied?

The only double blind randomised clinical trial I am aware of is this one, examining the use of hydroxychloroquine for the treatment of HIV-1-infected patients.  It finds significant reductions in viral load, but not improvement of CD4+ counts.  How much change could be expected in 8 weeks I do not know.  There are in vitro studies, such as this one looking at dengue virus.

In combination with azithromycin it has been examined for the use in COVID-19 (pre-print, not peer reviewed), but without a control group I find it hard to call it a clinical trial, and there are other criticisms of the work.


What is an apomorphy? What is a plesiomorphy? Can someone confirm these definitions? I want to know the correct definitions for the terms apomorphy and plesiomorphy. Unfortunately, there seems to be a variety of ways to define these terms depending on the language one uses. Thus, it has been hard to determine the correct definitions. I have settled on definitions that seem correct to me and also have examples. I would like confirmation from someone if I am understanding the definitions correctly.

Apomorphy -- any character state or trait novel to a species and its descendants. An apomorphy occurs when a taxon is selected to have a particular trait. Example: within the class reptilia, the suborder serpentes (snakes) has an apomorphy because its members have no legs.
Plesiomorphy -- an evolutionary trait or character state that is homologous within a particular taxon but is not unique to members of that group and therefore cannot be used as a diagnostic character for the group. Example: within the class reptilia, legs are a plesiomorphy for its members.

My Question:

Are these definitions and examples accurate?

That sounds pretty good. On this kind of things wikipaedia is very reliable.
You can also look at this very synthetic page:

https://www.enotes.com/homework-help/distinguish-between-synapomorphy-apomorphy-304128


How are Cytotoxic T cells transfered? We learned that Cytotoxic T cells are MHC dependent, and if CMH matchup doesn't occur between the T cell and the cancer cell for example, the former won't attack the latter.
If this is the case then how are T cells given through vaccines and transfers?

T cells are not transferred. Vaccines induce the host to expand their own T cells that are responsive to the antigens that are given.


What is the fundamental reason for death from too high or low internal temperature? I have read something about why we die from over/underheat, but always found too general reasons. Such that the liver fails. But why does the liver fail? I would like to know the most fundamental reason why not having the right internal temperature can make us die. Ignoring the very extremes where it is I think obviuos, like temperatures below 0°C and above 100°C when the water freezes and vaporizes.

So, a little bit of what I thought could be the reasons. If anything here is wrong, please correct my thinking.

As far as I understood, as the temperature changes, the speed of chemical reactions changes as well. Temprerature goes up, the reactions happen faster and if the temperature decreases, the reactions slow down. So if our body temperature changes, the speed of everything in our body should change as well. So with higher internal temperature we should just be more active, speedy and so, and with low temperature we should become slower. But that does not fit into the fact that we die from too high internal temperature. So, is it that the speed of different reactions changes in different rates, so the organism is not kept "in sync" and dies for that reason?

Or - as temperature changes, the volume of all materials changes as well. I think that's called thermal expansion. But different materials have different rates of that process. So as our temperature changes, something inside us just literally breaks or deforms too much and we die?

So why do we (and other organisms) die from not having the right temperature? Am I on the right track or am I completely wrong? Thanks for any answer.

Jakub

As mentioned in the comments, half of your question is answered elsewhere. Generally you are right, different processes change at different rates. Blood viscosity changes. Some complex systems, such as the heart, may completely fail to function. The other half of your question has a simpler answer. As heat increases, yes in theory so should enzyme performance. However enzymes have a tendency to denature if they get too hot. When heat is excessive, heat shock proteins are released which are naturally stable in hot conditions and which attempt to stabilize other proteins. This is only possible up to a limited extent, and sufficient heat will cause proteins to become entirely non-functional.


How do the variable portions of antibody genes look in cells which don't produce antibodies? There are several families of antibodies found in mammals.  They may have two or more antibody domains which contain heavy and light chains.  The variable regions of the light and heavy chains genes in the chromosome are spliced in antibody producing cells so that each cell produces a different antibody, with a unique sequence of amino acids in the variable regions.

Here's a cartoon:

The variable regions are disproportionately large here, but it gives some idea...

What I'm having trouble finding is how the DNA regions of these genes look in cells which don't produce antibodies.  Are they the same as that in the germline?  Do they undergo recombination but are not expressed?

Any help would be appreciated.

Perhaps you want to ask how VDJ recombination is regulated in non lymphoid cells..

Well even in immature lymphoid cells VDJ recombination is regulated. And also Ig genes are suppressed in T-cell and TCR genes are suppressed in B-cells..
Also, the recombination of Ig is suppressed in T-cell and vice-versa.

RAG-1,2(Recombination activating gene) downregulation partly does the job, but not fully.

Earlier reports say that transcription in the locus is essential and epigenetic regulation of transcription in turn regulates recombination.
But what it exactly means is that accessibility to the RSS (Recombination signal sequences) is limited in a repressed chromatin and recent reports say that nucleosomes are appropriately positioned over the RSS to control recombination.

Have a look at these:

http://www.cell.com/abstract/S0092-8674%2802%2900675-X

http://www.sciencedirect.com/science/article/pii/S0952791506000057

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC204470/


Are there any cases of observed extreme speciation Is there an observed (direct not indirect) speciation on record showing a species shift within the span of history of recorded science?

Could not fit in a comment…

What kind of observations will you accept to be an observation? If we can demonstrate showing genetic data that two current species where actually only one some time in the past would it represent an observation to you? Or does it has to be a lab experiment (experimental evolution)? Experimental evolution with big animals take much time, I am afraid we probably have no evidence (not counter-evidence) of a mammal species that evolve to be phenotypically speaking as different than a fruit fly and a june bug (example coming from your comment). Would you accept considering microorganisms (I have no example in head though right now)?

As you noted yourself I think, it is difficult to know how different (phenotypically or genetically?) should two sister populations (populations who derived from a common ancestral population) be so that you would consider that one of these populations at least evolved into another "kind" (compare to the ancestral population).


List of amino acid frequency of different foods? I'm trying to write a little application calculating the biological value of protein content of different meals using the amino acid frequency of different foods.

The idea is that the user can choose amount and type of different ingredients and finally obtains the biological value index for the meal.

For this calculation I'd need a list of amino acid frequencies of the different foods.

Any idea how I could obtain this?

My first idea was to just use the DNA of the different plants to extrapolate the proteins synthesized and then obtain the amino acid frequency from there but I know that genome and proteome is not correlating.

Any ideas / thoughts?

A reasonable starting place could be the Food and Agriculture Organization of the United Nations:
http://www.fao.org/docrep/005/AC854T/AC854T03.htm#chI.I

This source looks by no means complete or easy to parse, but some simple web scraping may help you wrangle the data into a database.


Do mantises stalk cicadas? The Chinese Idiom The mantis stalks the cicada, unaware of the oriole behind (螳螂捕蝉，黄雀在后), which the story behind the idiom comes from Shuo Yuan(说苑), refers to those who are attracted by immediate interests without thinking about the possible dangerous results.

In reality, do mantises stalk cicada? Moreover, are cicadas stalked by birds?

Yes, mantises hunt cicadas...

Mantis eating cicada. Source: Dreamstime.

...and yes, orioles hunt cicadas too...

Oriole eating cicada. Source: Bird Ecology Study Group.

.., and what may be more relevant to your idiom: orioles prey on mantises.

Oriole eating mantis. Source: Sustainable Adventure.