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Why don't mosquitoes evolve towards muting themselves?
Quite certainly, muted mosquitoes would be much more effective as far as their blood-sucking pursuits are concerned, since mosquito sound is predominantly responsible for sealing their fate (between the two palms of the hand). Muting themselves would certainly reduce the chances of being caught in the act. For instance, unless you notice by looking, leeches go undetected for long periods because there isn't any obvious sound emanating from them.
Thus, reasoning says - this should be favorable from the point of view of evolution, unless there is a some indispensable purpose served by this sound, which can not be otherwise served. This page seems to suggest that this is so from the point of view of mating. In fact, quoting verbatim:

Since female mosquitoes are larger, they flap their wings slower, and males know it. They use the distinctive pitch of the females' buzz to recognize them. Louis M. Roth, who studied yellow fever mosquitoes for the U.S. Army during World War II, noticed that males ignored females whenever the females were quietly resting, but whenever the females were flying, and therefore buzzing, the males wanted to mate with them. The males even wanted to mate with recordings of female mosquitoes or tuning forks that vibrated at the same pitch.

But mating signals could also be of other forms, like some chemicals secreted (I envisage something like pheremones). Why is making sound so important? Why can't this noise be either less intense, or lie outside the audio range for humans (their targets)?

Mosquitoes can fly and that is a greatly advantageous. The buzz is a tradeoff for their flying ability. I don't understand what exactly are you getting at.

@WYSIWYG: well, as a colloquial example, gliders, airplanes and choppers both fly, but do not make an equal amount of noise, do they? My point is - why can't the noise be either less intense, or outside the audio range for humans. (Thanks anyways, maybe I'll add this to the question.) :)

Maybe because most mammals are four-legged, thus they can seldom protect themselves against bites. Even though a cow might hear a mosquito land on it's back, can't do much about it. Humans on the other hand, are only here for as little as 200,000 years, which is not enough for much changes to occur.

@FloriOn - That's an interesting perspective. Thanks :)

This question is clear and there is no reason to close it even though the main answer might be pretty straightforward.

this is a frequent sort of question that arises on the site - why doesn't evolution eliminate obvious weaknesses.

Your question is really good, but in actuality, they do evolve towards muting themselves, actually, they have pretty much done "most of the work":
It is assumed that microscopic scales along veins and wind margin
play an important role as a silencer as downs on the flight feather of owl.

From this we can assume that the effectiveness of these scales are high, as they had plenty of time to evolve; thus the other factor they should alter to make them quieter is the frequency of their flapping $f$, which can be calculated from the following equation:
$$f=K m^{-1/6}$$
where $m$ is the mass of the animal and $K$ is the proportionality constant. The resulting number is around several hundred hertz (Remi.b observed a value around 440 Hz)
There are two options for them, either increasing the frequency up until our ear is incapable of hearing it which would be impossible as even the highest flapping frequency can hardly exceed 1000 Hz, which is nowhere near the required 20,000 Hz. By increasing their body mass they could decrease the frequency but the needed 15-20 Hz is pretty low compared to the actual several hundred, thus it would likely need a complete body structure change which is not something to happen in the near-future.
An another solution might be a different strategy in flying. Gliding attacks might pay off really well (that's why owls on the other hand can't be heard during flight), but even though there are some insects capable of such[1], it would need an immerse amount of time, not talking about the problems that might arise from the bumping into of our body.
I don't think that the mating signaling would be indispensable from an evolutionary perspective, but this statement of mine can't be proved.

These are the physical/biological difficulties of the problem, here is one from an evolutionary aspect: They are not likely to have experienced a strong selection against this feature, as most of the possible victims are incapable of doing much against a mosquito due to the absent of hands (and tails are seldom enough to stop them). The first possibly blood-sucking mosquito was found to be living 79 million years ago, while animals that might be able to "seal their fate" are much more recent, while not even having success most of the time.

https://www.jstage.jst.go.jp/article/jsmec1997/43/4/43_4_895/_pdf
http://www.geologica-acta.com/pdf/aghv3501a12.pdf
http://www.physics.emory.edu/faculty/weeks//lab/papers/jwang-arf05.pdf

Thanks, this is a very well researched answer. I'll wait for sometime and hear from others if they have anything to add to this, before accepting.

..they have not experienced strong enough selection to be silent fliers. people can only really hear those things when they fly close to your ears.

Could you please provide the reference for the flapping frequency formula?

@Hans It's in the first cited study, in section 4.1

Gliders do not actively fly and there is no work done by them in producing motion. Other flying machines do make a sound.
If a trait exists then it means that there is not enough pressure against it. You can hear a mosquito only if it flies close to your ears; otherwise, they seem to be undetectable by hearing.
To produce ultrasonic sounds the mosquito has to flap its wings too fast- which is energy intensive. Conversely, to produce just infrasonics, it has to flap the wings too slowly which may not provide it with enough thrust.
A recent study by Bomphrey et al. (2017) suggests that mosquito flight is different from other insects and the aerodynamics are rather complex. Mosquitoes are known to use low amplitude, high-frequency flapping that generates the buzz.
From the abstract:

Mosquitoes exhibit unusual wing kinematics; their long, slender wings
  flap at remarkably high frequencies for their size (>800 Hz)and with
  lower stroke amplitudes than any other insect group1. This shifts
  weight support away from the translation-dominated, aerodynamic
  mechanisms used by most insects2, as well as by helicopters and
  aeroplanes, towards poorly understood rotational mechanisms that occur
  when pitching at the end of each half-stroke. Here we report
  free-flight mosquito wing kinematics, solve the full Navier–Stokes
  equations using computational fluid dynamics with overset grids, and
  validate our results with in vivo flow measurements. We show that,
  although mosquitoes use familiar separated flow patterns, much of the
  aerodynamic force that supports their weight is generated in a manner
  unlike any previously described for a flying animal. There are three
  key features: leading-edge vortices (a well-known mechanism that
  appears to be almost ubiquitous in insect flight), trailing-edge
  vortices caused by a form of wake capture at stroke reversal, and
  rotational drag. The two new elements are largely independent of the
  wing velocity, instead relying on rapid changes in the pitch angle
  (wing rotation) at the end of each half-stroke, and they are therefore
  relatively immune to the shallow flapping amplitude. Moreover, these
  mechanisms are particularly well suited to high aspect ratio mosquito
  wings.

Bottomline is that evolution does not know where the best optimum is and it does not really try to proceed to a global optimum. If a trait is disadvantageous, it is selected against. Neutral mutations stay but do not get amplified unless they have some kind of advantage.

Note that the speed of wing flapping is exactly equal to the frequency of the sound produce. A mosquito flap at about 440 Hz (personal observation during my Bachelor degree). A young and healthy human can hear up to 20000 Hz. The mosquito would need to flap their wings 45 times faster to become inaudible (and would need to adapt its mating behaviour in consequences).

@Remi.b - Wow. That's fabulous information! Any comments about the second proposal (lesser intensity of sound, even though at the same frequency)?

@TheDarkSide for exactly the same reason as explained in the answer - there is no selection pressure to lower the volume. Additionally, since mosquitoes find each other by sound, lowering the intensity would decrease numbers of mating attempts, something that I'm fairly sure would not be advantageous to the species.


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Figuring out an honest indicator in intrasexual selection
In the first picture, the parameter $r$ seems to compare the direction and strength of two variables. In the second picture, $R^2$ seems to describe the variation of proportion of independent and dependent variables.

With this being said, are honest indicators determined by $R^2$?
Why is it a positive number for both graphs if we refer to the second picture?

I don't understand your question. I don't know if it is a stat question or a biology question. You have t give it more thoughts and split down to the individuals elements that are unclear to you. The r values are wrong. While R^2 is always positive, R can be positive or negative. It is negative when the slope is negative, positive otherwise.

Maybe, you are trying to understand what hones signalling mean. You could have a look at signalling theory and handicap principle as a start.

It's a biology question from general bio II that includes statistics. I want to know how we can determine an honest indicator in intrasexual selection based on statistics. an honest indicator comes from Zahavis hypothesis. Its pretty clear what I'm asking....I know what it means in terms of definition i just don't know how to interpret it in graphs.

Those graphs seem to just be teaching you what r and R^2 mean; there is no relationship to honest signaling except for the headers, and the data are all synthetic.

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How far in can non-extremophiles live, in Earth?
I am a high school student. I'm doing a project where I need to find a planet in our galaxy that might be habitable. Then I need to create an organism that could live on that planet and justify everything about it Ex: Sight, whether or not it can see and why or why not / Touch / Smell / Respiration / Central Nervous System / Cell Count... My final outcome must have these and a lot more.
I just need to justify and explain where it lives on the planet I have chosen. I found a planet (Kepler-422b) which was described as being one of the most Earth-like planets, in terms of size and temperature, yet found. Since it is very Earth-like, it made my job a bit easier. But the planet orbits a red dwarf star that is cooler than our star, and this planet is -40 degrees Fahrenheit (80 degrees cooler than earth) so my organism will have to live in the ground of the planet and rely on the core for warmth. But I do not know how deep organisms can go into the Earth. Can someone please help me? I have done a lot of research and spent a lot of time trying to find this but extremophiles are the only organisms listed.
Thank you so much for helping me.
An extremophile is defined as a microorganism, especially an archaean, that lives in conditions of extreme temperature, acidity, alkalinity, or chemical concentration. Like the Tardigrade. Im sorry I did not make this clear initialy

Can you define what is an extremophile? It seems difficult to answer question when this is not properly defined.

https://en.wikipedia.org/wiki/Gliese_422_b - It's like 10 times more massive than Earth - it's really not earthlike. Have you thought it out well? Also it's unconfirmed, so may don't even exist...

Welcome to Biology.SE and what a great project, it sounds fascinating!
A few years back there was an expedition that drilled down to the deepest layer of the ocean's crust. Down there they found hundreds of different species of bacteria (mostly Proteobacteria) surviving largely on hydrocarbons and other minerals found in the rock. The deepest (that was sequenced) was found 1391.01 mbsf (meters below sea floor) and survived at a temperature of about 102°C (215°F). Like I said, there were several species sequenced, so you could really use any of them that match your needs as at least a start to your organism.
This is the deepest point I know of that we have found life, and, considering your project, I don't think you have need to go much deeper. I assume Kepler-422b has liquid water (obviously not at the surface, but perhaps a few miles down)? If so, there is a chance that the water goes relatively close to that depth already.
I hope this helps and good luck!
CDB
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974637/
Edit: If you are looking for a multicellular organism that survives deep enough underground to rely on core warmth, I suggest Halicephalobus mephisto, a nematode living about 1.3 km underground at about 32°C (90°F). This is still considered an extremophile, however it is multicellular with a digestive tract, nervous system, etc. I apologize for the confusion in my initial answer and thanks to jamesqf for noticing my mistake. If you are not content with any extremophiles (even multicellular) please let me know and I will do my best to find something else. Again, I am very sorry for my error.

I think that living that far down makes them extremophiles, pretty much by definition.  And for the OP, the planet could have an ice-covered internal ocean, like Jupiter's moon Europa.

As far as I know these species of bacteria are not officially considered extremophiles, I could be wrong though. I will pin-point a specific species and research it's classification tomorrow to confirm this though.

@jamesqf it would appear that you are correct. The mere fact that these bacteria can survive in this environment makes them extremophiles. For instance, Ralstonia pickettii was one of the species found and it can survive high concentrations of heavy metals and low nutrition, making it both Metallotolerant and Oligotrophic, however this species is not officially classified as an extremophile. This situation seems to be a double edged sword; an organism living deep enough underground to keep warm would need to be Metallotolerant, however an organism living on the surface must be Psychrophilic.

Just out of curiousity, when you say "not officially classified", who/what is the official doing the classifying?

You know, I'm actually not sure. I assume that it would be the team who discovered it. Usually anywhere you get reliable information on classification will specifically note that it is considered an extremophile and cite what type, but I'm not sure who officially decides.

Thank you so much, this really helped a lot and saved me a lot of time! Your answer was great, I guess it was a little silly of me to think that an organism could live that far in the Earth and NOT be an extremophile. The Halicephalobus mephisto looks great, I will be able to use this very well. Again, thank you, all of you

No problem, I'm very glad I could help! Again, what an awesome project, from what you've said you seem to be doing a great job with it! Good luck and have fun!

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One Sample, Different Methylation Values
I'm hoping that somebody here can explain this unusual result that I'm getting with some pyrosequencing data. I have bisulphite converted a few samples a couple of times over the years for different projects. Recently I was collecting some of this disparate data together and I noticed that when the same pyrosequencing assay was used on these samples, those that were converted later had decreased methylation at the CpG sites of interest compared to the initial bisulphite converted samples. The original conversion was in 2010 and the repeat conversions were in 2014/2015. The assays are the same and it's difficult to blame this on PCR amplifying one clone over another since I've done technical replicates on each aliquot. Even the 2010 converted sample has the same result in 2015 that it did in 2010 but this is different from the 2015 converted sample.
We are using the same kit (Qiagen) for bisulphite conversion and haven't made a major change to our procedure (we follow the Qiagen protocol without modification). Has anybody noticed this phenomenon before? Is it possible that stored DNA would experience methylation changes? It seems more likely that the issue is technical but I'm having trouble figuring out exactly what that technical issue is.

In experimental troubleshooting questions like these it is difficult to provide an exact answer unless you specify the protocol. You should also add details such as storage conditions, how old was the bisulphite solution etc, level of difference between the two replicates etc.

Thanks - I added some detail. I unfortunately can't say too much about our pyrosequencing assays until we've published.

So just to clarify: You have a sample, converted some of it, stored some of it. Sequenced some of the converted sample(A). Wait five years. Sequence some more converted sample(B), convert some of the stored sample, sequence that (C). So A and B match but C is less?

I looked into this and if the effect is real, which it sounds like it is, it may be 5-formylcytosine.
Methylcytosine oxidizes into hydroxymethylcytosine, which reacts with bisulphite exactly like you expect (identically). Hydroxymethylcytosine further oxidizes to 5-formylcytosine, which behaves like unmodified cytosine (i,e. deaminates to form U). TET enzymes mediate this behavior in vivo but I can't find any data on spontaneous methyl group oxidation or what the kinetics might be like. This paper relies on the properties of 5-formylcytosine outlined above.
You could use this paper to test if that's true. Reduction with sodium borohydride converts 5-formylcytosine back to hydroxymethylcytosine, which reads as methylated under bisulfite sequencing.


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Why do viruses last longer on hard surfaces, like glass, than porous ones
All the papers I've read about survival of viruses outside of the host refer to longer survival times on hard surfaces without explaination. As a layman I would have thought that a virus (who's main environmental dangers are things like UV would survive better on rough or porous surfaces, where they are protected and can hide from the light and weather, not the other way round.
For example, one paper I read recently (although it's an old paper) showed Ebola virus surviving for 50 days on glass but not even 2 on rough materials. Can anyone enlighten me as to what it is about glass that makes such an ideal home for viruses to extend its lifespan by over 25 times?
More scientific papers would be helpful, but the medical community does seem to think that hard surfaces in general preserve viruses better than soft ones. The Mayo Clinic and UK NHS web sites both make that claim, without explanation.

Can you link some of the papers? That might be helpful.

Sure - the paper I mention is - Piercy, T.J., Smither, S.J., Steward, J.A., Eastaugh, L. and Lever, M.S. (2010), The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. Journal of Applied Microbiology, 109: 1531–1539. at link

Is it about roughness or material? Does it change between a flat glass and a rough glass surface? Because I think that the fact that glass is, in general, much less reactive than metal surfaces, for example, could explain why viruses survive better on it.

My first (purely hypothetical) thought is that porous materials would allow for ionic transmission in any direction, thus if water, ions or other bacteria would come in contact with the virus, it may affect it in a negative way. Glass is fantastically inert and impermeable.

The paper you cited is not about survival on smooth versus rough surfaces; it does, however, mention discrepancies in survival on metallic versus non-metallic surfaces.
From the article you cite (Piercy et al., 2010):

The lack of recovery of virus from metal substrates may be attributed to several factors; previous work (Sommer et al. 1999; Pawar et al. 2005) has shown the binding of micro-organisms to metal surfaces to be poor because of the high surface energy, high electronegative and hydrophilic properties of metal. Other research has also shown that positively charged metallic ions such as copper and silver have a high bactericidal activity (Friedman and Dugan 1968; Bitton and Freihofer 1977; Slawson et al. 1990) and hence by extrapolation may also have a high virucidal activity.

In short, it isn't exactly clear why viruses in particular might have poor survival on metal, but the electrical and chemical properties of metallic surfaces, as well as biological activity of metallic ions that are constantly leached from alloys like steel are all candidates.
The claim may also not apply to all viruses, and the results are not consistent across labs. For example, Sagripanti et al. 2010 find no effect of surface material (aluminum alloy, rubber, or glass) on Ebola, Venezuelan equine encephalitis, Lassa, and Sindbis viruses.
References:
Piercy, T. J., Smither, S. J., Steward, J. A., Eastaugh, L., & Lever, M. S. (2010). The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. Journal of applied microbiology, 109(5), 1531-1539.
Sagripanti, J. L., Rom, A. M., & Holland, L. E. (2010). Persistence in darkness of virulent alphaviruses, Ebola virus, and Lassa virus deposited on solid surfaces. Archives of virology, 155(12), 2035-2039.
Bitton, G., & Freihofer, V. (1977). Influence of extracellular polysaccharides on the toxicity of copper and cadmium toward Klebsiella aerogenes. Microbial ecology, 4(2), 119-125.
Friedman, B. A., & Dugan, P. R. (1968). Concentration and accumulation of metallic ions by the bacterium Zoogloea. Dev. Ind. Microbiol, 9, 381-388.
Pawar, D. M., Rossman, M. L., & Chen, J. (2005). Role of curli fimbriae in mediating the cells of enterohaemorrhagic Escherichia coli to attach to abiotic surfaces. Journal of applied microbiology, 99(2), 418-425.
Slawson, R. M., Lee, H., & Trevors, J. T. (1990). Bacterial interactions with silver. BioMetals, 3(3), 151-154.
Sommer, P., Martin-Rouas, C., & Mettler, E. (1999). Influence of the adherent population level on biofilm population, structure and resistance to chlorination. Food microbiology, 16(5), 503-515.

Maybe I should have been clearer in the title question, my mistake. I read and understood the effect of metals, my main question is in the final paragraph, why glass, so much smoother than all the other materials which are rougher.

@Isaacson Do you have a paper that shows that glass specifically is best, or that says it is better because it is smooth? Most likely it is because it is quite inert, unlike metals. If you are comparing glass and metal, though, it doesn't really matter which you focus on. You could say "survival on metal is shorter because it does X, Y, Z" or you could say "survival on glass is longer because it doesn't do X, Y, Z": the answers are the same because it's a matter of comparison. Or am I still misunderstanding your original intent?

(also note the point I made at the end of my answer, which was a reference to a paper that showed for several viruses no difference between glass, rubber, and metal)

Yes,thanks. I don't have the papers to hand at the moment I will have to look them up again (this question is quite old) but it's mainly that all the papers I read on the subject seemed to cite a few days survival and then suddenly there was this one 50 day survival time on glass. I presumed it was the glass because I had read elsewhere that viruses like norovirius survive longer on hard surfaces too, but maybe it was nothing to do with the glass.

Ah okay - I didn't initially notice the age of the question because it just got bumped - I did see April but forgot we are in 2017 (this is really easy to do as an academic in the US, I might add). The paper you linked did show the longest hard-surface survival on glass, but that was just one sample with just one of the viruses, and they didn't try to conclude statistically that it actually survived longer than the plastic, just that it was clear that both those surfaces were much better than metal. If you find something else I'm happy to amend the answer as best I can!

No, that pretty much answers it, if you think it's most likely to be just an odd result and unrelated to the substrate, that's pretty much the answer, unless I can remember what I read that made me think it was more of a general trend.

Just to clarify, I don't think it's unlikely that glass could be a nice place for a virus to rest, I just don't think it is a magical home that provides any sort of order-of-magnitude increase in survivability over other surfaces that are also fairly inert, regardless of their actual microscopic texture.

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Why are spiders afraid of flies caught in their web?
I recently noticed a fly got caught in a spider web in my house. The fly was very energetic and, even though caught, continued to flap it's one wing (which I think might have been partially free) with hyper-speed.
Initially I thought it was just trying to get free from the web but then I noticed that when the tiny spider (it was smaller than the fly) approached it to, presumably, try to inject its venom the fly started to again energetically flap it's wing and it scared the spider off.
I was wondering - why did the spider got scared? I know animals do not perceive threats quite like us and even a big lioness might give way to a tiny mongoose if the mongoose threatens with a fight (I'm guessing both because unnecessary fighting expends precious energy and any wound can be bad with no hospitals around) but still as far as I know the fly can't harm the spider in any way even if it is free and much less when it is bound and while it would be smarter for the spider to just sit and patiently wait for the fly to drop out of exhaustion he is also risking it getting free, eventually.
So why are spiders scared of flies caught in their web?

from https://www.researchgate.net/figure/234696071_fig5_Figure-1-Differences-in-attack-strategies-upon-safe-and-dangerous-prey-in-orb-web

The linked article is pretty cool.  Bottom line: predators need to be careful.  If they get hurt they cant hunt and they starve.  Spiders have different strategies depending on perceived dangerousness of a prey item.  The linked article, for example, categorizes dipterans (flies) as nondangerous to spiders but orthopterans (crickets) as dangerous.  How are crickets dangerous?
For your spider I can think of 1 of 3 things.
1: Fly is dangerous to spider in a way not obvious to you.  Maybe it is poisonous, or can bite, or has sharp spines on the leg.
2:  Fly is perceived by spider as similar to dangerous prey.  I have watched spiders address wasps in their webs and the spiders are careful.   If there are flies that mimic the appearance of wasps / bees to get respect, why not one that behaves in the web like a wasp to get respect?  A cool idea and testable too.
3:  What you see is the danger.  A big fly thrashing around might be enough to damage the spider.  A spider not desperate for food might not want to risk getting hit.  Spiders are not that durable.  That makes sense to me.


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Recommend any Molecular lab LIMS (Laboratory Information Management System)
We are looking to develop or customize a LIMS for our molecular lab. Do you know of a LIMS that you've used in a molecular lab before, or one that could be used.
Thanks for the help
(Edit)
Some of the attributes we'd like to store include:
    Patient information (Name, demographics, test ordered)
    Sample information (Accession #, Case ID, sample type (blood,bone, etc.) )
    Test information (Kit used, Kit lot #, associated expiration date)
Ideally this is Software as a Service so its usable on multiple operating systems.

What are your precise requirements? online/offline ? Lab notebook or it should handle inventories also? Linux or MS or cross platform?

We use Quartzy to manage all of our lab supplies and reagents. As far as I know though, this does not allow you to also store things like patient records, or lab notebooks.

What kind of management? Orders? Stocks ??

I just added some additional info. Hope this helps clarify


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Can I leave BL21(DE3) cells in room temperature?
I am preparing competent cells, and I finished inoculating a single colony in SOB. It has been incubating at 37 degrees Celsius for almost 16 hours since, and it's getting very late where I live. I wanted to do the large-scale inoculation a few (at least 7) hours from now instead of right away, but I do not want the cells to start dying. Can I take the cells out of the incubator and leave the cells in room temperature? I'm hesitant about this because even at room temperature, wouldn't cells still be growing, making it possible for cells to die as well? What extra steps, if any, should I take before using the cells?

Don't do this. User fresh cells thoughout the process, everything else can affect your transformation efficiency in the end.

What would you suggest?

I always did the preculture (picking a single colony from the plate) overnight (12-16 hrs typically) and then started the main culture from which I harvest the cells for the competent cells the next morning. Here you need to carefully check the OD anyways to not overgrow the cells.

I meant to do that, but I end up having to do the preculture in the morning (long story), so now I feel like I should either start harvesting or (as someone suggested to me) leave it in room temperature.

I would use a fresh overnight culture then. A colleague tested this a while ago and the cells which are stored for a while give less efficient transformation rates.

What kind of inoculation? What is the final purpose? It may not be a problem at all. Ask someone in your lab to take the cells out and keep them in 4⁰C

If you leave the cells at R/T what are you worried might happen?  This strain is a lambda lysogen that produces bacteriophage T7 RNA polymerase (correct?). Therefore it stands to reason that you wish to express some foreign gene product under the control of the T7 promoter, so we are talking about a transformation where you already have the plasmid in hand and are just changing hosts.  So you don't need the competent cells to have a transformation efficiency greater than 1EE8 per ug--1EE6 per ug would be more than enough. Leaving them out at R/T might be okay, or it might ruin them.

I have not transformed the cells yet. I was told to follow a protocol to make the cells competent before transformaton. In a few hours I will be cleaning the cells and planning to perform transformation. Also, wouldn't putting the cells in 4 degrees Celsius form ice and cause damage to the cells upon thawing?

4 C° is fridge temperature, above the freezing point of water. Are you thinking of 4F° or perhaps -4C°?

Yes, I know it is fridge temperature, which is why I was worried that it could freeze and damage the cells upon thawing. The overnight cells ended up alright, although their growth curve lagged a bit, but overall it was OK. Thank you all for your inputs.

Pure water freezes at 0C, but the buffer that render the cells competent for DNA transformation contains divalent cations (usually Ca++). These ions will cause freezing point depression (like sprinkling rock salt on an icy sidewalk). So I would not expect the bacterial cells to freeze until the temperature was well below 0C. You also need to take into account that the bacterial cells contain lots of ions (all of the proteins, for example) and is about 150 mM in total (various physiological ions). Finally, if your recipe includes glycerol that also depresses the freezing point further.


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Why don't our cells merge when their phospholipid membranes touch each other?
Membranes of our cells consist of lipid bilayer (with some other components mixed in).  Why wouldn't those lipid bilayers glue to each other and make the cells merge? If you suppose that it's due to additional components in the membrane that prevent them from gluing together, consider the case of liposomes, which don't contain additional components, but seemingly don't glue as well.
I'm primarily interested in quantitative physical chemistry aspect of the matter.

Phospholipid bilayers found in cells are usually negatively charged. The phosphate groups repel each other by like charges and prevent two membranes from coming too close to each other. Membranes are also full of proteins and often coated with carbohydrates, which serve to keep membranes from interacting too strongly. See this diagram of a membrane bilayer:

Even this diagram is probably cleaned up.
From a more physical chemistry perspective, the energy barrier for flipping a lipid in a bilayer is pretty high, since the polar head group doesn't like passing through the hydrophobic layer. Bringing two membranes together would require overcoming the charge-charge repulsion and flipping around the inner two layers of lipids, so you go from 4 layers to 2.
Interestingly, there are mechanisms for fusing membranes, such as using cationic lipids. These would turn charge repulsion into charge attraction. The lipid ion pairs tend to have shapes that don't support bilayer formation, and tend to prefer micelle or inverted micelle shapes. These have been utilized to break down vesicle membranes and allow large molecules to pass through, like DNA or proteins, and are used in genetic modification of cells.

Also, SNARE proteins facilitate membrane fusion.

well it's based on the tissue type for example take loose connective tissue which lies under epithelium they don't merge because of the profound matrix separating them while in the epithelium in cuboidal and columnar epithelium at side corner and upper portion of their membranes the two neighboring cells fused completely preventing any flow of material whatever may be the size it's called tight junction and is due to the physical change in lipid layer of both cell causing this adherence.
or if by merging you mean that the cells should remove their barriers (side membranes) to make their self one cell it is also depending on tissue like macro phages becoming giant cells by merging and forming one cell.

Yes, I mean why don't they make giant cells by merging?

well it's due to the enzymes synthesized by macrophages which other cells doesn't show this charesteristics and this fusion doesn't happens itself unless there is a stimulator like bacillus anthracis (causer of tuberculosis) when it enters the body the macrophages can swallow them but can't lyse them so they have to merge... so in that case the alterer of this phenomena is the bacteria mentioned by indirect stimulation of those gene which synthesis those enzymes which take part in fusion of macrophages...so the bottom line is not every cell can synthesis those fusion making enzymes.


text:
Can we take advantage of nanopore sequencing systematic errors to predict secondary structure motifs?
One of the methods of single-molecule sequencing, Nanopore sequencing, is based on traversal of DNA strand through a nanopore. Nucleotide is determined by measurement of ion current (when nucleotide passes through the pore, it decreases the current of ions through the pore, which can be measured).
The method is known for producing systematic errors. I.e. if you sequenced the same molecule twice and during the first run Adenine in 255th position was confused with Guanine, it will be confused again if you repeat the experiment.
I wonder, if it's possible to make use of information about location of errors to predict secondary structure of DNA/RNA etc.? It is natural to suppose that presence or absence of errors is determined by the context, where a nucleotide is located. If I want to validate the hypothesis that same errors are produced by the same motifs of secondary structure, where can I get the raw data to validate this theory?


text:
How are the physiological properties of mitochondria measured?
this is my first question on BiologySE. I am a Physics and Mathematics student currently doing a project on cell growth simulation. I am doing literature survey and I have a question about cellular biology experimental methods.
I understand that the membrane potential is a measure of mitochondrial functionality (higher potential means more efficient electron transport chain). Additionally, the mitochondrial volume is also an indicator of mitochondrial efficiency (higher volume, higher area, more places to do electron transport).
I would like to have some points elucidated.
In particular, can these mitochondrial membrane potential and volume...

be measured for a single cell, or only in a population?
be measured non-destructively, leaving the cell alive?
be measured simultaneously, or experiments measuring one necessarily make the other unavailable?

I am thinking mostly of in vitro experiments of course.

Note that mitochondrial shape would also matter.

A simple method would me to express a fluorescent protein in the cell that specifically localizes to mitochondria. mito-dsRed is a Red Fluorescent Protein which has that property; it can be expressed from a plasmid.
Using fluorescent microscopy and image analysis, you would be able to measure the geometric properties of the mitochondria. This can be done at a single cell level too (using confocal microscope) and non-destructively. Volume can be measured by what is known as Z-stacking— an automated technique by which the microscope takes several 2D snaps at different planes and stacks them to construct a 3D image.
You can implement this in live cells too; this method is called live cell imaging.

Could you say something about the membrane potential too?

@AndreaDiBiagio There are some voltage sensitive dyes, that can be used for that purpose but I don't know much about them. I'll have to check.


text:
What happens to a virus SARS-CoV-2 on an object?
Many articles say that "the coronavirus" — they probably speak of the SARS-CoV-2 — can "remain alive" for so many hours on some surfaces, so many days on some other surfaces. For example, "the virus lives 5 days on glass".
I think that this is a bad choice of word. All these articles speak about the virus SARS-CoV-2 as if it were a living being. But I think it is not a living being. The virus SARS-CoV-2 does not "live" on a glass surface. It just is there.
When a virus SARS-CoV-2 is on an object, what happens to it? If it is not there anymore after 5 days, why? What does time do to a virus?

This is almost a duplicate of Why does the SARS-CoV2 virus not remain infectious forever? Or does it?. Check out that question to see if the answers there answer your question

@Charles - This other question is interesting. But on its page there is no answer to my question. Especially, on flat glass or steel surfaces, what happens?

Edit: What does time do to a virus?

The linked duplicate asks the same question: "All these articles speak about the virus SARS-CoV-2 as if it were a living being. But I think it is not a living being." and the answer there is "Rubber bands (for example) aren’t alive either, but there are several ways they can be destroyed, including physically pulling them apart or just by having them exposed to air enough. Viruses are the same, conceptually." If you want to ask a different question I'd strongly recommend removing the trivial bits about viruses not being "alive" that implies that this should somehow make them invulnerable.

Those articles simply refer to the viability of the virus, i.e. whether it can still infect a host thereafter. (Sometimes this is referred to as "survival" of the virus.)
A unviable virion is not quite the same as it being "not there" at all, although it is so from the perspective of a host that doesn't get infected.
Those viability [in the environment] studies use a quantitative measure of how much of the virus (i.e. how many virions) are still viable after some time on some surface (or even in "the air"), e.g.

SARS-CoV-2 remained viable in aerosols throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air. [...]
SARS-CoV-2 was more stable on plastic and stainless steel than on copper and cardboard, and viable virus was detected up to 72 hours after application to these surfaces [...], although the virus titer was greatly reduced (from 103.7 to 100.6 TCID50 per milliliter of medium after 72 hours on plastic and from 103.7 to 100.6 TCID50 per milliliter after 48 hours on stainless steel).

So they are measuring the time to some [chosen] statistical threshold of viability. For reference as to their particular method:

The TCID50 (Median Tissue Culture Infectious Dose) is one of the methods used when verifying viral titer.
TCID50 signifies the concentration at which 50% of the cells are infected when a test tube or well plate upon which cells have been cultured is inoculated with a diluted solution of viral fluid.

Which part of the virus machinery breaks first might depend on the environment. On copper, for example, it has been found that for "common cold" coronaviruses (e.g. HuCoV-229E):

Exposure to copper destroyed the viral genomes and irreversibly affected virus morphology, including disintegration of envelope and dispersal of surface spikes. Cu(I) and Cu(II) moieties were responsible for the inactivation, which was enhanced by reactive oxygen species generation on alloy surfaces, resulting in even faster inactivation than was seen with nonenveloped viruses on copper.
[...]
Coronavirus was exposed to metal surfaces and recovered, and the positive-stranded viral RNA genome was extracted and purified. A one-step reverse transcriptase real-time quantitative PCR (RTqPCR) was performed to detect a 139-bp region of ORF1 within nonstructural protein 4 (nsp4). Virus that had been exposed to copper and brass surfaces demonstrated reduced copy numbers of this fragment with increasing contact times. [...] . Comparison of the entire viral genome by agarose gel electrophoresis confirmed that nonspecific fragmentation occurred on copper and brass, with fragments becoming smaller with increasing contact time.

See also related q here on virus survival in small droplets, where a different inactivation mechanism is suspected.
In general, all viruses start to degrade outside their hosts at temperatures above -20C, even in the absence of some more specific environmental stressors (like unfavorable humidity, reactive surfaces like Cu, etc.) In suitable hosts, this temperature-based degradation is more than offset by the virus' multiplication.

Thank you. I have added to my question: What does time do to a virus?

@NicolasBarbulesco: Time does nothing unless the temperature is high enough or there are some other "nasty" environmental factors. Influenza viruses have been preserved for over 50 years in cryogenic conditions (once unfrozen they are viable), some viable viruses have been recovered from 30,000 years-old permafrost;.see end of my answer and the med SE q linked from there for details. Are you asking for details about temperature-related degradation (as it's the most general mechanism)?

From What happens to viruses that causes them to die?:
TL;DR: Factors such as UV light and heat causes the mix of RNA, fatty membrane, and protein making up the viruses to steadily break down.

More details:
https://www.sciencefocus.com/nature/do-viruses-die/:

Strictly speaking, viruses can’t die, for the simple reason that they aren’t alive in the first place. Although they contain genetic instructions in the form of DNA (or the related molecule, RNA), viruses can’t thrive independently. Instead, they must invade a host organism and hijack its genetic instructions.

https://www.sciencealert.com/how-long-does-coronavirus-last-on-surfaces:

Just hanging about in the atmosphere, the effect of factors such as UV light and heat causes the mix of RNA, fatty membrane, and protein making up the [viruses] to steadily break down in a few hours [or less/more].

https://www.statnews.com/2020/03/19/coronavirus-survives-on-surfaces-how-to-protect-yourself/ (mirror):

Viruses covered in “envelopes” have the most trouble surviving outside a living cell. On surfaces, the surrounding light, heat, and dryness break down the envelope, killing the virus. (Porous surfaces pull moisture away from viruses that land on them, accelerating the destruction of the envelope.) Most rhinoviruses have such envelopes; so do some influenza viruses. Norovirus doesn’t, enabling it to last longer in the environment.

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


text:
Multiple transcripts encoding for one protein
Trying to get a better understanding of the process of DNA to proteins.
So when we have a gene, it is read from the 5' to 3' end, only translating the exons to mRNAs. A single gene can have multiple exons, and use alternative splicing to create different transcripts. A transcript may result in mRNA (not necessarily right? Also other kinds of RNA?) which is translated to amino acids. Finally folded to a functional protein.
My question here, are there different transcripts (say in different genes) that encode for the same protein?

Yes, they arise because of gene duplication but usually the protein is not exactly similar but quite similar. These genes are called paralogs.

yes, for example, if one gene came from you mother and another from your father, they might be different enough to cause disease (see sickle-cell anemia or cystic fibrosis).

As I understood it, a transcription is a combination of exons being used for, for instance, creation of proteins. I'm not referring to point mutations and such, because than another protein will be made by the transcript. Most probably not a protein which is created in another gene.

Gene duplication accounts for different the same proteins to be created in different parts of the chromosome, in an extreme case on a different chromosome. But in principle, the genes are the same, hence the transcript is the same. Are there, naturally (so we all have) different genes encoding for the same proteins

Any mutations in the 3' UTR of a transcript for a paralog would result in a different transcript which encodes for the same protein.

Just a point of clarification: you say "it is read from the 5' to 3' end, only reading the exons" but this is not the case. The cell's transcription machinery reads the entire gene until it comes to a "stop" sequence. The resulting pre-mRNA is then spliced to produce the actual mRNA(s) that are translated into proteins. It is during this splicing that introns are cleaved out.

@MattDMo you're right. I skipped some steps...

@TomD interesting links! :-)


text:
Cut-off values for LD, LOD and D-prime as algorithmic input
I created an algorithm to generate SNPs for random people of different descents - based on HapMap data. While this works good, there is something else I want to take into consideration. So if a SNP has a MAF of 0.01, with an LD of 1, the generated results will, in most cases be sufficient. This is not the case for a MAF of 0.4 and LD of 0.8.
The HapMap LD files have, besides the LD data, also LOD and D-prime. The question is, is there a set of parameters so that as much of the relevant LDs are filtered out of the total set?
I want to filter this out, since, for example, there are LDs described with a value of 0, or an LOD < 1, and problematic D-primes.
Trying to rephrase the question:
Given a huge set of LD information (250GB), which are not filtered on statistical power, I want to make a subselection of LD information that are 'relatively' descriptive of the link with respect to another SNP. So I need to have a set of parameters to filter the LD information from HapMap. Of which possible values are LD, LOD, and D-prime.
Eyeballing the LD dataset, it doesn't gives a good instinctive boundary. A problem with using the data as is, is that both the D' as LOD can be both high and low. I know the parameters have an interdependence, but not a one-to-one mapping.
Does anybody have experience in filtering non-descriptive LD values from (for instance) the HapMap LD dataset?

I don't get your question. LD, LOD and D' are not independent parameters but scores describing the heritability linkage between SNPs. For GWAS SNPs are typically pruned at an LD linear $r^2$>0.8 to ensure independence but I don't think this is really relevant for the simulation you are doing. Also I don't see why a LD value of 0 is problematic, this means that two SNPs are completely independent.

@cagliari2005 I know what LD means, but working with lower LDs make generating alleles for SNPs that were generated before harder, since the MAFs differ. Wrt D-prime, values of -1 and 1 seem good, but only if either the MAFs are similar, or the population size is big enough. LOD of 3 seem to make sense, but for certain purposes possibly to restrictive


text:
Could Physarum polycephalum consume regular toenail fungus?
I just watched this video on physarum polycephalum, aka the "blob" and noticed how it consumes white fungus. Could it do the same maybe with human toenail fungus?

I am afraid your question is expressed in non-scientific terms, and requiring one to watch an external video to understand it, is not acceptable for this list. Your question is likely to be closed for lack of clarity unless you edit it so that it becomes comprehensible in itself. “Blob” indeed!

The site shows a related question that seems to be accepted : https://biology.stackexchange.com/questions/46192/what-is-this-white-stuff-inside-apples?rq=1 Your proposal sounds like a double standard :) I edited the question nevertheless.

— Unconvicted criminals do not create precedent for criminality. I know nothing about the question you refer to, and have no obligation to examine every question on this list. To accuse me of double-standards is absurd and offensive. Comments are to help people improve their questions, and I have done so in a manner that informs you of the “law”, not its transgressions. A more civil response would be to say thank you.

Thanks, of course :) The question was understandable though in layman terms, and that was the point. Science has to be inclusive and avoid scaring layman away.

Toenail fungus is deep inside the toenail.
Physarum would probably love to eat delicious toenail fungus if it could get at it.  But that fungus is down infiltrating the structure of the toenail itself, which is why topical treatments to the nail are (usually) ineffective at curing an infection with this fungus.
Toenails are durable and pretty impervious and the toenail fungus is safe down in there.  Physarum is a detrivore and I do not think has the enzymes necessary to penetrate the toenail and get to the fungus.  If it did I suspect it would be happy to eat toenail, fungus and all.  I would not want to have something like that on my toe.


text:
What to call a trait that has current utility but unclear evolutionary origin?
I'm looking for a commonly used term to describe a trait that has clear current utility but an evolutionary origin that is uncertain and that we do not necessarily wish to emphasize in our description (e.g. to avoid unnecessary speculation):

Adaptation emphasizes an origin driven by natural selection.
Exaptation emphasizes an origin driven by co-option.
"Aptation" fits the bill, but it seems cryptic and rarely used.

Thank you for your help.

Can you give an example of such a trait? It's not clear to me what you are describing?

I have rephrased the question to make it more precise. A vast number of traits have some function but an uncertain evolutionary history (that we often do not wish to emphasize).

@kmm, maybe woman breasts? It's still unclear why are they prominent. But that's only if "being sexually succesful" counts as current utility.

Intelligent design.

As you point out, people have sampled other terms like "aptation" but these terms are not commonly used.
In order to not imply anything about the evolutionary history, since it is unknown, I think it makes most sense to refer to these simply as traits or phenotypes (or genotype for that matter, depending on the approach you are taking). If you wish to emphasize that these traits are beneficial to the organism, it is sufficient to call them beneficial traits or use other adjectives like useful, positive, etc.


text:
What happens to the food you accidentally aspire?
I'm well aware of the health effects of aspirating solid food and liquids, but I'm interested in the reaction of the body on the biological level to the strange body on our lungs.
After I almost aspirated corn, I started to wander: what does the body do when food got on our lungs?
Will it be eventually absorbed? Destroyed by our white cells? Or just lie there forever until it fully decomposes?
The body has mechanisms to prevent food to get into the lungs, so the body is aware that eventually some food will get into the lungs. As a result, it makes sense to believe that our body would have a mechanism to deal with such issue if all other mechanisms fail ( coughing and etc.,) yet I couldn't find anything on Google.

https://www.youtube.com/watch?v=I40Qr9bOLOY

wow that's terrifying...I want to see a doctor now lol

Don't worry, this outcome is very rare. :D

I still don't like the idea of having corn inside my lungs, and I can get quite paranoid with thinking on that lol

You mean you really inhaled corn?

People can drown because of aspired food. If they don't then it can cause diseases, for example pneumonia. In extreme cases a tree can grow in the lungs. There are other aspiration/inhalation related diseases like silicosis or asbestos lung cancer. So it depends on the composition of the object (or liquid or powder) and other factors whether it causes a disease or not. I did not find anything about what exactly happens with these objects in the lungs. Probably the lung tries to get rid of them mechanically, if there is no success in that, then they cause a local inflammation, which can lead to diseases if it becomes chronic and/or the object contains pathogens.

Common presenting symptoms (information available in 36 cases)
  included dyspnea (14), fever (9), and cough (6). A history of
  recurrent pneumonia was present in 9.

2007 - Pulmonary Disease due to Aspiration of Food and Other Particulate Matter: A Clinicopathologic Study of 59 Cases Diagnosed on Biopsy or Resection Specimens

The annual overall inpatient cost associated with pediatric bronchial
  foreign-body aspiration is approximately $12.8 million. Combined, the
  rate of death or anoxic brain injury associated with pediatric foreign
  body is approximately 4%.

2014 - The national cost burden of bronchial foreign body aspiration in children

Gastric aspiration is a high-risk condition for lung injury.
  Consequences range from subclinical pneumonitis to respiratory
  failure, with fibrosis development in some patients. Little is known
  about how the lung repairs aspiration-induced injury.

2015 -Resolution of Lung Injury after a Single Event of Aspiration : A Model of Bilateral Instillation of Whole Gastric Fluid

Aspiration is a common but underrecognized clinicopathologic entity,
  with varied radiographic manifestations. Aspiration represents a
  spectrum of diseases, including diffuse aspiration bronchiolitis,
  aspiration pneumonitis, airway obstruction by foreign body, exogenous
  lipoid pneumonia, interstitial fibrosis, and aspiration pneumonia with
  or without lung abscess formation. Many patients who aspirate do not
  present with disease, suggesting that pathophysiology is related to a
  variety of factors, including decreased levels of consciousness,
  dysphagia, impaired mucociliary clearance, composition of aspirate,
  and impaired host defenses.

2014 - Aspiration-Related Lung Diseases
2012 - Aspiration and Infection in the Elderly
2015 - Pediatric foreign body aspiration: A nidus for Aspergillus colonization
2012 - All that wheezes is not asthma: a 6-year-old with foreign body aspiration and no suggestive history


text:
Which kind of caterpillar is this?
Which caterpillar is this? It was found in mid Europe during this time (April). Size about 2cm in length.

That ain't a caterpillar buddy. Thats a millipede.

Caterpillars have six true legs, and only six. That thing looks like it has two pairs of legs per segment, so... like @PrittBalagopal said.

I see. Any idea which kind of millipede it is? I know that there are more than one kind -- but maybe some "popular" one.

"in mid Europe" seems a big vague for me, some more details like country, city and natural habitat would be a bit more helpful.

Actually it's Germany

Based on the body structure and double pair of legs per body segment, this is a millipede.
Based on the small size and spacing between body segments, it could possibly be in the Paradoxosomatidae family. You could check by examining the specimen more closely:

Most species possess a groove or furrow ("sulcus") on the dorsal surface between the keels (paranota) on each segment.

Although the color is wrong, this millipede reminds me of the somewhat-cosmopolitan invasive, the Green house millipede (Oxidus gracilis), which is about 1.8 to 2.3 mm long.

 Source: NCSU Plant Disease and Insect Clinic; Credit: Matt Bertone
Due to the color difference, I cannot tell definitively whether this is your species or not. Your poor picture quality makes this more difficult. However, I thought I'd provide this post for you as a jumping off point. good luck!


text:
Why does the pH decrease, when adding pancreatin to different types of milk (cow milk, soy milk etc.)?
I'm experimentally observing how pancreatin affects the pH in different types of milk.
Why does the milk's pH decrease when I add an enzyme solution to different types of milk (e.g., cow milk, soy milk etc.)?
I am not sure how to explain this reaction.
Thank you for your help.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

@Chris This is more of an experiment than homework.

I have edited your question, removing the word level after pH. Also named the enzyme mixture in the title to make it specific, although this pancreatic preparation is so crude it hardly deserves a name.

Isn't it something to do with making cheese? That's what upsets vegetarians? Is it the same as the renet reaction? Try googling that.

the pancreatic fluid contains lipase which breaks down the fat in the milk in to fatty acids and glycerol. The fatty acids produce lower and create a more acidic pH.

Please don't answer questions when others have flagged lack of effort on the part of the poster. It is clearly a homework question, so that if she used your answer she would be getting undeserved credit. Fortunately the fact that she did not respond to the original comments suggests her deadline is long past and she has no further interest in the question. Which is why I would ban all homework questions if I had my way.

@David Which I'm glad you don't because some people don't have a teacher they can ask and the answer might not be in their textbook!

Please add some references! :)

@L.B. — l recognize my view is not list policy, and meta would be the place to discuss this, but there is no reason for not drawing attention to the characteristics of many homework posts.

@David There is that. And also I don't appreciate blatant homework questions. Just making the point that there are people like me who have questions regarding homework (and are either self studying or homeschooled and so don't have a teacher) who are afraid to ask for fear of a downvote and therefore, loosing reputation.

@L.B. — OK. I'll try to be more tolerant in future.


text:
Are lanternfish real?
Is there a real lantern fish existing in the world? If yes, kindly share a picture if one exists. I searched online for images, but most of them seem to be fake. The pictures I have seen on the internet were of a fish with a hanging lantern over its head. Are these possibly real pictures?

Do you have a picture? And yes, these fish are real.

Fish you are referring to by description "fish with a hanging lantern over its head", are not lanternfish. Fish with "lantern" bait above head are members of group of fish named anglerfish (Lophiiformes).
You can find more information about them here: https://en.wikipedia.org/wiki/Anglerfish
Lanternfishes or myctophids are smaller fish that use bioluminecence for communication during mating season.
https://en.wikipedia.org/wiki/Lanternfish

Any added image would be appreciated :)

As Domagoj mentions in his answer, it sounds like you are actually referring to an anglerfish (family Lophiiformes) and not a lanternfish (family Myctophidae).
Assuming this is the case, you can see video footage of the Black Seadevil (genus Melanocetus), a deep-sea anglerfish here.
I've copied some footage from the video (from MBARI*) below as gifs:

The Aquarium video provides the following description:

Deep-sea anglerfish are strange and elusive creatures that are very rarely observed in their natural habitat. Fewer than half a dozen have ever been captured on film or video by deep diving research vehicles. This little angler, about 9 cm long, is named Melanocetus. It is also known as the Black Seadevil and it lives in the deep dark waters of the Monterey Canyon. MBARI's ROV Doc Ricketts observed this anglerfish for the first time at 600 meters on a midwater research expedition in November 2014. We believe that this is the first video footage ever made of this species alive and at depth.

You can see footage of another species of anglerfish here.
*MBARI = Monterey Bay Aquarium Research Institute.


text:
can you identify this plant?
I would like to learn how this plant is called. It grew together with the beans I had planted. The body of the plant grew overnight while the leaves took a couple of days to develop. I decided to keep it in a small pot I had laying around to see if it will develop any further....

These are cotyledons from some species of dicot. However, many species of dicots have very similarly shaped (in this case having a retuse tip) and sized cotyledons. You will almost certainly not be able to ID this plant unless you allow it to grow to the point that its first true leaves (those that have the "normal" morphology characteristic of your species) have grown. These should follow soon after the cotyledons if the plant is properly cared for. DO NOT damage the plant if you want to be able to properly ID this species. Please update us when true leaves have grown.

@theforestecologist - Shucks. I thought I said that...

@anongoodnurse oops sorry missed that. I wasn't going to comment at all and was just going to wait this question out until the OP (hopefully) posted new pictures showing the true leaves. I just saw someone had posted an answer making a guess (I admittedly only read down to your first picture), so I thought it was a good time to clarify in the comments that these cotyledons would make ID difficult.

That was some interesting information. I didn't know that some plans' first leaves do not represent the final ones! I will wait for it to grow and I will post a picture of its real leaves. Thanks again!

@GeorgeTsak Any luck growing true leaves?? :)

@theforestecologist Unfortunately the plant got hit by direct sun and it dried up within a couple of days...

It resembles a kiwi fruit seedling though it is hard to tel

Looks a lot like a radish seedling to me.

However, if I'm not mistaken, it doesn't even have its first true leaves yet, making identification very tenuous.
It can also be any number of brassica species, e.g. mustard (l) or cabbage (r):

If you can't wait to see what it grows into, smash one of the "leaves" between your thumb and a finger. If it's a radish, it will smell like one. If it does, taste the other leaf. If it tastes radishy, you have your answer without waiting. If you want to wait, however, doing that would kill the seedling.
Brassica seedlings will also taste spicy, but not like a radish.
Based on the number of "weeds" in the brassica family, I'd guess it belongs in that group.
I included these diverse possibilities to illustrate how difficult identifying a plant without true leaves is. :)

Good picture examples showing the similarities of plant "seedling" cotyledons. I agree that specific ID is tenuous if not impossible. However, as I commented under the OP's question, I'd recommend NOT crushing the "leaves" and instead waiting for true leaves to grow in order to have a better chance of IDing the species.

I think it's a mustard too. But mustard shoots have whiter and weaker stems, right?


text:
Calculating chromosome number in meiosis: Why is the crossbreed between a fox and a dog (dox) sterile?
Given the following example/question (originally found here):

I worked out the haploid number of the dox to be 29 and the diploid number of the dox to be 58. 58 is an even number, so surely 29 homologous pairs of chromosomes can form for the dox to be fertile. Why is it sterile?
Thanks

Please add the original question as a text and not as an image. Moreover, the image is also not posted in SE and any user has to go to an external site.

I would rework the the title of your question as in its current form it doesn't properly reflect the content of your question.


text:
ID a shell from Puerto Rico
I recently found this in Rincon Puerto Rico on the beach.
I assumed it was a baby sea turtle shell or some kind of turtle. Someone that frequents Puerto Rico said it was not. Does anybody know what this is?

Welcome to Biology.SE. Nice pictures fo ID. Would be good to see the other side though.

Well it doesn't appear to be any of the marine species or native freshwater species of turtle that frequent Puerto Rico.

This is the shell of a marine mollusk called a chiton.

They are also sometimes known as sea cradles or "coat-of-mail shells", or more formally as loricates, polyplacophorans, and occasionally as polyplacophores.

In Puerto Rico, they call these animals "Quitones."

All chitons bear a protective dorsal shell that is divided into eight articulating aragonite valves embedded in the tough muscular girdle that surrounds the chiton's body.

My initial guess as to the species is: Chiton tuberculatus.
 (Disclaimer: I know almost nothing about these animals, so this is at best a guess).

 Source: NATURAL HISTORY MUSEUM ROTTERDAM

 Source: NATURAL HISTORY MUSEUM ROTTERDAM
You can find additional images that look even more like your specimen here and here
According to Wikipedia:

This species can be found under rocks and in spray zones of rocky shores, in the intertidal, shallow subtidal zone of Western Central Atlantic (USA, Colombia, Bermuda, Mexico, Venezuela and the West Indies)

This includes Puerto Rico

Based on Fig 1 of Crozier (1918) showing typical sizes of various ages of C. tuberculatus, you have a fairly young specimen (likely only a few years old).
The Quitones of Puerto Rico by Cedar García Ríos (ISBN: 1-932271-16-3) is probably a good tool for definitively IDing your specimen to species.


text:
Can neurons be inhibited with electric current?
It is well known the electricity can be used to fire neurons. But can it be used to inhibit neuronal firing? This is in the context of extracellular stimulation. In extracellular stimulation, it is known that there is a threshold for stimulation and a threshold for damage(electroporation). Is there a threshold in between these two which inhibits neuron firing without any damage? Please provide reference for your answer.

Generally it's not appreciated to edit the question such that an exisiting answer becomes obsolete.  -1

I apologize, but your answer made me realize the incompleteness of my question. Thanks.

In practice, focal electrical stimulation of the brain can be used to prevent or abrogate seizures.  There is a device marketed for this.
from https://www.scientificamerican.com/article/implant-epilepsy-seizure/

NeuroPace's Responsive Neurostimulation System (RNS), an
  electrical-stimulation implant with two leads, each containing four
  electrodes, placed in the brain at the seizure focus. The RNS detects
  electrical activity that denotes the start of a seizure and delivers
  direct electrical stimulation to interrupt the activity and normalize
  the area.

It is not immediately obvious to me why this would work.  The linked review describes how this was first observed empirically.  My understanding is that the electrical stimulation causes polarization such that the nerve cannot immediately fire again as part of the epileptic focus.  Sort of like a counter burn if you are fighting a wildfire.
Sun FT et al.  Responsive cortical stimulation for the treatment of epilepsy.Neurotherapeutics. 2008 Jan;5(1):68-74.

In the 1990s, Durand and colleagues demonstrated success in
  suppressing spontaneous inter- ictal bursts in vitro by providing
  responsive stimulation directly in the epileptogenic region. Their
  result sug- gested that the mechanism for suppression is an inhibi-
  tory polarization caused by the transmembrane currents generated by
  the applied pulse. These trials in animals laid the groundwork for
  responsive stimulation therapy for epilepsy.

My answer explains how this would work - via depolarization block.

Yes, but maybe not how you think.
It is important to recognize that voltages refer to potential differences. When we say the "a cell is at -65mV" for example, we mean "The potential difference across the cell's membrane to the extracellular space is -65mV." When you stimulate electrically, you create a transient electric field, whereby the extracellular space is no longer effectively isopotential.
Let's imagine for the sake of some neuron that this field strength is on the order of 40 mV across the membrane. If this electric field is perpendicular to some neuronal process, the voltage across the membrane will be about -105mV on one side, and -25mV on the other side. The -25mV side is now depolarized enough to open voltage gated sodium channels, and some current is flowing into the cell. Once the shock has passed, positive current will continue to flow through those open channels and open more channels. It doesn't matter much that the other side is transiently at -105mV, all that matters is that you opened a bunch of voltage gated sodium channels which starts a positive feedback loop.
Therefore, transient electrical simulation will almost always be excitatory. There are two exceptions:
1) Neurochemical inhibition. If you excite a particular brain region that is specifically inhabited by inhibitory projection neurons, you will primarily excite those inhibitory cells and therefore cause excitation elsewhere. Of course, in this case, the electrical stimulation itself is still directly exciting cells, they just happen to have inhibitory effects elsewhere.
2) Depolarization block. If you continually stimulate the same population of neurons with a high-frequency stimulation, you can put neurons in a state called "depolarization block." Voltage-gated sodium channels have a chance to inactivate whenever they are activated. If you inactivate enough channels, there aren't enough available to produce an action potential. Therefore, if you can keep a cell pretty much constantly depolarized by continually stimulating, you can prevent action potential propagation because too many of the voltage gated channels in the axon initial segment are inactivated.

Short answer
Yes.
Long answer
Neuron activity can indeed be inhibited with the correct type of electrical input stimulus.
In fact you can play around with various electrical signalling stimuli yourself, and observe the results not just for a single neuron but the entire network, yourself:
https://www.neuron.yale.edu/neuron/
The link above is a simulation environment that tried to emulate neuronal activity based on user defined signalling stimuli. Not only can you inhibit signals, but you can totally control macroscopic behaviors: e.g. excitation of entire regions of a prototypical neuronal pathway.

Are you referring to injecting current into a cell directly? That isn't what the OP asked.

Oh my bad... ty


text:
Varied Carpet Beetle Larvae
I keep finding what I'm 99% sure are carpet beetle larvae on my walls, of all places. Yet when I look around and search thoroughly, I cannot find any signs of an(y) adult Beetle(s). Why/how is this happening and if it's not a carpet beetle larvae, then what is it?

Maybe attach a photo of one to this question?  That would help with the second part.

The eggs of carpet beetles would be exceedingly small. What makes you so sure? Also, seeing eggs of an insect, but not finding the adults would not be unusual at all.

I saw dozens of carpet beetle larvae in an old home I live in for more than a decade but never did I once see the adults. It can happen. See here for a visual.

Related: What kind of insect can this be?..., Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug...,
How to protect my mounted insects..., What is the name of the critter depicted..., What small insect is this?, What bug is this...


text:
Why does the ring finger not move independently?
Why is it that we need to move little finger in order to move ring finger with it? For example, put your palm on a table and fold your middle finger inside. You won't be able to move your ring finger unless you move your little finger along with it. Why? Paul Gilbert and Buckethead and various other guitarists are the only people that I'm aware of that use the ring finger and looks independent. Is it possible to have surgery to make the fingers independent or is it not functional to do that?

I'm not sure what you mean. Do you think piano players can't use their fourth and fifth fingers independently? Surgeons? (A surgical knot is performed primarily by the third and fourth fingers.) Other occupations requiring manual dexterity?

I'm no expert on the topic, so I'm not going to officially answer your question. But from what I know, all your finger extensions are controlled by a single extensor muscle - the extensor digitorum. However, only your index and pinky have an extra extensor muscle, making extension easier for those fingers. For flexing movements, you have 1 flexor muscle that controls a couple fingers and another flexor that controls the rest - the lack of flexors makes it harder to control. Getting surgery to alter your fingers' movement would probably be unnecessarily risky and probably not possible

It mainly because of Paul Gilbert who is the only person along with many others who uses his first, ring and pinky very well.

I have no problem moving my ring finger without moving my pinky...

indeed, here is another pic of the ulnar nerve. https://www.healthlinkbc.ca/sites/default/libraries/healthwise/media/medical/hw/h9991344_001.jpg

The reason for this phenomenon is in both the muscular structure and neural connections of the little and the ring finger. Lets start with the following diagram:

As you see (click on the image to see full version), the fingers contain extensor muscles for movement. However, the index finger and the little finger have separate extensors, because of which they can move more independently as compared to the middle finger and ring finger, which contain a common extensor muscle called extensor digitorum. Some people lack the interconnections between these extensors, and can thus move their ring finger quite easily. One can also achieve this through practice.
Now, as to why the ring finger moves easily when moved along with another finger, have a look at another image:

The fingers are connected to brain via two nerves:

radial nerve, which connects with thumb, index finger and one side of middle finger
ulnar nerve, which connects with little, ring and the other side of middle finger

As you see, the branching between these nerves is what causes dependence of the fingers on each other for movement. Since the nerves for ring finger and little finger are intertwined, it becomes difficult to move each of these fingers separately. Similarly, you may find it easier to move your ring finger along with your middle finger. But you can easily move your middle finger independently because it gets signals from radial as well as ulnar nerves.
Thus, it is the combined effect of muscular and neural anatomy of ring finger which causes this effect.
PS: Since the effect is due to the neural and muscular anatomy of the ring finger, I don't think surgery would help in this case.
References:

Wikipedia contributors. "Extrinsic extensor muscles of the hand." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 29 Jan. 2017. Web. 27 May. 2017.
Ross and Lamperti, 2006, p. 300
Flexor Tendon Anatomy - Medscape
Wikipedia contributors. "Median nerve." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 1 May. 2017. Web. 27 May. 2017


text:
Examples of animals with 12-28 legs?
Many commonly known animals' limbs usually number between 0 and 10. For example, a non-exhaustive list:

snakes have 0
Members of Bipedidae have 2 legs. Birds and humans have 2 legs (but 4 limbs)
Most mammals, reptiles, amphibians have 4 legs
Echinoderms (e.g., sea stars) typically have 5 legs.
Insects typically have 6 legs
Octopi and arachnids have 8 legs
decapods (e.g., crabs) have 10 legs

....But I can't really think of many examples of animals containing more legs until you reach 30+ legs in centipedes and millipedes. Some millipedes even have as many as 750 legs! The lone example I am aware of, the sunflower sea star, typically has 16-24 (though up to 40) limbs.
So my question is: what are some examples of animals with 12-28 legs?

One will need a good study of the distribution of number of legs (and the sample size used to build this distribution) before saying anything. For the moment the presence of a "distributional gap" is an opinion and is not evidence-based. I am voting to close as such. The question is interesting though!

@Remi.b: you're right about your points concerning distribution. So instead, I've modified the question to focus on simply: why are there not examples (or more examples) of animals with between 12-28 legs. ...Visualizing the distribution of species and their leg numbers would be very fascinating, though wayyy too much work to do accurately).

Yes, I realize how much work it would be but without that it makes little sense to speculate on why are there not examples (or more examples) of animals with between 12-28 legs unless we know whether or not this is to be expected from the little sample size (taken pseudoreplicaiton into account) that is available.

As a couple of counterexamples, species in the classes Symphyla (Pseudocentipedes) and Pauropoda within Myriapoda have 8-11 and 12 leg pairs respectively, so between 16 to 24 legs (sometimes with one or two leg pair stronlgy reduced in size).

(species in Symphyla, from wikipedia)
Another common and species-rich group with 14 walking legs (7 leg pairs) is Isopoda.

(Isopod, picture from wikipedia)
You also need to define 'legs' for the discussion to be meaningful. As you say, decapods have 10 legs on their thoracic segments (thoracic appendages), but they can also have appendages on their abdomens (Pleopods/swimming legs), which will place many decapods in the 10-20 leg range.

(Decapod abdominal appendages/legs in yellow, from wikipedia)
So overall, in Arthropoda, having 12-28 legs doesn't seem all that uncommon. There are probably other Arthropod groups besides those mentioned here that also have leg counts in this range.
However, for a general account, the most likely answer (if there is indeed a relative lack of 12-28 legged animals) is probably evolutionary contingencies and strongly conservative body plans within organism groups.

Also velvet worms.

The now-extinct, Hallucigenia had 7-pairs (or 14) legs.


text:
What is this feather like bug with no legs?
Seen on leaf in North Texas, USA in April 2017. Critter will attach itself to any object put next to it.

Could it be a feather? What made you think it's an animal?

Can you see any features that appear animal in nature? Eg. Head, eyes, antennae, mouthparts. Could you describe them if yes?

It is a specialized feather called "down" (like in down pillows, etc.)

Down feathers have a rachis that is shorter than their longest barb. They are completely plumulaceous and have a fluffy appearance, which results from filamentous, noninterlocking barbules.

Anatomy, Clinical Presentation, and Diagnostic Approach to Feather-Picking Pet Birds

This indeed simply looks like a feather.

 Source: Pattaya Daze
Many predators, particularly hawks and other birds of prey, will typically pull these whimsical down feathers off of their prey before eating.

 Source: Kruger Sightings

 Source: Tom Strong Reviews


text:
What are these bumps on tomato stem?
What are the bumps on this tomato stem? They are way off the ground so I doubt they are air roots.
What are they, what function do they have and why do they form?

Those bumps are aerial surface hairs, a type of trichome. They are epidermal outgrowths.
Therefore it's vines are of pubescent type.
In addition to facilitating better exchange of gases, it also facilitate the vining process, turning into roots wherever the plant is in contact with the ground and moisture, especially if the vine's connection to its original root has been damaged or severed.

Sources:
1:https://en.m.wikipedia.org/wiki/Trichome#/search
2:https://en.m.wikipedia.org/wiki/Tomato

I'm very skeptical of the claim that these trichomes facilitate gas exchange or vining, or become roots. The long spiky trichomes are almost certainly for defense. The shorter fuzzy trichomes may serve to increase the air boundary layer, thereby decreasing moisture loss, but one can see that many of these shorter ones are gland-tipped, so they are probably also involved in defense. Trichomes come from only the outer epidermis cells, so they themselves wouldn't "turn into roots", though they do come from a similar developmental process as root hairs, which may explain the confusion.


text:
Can you identify this bee?
Found on the ground on dried cottonwood leaves in southern Utah.

It looks like a species of Megachilidae family of bees, solitary and leaf eaters, covered in pollens.
It could be from Genus Megachile.
All its identifying features are hidden though:

T1 segments have 2 “sides”, one that faces forward or faces the thorax and one that faces the top.$^1$
In Megachile, the “corner” where the forward side and the top side meet is severe. It creates a flat or concave appearance like a circular shelf.$^2$

This genus it comparable to Lithurgopsis which

has a more gradual transition to the "sides" of T1.$^3$

(Source: bugnet)

@MikePasichnyk I didn't ID this correctly. Your bee shouldn't be a leaf eater, as the  pollen-carrying structures of this family are restricted to the ventral surface of abdomen. So it is anything other than this family. I'd like to remove this answer which is possible only if you uncheck it.

Tyto is correct, it's not a megachilid. It looks like it's probably in the genus Andrena to me, you can see deep, hairy fovea at the top of the head.


text:
More *total* oxygen absorbed by breathing fast or slow?
I have heard that human lungs capture/absorb/process more oxygen by breathing slower.
A) Is the above true?
B) If so, if my primary concern was absorbing the most total oxygen (not most efficient), would it better to breathe deeply and quickly or deeply and slowly?
C) Are there any other considerations (e.g., will fast, inefficient breathing make me feel more tired even if I'm taking in more oxygen)?
D) Is there any "ideal" breathing rate (such as for sports) that is a good balance between volume of air intake and efficiency of absorption?
Thanks.

Can you be more specific in stating the desired goal? Is it for a specific time frame/event? Our rate (and depth) of breathing affects CO2 levels well before O2 levels, and we function best within a certain narrow range. "More oxygen" does not equal "better" except in certain circumstances (e.g. Carbon monoxide poisoning, high altitude climbing, etc.)

Your body naturally optimizes breathing rate/tidal volume to minimize energy spent for what level of exercise imposed on it while also maintaining less than a critical level of $PaCO_2$.


text:
What kind of larva is this? (Southern CA, USA)
I need help identifying this larva:

(Click images for full size versions).
There's about a dozen of them in my parents' bathtub and I'm not sure what they are or where they are coming from.
They are about a centimeter long, maybe a little less. They look flat and are hardly noticeable. When they are upside down they look more like a maggot.
My parents didn't even notice until I pointed them out. They move around very little and stay at the bottom of the tub. I haven't seen them anywhere else.

3 Important questions: 1. Is your parent's home currently under renovation/construction? 2. Have you noticed any insect damage in the bathroom or nearby? 3. Have you seen any flying insects in or outside their home?

Also, a definitive length may rule out certain species...

That looks a lot like a Common Southern California Termite. I would check any wood that you have around your home just to prevent any damage. If you want more information just look it up online, but that's most likely what it is.

Note the eyes, the short, segmented antennae, the mandibles (better seen in your second photo.)

Please add a link to an image of your id/ add an image directly. Also mention why do you recognize it as one. That would make your entry complete. Thank you for writing an answer.

Hi Askansce. I edited your post to bring it to our site's requirements. Feel free to roll back if you desire. :)

@anongoodnurse, thanks for the help. I'm really new to all this and don't quite know the format for everything just yet. I definitely appreciate the assistance :)

 Short Answer
These look like termites, and based on appearance and size they are likely Drywood Termites of the family Kalotermitidae.

Specifically, these appear to be either workers or "pseudergates$^†$", and likely those of the species western drywood termite (Incisitermes minor).

 Source: UCANR

However, without mature soldier or swarmer specimens, conclusive species ID is very difficult.
 Long Answer
General Termite ID
According to Orkin, there are 3 distinct groups into which termites are divided: subterranean, drywood, and dampwood.

Since the worker termites in these groups more or less look the same, the appearance of the reproductive caste (alates) [or swarmers] and soldiers is important..

In other words, it will not be possible to properly ID your specimen without pictures/descriptions of the soldiers or swarmers.

However, It is critical to identify the species of destructive termites to formulate an appropriate control program.

According to this UC IPM page, there are at least 23 different species of termites in California.
I'll give you support for the options that I think are most likely:
 Option 1:
My initial guess is that you have some species of drywood termite (family Kalotermitidae), because these are common.

Based on the following picture (and numerous others from a google search), your specimen looks more like the size/shape of a drywood species vs. either dampwood or subterranean:

 Workers (from left to right) of subterranean, Reticulitermes hesperus; drywood, Incisitermes minor; and dampwood termites, Zootermopsis nevadensis. [Source: UC IPM].
Without swarming specimens, further confirmation will be difficult.

However, drywood termites have very distinct hexagonal 1mm-long fecal pellets called frass that you could try to locate to confirm.

 Zoomed in frass (or fecal pellets). Sources: Termiteweb and UC IPM

 Fecal pellets collecting under a door Photo by B.J. Cabrera, University of Florida
Do you have this??

However, even given that initial guess, another UC IPM page suggests that drywood termites are not often seen:

Drywood termites are cryptic insects that are difficult to detect. They live deep inside wood; and except during periods when they swarm or when repair work is being done on infested homes, they are seldom seen.

So my guess could be wrong....

Possible Candidate Species
If your specimen is a drywood species, it is most likely the western drywood termite (Incisitermes minor).

 Source: Himmi et al.(2016)
From UC Berkeley:

Pest Status: Second most destructive termite in California.

Key Characteristics:

Present throughout California, but most prevalent in southern CA.
~ 1 cm long
Live in and eat dry wood (typically found throughout wooden structures of homes)
Nests of most species remain entirely above ground and do not connect to the soil.

For more info, see here.

 Option 2:
Subterranean termites (typically of the family Rhinotermitidae ).

Shelter tubes (sometimes called mud tubes) are the most commonly seen evidence of a subterranean termite infestation.

Common species:

Western Subterranean Termite (Reticulitermes hesperus) [also see here].

The most destructive termites found in California [Source: UC IPM page].
Unlikely your species because they typically are only about 0.3 cm long. [Source: Termite.com].

Formosan subterranean termite (Coptotermes formosanus)

 Source: Nolawoman

Invasive termite from China, that has invaded US (including CA).
Nicknamed the super-termite because of its destructive habits due to the large size of its colonies and its ability to consume wood at a rapid rate
Again, these are likely too small to be your specimen as the body length is approximately 4-5 mm. [Source: CABI].

Conclusion
Based on size, it is more likely that you have a drywood species vs. a subterannean species.
However, again, without more evidence (frass vs feeding tubes and/or pictures of mature soldiers/swarmers) a definitive ID will be difficult.
I advise that you contact a local exterminator or termite expert to have them check your parent's house more closely.
Good luck!

$^†$  Note: "pseudogate" = a blind wingless nymph performing some of the functions of a worker. [See here].


text:
Why don't we build up an immunity to sore throat?
We often get sore throats once or twice a year, and it clears in a few days sometimes without any antibiotics. I was wondering why doesn't our body become immune after clearing a sore throat?

Sore throat is mostly a symptom of viral infection. So this post is relevant.

 Short Answer

It should be noted that there are many non-pathogenic causes of sore throat, and I would suspect that you are not always distinguishing these causes from actual illness.

In most cases, it would not be possible to build a response (immunological or otherwise) to avoid reacting to these stressors.

Bacteria and viruses mutate frequently in ways that make your immune system unable to properly recognize them to ward off initial infection.

Your immune system recognizes specific pathogens based on structural characteristics. If those characteristics change when pathogens mutate (which happens fairly frequently), your immune system will not recognize it as readily (or initially at all).

 Long Answer
Sore throat is most commonly attributed to pharyngitis, or the inflammation of the back of the throat called the pharynx.
Causes
Sore throats can be caused by many things. (e.g., see here, summarized below):
First off, a sore throat can be the result of many things unrelated to illness:

Allergies
Dryness
Irritants
Excessive talking,singing,shouting,etc.
Muscle Strain
Gastroesophageal reflux disease (GERD)

As a result, at least 30+% (higher in adults) of reported sore throat cases (and supposedly many more unreported cases) are not due to any type of illness.
Further, a number of pathogens can cause a sore throat:

Viruses

Rhinovirus, coronavirus, influenza, parainfluenza, adenoviruses, Epstein–Barr, etc.
(see here for one estimate of relative etiologies).

Bacteria

A number of bacterial infections can cause a sore throat. The most common is Streptococcus pyogenes (aka "Strep A").

It turns out that pathogen-caused pharyngitis is fairly common. Supposedly 10% of adults with sore throats have strep, and around 70% of children pharyngitis cases seen by doctors are either virally or bacterially caused.

However, it should be noted that only 20-30% of children and just 5-10% of adults have bacteria to blame for their sore throat, with viral infections being much more common. (source: IDSA).

Sore Throat Frequency
It turns out that sore throats are fairly common; Jones (2004) determined that about 7.5% of people have a sore throat in any three-month period. Further, on average, adults get a sore throat two to three times a year and children about five times a year (Tamparo 2011 and Rutter & Newby 2015), so your personal experience is fairly average.
Because viral causes and non-pathogenic causes make up an overwhelming percentage of overall sore throat cases, it shouldn't be surprising that most sore throats clear up without the use of any antibiotics.
As for those that are caused by pathogens:
Why no Immunity?
Bacteria and viruses both mutate fairly quickly (see Antigenic Variation, Antigenic Drift and Antigenic Shift), so it shouldn't be surprising that you're capable of having an immune response to pathogens throughout life.

If we consider just strep alone, it mutates/reemerges with improved fitness frequently (e.g., see Bao et al 2016 and their citations)
And see Sanjuán et al. (2010) for a reviewof viral mutation rates.

So not only are there a number of pathogens that can cause sore throat, but each of these pathogens can mutate. That leaves you with a fairly sizable number of potential invaders that can illicit a sore throat.
Let's See How Your Immune System Responds:
Your immune system contains cells that can be split into two broad groups: cells that belong to the adaptive immune system, and cells which belong to the innate immune system. [See here for a simple explanation].

Innate Immune system: consists of cells responsible for initial detection of pathogens, recruitment of other immune cells, activation of the complement system, engulfment and (more immediate) destruction of pathogens.
Adaptive immune system: consists of cells which coordinate to develop a memory of the infections they've seen previously in order to mount a faster, more pronounced immune response to repeat pathogens.

Depending on the kind of foreign invasion, two different immune responses can occur in either of these 2 broader "systems": either a humoral response involving antibodies or a cell-mediated repsponse.

A general feature of the immune system is that these mechanisms rely on detecting structural features of the pathogen or toxin that mark it as distinct from host cells (see Chaplin 2010 for a review). The mechanisms permitting recognition of pathogenic/toxic foreign structures can be broken down into two general categories:

hard-wired responses encoded by genes that recognize molecular patterns shared both by many microbes and toxins that are not present in the mammalian host. This is the innate system described above.
responses that are encoded by gene elements that somatically rearrange to assemble antigen-binding molecules with extreme specificity for individual unique foreign structures. This is the adaptive system described above.

Antibodies recognizes a unique/specific molecule of the harmful agent, called an antigen, and binds to it to tag it for immune attack.

Because the adaptive system is composed of small numbers of cells with specificity for any individual pathogen the responding cells must proliferate after encountering the antigen in order to attain sufficient numbers to mount an effective response against the microbe or the toxin. [Source: Chaplin 2010].

This means that you can still experience some mild symptoms due to the invading pathogen.

The important take-away from all this, though, is that your immune response relies on structural "markers" on pathogens in order to recognize them. This is true for both innate and adaptive immune responses. If the physical/structural properties of a pathogen change (due to antigenic processes and mutations as mentioned above) your immune system will be slower (and possibly ineffective) in responding to an attack.

The result, then, could be another one of those sore throats...

Citations

Bao, Yun-Juan et al. “Phenotypic Differentiation of Streptococcus Pyogenes Populations Is Induced by Recombination-Driven Gene-Specific Sweeps.” Scientific Reports 6 (2016): 36644. PMC. Web. 17 Mar. 2017.
Chaplin, D. D. (2010). Overview of the immune response. Journal of Allergy and Clinical Immunology, 125(2), S3-S23.
Jones, Roger (2004). Oxford Textbook of Primary Medical Care. Oxford University Press. p. 674. ISBN 9780198567820. Retrieved 4 August 2016.
Rutter, Paul Professor; Newby, David (2015). Community Pharmacy ANZ: Symptoms, Diagnosis and Treatment. Elsevier Health Sciences. p. 19. ISBN 9780729583459.
Sanjuan, R., Nebot, M. R., Chirico, N., Mansky, L. M., & Belshaw, R. (2010). Viral mutation rates. Journal of virology, 84(19), 9733-9748.
Tamparo, Carol (2011). Fifth Edition: Diseases of the Human Body. Philadelphia, PA: F.A. Davis Company. p. 356. ISBN 978-0-8036-2505-1.


text:
What is this bizarre in-growth in this red bell pepper?
I just chanced upon a rather strange red bell pepper (or capsicum?):

The green formation is bulbous to touch, just the like the outside of the bellpepper, and it has the same smell as one. I'm no biology expert, but I have a feeling that's a tiny ingrown bellpepper in there. My mom thinks it's a strange genetic experiment and wants me to throw it away!
What is that strange growth, and what might have caused it? Is this safe to consume?

These are "baby fruits" which are safe to eat. It's a quite common phenomenon.

This is very likely to be parthenocarpy, which is an “internal proliferation” and varies from an irregular fruit to an almost carbon copy of the larger pepper. What is known is that it shows up in seed lines through natural selection and is unaffected by weather, pests, or other external conditions. Please see page 27 of this document.