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Why do cells use microRNA to break down mRNA, instead of not transcribing it in the first place?
As I understand it, microRNAs are used to ensure that certain genes are only expressed when needed. The way this apparently works is that when the translation products of an mRNA are not required the appropriate microRNA is transcribed to bind to the mRNA and initiate its nucleolytic degradation.
My question is if the cell can detect that the product of a specific mRNA is not required why is the mRNA transcribed it all, rather than synthesizing it and then synthesizing another RNA to silence it?

Hi Sam. I rolled back your recent edit, but I understand your frustration. Yours is an interesting question, though, as it stands, it is practically impossible to answer. If you reduce the scope of your question, you may find someone willing to take a crack at it. For instance, instead of asking why microRNAs exist (redundancy?), perhaps you can ask whether microRNA regulation is energetically beneficial from the cellular perspective, relative to control at the levels of transcription (TF abundance and binding) or translation.

@acvill: I disagree. It is not impossible to answer. miRNAs allow a cell to rapidly remove any present mRNA in order to react quickly. Furthermore, every mRNA is subject to constant production/degradation (RNA Homeostasis, Pelkmans 2022). This question is about RNA biochemistry. This does not contain an answer.

@markur your comment addresses how miRNAs help maintain mRNA homeostasis. The question asks why miRNAs evolved as a control mechanism. We can speculate, but, generally, it’s very difficult to know why a particular trait or pathway evolved alongside / in lieu of another.

@markur if you believe the question should be reopened, feel free to submit an edit.

@acvill ok cool, I submitted an edit, let me know if I did something wrong. And sure, I get why one might consider this question is related to "traits". However, I feel it's unfair to depict this question as speculative, considered that there is just so much knowledge about how and why RNAs are produced and regulated and degraded etc.

@acvill — I disagree. The question is from a naive user ("I am learning" or something of the sort) who seems not to realize that if you light a candle and finish the game you may want to snuff the candle out as well as not lighting another. Of course the question of why one mechanism rather than another for a specific gene is speculative and has to be considered on a case by case basis, but I think that can be mentioned, with examples of other regulatory mechanisms. There is also the point of circuits and oscillations with multiple regulatory controls (that I do not understand). Try my edit.

@David that's a good edit. I'll vote to reopen.

Simple Answer
Switch On: To start expressing a protein-coding gene — synthesizing its product — you have at some stage to synthesize its mRNA — transcribe it.
Switch Off: To stop expressing a protein-coding gene it makes sense to stop making more RNA, as the poster suggests. But that may not be enough! Many eukaryotic mRNAs have half-lives ranging from hours to days, so that merely stopping transcription will not immediately stop the protein being produced. If it is important to stop synthesis immediately, something else is required. Nucleolytic degradation of the mRNA initiated by microRNAs is one way to do this.
More than one way to kill a cat
Why is this not more widespread? The answer is that this is only one of a variety of means to regulate gene expression. Others include having mRNAs of shorter half-life (as in bacteria), controlling mRNA translation, inactivation of the protein (if it is an enzyme) or degrading the product by proteolysis. Which method is employed depends on evolutionary chance, the nature of the system, whether it is advantageous to be able to resume activity quickly etc. So systems regulated by microRNA need to be considered on a case-by-case basis.
And although I am not competent to write on this (additions solicited) I am led to believe that mathematical modelling shows that the existence of a variety of regulatory mechanisms can allow a smoother and more buffered response to a variety of stimuli.

The key differences are:

miRNA act very quickly (hours, day). Transcriptional repression stops production, but doesn‘t remove the gene‘s signal since the mRNA is still there.
one miRNA can target multiple (even hundreds of) different transcripts  coming from different genomic loci, causing significant changes to the transcriptome at once. That‘s needed for differentiation processes (see let-7: Balzeau 2017). Transcriptional repression can‘t handle that, since that would impose more extensive requirements on promoters/enhancers. (Ni & Leng 2015)
miRNA evolved from an anti-viral system (RNA interference) that degrades viral dsRNA. Its machinery is multifunctional.
miRNA can be transported between cells within extracellular vesicles. That way, intercellular communication causes quick changes to transcriptomes. Transcriptional repressors can‘t do that as easily, since they‘re localized to the nucleus and not the cytosol.


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A cup of milk dregs has turned a deep blue color. What is growing in it?
Ok, so yes this is gross and all. But it was too amazing to me to keep to myself. I left a cup with a small amount of leftover milk from "honey bunches of oats" out for like 2-3 days and this is what I found:

It's a shiny (might I say pretty?) paint-like shade of turquoise. Can anyone identify what is growing is cup or shed light on what happened? I've never seen milk go off like this before.

source: Stack Exchange

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

sort: votes


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Expected variant allele frequency of mutation present on 2 out of 3 copies of a 70% purity cancer sample
I am reading Nik-Zainal et al., 2012.
In such paper, (for sample PD4120a - a 188-fold depth ER+ breast cancer tumor), it is stated that:

The sample has 70% tumor purity.
The genome has one triploid chromosomal region.

The final point I don't understand is why "mutations occurring on the triploid chromosomal region before duplication would be present on two of three copies - with an expected variant allele fraction of ~55%."
If I correctly understood VAF calculation, such mutations should have expected VAF of $2/3 p$, where p is the purity. Therefore, $0.7*2/3=46.7\%$.
Why is this different from the reported expected VAF?

Migrated from Bioinformatics SE at author request

I'm sorry I did not read the article. But in the case that it is only the tumor which has the duplicated chromosomal region, I think you will have an increased contribution of the mutation relative to the normal. I'll try to illustrate with an example:
Let's say the total sampled number of cells is 100. Tumor purity makes it 30 normal cells and 70 tumor cells.
30 normal cells contributes 2 normal copies: 60
70 tumor cells contributes 1 normal copy and 2 mutated copies: 70 and 140
If we calculate the expected frequency of the somatic mutation we get:
140 / (60 + 70 + 140) = ~ 52%
Still not 55! But it's the best guess I have.

Thank you, this does indeed make sense. I will see if anyone else has a closer results + explanation.

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


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What are these most tiny bugs called
These bugs are the smallest bugs I've ever seen in my life and they are very annoying, throughout the day, I just feel sudden scratches on my body and when I look closely, the cause are these bugs moving on my body, they are making me lose my mind. They are hard to kill, putting pressure when they are between my fingers does not kill them, I need to press them against hard flat surface to kill them. They go inside my laptop, from the keyboard holes and touchpad which could possibly damage it and they are everywhere and there's a lot of them.
Here's an enlarged image of one of them moving on my monitor's screen:

The rest of the images are not zoomed in so you can get a sense of how small they are, please zoom in on them as you wish:

What are these bugs called?
I've been googling a lot, the closest I could come up with was bed bugs and Argas reflexus and they are not either of those.


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What forms a mutation hotspot?
From https://en.wikipedia.org/wiki/Recombination_hotspot#:~:text=Recombination%20hotspots%20are%20regions%20in,that%20of%20the%20surrounding%20region.
I understand that hotspots may arise when certain regions are enriched with particular repeats, or if certain loci are located in chromosome regions that facilitate recombination.
But I'm not sure I understand this paragraph and the implications it may have:
"Recombination hotspots do not seem to be solely caused by DNA sequence arrangements or chromosome structure. Alternatively, initiation sites of recombination hotspots can be coded for in the genome. Through the comparison of recombination between different mouse strains, locus Dsbc1 was identified as a locus that contributes to the specification of initiation sites in the genome in at least two recombination hotspot locations. Additional crossing over mapping located the Dsbc1 locus to the 12.2 to 16.7-Mb region of mouse chromosome 17, which contains the PRDM9 gene. The PRDM9 gene encodes a histone methyltransferase in the Dsbc1 region, providing evidence of a non-random, genetic basis for recombination initiation sites in mice. Rapid evolution of the PRDM9 gene explains the observation that human and chimpanzees share few recombination hotspots, despite a high level of sequence identity."
I interpret this as there is a locus "Dsbc1" that plays a role in determining which place in the genome gets to have a recombination site (or makes that site more prone to recombination), and that the PRDM9 gene difference between chimps and humans causes our recombination sites to be different to those of chimpanzees. If I'm correct here, does that mean mutations to this or similar genes can have downstream effects on the mutation rate and thus how conserved another gene is?

There are many examples of genes that impact DNA processing and thus mutation rate globally. See pol delta (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2169052/), mutS (https://elifesciences.org/articles/22939), etc.

@MaximilianPress Yes, I'm guessing genes encoding DNA repair proteins may have the same effect, but I was thinking more about genes that determine hotspots (or make an existing spot hotter), and how this may impact the "conservativeness" of gene regions.

Yes, there are such cases. Another example would be homology-directed repair
(HDR) genes, where HDR targets rejoining of DNA breaks to regions sharing homology with each other. https://www.nature.com/articles/s41467-019-11105-z. This is one of the reasons why pericentromeric and other repetitive regions have high structural variability.

Latin -us singular, -i plural (for the particular declension to which locus belongs).


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Source for "The human body recycles its body weight of ATP each day"?
I have read in many biology textbooks and scientific journals that "you create your own bodyweight in ATP each day", but they are all just stated as facts.  I have yet to see a study or article that explains how this was determined and what assumptions or observations were used.
For example in the Wikipedia ATP entry "Other processes regenerate ATP so that the human body recycles its own body weight equivalent in ATP each day."  This has a footnote which links to Opening and Closing the Metabolite Gate in PNAS.  Once again it is just stated as a fact "On any given day you turn over your body weight equivalent in ATP" this time with no footnote.
Has anyone come across anything with actual calculations of how this was determined?  Is it based on calories eaten, or oxygen consumed, or extrapolation from a single cell, or something else?

If this doesn't work out as a question here on biology, then our sister-site [skeptics.se] would certainly take it. You should take the [tour] and refer to the [help] on each site before posting (in an ideal world).

As @Domen demonstrates in his answer, it is quite easy arithmetically to come up with this sort of statement. But why are you interested in it? It is just hyperbole used by the self-important to imply their topic is of importance. It may or may not be, but this sort of thing doesn’t make it so.

Hi @david, I agree with you that the weight part of this is stupid. I think it misses the really impressive part which is how many times the body is converting ADP to ATP.  Something like 6x10^25 a day, or 150 million /every cell in the body (excluding RBCs) /second !  I asked my question because the "body weight in ATP" is commonly stated and I hoped someone knew where it came from.  I disagree it is "quite easy" to determine due to uncoupling proteins and mitochondrial membrane permeability that make heat rather than ATP from protons.  And other things I am unaware of, hence my question.

But are big numbers really impressive? How many water molecules are there in a filled tumbler? A lot. And someone will always say "Wow". But one hopes only the first time. Yes, the microscope world is amazing, but the aim of investigating it is rather wider than finding throw-away lines with which to start a lecture.

The following is a back-of-the-envelope calculation to get a reasonable order of magnitude.

An average person has a daily caloric intake of $E \approx 2000 \; \rm kcal$.
Assume all of the caloric intake goes into the production of $\ce{ATP}$.
The free energy cost1 for synthesizing $\ce{ATP}$ from $\ce{ADP}$ in cellular condition is $\Delta G \approx 50 \; \rm kJ/mol \approx 12 \; \rm kcal/mol$.
Molar mass of $\ce{ATP}$ is $M(\ce{ATP}) \approx 500 \; \rm g/mol$.

Therefore, each day our body produces:
$$m(\ce{ATP}) = \frac{E}{\Delta G} \times M(\ce{ATP}) \approx 85\; \rm kg,$$
which is approximately the mass of a human body.

1 http://book.bionumbers.org/how-much-energy-is-released-in-atp-hydrolysis/

Wow............

While this calculation works out, I think it's worth considering that it's kind of bizarre to think this way for any purpose besides trivia. If a 70 kg person takes about 1000 steps over an 8-minute run, you could say that they've moved 1000X their body weight = 70,000 kg in 8 minutes, but has that actually told you anything about how much useful work they've done? Not really, you've come up with an impressive number but it hasn't really meant anything without other context.

@BryanKrause Well, yes and no. You example is meaningless, but the ATP production is, I think, not. It means that indeed there is an enormous churning and recycling of compounds in our body. (I for one would not have thought that it's so much, hence my previous comment.) For example, it becomes clear that the ATP, once it has delivered its energy load, must be readily available to be "recharged" -- we see from the numbers that it cannot be metabolized and excreted, for example.

@Peter-ReinstateMonica Sure, but there's nothing in ATP that comes from the food being 'burned' for energy, it's just part of the "machine". Why count just the ATP, and not all the other molecules that were part of some chemical/electrochemical reaction in the process? What if you summed up the mass of a weak acid/base in solution every time a proton bounces on/off? I do see your point, though, that it may be useful to countering some particular misconceptions of what happens in a cell at a molecular level, which can be quite difficult to intuit.

@BryanKrause Yes, true, it's mostly within the cell, and there it is less meaningful. Although (excuse my layman-ness) I suppose it's the product of some oxidation of glucose or such in the cell?

But note the conjurer’s sleight of hand. The molecular weight is immaterial. If Adenosine had a MW of 1 million, the fact would  remain that all that is happening is one phosphate is being added and taken away. I edited the title to try to show how this sort of statement morphs into nonsense.

@David True, it's not that 80 kg of mass is synthesized from scratch!

Yes, David's slight of hand point is basically the point I was trying to make about the jogger. It doesn't really matter what the weight of the phosphate is, either, you could do the whole thing with just a rearrangement within one molecule, too, without any appreciable change in mass.

@BryanKrause, I agree that such calculations and final results can be a bit misleading if one isn't careful when interpreting them. However, I think that the "usefulness" of this particular one can be revealed if you actually see it from another perspective: "How much ATP do I need to power (by converting ATP to ADP) a human being for one day?" This interpretation then gives you some rough idea on the amount of ("useful") energy that ATP can store (or more precisely, its energy density), which you can compare to the energy density of food (2000 kcal ≈ 85 kg of ATP ≈ 800 g of bread ...).


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A study claims that the consumption of fish increases the likelihood of getting skin cancer, does this have any relation to their omega-3 content?
A study claims that fish consumption increases the likelihood of getting skin cancer.
Since another older study claimed that omega-3 consumption increases the likelihood of prostate cancer is there any evidence that omega-3 is at least partly responsible for the increased likelihood of cancer assuming that the result of the first study is accurate?

The study doesn’t mention fish (that I saw on glancing at it) at all. How did you jump to fish? Also, can you support your statement about omega 3 fa? There’s a good chance you missed something. Thanks.

There are academic-ish articles that you could have referenced such as this which suggest a link, but with indeterminate cause as far as I can tell (they guess it's toxin contaminants).

The summary article states Data showed that the risk for developing SCC and BCC was associated with a higher intake of polyunsaturated fats. While the risks of SCC, BCC, and melanoma were associated with a higher omega-6 fat intake, omega-3 dietary fat intake was found to be associated with risk of BCC but not with SCC or melanoma. No other fats were associated with melanoma risk.

Honestly spoken, I doubt the results of this study and there are a few reasons for this. To start with, we have to recognize that the authors did quite a lot of work to exclude bias and false conclusions. They did their study as a prospective study which means they collected the data first (questionnaire on eating habits) and watched the people afterwards to see the outcome. This avoids wrong conclusions or bias in terms of what has been eaten. Also, the sample size is sufficiently large, which is often problematic in such studies.
To categorize the results: In this study, the effect size was not very strong, the hazard ratio was 1,22 (with a 95% CI = 1.11-1.34 ) meaning a 22% higher risk of developing melanoma. The absolute lifetime risk for developing melanoma in the US for white skinned people is about 2,6%, putting a 22% increase on top would translate in a absolute risk of around 3,2%.
However, some points are to be criticized, some mentioned by the authors. First, this is a study which relies on a self-reported questionnaire on their fish consumption in the year before and then tracked the participants for 15 years. This is not very hard data, since I would probably misjudge the amounts of the different stuff I ate and drank over the course of the lase year. Additionally it does not factor in changes in lifestyle (some people may become vegetarians, I personally ate a lot more fish when I lived close to the sea since it was easily obtainable and so on).
Then there are factors which are a lot more important for developing melanoma. This includes exposure to UV radiation (sun and sun tanning booths), mole count and if you are lightskinned/have red hair. For the later the absolute risk for getting melanoma is about 400% higher than for people with dark hairs. Also the UV exposure: The study did not ask for the personal habits on UV exposure (meaning working outside a lot like gardening or other outdoor activities or using tanning booths), they calculated the UV associated risk by the median UV radiation based on the place of living at the beginning of the study. As far as I can see they did no further correction for places of living for the following 15 years which might have brought a much higher (or lower exposure). Not correcting for these importants factor contributing to the development of melanoma is very problematic and can skew the whole statistic. What happens if the group of "fish related melanoma" contains disproportionately many redhaired people?
Some points are just curious. The authors distinguished between canned tuna, fried and non-fried fish and found a correlation to the development of melanoma only between non-fried fish and canned tuna. This is an observation for which they do not really have an explanation.
Additionally the median age in which melanoma where first detected was 70,1 years, according to the American cancer society this age for the whole population is around 65 years of age. This might not be significant but is at least odd.
The authors themselves speculate about some toxins like arsenic, mercury or polychlorinated biphenyls which have been connected to melanoma in recent studies, but fail to explain why this would not cause problems with fried fish.
Taken together, this is a relatively weak link which is not supported by strong indications while there are other, strong causes of disease which have not been analyzed further. If there is such a link, I think this is a very weak and not very important one.


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What could be a refuge in host-parasitoid models
I was reading about refuge effect in host-parasitoid models and  I found somewhere that refuge does not have to be only a place in habitat where hosts can hide, but also some "situation" that allows them to be protected from parasitoid. So let's assume that the hosts are divided into two groups that live at the same place. The first group is for some reason protected from parasitoids and will not become parasitized (so they are in some kind of refuge, but not necessarily in physical refuge). Another group is exposed to parasitoids and may become infected. We can also assume that the hosts are in the same stage of development e.g. all of them are adults.
My question is: What would be an example of non-physical refuge in real life?
I would be grateful for any help.

The most typical situation is a size refuge, i.e. prey/hosts that are too large or too small to attack (or possibly too small to be useful) are not attacked, or are attacked less, than hosts that are the natural enemy (parasitoid/predator)'s preferred size.
Walde et al (1989) considered whether an observed spatial refuge pattern (less parasitism on the trunk and woody branches of trees) could be explained by a size refuge (i.e., hosts on the trunk and woody branches were smaller on average, so may have escaped predation due to their size)
Depending on what you mean by "situation" and "non-physical", other examples are

inversely density-dependent attack rates: if hosts occur in patches of different population density, and if natural enemies are not disproportionately attracted to high-density patches, then hosts in higher-density patches will have lower per capita rates of parasitism (because the risk of parasitism is shared by all of the individuals in the patch) (Price 1988)
gall wasps in galls with thicker walls are better protected from parasitoids (Ito and Hijii 2002)

Ito, M., and N. Hijii. “Factors Affecting Refuge from Parasitoid Attack in a Cynipid Wasp, Aphelonyx Glanduliferae.” Population Ecology 44, no. 1 (2002): 23–32. https://doi.org/10.1007/s101440200003.
Price, Peter W. “Inversely Density-Dependent Parasitism: The Role of Plant Refuges for Hosts.” Journal of Animal Ecology 57, no. 1 (1988): 89–96. https://doi.org/10.2307/4765.
Walde, Sandra J., Robert F. Luck, Dicky Sicki You, and William W. Murdoch. “A Refuge for Red Scale: The Role of Size-Selectivity by a Parasitoid Wasp.” Ecology 70, no. 6 (December 1989): 1700–1706. https://doi.org/10.2307/1938104.


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Can whales send each other [3D] images?
Russell Arnott, apparently an oceanographer, who currently works as a project manager at the Sainsbury Laboratory, Cambridge University (UK), wrote in his piece Whales and Waves (2016, p.2):

New research from the DAREWIN Institute postulates that once a whale has obtained an image of an object using sound, it can then send a holographic image of what they saw to another whale using sound.  That’s like sending a 3D-picture to your friend using only your face.

Although that article is available on Academia.edu, and Russell Arnott does indeed apparently currently work for Cambridge University, the article is not from a published academic journal. With my meagre understanding of biology I've tried to hunt down articles on this in peer reviewed journals or academic books but have drawn a blank.
Is there any research which suggests that whales may be able to send each other three-dimensional images, or in fact, images of any sort at all?

whales uses sonar and it might be possible for other whales to see the return signal/picture,it is sort of scary if it is done in any other way than this.

Computers transmit topographic maps, 2D images and 3D files with colors and measurements at high bandwidths, Animals transmit symbols as language. If you mix the notions of 3D and symbols, it's like saying the whale's don't need to define the seabed or a shoal of fish when they speak, they provide a high bandwidth topographic map, and that's a muddled suggestion without data. Given their soundwaves and the precision of analogue time measurement, they could speak all day to transmit only a small topographic scan.

To send a holographic image using speech, you have to convert the information of the image from an echogram to vocal soundwave and back to an echogram, using analogue time measurement process the data. for a 3D image, whales also have to take multiple echograms from different locations, think about them, then synthesize them into one low bandwidth voica call going through a different sensory pathway, using analogue time for precision, and no mammals have very precise timing to "send images" using sound.

@bandybabboon Apart from humans animals don't use language. And my interest in this question is precisely because it throws light on why humans need language to communicate and why we have verbs.

Holographic is a very uncommon word to use for animal communications. 3D scenes definitely require adding together more than one echogram.

Dolphins, primates, prairy dogs, elephants and many other animals communicate symbols, maybe called signalling systems not language.

I would be highly skeptical. First one must ask what is meant by a 3D image. On one hand, humans are perfectly able to transfer this type of information, but not as an image. Expressions, such as "red, guitar-shaped, covered in iridescent fish-scales and with an orange coming out of the hole in middle" will create a clear (albeit confusing) image in the head of the reader/listener. However, it is not the image that is transferred, only attributes of the object allowing the receiver to reconstruct the image based on previous experience. It is not inconceivable that some animals can do the same to a lesser degree, although it requires a well-developed language, not consistent with what we know about how (little) sperm whales communicate with each other.
On the other hand, if what is meant with a 3D image is a detailed representation of the actual shape of an object, it would be unlike any other known form of communication between animals and raises a wealth of questions that must be answered, such as how this image is represented neurally in the brain of the sender, how it is encoded in an acoustic signal transmitted to the receiver, and how the receiver then decodes this information to recreate the image. Quote Carl Sagan: "Extraordinary claims require extraordinary evidence".

As somebody familiar with production of the first digital 3D images, Russell Amott's suggestion of whales communicating in image format seems entirely possible.  Perhaps the people at CETI (organization studying whale communication) need a few top geophysicists to consider the problem of how to decode whale language?  Why not try running whale communications through seismic data processing algorithms?
Consider that a whale spends a large, continuous amount of time decoding sonar clicks into a 3D spatial understanding of its surroundings.  Sonar works by measuring the phase shift in sound REFLECTIONS.  Consider that in order to produce the loudest sounds it modulates sound also through internal reflections within its own biology (i.e. "junk" of a sperm whale).  Is it not reasonable to consider that a whale would evolve to produce sounds analogous to what it hears and decodes?
This would be a great problem to get some interested Geophysicists to attempt to solve.  I believe this is a more probable manner in which to decode whale communication than trying to use purely human language models.
Imagine if you could transfer 3D images into somebody else's head?   No need to go to the movies.  Wow.  Maybe that's why a sperm whale's brain is six times larger than a human's?

I'm confused why this is getting any upvotes. There is no citation of any relevant information here, purely speculation, and it is simply not physically possible to transmit echolocation sounds the way they are heard, because they depend on arrival times at the listeners ears; regardless of what you hear, you can't transmit without separate speakers that can control the arrival time at each ear and also encode spectral cues that are distinct by the individual listener, only meaningful to that listener, and applied to any sound that comes in according to the direction of that sound.

@BryanKrause But I can hear someone singing and receive that signal through two ears at different times mediated through my own personal biological equipment and still transmit version of what I've heard with meaningful accuracy. The sound that's coming back to a whale/porpoise/dolphin originated from that mammal from roughly the same area as it's received (and the reception isn't anyhow simply directly through the ear , but is also transmitted through fat in the jaw to the ear). The buzzes going outwards are made by the mammal itself. It is not unreasonable to suspect ...

@BryanKrause ... that the incoming signal can also be reproduced. If what is being received by one mammal is reproduced to another, it does not mean that that other mammal will not be able to understand that the original receiver is transmitting what they 'heard' fro their own point of view. I also do not see that two ears are necessary for decoding the original signal to reproduce a three dimensional representation. One might do adequately on its own.

Just because a person shines a torch and others see what the light hits and reflects off doesn't imply communication. @Araucaria Whilst I see that this answer touches upon unknown neural and conceptual processes that occur (or may occur) in whales, it doesn't seem to answer the question about communication, nor is it supported with even minimal references.

@JiminyCricket. That isn't a good description of what I described, which involved an animal resending the signal they received - handing over a polaroid in your analogy. The 'communication' seems to have been imported into the discussion by you! However, as a relevance theorist working on human linguistic communication, all that would be needed would be for the sender to be ostentatiously and self-consciously trying to affect the receiver's stock of assumptions about the world, and for the receiver to be aware f this intention, and for the receivers recognition to be understood by the sender.

@Araucaria Read more carefully what I've said and think about how the spatial representation of the world relates to the spatial representation of the ears. You cannot deliver that signal because it needs to come from all the real physical places at once. You can't generate a mimic of it from one place, it's not physically possible,  because sound travels freely: the right ear is going to receive the signal you intended for the left and vice versa.

I have direct knowledge of programming 3D images and know the maths processes inside out. digital is far less useful than analogue, that's why humans don't transmit numbers to each other when they describe scenes, and whales deffo wouldnt either unless they favor low resolution and efficiency.

This just seems like a weird and potentially hyperbolic way to state a postulate that whales use language to convey things to one another that they have observed via echolocation. Don't overthink it.

There are currently no serious claims of that type by any scientists who use the scientific method.
If it's an inaccessible, unevidenced, unpublished, unreviewed, unauthored claim of a theory, that nobody has written about from the science community, publicly attributed to no researcher titles, you can presume it is not real.
1/ The linked article quote "is for an audience of 15 years old average GCSE Students."
2/ "DAREWIN" 3D, i could find zero results related to any related research. No data is available on that theory from DAREWIN. Please comment if you find anything else than that one single statement meant for a school project.
I know about the TF dimensional limitations of sound. The article suggests that the whale sounds work like sonic modem rather than a language.
I programmed 3D graphics, vectors, maths and geometry for more than 5 years and sound waves for 8 years, including dolphin TimeFreq graphs, data transmission using sound clicks.


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How to get an adaptive landscape from a fitness function?
In Schluter (2000), it is mentioned that one can convert a fitness function (see image (a)) to an adaptive landscape (see (b) and (c)). The key is to calculate the mean phenotype of a population and calculate the mean fitness value for that population (based on the fitness of each individuals). The shaded area in (a) under the 2 peaks curve is a population distribution of phenotype z. But like the image shows, how can one draw the adaptive landscape if you have only one population?
I get that the fitness landscape can be calculated with splines and the results plotted as the predicted values of the spline analysis. But how can one generate an adaptive landscape? In the lab, it would be to generate new populations with the whole range of phenotypes and get the mean fitness of the population. But for organisms that sampled in the wild, it is not possible to get the full range of phenotypes and thus calculate different mean fitness across the whole range of phenotypes. How to get a adaptive landscape with phenotypes (and possibly from populations found in the wild?).


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Can a dead fish be made to twitch via electrostimulation?
Galvani in the 1700s famously showed that a dead frog can be made to twitch by electric stimulation. The hind legs are particularly susceptible. Salt helps in the activation, as shown in these videos:
https://www.youtube.com/watch?v=sJifWqUa2pY
https://www.youtube.com/watch?v=2YZJt_Bw3eo
Can the same be accomplished with a fresh dead fish? Fish are more easily available for demonstrations to children. Have you tried this, and if so which part of the fish is most readily stimulated?

This is quite immediately post-mortem; we aren't talking grocery store frogs, if that's what you're thinking.

With fish, the hearts can be stimulated to beat just by prodding them.
Learnt a long time ago, preparing fresh fish given to me by others.

Works with mammals, including humans, too.


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Examples of natural graded transcriptional responses to extracellular ligands
In this paper (1) from 2001 the authors show that the mating pathway in budding yeast yields a graded transcriptional response to increasing concentrations of pheromone, and claim that:

To our knowledge, this is the first example in eukaryotes that extracellular signals can be propagated in a simple graded fashion.

Here's another paper (2) from 2005 showing the same thing, but with single-cell fluorescence microscopy instead of flow cytometry.
Given that these papers are around 20 years old, I assume other pathways with similar signaling dynamics have since been found, but I'm struggling with finding good examples.
Is anyone aware of other pathways where the dose-response relationship between an extracellular stimulus and a transcriptional response is graded, as opposed to bistable? The organism is irrelevant, as long as it's a eukaryote, it's a natural (i.e. not synthetic nor mutated) pathway and the results have been shown by some single-cell analysis technique.

Poritz et al. (2001) PMID: 11571757
Colman-Lerner et al. (2005) PMID: 16170311


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Ecology: Indices to calculate species overlap in a community?
Experimental design: I sampled the abundances of four species for each month of the year. I did this across 6 sites. I want to calculate the temporal niche overlap for all the species at each site. Ultimately, I want to compare overlap across sites.
I want to compare the extent of overlap of species abundances in the following two secanrios. In the first scenario, species barely overlap so the index or overlap value should be zero. in the second case species fairly overlap in their abundances as shown below (Note: My data has absolute abundances not relative. The graph is only for representation).

I found Pianka's index (from Gotelli 2000) to be one such index that estimates the extent of overlap. However, on closer reading, I find that takes the resource utilization matrix as input and returns the average pairwise Pianka's niche overlap index averaged over each species pair as so:
$$O_{kl} = O_{lk} = \frac {\sum\limits_i p_{ij}p_{ik} }
    { \sqrt{\sum\limits_i p_{il}^2 \sum\limits_i p_{ik}^2}}$$
I am not sure if I can use it to compute the overlap of species abundance distributions alone. I am wondering are there any other indices that I can use to do a similar computation? Is there a statistical route that I can take to capture a breath of overlap?
Specific questions (in response to Ben Bolker's comments):

I want to calculate a single number for the overall overlap. It has to be able to deal with 0s.

I would be curious to know the overlap coefficient for each species pair. My guess is that I can use a alpha-diversity index like Shannon’s diversity index.

Would it be incorrect to use Pianka's niche overlap here? Why can't I?

Might be handy http://www.zo.utexas.edu/courses/thoc/sppdiv.html

https://en.wikipedia.org/wiki/S%C3%B8rensen%E2%80%93Dice_coefficient ; can you be a little bit clearer about your experimental design? i.e., do you have a set number of observations over the course of the year (e.g. one per month)? Do you want a single number for the overall overlap, or a coefficient for every pair of species? (I'm assuming that you have "the abundances of 8 species", not "8 observations of species abundance for n species")

@BenBolker  I have updated my answer based on your question. TLDR: looking for a single coefficient for all the species. I have 6 different sites, so I am trying to compute the overall overlap (across the year) at each site. The Dice/ Jacard etc calculate for two species at a time not overall. Pianka or Czekanowski niche does across all species. One of my questiosn is why can't I use pianka's index here?

I am confused now: Do you care about niche overlap or pure temporal overlap? In the former case, you obviously need to take resource consumption (and similar) into account. For example, foxes and trees can exist simultaneously while having zero niche overlap. With that being given, what’s wrong with Pianka’s overlap index? In the latter case, why do you write niche overlap in your first sentence?

If you only care about direct overlap, this sounds like a case for classical correlation coefficients. These answer you whether a high abundance of Species A coincides with a high abundance of Species B. The known advantages and disadvantages of the respective correlation coefficients apply, e.g., ranked correlation coefficients being less sensitive to outliers.
Beware that when you want to determine the significance of your results, you need to take into account that your individual data points are correlated through time. For example, if Species A and B have a high abundance today, they probably also have a high abundance tomorrow. Therefore you cannot apply standard ways to obtain significance as those assume uncorrelated data points and you would commit pseudoreplictation. However, it is quite easy to implement a computational null model that preserves the temporal correlations while destroying the ecological correlations (i.e., between species): For example, you can randomly shift one time series if your data is cyclic (e.g., capturing a strictly yearly cycle) or sufficiently large that border effects do not matter. Or you can use time-series surrogates to create null-model data with an identical frequency structure.
Things become more complicated if you care about close overlaps, like Species A being abundant in the month after Species B was abundant. Here, you can use tools like cross-correlation, but this really depends on what exactly your constraints are and what you want to know.


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Percentage of nervous energy used by human eyes
I am reading a book 'How to stop worrying and start living' by Dale Carnegie. I stumbled across this statement below and I couldn't find any research article to backing this claim. Does anyone know if this claim is reasonable or not? Following is the claim:

The reason the eyes are so important in relieving nervous tension is that they burn one fourth of all nervous energies consumed by the body.

"Nervous energy" might seem not to refer to refer to calories as much as fidgeting and muscular tension. Could you clarify the disjunct between the question title and the image text. We discourage text images, as those using a text reader for reasons of accessibility are less likely to be able to read it, if you can use the quote function and type the text in, that would be preferable.

Thanks for editing in the quoted text, but as I indicated, the phrase "nervous energies" is idiomatic, it doesn't refer to Joules or calories, it refers to muscular tension and restless fidgeting. Could you make the title agree with the body of the question. We also require that you show your prior research, once you've worked-out what question you're asking that is.

I couldn't find any information about this topic while doing my research that is why I thought I could ask in this forum

This seems very...non-rigourous. To be honest, I've heard what I can only refer to as quacks speak in a similar manner.

But the question is very unclear, the title being different from the body of the question - please begin by editing so that it's making sense.

Could you do it, I don't know how to frame it better

There is no metric known to me that fits the description "nervous energies". It's the sort of unchallengeable rhetoric that self-help gurus come up with that gives the impression that it's in some way scientific, but the meaning is more intuitive than quantifiable by science. If you can find a metric for "nervous energy" then I'd be surprised if it had a sound methodological underpinning. Don't let that stop you trying though.


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Why don’t animal cells fall apart when they are out of water?
Cell membranes are formed because of the phospholipid's shape and properties. The hydrophilic heads will arrange themselves to surround the hydrophobic tails, so the hydrophilic heads always face the water while hydrophobic tails are shielded. But out of water, there is only water on the inside, and not outside, so shouldn’t the cell membrane just fall apart when the cell is out of water?

But do animals really dry out without dying? I mean...early land animals like amphibians die if their skin dries out and more developed land animals have mechanisms to protect from drying out while the insides of animals are universally wet.

Why would a cell membrane fall apart when out of water? interaction forces between neighboring phospholipids don't disappear.


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Is it better for a person's stomach to have 1 big meal or 2 small meals? Does this change as a person gets older?
Is it better for a person's stomach to have 1 big meal or 2 small meals? Does this change as a person gets older.
Also what about water? Is it the same way or different and why?

How do you define 'better'?

"Also what about water?" Try drinking all you daily water in one go. Your body will instantly let you know it's not okay with that.

I’m voting to close this question because it is both unclear (see comment by @user438383) and seemingly asking for a medical opinion. Please take the [tour] and then consult the [help] pages for additional advice on [Ask] effective and appropriate questions on this site and then delete or [edit] your post accordingly.


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Bug Identification North Carolina Help
I found this bug up in North Carolina and it freaked me out because I found it inside. Would anyone be familiar with this type of bug?
I apologize for the bad angle, it is not a bee at all, but had a striped body, which made me curious!

Welcome to Biology.SE. Unfortunately I think it is unlikely that this can be identified based on the poor quality of the image and the specimen. It might help if you [edit] in why you are sure this wasn't a bee. Please take the [tour] and consult the [help] starting with [ask] for details including the expectations for questions on this site. See also the species-id tag info page for suggestions about how to ask this kind of question — for example including a size estimate is very important.

If you still have the specimen, please take a better picture, e.g. a “bird’s eye view” if the insect were still alive. It’s hard to make out any distinguishing features.


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Test for e. coli in murky water
We had some tests done on some stream water. In the results report, the lab said:
The coliform/e. coli test was requested and [we] attempted to test for the bacteria but the sample was too dark in color to run the test, therefore, a result for coliform/e.coli is not available. This test requires a sample with little or no sample color to successfully read the color change that is performed during the test.
The test method is SM 9223B
Is there an e. coli test that can be done on murky water?


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Can typed-switched B cells recognize the tertiary structure of antigens?
As T helper cells are responsible for isotype switching but Th cells are MHC class 2 restricted and MHC only presents denatured peptides (up to 30 residues, no folding), does that imply that only IgM can recognize tertiary structure? If IgG and the like can, how was that naive b-cell able to present a tertiary structure recognizable by a Th and thus typed-switched.

MHC and B cell receptors/antibodies are totally different things, and recognize completely independent antigens. I think you're mixing up the two.

But doesn't it take a Th cell specific to the same antibody as a B cell to cause the B cell to type switch? And the Th is immune restricted to class II MHC.

Th cells are not "specific to the same antibody" as B cells because T cells don't care about antibody/BCR recognition sites. B cells are activated by Th cells that recognize the same antigen (a protein, for example), but not the same epitope. BCRs/antibodies and MHC (I or II) have very different epitopes. A B cells Class II doesn't necessarily display the same peptide its BCR recognizes.

Sorry, meant antigen, typo.. how does the Th cell know it recognizes the same antigen as the B cell (or vice versa)?

Ah, didn't realize that b cells endocytos BCR-bound antigens and present on MHC class 2.. makes sense.

B cells endocytos BCR-bound antigens and present them on class II MHC. Previously activated Th cells then activate the B cell.

We're looking for long answers that provide explanation, context, and include references to reliable sources. Don't just give a one-line answer; explain why your answer is right with appropriate citations. Answers that don't include explanations may be removed. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] (and [Ask]) effectively on this site and then delete or [edit] your answer (and question) accordingly.


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How does a neuron change its function, without changing its synaptic connections?
How does a neuron change its characteristics in order to change its function, without changing its connections with the neural networks? Basically, do any organelles change their properties and are there any major chemical modifications that could cause it and explain it?
I tried looking everywhere on the internet but I couldn't find any, perhaps neuroscientists still don't know yet.
My initial idea was that some changes of some organelles inside the neuron caused the change in function of the entire neuron. Or that there were some chemical changes that could cause the presence of a molecule that controls the global function of the neuron more than some other.
Thanks a lot for your help and answers.

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] this to be a single question and tell us: where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions are subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

Hello. I have spent some couple hours searching for answers. I tried looking for the list of the organelles of neurons to see their functions and if they have any relationship with brain plasticity, but couldn't find any that actually participate in the manifestation of structural plasticity directly. But I didn't find anything useful. My other theory was that there were some major chemical modifications, and because the function of a neuron was based off the chemical properties of it, then its function would change if the chemistry in the cytosol for example changed. I'm no biologist, sorry.

Also, I think the two other questions are just extensions of the first one. It's just to clarify my question.

If you mean what other functional changes at the level of neurons exist, excluding synaptic plasticity, what is left is called homeostatic plasticity. That is a vast subject that includes alterations in intrinsic excitability, resource allocation (e.g. mRNA), and even hetero-synaptic plasticity, depending on how you define synaptic plasticity. Unfortunately, this subject is too broad for me to put the effort required to write an answer for this site.

The keywords are Synaptic plasticity, LTP, LTD, and STDP, among others. The organelles includes release pools, receptors, scaffold proteins, etc.
Actually there is a huge body of literature around this topic. It will take years just too roughly understand what's already done.

Thank you. But for LTP, LTD, and STDP, don't they only cause functional changes, that means between the neurons and not actually in the neurons? Just asking for a clarification thank you.

@eengeeneer a small part is indeed carried out "between the neurons", i.e. synaptic-clefts, even astrocytes could be involved. But the majority of events, including pools, vesicles, receptors, scaffolds and signaling cascades, happens inside the pre- or post-synaptic neuron.


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How can drone bees be born from unfertilized eggs?
I am learning about Drone bees and I keep reading that they are born from unfertilized eggs.
Now here is my question: if eggs are gametes and therefore reproductive cells, how can they turn into a new living being without being fertilized? If that is possible, then it would mean that the gamete is already a living being/bee from the moment of its creation.
What am I missing? Is there some "activation" process that substitute the fertilization in the case of bees?

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


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Examples of bifurcations in real-life systems
Does period-doubling bifurcation and Neimark-Sacker bifurcation happen in real-life systems? Are there some examples? I'm particularly interested in biological host-parasitoid and predator-prey models.
As far as I know, Neimark-Sacker bifurcation is interpreted as oscillatory behaviour of system, while period-doubling represents the situation when cycles of period 2, 4 etc. appear. It may lead to chaotic, unpredictable behaviour of system.

I'm going to limit my answer to biology since that's what I know about.
This is a surprisingly hard question to answer, especially in ecological (including epidemiological) and evolutionary systems, because it's very hard to be sure that you know enough about an ecological system to prove that the dynamics you're seeing are chaotic, let alone reliably inferring the existence of bifurcations. In ecology, the most reliable examples I know of are experimental, i.e. Fussman et al. 2000 (Hopf bifurcation — I do know that's not what you're looking for) and Cushing et al. 2001 (period-doubling bifurcations).
Beyond that, I looked for reasonable-seeming papers that at least referenced a particular biological system. This is not a perfectly reliable approach, as lots of modeling papers will use an empirical system as loose "inspiration" for a purely theoretical investigation of some model or set of models.

it has long (since the 1980s) been suggested that infectious disease epidemics can undergoing period-doubling bifurcations due to seasonal forcing or many other mechanisms (Aron and Schwartz 1984) [classically measles, with its very high $R_0$ and seasonal forcing through aggregation of school children, was the poster child for this phenomenon], although strong evidence that this is the dynamical mechanism for a particular disease is hard to pin down. Aguiar et al (2009) gives one example that involves some reasonable biology for dengue.
Guill et al. 2011 (Neimark-Sacker, Pacific salmon) and Kamimoto et al. (period-doubling, red coral) are two papers that are based at least loosely on evidence from real ecological systems, and use models to illustrate the plausibility of certain bifurcations
chaos and bifurcations are a little easier to pin down for within-organism dynamics, because the systems are more controllable/easier to experiment on/the models may be a little more tightly linked to the actual biology (although this may be my ignorance speaking), e.g. Ryashko and Slepukhina (2017) mention Neimark-Sacker bifurcation in the context of stochastic neuronal dynamics; Quail et al 2015 discuss period-doubling in (stochastic) cardiac systems.
two other examples of putative period-doubling bifurcations: cAMP waves/communication in slime models (Dictyostelium) (Goldbeter and Martiel 1987) and katydid chirping (stridulation) (Sismondo 1990).

Aguiar, Maíra, Nico Stollenwerk, and Bob   W. Kooi. “Torus Bifurcations, Isolas and Chaotic Attractors in a Simple Dengue Fever Model with ADE and Temporary Cross Immunity.” International Journal of Computer Mathematics 86, no. 10–11 (November 1, 2009): 1867–77. https://doi.org/10.1080/00207160902783532.
Aron, Joan L., and Ira B. Schwartz. “Seasonality and Period-Doubling Bifurcations in an Epidemic Model.” Journal of Theoretical Biology 110, no. 4 (October 21, 1984): 665–79. https://doi.org/10.1016/S0022-5193(84)80150-2.
Cushing, J. M., Shandelle M. Henson, Robert A. Desharnais, Brian Dennis, R. F. Costantino, and Aaron King. “A Chaotic Attractor in Ecology: Theory and Experimental Data.” Chaos, Solitons & Fractals, Chaos in Ecology, 12, no. 2 (January 2, 2001): 219–34. https://doi.org/10.1016/S0960-0779(00)00109-0.
Fussmann, G., S. P. Ellner, K. W. Shertzer, and Jr N. G. Hairston. “Crossing the Hopf Bifurcation in a Live Predator-Prey System.” Science 290 (2000): 1358–60.
Goldbeter, A., and J. L. Martiel. “Periodic Behaviour and Chaos in the Mechanism of Intercellular Communication Governing Aggregation of Dictyostelium Amoebae.” In Chaos in Biological Systems, edited by H. Degn, A.V. Holden, and L.F. Olsen, 79–89. Springer, 1987.
Guill, Christian, Barbara Drossel, Wolfram Just, and Eddy Carmack. “A Three-Species Model Explaining Cyclic Dominance of Pacific Salmon.” Journal of Theoretical Biology 276, no. 1 (May 7, 2011): 16–21. https://doi.org/10.1016/j.jtbi.2011.01.036.
Kamimoto, Sayomi, Hye Kyung Kim, Evelyn Sander, and Thomas Wanner. “A Computer-Assisted Study of Red Coral Population Dynamics.” arXiv, September 30, 2020. http://arxiv.org/abs/2008.08011.
Quail, Thomas, Alvin Shrier, and Leon Glass. “Predicting the Onset of Period-Doubling Bifurcations in Noisy Cardiac Systems.” Proceedings of the National Academy of Sciences 112, no. 30 (July 28, 2015): 9358–63. https://doi.org/10.1073/pnas.1424320112.
Ryashko, Lev, and Evdokia Slepukhina. “Noise-Induced Torus Bursting in the Stochastic Hindmarsh-Rose Neuron Model.” Physical Review E 96, no. 3 (September 14, 2017): 032212. https://doi.org/10.1103/PhysRevE.96.032212.
Sismondo, Enrico. “Synchronous, Alternating, and Phase-Locked Stridulation by a Tropical Katydid.” Science 249, no. 4964 (July 6, 1990): 55–58. https://doi.org/10.1126/science.249.4964.55.

Thank you very much for the answer and references!


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How does tetracycline transactivator localize to the nucleus? Where is the nuclear localization signal?
Proteins typically use a nuclear localization signal (NLS) to localize to the nucleus. Tetracycline transactivator (TTA) needs to work in the nucleus, but I did not find an NLS in the structure.
Tetracycline transactivator is a fusion of tetracycline repressor of E. coli (P04483) and  VP16 of HSV (although by blast I only found P04483).

The Tet-Off system makes use of the tetracycline transactivator (tTA) protein, which is created by fusing one protein, TetR (tetracycline repressor), found in Escherichia coli bacteria, with the activation domain of another protein, VP16, found in the herpes simplex virus.2. Source

There can be multiple NLS's, but the ones I checked I did not find here.
Elements

TetR is a protein from  E. coli, which has no nucleus, and the above sequence is a perfect match to P04483, so NLS is not expected here.
VP16 is from HSV, and it is reported to use HCF-1 to locate to the nucleus.

VP16 itself does not possess a nuclear localization signal; it is transported to the nucleus by HCF-1 and then binds to Oct-1, which can also recognize the same target sequence.
- Since only a domain of VP16 is (f)used in TTA, I am not sure if this is present.

Vaysse 2013 explicitly added an SV40 NLS to TetR, although for a completely different reason (translocate the plasmid DNA in to the nucleus during transfection).

Sequence of Tetracycline transactivator (advanced)
tccagactggacaagagcaaagtcatcaactctgccttggagctcctgaatgaagttggcattgagggcttgaccaccaggaagctggcccagaagctgggtgtggagcagcctaccctgtactggcatgtgaagaacaagagggctctgcttgatgccctggccattgagatgttggacaggcaccacacccacttctgccctctggaaggggagtcctggcaggacttcctgaggaacaatgccaagagcttcagatgtgccttgctctcccaccgggatggtgccaaagttcacttgggcaccaggcctacagagaagcagtatgagaccctggagaaccagctggcattcctgtgccaacaaggcttctccctggaaaatgccttgtatgccctctctgctgtgggccacttcaccttgggctgtgtgctggaggaccaggagcaccaagttgccaaggaggagagggagacccccaccactgactccatgccaccactgctgcggcaagctattgagttgtttgaccaccaaggggctgagcctgcattcctttttggcctggaactgatcatctgtggcctggaaaagcagctgaaatgtgagtctggctctcacgtgcccaaaaagagaaagcacgtgcctgctgatgccttggatgattttgacctggacatgctgcctgctgatgccctggatgactttgatttggacatgctccctgctgatgcacttgatgattttgacctggatatgctg

I noticed after writing my original answer that your DNA sequence is not tTA (TetR-VP16). I've expanded my answer to account for this, but you might want to provide the source for your DNA sequence.

Hi! It is the Synthetic construct improved tetracycline-responsive activator mRNA, complete cds; GenBank: DQ414432.1

If you follow the authors' references you'll see that the sequence you provided is not tTA, but instead itTA (improved tTA). From PMID: 15548671:
The itTA sequence, generated by assembly PCR, encodes three F-domains (PADALDDFDLDML) in place of VP16

Proteins with a molecular weight less than ~30 kDa(*) can diffuse freely through the nuclear pore (see for example here (1) for a review on nuclear transport).
Assuming that the sequence you provide for tTA is correct (EDIT: it is not, see edit below), the protein would have a molecular weight of 28.64 kDa, i.e., below the size limit. In other words, it seems like an NLS is not essential for tTA entry into the nucleus, which is evident from this paper (2) where they use tetracycline to regulate expression from a tTA-dependent promoter in HeLa cells.
Having said that, in this paper (3) (unfortunately paywalled) they create a tTA-nls derivate of tTA by fusing an NLS (KRPRP) to its N-terminus. No data on nuclear localization is shown in the paper itself, but they refer to a thesis (4) where nuclear enrichment of tTA-nls has apparently been shown.
So, although tTA can enter the nucleus without an NLS, including one will cause it to actively localize into the nucleus, possibly improving its transcription factor activity.
(*) This is a number I've heard before, and apart from finding it in the review I haven't bothered looking up the original reference. There are more accurate ways (5) of defining the free diffusion barrier, but I'll stick to ~30 kDa for the purpose of this answer.
EDIT: I did a bit more research, and it looks like the DNA sequence you provide is incorrect. The first part does encode for TetR (2-207), but the second part is not something I could identify, but it is certainly not VP16 (see EDIT 2 below).
In the original paper (2), two versions of tTA are created. In both cases they use an N-terminal region of TetR (1-207):
>TetR (P04483) 1-207
MSRLDKSKVINSALELLNEVGIEGLTTRKLAQKLGVEQPTLYWHVKNKRALLDALAIEMLDRHHTHFCPLEGESWQDFLRNNAKSFRCALLSHRDGAKVHLGTRPTEKQYETLENQLAFLCQQGFSLENALYALSAVGHFTLGCVLEDQEHQVAKEERETPTTDSMPPLLRQAIELFDHQGAEPAFLFGLELIICGLEKQLKCESGS
They then use two different fragments of VP16 and fuse them C-terminally directly to the above TetR fragment:

Long VP16 fragment (363-490)
>VP16 (P06492) 363-490
AYSRARTKNNYGSTIEGLLDLPDDDAPEEAGLAAPRLSFLPAGHTRRLSTAPPTDVSLGDELHLDGEDVAMAHADALDDFDLDMLGDGDSPGPGFTPHDSAPYGALDMADFEFEQMFTDALGIDEYGG

Short VP16 fragment (406-490)
>VP16 (P06492) 406-490
HTRRLSTAPPTDVSLGDELHLDGEDVAMAHADALDDFDLDMLGDGDSPGPGFTPHDSAPYGALDMADFEFEQMFTDALGIDEYGGF
The trailing phenylalanine (F) in the second sequence is not part of the original VP16 sequence, but gets added as a result of their method of cloning.

As far as I can see, they only use the longer version of tTA in the paper, and show that it works in HeLa cells. This is despite the fact that this protein actually has a molecular weight of 36.92 kDa. This is above the ~30 kDa size limit I mentioned earlier, but since this limit is only approximate and tTA clearly works, I think it is still safe to say that tTA freely diffuses through the nuclear pore (albeit not as efficiently as a smaller protein might).
EDIT 2: after the Op provided the reference for the DNA sequence (GenBank: DQ414432.1), I was able to identify the ORF from this source paper (6) as  "improved tTA" (itTA), and the C-terminal fragment as three F-domains (PADALDDFDLDML).
References

Kim YH, Han M-E, and Oh S-O (2017) PMCID: PMC5509903.
Gossen M and Bujard H (1992) PMID: 1319065.
Gossen et al (1995) PMID: 7792603
Kistner A (1993) thesis, University of Heidelberg, Germany.
Matsuda A and Mofrad MRK (2021) PMID: 34339633.
Krestel HE et al (2004) PMID: 15548671.

Wonderful, thank you so much! It is a very clear and precise answer; much appreciated!


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Seasonal fur shedding
How does an animal's (specifically dogs and cats) body "know" to shed fur in the spring and retain fur in the autumn?
Google just tells me that it happens, not the biological process of turning off the follicles and then turning them back on.

Their seasonal (colour) moulting is controlled by pituitary hormones, including prolactin, melatonin and alpha-melanocyte stimulating hormone (α-MSH), together with glucocorticoids, gonadal steroids and thyroid hormones (Zimova et al., 2018).
From the link:

We found that across species, ... photoperiod is the main driver of the moult phenology

In other words, daylight getting longer is a signal of spring/summer; daylight getting shorter is a signal of fall/winter.

Thanks for the editing from Bryan and Ron. I'm not experienced in this field and I learned from your contribution :-)

@BryanKrause but my indoor cats shed in the summer.

@RonJohn Do your indoor cats see daylight?

@BryanKrause much less than they see indoor light at night, or a dark room during the day.


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Does the SARS-CoV2 spike protein passively diffuse through the nuclear pore complex?
I found this thread which is worth reviewing as context to my question(s) since there is some overlap in potential discussion, although it's concern is with mRNA ingress rather than spike protein.
Does the mRNA of the covid19 spike protein contain any nuclear localization signals
It focuses on nuclear localization signals, but there are other mechanisms by which proteins or small enough macromolecules may ingress through NPC's (nuclear pore complexes)
First, see:
Which is bigger, mRNA or the protein it codes for?
http://book.bionumbers.org/which-is-bigger-mrna-or-the-protein-it-codes-for/
mRNA is, somewhat paradoxically (although not really) larger, mass wise, than the proteins it codes for.  And passive diffusion is influenced by molecular weight (a fair model,) so before being concerned about the larger mRNA sequence, we should first be concerned about the manufactured spike protein (either by wild type SARS-CoV2 or vaccine) both produced at the ribosomes of the ER.  An additional concern though could be the geometry / spatial extent of the mRNA or spike protein (in both it's conformations); ex: since mRNA may typically be more linear than globular, passive diffusion curves will be substantially modified as most NPC diffusion curves I've perused all consider globular macromolecules.
Second, see for proof of concept where an accessory protein on SARS-CoV is found to ingress via passive diffusion:
SARS-CoV 9b Protein Diffuses into Nucleus, Undergoes Active Crm1 Mediated Nucleocytoplasmic Export and Triggers Apoptosis When Retained in the Nucleus (2011)
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0019436

Background 9b is an accessory protein of the SARS-CoV. It is a small protein of 98 amino acids and its structure has been solved recently. 9b is known to localize in the extra-nuclear region and has been postulated to possess a nuclear export signal (NES), however the role of NES in 9b functioning is not well understood. Principal Findings/Methodology In this report, we demonstrate that 9b in the absence of any nuclear localization signal (NLS) enters the nucleus by passive transport. Using various cell cycle inhibitors, we have shown that the nuclear entry of 9b is independent of the cell cycle. Further, we found that 9b interacts with the cellular protein Crm1 and gets exported out of the… Show more

Simple rules for passive diffusion through the nuclear pore complex (2016)
https://rupress.org/jcb/article/215/1/57/38760/Simple-rules-for-passive-diffusion-through-the

Recent in vitro studies over the last two decades also suggested a relatively sharp threshold of 30–60 kD (Keminer and Peters, 1999; Ribbeck and Görlich, 2001; Mohr et al., 2009; Ma et al., 2012), although such in vitro systems have recently been shown to be quite sensitive to the precise experimental conditions (e.g., the concentration of transport receptors and the nuclear factor Ran; Ma et al., 2012; Lowe et al., 2015). Larger molecules up to 230 kD in size have also been observed to permeate the NPCs in vivo on the time scale of many minutes to hours (Wang and Brattain, 2007; Popken et al., 2015).

SARS-CoV-2 spike protein: pathogenesis, vaccines, and potential therapies (2021)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8326314/

SARS-CoV-2 S protein is a class I fusion transmembrane structural glycoprotein that is composed of S1 and S2 subunits [ 71 ]. It is a homotrimer with a size of 180-200 kDa

Back to a quote from Rockefeller University press paper above, I found this very interesting:

Nonetheless, the prevailing functional model of passive transport, which we term the “rigid barrier” model, is that of a barrier with a firm size threshold of 40 kD for passive diffusion (Christie et al., 2016; Knockenhauer and Schwartz, 2016; Musser and Grünwald, 2016; Schmidt and Görlich, 2016). According to this prevailing view, the slow permeation of larger macromolecules across the NPC is regarded as residual leakage beyond such a firm threshold (Kirli et al., 2015; Fig. 1 A, red curve). However, this supposed “leakage” may be also interpreted by an alternative “soft barrier” model of transport. In this model, passive transport rates are expected to decrease much more gradually with increasing molecular mass than previously realized (Fig. 1 A, black curve).

Note that last part, which is somewhat telling (and the curve in the paper)
So invoking:

Larger molecules up to 230 kD in size have also been observed to permeate the NPCs in vivo on the time scale of many minutes to hours

And

It is a homotrimer with a size of 180-200 kDa

Could spike protein manufactured at the endoplasmic reticulum ingress by way of passive diffusion into the nucleus or not?  If so, has this been studied?
Is it possible to be unconcerned because such a small 'negligible' quantity would ingress as such (without a NLS)?
Does the geometry / spatial extent of the spike protein (or secondarily, mRNA) itself augment how it would passive diffuse through a normally protected protein complex?

Welcome to the site. What would be your concern if the protein was capable of entering the nucleus?

Thanks bob1.  I'm not sure.  I'm just trying to understand the mechanism and validity of the idea (summarized by the title of the post) before hypothesizing potential outcomes if it were possible.

Ok, was just trying to see if there was some motive behind the question. Generally proteins of the spike sort aren't freely floating and are actively transported to the surface of the cell for virion assembly. However, if it were free-floating I don't see that it couldn't occur via passive diffusion,  but I'll let a better cell biologist answer.

Fair enough on diffusion.  "Generally proteins of the spike sort aren't freely floating".  Have a source for this?  What is different about 9b accessory protein as described in the paper cited in my original question?  Yes, all of the sub-unit proteins are 'expected' to be shuttled for virion assembly, but it appears this doesnt always happen.  Also, according to, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7112327/, the earlier studies theorized assembly at intracellular membrane, but later ones suggest the tubes between ER and Golgi Apparatus as the location of coronavirus morphogenesis.

On that last bit, its definitely more complicated, as some sub units also appear to be assembled elsewhere, for instance, in the cytoplasm, which would be where passive diffusion through NPC becomes more possible.  Depending on the protein, this would naturally vary.  That particular paper describes S protein migration oddly, at least in my opinion: "During its transport to the cell surface, either alone or as part of virions, the S protein undergoes further modifications".  So it could be either?

What I meant by "not free-floating" is that they are generated at the ribosomes and directly transported on the RER; but I see that ribosomes can be not associated with the RER, so that could be a source. Of interest: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC249107/ https://link.springer.com/chapter/10.1007/978-1-4684-5823-7_3.

9b is tiny - only 98 aa (~17 kDa), vs the ~1270 (180-200 kDa) of spike, so much much smaller and therefore more easily diffused and small enough to pass through passive transporters.

The crux of the concern stems from me running into this statement in the paper and  comparing to the approximate size of SARS spike protein: "Larger molecules up to 230 kD in size have also been observed to permeate the NPCs in vivo on the time scale of many minutes to hours".  This would suggest a lower concentration gradient through the NPC, but it appears at least theoretically possible.  The molecular mass simplification doesnt account for spatial extent, and the full length spike protein is suggested to be more axial / rod-like so this also may allow for more permeability.

With small enough molecules (ex: 9b or maybe smaller), concentration in the cytoplasm versus nucelus may reach equilibrium.  For larger masses (and the 'more' globular), equilibrium wouldnt reached, but the question still remains: is it theoretically or experimentally possible for any amount of S protein to passively diffuse through, of course, without a NLS? (Noting the paper with the 230 kD upper bound might need to be recreated / observed in-vivo)

Welcome to Biology.SE. Could questions are problematic since you can often find (or hypothesize) biologically irrelevant conditions under which the answer is "yes". I've therefore modified your question title — if you dislike this change feel free to revert it, but if so please clarify why and what conditions are of interest.


text:
Would the environmental pressures imposed by humans make the housefly of today significantly harder to swat than their ancestors of 1000 years ago?
For context, I am primarily referring to Musca domestica.
Recently the thought occurred to me that due to short life cycle of the common housefly, and due to the fact that such flies have interacted with humans for thousands of years, it would be rather likely that human beings have served as an environmental factor that have affected the evolution of houseflies. Because of the short life cycle of the common housefly, would they been able to rabidly adjust to the environmental pressure of humans swatting them? Would the housefly of today be noticeably harder to swat than the flies of a thousand years ago? Would their be any way to know for sure?

I'm wondering how much of a dent in the fly population swatting makes. Perhaps you might show your research into the relative swat/survival rate (we're meant to show our prior attempts to answer when asking anyhow). Please take our [tour] and refer to the [help] for our guidelines.

@JiminyCricket Hi! Thank you for your response. I do not understand what you mean by providing my research. Do you mean research done by myself on the topic, research that might help with finding an answer, or my own research?

Suggestions; perhaps what you can find online about population density in your selected area (urban?), mean survival numbers to adult fly stage per generation, anything about mutation rates (?), and the likely numbers that you'd need to swat in order to make a dent in the population constituting selective pressure. Whatever you can't find/deduce, perhaps we can fill in some of the details, remembering that no population is going to be completely isolated, because - flies.

Cows have been around for ten thousands years,. Wildebeests for millions. Both have built-in fly swatters. They don’t seem to be swatting furiously. How could we possibly know? It’s not like records have been kept on attempts/successful-hits ratios. The answer is, “Maybe, who knows?” I’m sure there’s plenty of research on domestic flies and their abilities. This site requires that you show some effort to answer your question.

@JiminyCricket. Hello, thank you for your quick reply.
I have some studies that might be relevant to answering this question:
I found that study that shows that Musca domestica adapts very quickly to existential evolutionary pressures: https://onlinelibrary.wiley.com/doi/abs/10.1002/ps.5409
I also found this article that shows the average flight range of Musca domestica: https://eprints.um.edu.my/5793/
Finally, this article explains the mutation rate of Musca: https://portlandpress.com/biochemj/article-abstract/359/1/175/38665/Identification-and-characterization-of-mutations

Ah, that's great, can you now [edit] the question with any relevant info you found (plus the links). I'll make a point of checking back later, see if i can help at all.


text:
Why does the luminal test need hydrogen peroxide?
In the chemiluminescent reaction of Luminol in an aqueous solution, the luminol needs to react with molecular oxygen to produce a photon of blue light. In the technique, the hemoglobin of blood decomposes hydrogen peroxide to produce oxygen, which then react with the luminol.
My issue is; wouldn't there already be oxygen present within the blood itself or from the environment that would react with the luminol itself? Am I missing something?

wouldn't there already be oxygen present within the blood itself or
from the environment that would react with the luminol itself?

I'd say that's the exact reason why peroxide is added.

Without peroxide, the oxygen in blood stain may not contrast clearly enough with environmental oxygen, and you got uniform background (if detectable) luminescence everywhere.

With peroxide, the iron in blood stain suddenly produce huge extra amount of oxygen, and everywhere else the background is kept low, which gave away where the stains are.

That's if you are looking for the blood (with the help of oxygen). If you are looking for the oxygen itself, there should be other methods (electrochemical  sensors, etc).


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Why does plasmid cloning efficiency go down with increased size of insert?
I am setting up a cloning experiment. Briefly, I ran PCR on a gene of interest, cloned it into a vector (pGemTeasy) and bulked it up in bacteria. I have been advised to limit the size of my fragment to <10kb.
Say I have two scenarios:
1 - Insert = 2kb
2 - Insert = 10kb
Assuming we use optimal ratios fragment/plasmid in both scenarios. Why does the efficiency go down?
Here is a ProMega tech note showing the phenomenon for my vector.

Related (not identical) question: https://www.researchgate.net/post/Strategy_to_clone_larger_inserts_2-6_kb_into_T_Vectors_pGEMR-Easy

This article may have the answer but I don't have time to go through it now: https://academic.oup.com/nar/article/27/3/910/2902439

I suspect, but don't have any proof, that it is the physical difficulty of getting both ends ligated to a single strand - think of it like this:
Your 10 kb is essentially a long string, ligate one end to your vector, now try to get the loose ends of that now ~13 kb string in proximity to the same. All in a tube with (assuming nanomolar concentrations) approx 1011 other molecules all trying to do the same. Chances are that the loose ends will encounter another molecule and end up ligating to those rather than the end that will result in a closed circular plasmid.
In contrast, with shorter molecules, having the insert and vector ligated at one end should constrain the number of potential interactions by relative proximity, making it more likely that the loose ends will interact and ligate to form the circular plasmid.
Now, I am sure that this isn't the complete answer, as there will be DNA topology, reaction conditions, etc. to take into account, but I think it is a good approximation of the problem.


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Are fairy rings documented as a growth pattern in ferns?
I planted an Onoclea sensibilis, a single plant, in my garden. After the first season, there was signs that a fairy ring was forming. A few years later it was mostly complete, but then was obscured in the following years by the growth of the next generation ferns on the ring.
I have not seen any documentation in my field guides that sensibilis or any other fern creates a fairy ring.
I would believe that the fairy rings would be rare in the field.
Where would I find documentation on fern fairy rings?

As this was the only result I could find about Onoclea sensibilis fern ring I wanted to add a reference to a wild fern ring I found of the species. This was found in the fall, 2022, in WV during a hike. I do not know the age of the patch of ferns.
This response, I hope, should act as an answer to the question for documentation of a sensibilis fern fairy ring.
As reference and showing ownership of copyright, I originally posted this image on instagram here: https://www.instagram.com/p/CiTl_VvjXq5/


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DNA from Egyptian Mummies Evolution vs Human of Today
Comment: I ask my biological questions from the point of view of mathematical proportions. I am not a biologist.
Are there significant differences in DNA from Egyptian Mummies vs. those available from humans today (5K years aprox)?
Related to this question, I found this answer https://biology.stackexchange.com/a/20301/13003, but just because of lactase tolerance it takes around 7K years!!! which for me is very slow! (without taking into consideration that tolerance probably is only adaptation or this change is detectable at DNA level?)
To get back to Homo Sapiens (300K years) we would have to revert in 60 (300K/5K) similar time ratios.
I found this question Are there differences in DNA between humans of today and humans from 2000 years ago?
Obviously the changes are not homogeneous, perhaps some occurred faster than others, however, the fact that such changes have not been detected in 5K years exerts pressure for the changes to occur almost immediately; that is to say, the Homo Sapiens species appears and immediately there must be changes at the DNA level.
Not only the immediacy of the change, but also the amount of accumulated changes between Homo Sapiens and modern man (ie, simultaneous DNA changes between a subject and his great-great-grandparents).
If changes in climate, environment and food are determining factors, it implies an instability of the DNA (few generations to present a change).
Personally, the fact that no change in DNA has been found for at least 5K years casts doubt on whether we came from Homo Sapiens.
Same calculation could be derived from Homo Sapiens. 66M years after the destruction of the meteorite. 300K years for changes in the DNA of Homo Sapiens and the Human of Today. That produces 220 time ratios (66M/300K).
Comment: I personally think we would need more time ratios to get from a species after the destruction of the Meteorite to Homo Sapiens 300K years ago
What other considerations should I take into account for a more biologically appropriate analysis?

For this to be an answerable and appropriate question on this site you would need to: 1) define what you mean by "significant", 2) make this clearly focused on a single question, 3) remove nonsensical statements like "Personally, the fact that no change in DNA has been found for at least 5K years casts doubt on whether we came from Homo Sapiens.", and 4) provide a clear explanation of any of the numerous assertions you've made that you think are essential to your question. Please take the [tour] and consult the [help] starting with [ask] for details.


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Can you identify this dead bug?
I found this bug in the kitchen and already killed it. It's in austria area. Can someone tell me if it's dangerous?

Welcome. Could you give us some idea of scale, tell us what you found it on or near, was it eating anything?

Photos of the other side?

Looks like an Ectobius_vittiventris, a so called 'Bernstein Waldschabe' which is recently invading Austria. I might be extending this comment to an answer once I have sufficient time on my hands to provide sources and proove.. Greetings from Vienna, we have lots of them too in the surounding suburbs. It feeds on decomposing plant material, so don't worry it's not dangerous to humans - rather the other way around ;)

Looks like an Ectobius_vittiventris, a so called 'Bernstein Waldschabe' or 'amber wood cockroach' in English, which is 'recently' invading Austria and Southern Germany, especially in hot and dry summers.

Image info: Author: Amada44, Licensed: https://en.wikipedia.org/wiki/en:GNU_Free_Documentation_License
In size, shape and color, the amber forest cockroach is very similar to the German cockroach Blattella germanica, which is feared as a hygiene pest and is usually controlled. The most striking difference is the uniform brown pronotum in the amber forest cockroach, which in the German cockroach has two dark longitudinal stripes.
Source
From Wikipedia:

It is a species of wood cockroach originally from southern Europe . It is completely harmless to humans and does not appear as a storage pest, as it only feeds on decomposing plant material and perishes within a few days in human dwellings due to a lack of food. Its original range is south of the Alps, but this species seems to have established itself permanently north of the Alps and in southern Germany.

From Wikipedia:

The natural habitat of the amber forest cockroach is outdoors in low bushes and in gardens under pots. It feeds on decomposing plant material. Warm, dry summers can encourage mass reproduction. Then the probability is high that the animals can also be found in apartments.

Since it feeds on decomposing plants it's not dangerous to humans - rather the other way around ;)


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

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

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


text:
Can features of modified plasmids be divided into prokaryotic features and eukaryotic features?
Here's what I understand and please correct me if I am wrong:
Plasmids modified for gene therapy or genetic engineering should contain factors for certain functions in prokaryotic cells. For example, it should contain an origin of replication for amplification in prokaryotic cell as bacteria.
In the same time, if it's being made to alter a mammalian cell, which is an eukaryotic cell, it should contain features that helps in expression of a certain gene as Kozak sequence
So is it right to say that we can divide features in the architecture of plasmids into features that serve prokaryotic functions and others that serve eukaryotic functions?
are these functions restricted to replication in prokaryotics and expression of genes in eukaryotics?

Plasmids are prokaryotic. If used as vectors for cloning they are still prokaryotic as regards their replication transcription and translation. The inserts in the vectors have the characteristics of the organism from which they originated. If the purpose is to introduce the insert into a eukaryote and hope to have it expressed then it will obviously require the transcriptional and translational signals to allow this occur, and these differ from prokaryotes to eukaryotes. You seem to understand this, so I don't quite see what your question is.

Not to be nitpicking, but while I agree that for cloning purposes plasmids are to be considered prokaryotic, eukaryotic plasmids do exist. The yeast 2-micron plasmid is one example (PMC213983).

@david i want to know if my reading is correct and also i want more specificty:
are these functions restricted to replication in prokaryotics and expression of genes in eukaryotics?

Unfortunately I don’t think you have a specific biological question in the terms of this list.

are these functions restricted to replication in prokaryotics and expression of genes in eukaryotics?
Probably. We still use bacteria to make large quantities of plasmids, so we need to keep the essential prokaryote parts such as origin of replication. Also, we need selection markers markers such as antibiotic resistant gene fro pro and sometimes eukaryotes.

Welcome to Biology.SE. This looks like it could become a good answer, but answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus inappropriate for this site. This is a good example of how to format references. In addition, it is best to leave poor questions unanswered. ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site.


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Biological basis for the illusion of being pulled uphill on a *magnetic hill* when, in fact, one is coasting downhill?
A "gravity hill" is one where a downhill slope appears to be uphill, such that an object such as a car will appear to roll uphill when in fact it is moving downhill.
This is described in a wikipedia article as a feature of the lie of the surrounding land.
What relevant feature of the land would cause this misperception/illusion in human beings? I assume it’s related to some aspect of vision, but would have thought our proprioceptors would feed us opposing information, inducing discomfort of some kind.
What is the biological basis of this illusion?
Edited to add my research: the phenomenon is explained here as a gentle decline between two steeper declines. The illusion is explained as comparable to the Zöllner illusion in which  lines intersected by oblique line segments appear to tilt (Kitaoka, 2007; Oyama, 1960; Robinson, 1972/1988; Zöllner, 1860).

The American Psychological Association’s definition of the Zollinger illusion is

a visual illusion in which parallel lines appear to diverge when one of the lines is intersected by short diagonal lines slanting in one direction, and the other by lines slanting in the other direction.

The illusion in 2 dimensions is clear. But how does that translate into the 3D illusion? Are the “parallel lines” the edges of the road? Or is the road the line (visually implied) transacted by oblique angles of the landscape?
If That question is confusing, it’s because I am confused. Sorry.
This is not original to me but the original poster chose to leave in a huff. Now I really want to know, because when I was a girl, my mom told me great stories about the strange things she herself had experienced. One of the stories involved being pulled uphill in a car placed in neutral at the bottom of a hill. TIL… it was true, for her at least!

I don't have any sources, but usually these sorts of things in the outdoors are related to the layout of the landscape, perhaps with a horizon that appears horizontal, but isn't actually, or maybe with a horizon that is steeper than your brain interprets. I've been on one in a "puzzle world" with a chair that rolls "up" the slope, but it's actually that the wall decor and floor are sloped.

I recall doing instrument flying (IFR) in pilot school and how difficult it is to maintain spatial orientation without a visual horizon. Under these conditions, it is actually impossible to maintain level flight without reference to the instruments, especially the attitude indicator/artificial horizon. I have heard of plane crashes caused by instrument failures during IFR flight: the pilots thought the plane was straight and level when in fact it was in a banking dive. I don’t know if this is related, but it seems like it could be.

@bob1 - I didn’t consider the horizon. I just assumed (a dumb thing I often do) it would be hilly. Good point.

I've found some footage of the one I went to here (youtube; timestamped, but it's only 2min anyway) with a couple of similar illusions. Not easy to see what's going on though, other than a sloped floor and ceiling.

@bob1 - write this as an answer! It may not say exactly what is going on. But your comments do help (as did canadianer’s) and the bounty should go to one of you!

I don't have any proof, but these illusions are typically by visual effects, much like was postulated in the question.
Basically it is a matter of subverting the expectations of the viewer. In most cases this seems to be through a horizon that the viewer interprets as horizontal, but isn't.
An couple of examples of this can be found at Puzzling World in Wanaka in New Zealand, where there are illusions of balls rolling up a pool-table, and a rail (with chair) that the chair rolls "up". Footage of these can be found at this timestamp on Youtube. In both these cases, the floor and/or ceiling are sloped, but the eye interprets them as horizontal (I think through expectations/familiarity).
As commented by @canadianer on the question, pilots doing instrument flying find it difficult to maintain spatial orientation and level flight if their instruments fail and tend to bank the plane, and in some cases dive/rise, when flying without artificial horizons.

The YouTube video is impressive! The brain is a funny thing, and I think you’re right when you say familiarity is behind it. Much more simple example of familiarity is interpreting a broken circle as a circle still. No reason to think illusions can’t be very complex.


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Variant Allele Frequency (VAF) peaks for clonal CNAs
I am reading an overview of the CNAqc package, which defines how the algorithm computes "Variant Allele Frequency (VAF) peaks for clonal CNAs."

mutations present in a percentage $0<c<1$ of tumour cells, sitting on a segment $nA:nB$;
tumour purity $\pi$;
a healthy diploid normal;

Since the proportion of all reads from the tumour is $\pi(n_A+n_B)$, and from the normal is $2(1-\pi)$. Then, mutations present in $m$ copies of the tumour genome should peak at VAF value
$$v_m(c)=\frac{m \pi c}{2(1−\pi)+\pi(n_A+n_B)}.$$

However, I don't understand exactly the definition $n_A:n_B$ in this context.
Are $n_A:n_B$ the number of reads coming from alleles $A$ and allele $B$ in the tumor? But then, why the normal has only $n = 2$?

Migrated to Biology at the request of the question author

On a further inspection on the associated paper, $n_A$ and $n_B$ are the allele-specific copy numbers.
And it definitely makes sense that we have 2 (diploid) for the normal component.


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What is the difference between ‘classical’ and ‘non-classical’ pathogen resistance genes in plants?
I have stumbled across a mention of classical resistance genes against pests in plants, however the classification seems a bit vague.
What would be classified as classical resistance genes and what as non-classical in plants?
Edit:
Found it here:

'For example, the identification of classical plant resistant genes in
Arabidopsis and other model dicots facilitated the successful cloning
of multiple wheat rust resistant genes (Ellis et al., 2014; Wulff and
Moscou, 2014).'

Schwessinger, Benjamin, et al. "Focus issue on plant immunity: from
model systems to crop species." Frontiers in plant science 6 (2015):
195.

Where have you stumbled across the mention, and what was said about it?

@BryanKrause i originally encountered it at a conference but then also found it here:
Schwessinger, Benjamin, et al. "Focus issue on plant immunity: from model systems to crop species." Frontiers in plant science 6 (2015): 195.
'For example, the identification of classical plant resistant genes in Arabidopsis and other model dicots facilitated the successful cloning of multiple wheat rust resistant genes (Ellis et al., 2014; Wulff and Moscou, 2014). '

I edited to reflect that the reference is to classic genes rather than to classic immunity.
Note that this is not a formal definition but rather an informal way of talking about the state of the scientific literature: "classic" or "classical" is a way of referring to the first-described, standard, or most familiar example of a phenomenon.
The term "classic" has no biological salience, but rather has salience for the history of science and what is in textbooks (e.g. the necessarily subjective human perception of nature).
See e.g. this blog post discussing this loose way of writing.


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What is the difference between a macrophage and dendritic cell?
I am aware that both these cells (monocytes) are phagocytes and are able to present antigens upon their own Class II - MHC integral proteins.
Other than their difference in structure (size and shape), what other differences do they have? For example, do they engage with T-Cells differently?

Macrophages can only activate the general T - Cells while dendritic cells can activate memory T - cells as well. Also, dendritic cells don't survive after their effector function while macrophages do. The main difference is the fact that dendritic cells present pathogens to T-cells while macrophages initiate the main response of removing the pathogen and then presenting their peptides to other cells.
This link might be helpful as well.

Hi Shadan. Thanks for answering. To improve your answer, please include credible references to support specific statements, otherwise the answer to such a rather specific question is suspect and will be downvoted. Scientifically, using phrases like "from what I know" and "I would say..." are unfortunately worse than unhelpful, they cast doubt or confusion, and take away from the link that you share at the end, which you may have quoted to answer the question very elegantly!