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Hemoglobin question- how many alleles?
So I know that Hemoglobin is made of 2 alpha and 2 beta subunits. The alpha consists of 2 genes on chromosome 16, and the beta of 1 gene on chromosome 11.
So why does Hemoglobin only have 4 alleles? Why is it not 6? In my way of thinking each alpha subunit consists of 2 genes, so 4 total. And each beta subunit consists of 1 gene, so 2 total. Together that makes 6. Confused! Thanks in advance

Can you cite where you are getting the idea that there are only 4 alleles across the three genes you are referencing? There are certainly disease-involved and normal alleles at all three genes so there are certainly more than 4 alleles across the three genes. I'm suspecting your source is talking about something more narrow. That said, Remi.b's answer is still good to consider.

Meaning of Allele
The word "allele" is often used with two slightly different meanings in biology.
The first, probably more appropriate usage is the one in Remi.b's answer: an allele is a variant of a gene in a population; there are many many possible alleles for a given gene, depending on the length of the gene, though typically only a few are common in a population and even fewer may be known.
The second use of the word "allele" is to mean "copy" of a gene; because those copies can be different, in this context an allele is a potential variant of a gene in an individual. For a diploid organism like a human, you might say that an individual has "two alleles" but what you really mean to say is that individual has "two copies of a gene, which could be the same or different alleles." The relationship between the two copies is called zygosity. I'd argue that this is a slightly sloppy use of the term, but nonetheless it is common and if you understand the meaning it is still clear.
Genes for hemoglobin
For hemoglobin, there are at least 3 important genes: two each encode alpha subunits, and the third encodes the beta subunit (there is also a delta and gamma subunit, but we can omit discussion of those for now).
For the beta subunit, each individual has two copies of the gene, which in human populations are typically thought of as one of two population alleles: either a normal allele or an allele associated with sickle cell anemia. Individuals with two of the sickle cell alleles will have sickle cell anemia.
For the alpha subunit, each individual has two copies of two different genes. There are alleles for each of those genes that produce non-functional products. Individuals with alleles that produce non-functional alpha subunits, for either gene, have Alpha-thalassemia. The severity of Alpha-thalassemia depends on how many alleles are present across the two genes that do not product functional alpha subunits.
Why 4 alleles for hemoglobin??
I suspect if you read somewhere that there are "4 alleles" for hemoglobin, that source was probably talking about Alpha-thalassemia in particular, in which case there are indeed 2 copies of 2 different genes so that an individual has four possible alleles. The severity of Alpha-thalassemia depends on the total number of defective alleles across the two genes, where having 4 defective copies is fatal, and having just 1 defective copy is not noticed clinically.
In the population, however, it is likely that there are actually many other alleles for each gene. For the purpose of describing disease, however, we can group these into "functional" and "non-functional" and say that there are two population alleles for each of these two genes.

An allele is a variant at a given locus. If at a given locus, there is no variance in the population, then the entire population is fixed for a single allele. If there are different variants in the population, then there are severeal alleles in this population.
A locus can be defined as a DNA sequence of any length. For a locus of size n the maximum number of alleles is $n^4$ and the minimum number of alleles is $1$. In practice, that being said, we sometimes group allele together and hence the maximal number of alleles is somewhat lower. But let's not go into these details.
The point is that it does not matter how many subunits you want to consider. The number of alleles is simply the number of variants that exist in the population. If for the hemoglobin, there are 6 alleles, then there are 6 alleles!


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What is this underwater creature?
West Bali, about 10 meters deep. Body is roughly 10 cm across.
Does not move.

Is that "does not move " in the timeframe you allowed? Or based on a timeframe of months of continuous observation.

Lack of movement suggests it's not a sea slug. Possibly a strange tunicate?

I am convinced this is a nudibranch. The features that indicate this are the rhinophores (antennae-like sensory structures at the "peaks"), the cerata or brachial plume (hard to tell which based on this photo, but these are translucent extensions just visible in the "valley" between the two "peaks", if you zoom in). A look here and here shows there is a huge diversity in morphology, but many nudibranchs have some form of these structures. Also, the shape of margins around the edge of the animal matches that of many nudibranch species. These are mobile animals but it is possible it just was not moving during your observation.

I would say that it is a sea hare of some type based upon its appearance and location above course sand. While it was not moving, that could just be a factor of when it was observed. I wouldn't expect a tunicate to have this appearance or be affixed to sandy sediment.

Welcome to Biology.SE. You are more likely to get a positive response to this answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion and is thus inappropriate for this site. ——— You may also wish to take the [tour] and then consult the [help] pages for additional advice on [Answer] and [Ask] effectively on this site.

source: Stack Exchange

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

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Help me identifiy this insect
I found this insect in Pune/India. It looked like a fly, and it was running over a leaf.
Size is about 2mm-3mm. Is it juvenile of some fly species or is it not even a fly?

Yes, this looks a lot like a fly (six legs, two wings, shape of the body and head), but I am clueless what kind.

Another possibility is a Hymenopteron of the superfamily Chalcidoidea (parasitoid "wasps"); I base this on the clubbed antennae, small size, and what appears to be very reduced wing venation.  If this guess is close to correct, good luck getting the animal much further (a good stereoscope is practically a requirement just to get to family, and going deeper than that may require a compound microscope -- as for species, what we see here may or may not have a formal name; there are LOTS of Chalcidoids).

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


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Comprehensive database of cell types
Wondering if there is a comprehensive list/database of cell types, similar to this wiki list of cell types in the human body. It lists probably 100+ different types, but this is just for a human. If we include all animals, and plants, and bacteria, and single celled organisms, etc. then the list would probably get larger.
Wondering if any such aggregation exists, either just as a collection of lists or as a database of cell types. Doing a search returns CELLPEDIA, but the last results are from 2011, so it looks like it never came to be. I also saw MorphoBase, but it didn't look like it was there either. But something like that would be good, otherwise just a list. Basically like a cell taxonomy.

A currently active cell database is SHOGoiN, which says it is a significant extension of the world-first human cell database, CELLPEDIA.  It focuses on human cells but also has information on mouse, sea urchin, and C. elegans.
The site says:

The database consists of several modules that store cell lineage maps, transcriptome, methylome, cell conversions, cell type markers, and cell images with morphology data curated from public as well as contracted resources, based on sophisticated cell taxonomy.

Wondering if you know of anything similar for plants/bacteria/single-celled organisms.


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Antiparallel DNA Strands - Error Correcting Code?
Let me quote Wikipedia.org:
"The two strands of DNA run in opposite directions to each other and are thus antiparallel."
There is a practice or method used for error correction with regard to parking tickets: First the number plate is written down from left to right, then again but in reverse (right to left) order.
So my question is: to what extent does the antiparallelity of both DNA stands constitute an error correcting code?

I can flesh out my answer a bit more if you don't have enough biology background to connect with the info in the linked article

Double-stranded DNA does have redundancy giving a basis for error-correction, but it has nothing to do with the antiparallel nature of the DNA.
Each strand has an orientation, that is the pieces of the backbone are not symmetric and so chemical reactions have to happen in one of the two possible orientations along the strand.  One end of a strand is called the 5' end and the opposite end of the strand is the 3' end.  The two strands of a DNA molecule run in opposite directions (antiparallel), with the 5' end of one strand being adjacent to the 3' end of its partner strand.  The two strands do not contain the same codes in opposite order like your license-plate coding example.
The redundancy is only pair-by-pair.  A nucleotide in one strand is paired with a unique complement nucleotide on the other strand.  It is thus redundant like bit-for-bit odd parity is redundant.  This redundancy allows errors to be detected from a mismatch in what should be a pair, and a damaged nucleotide can be replaced with the correct nucleotide by using the complement of the nucleotide on the other strand.

As you have intuited, complimentary base pairing gives DNA molecules 2-fold redundancy. That is, given the base present on one strand, we can always deduce the base that should be at the corresponding position on the other strand.
Cells take advantage of this redundancy to perform error correction through DNA repair processes. Here is a textbook section that introduces how DNA damage is sensed and how cells can use the complementary base on the other strand to guide repair. It also details how cells can determine which base is "correct" when a mismatched base pair arises during replication.
https://www.ncbi.nlm.nih.gov/books/NBK9900/


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Rod and cone photoreceptors are neurons?
i mean the photoreceptors have axon and dendrite and body cell or it is not neuron
any more   . can we say outer segment of photoreceptor cell is dendrite ? of course these have body cells but i am not sure they are neuron or not

Photoreceptors are considered neural based on embryonic origin: they derive from neuroepithelial cells like neurons do.
Neuroepithelial cells also produce non-neuronal cells like some glial cells.
It doesn't make much sense to worry too much about whether a rod/cone photoreceptor is a neuron or not. They don't have long axons or dendrites, but they need not have either to be called a neuron. They make synapses, but these synapses are highly specialized and different from other types of neurons; that isn't sufficient to not call them a neuron. They don't fire action potentials, but they need not fire action potentials to be called a neuron. They do release neurotransmitter, but there are other cells that also release neurotransmitters that are not considered neurons. Ultimately, deciding whether a cell is a neuron or not is a matter of semantics, not biology.
Most texts I am familiar with consider them neurons because of their neural origin, which differentiates them from other sensory cells that derive from other tissue.


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Why do seeds grow upwards?
Why do seeds grow upwards?  Surely gravity would pull them towards the earth's core?  Can anyone shine any light on this? Do seeds that are planted deeper grow more quickly.

While the general question is good, still, the part about "Surely gravity would pull them towards the earth's core?" could be applied widely to many other things. Why aren't you pulled toward the core? Why aren't you sinking into the dirt? Why don't you grow downward? Why does water evaporate upward into the air? Why do particles get ejected away from the sun? Gravity attracts, yes, but that does not mean that everything is always moving toward it at all times. If that were true, everything would collapse into tiny points and be like black holes.

one could argue that we do grow downwards, but for every bit we grow downwards, the earth pushes us back up

@Aaron  Nicely considered and said!  Yay!

It is a reaction to gravity, it is called geotropism or gravitropism. The roots tend to grow in the direction of the gravity (positive geotropism) and the stem is going against gravity (negative geotropism).
The mechanism works with auxins, or plant growth hormones. They are pulled by gravity toward a side of the plant and will either stimulate or inhibited growth in that area.

For a longer view, reflect that plants which didn't evolve some mechanism to grow upwards (and their root systems downwards) would be pretty much restricted to floating on ponds and such.

is correct, but doesn't provide any support or citation.

@jamesqf or having a 50/50 chance of getting it right anyways.

Because of a force known as geotropism - it is a reaction to gravity. The upward growth of shoots from seeds is known as negative geotropism whereas the downward growth of roots is known as positive geotropism.
The act of a seed to decide which way is up, or to orient itself, is geotaxis - it detects which way is down and up, in other words, because of gravitational force. see here https://www.sciencefocus.com/nature/how-do-seeds-know-which-way-to-grow/
And no, seeds which are planted deeper don't grow faster - each kind of plant seed needs to be at an optimal depth in order to germinate. Ever noticed you get lots of weed germination in freshly dug areas? That's because seeds sitting too low down in the soil which might have been there ages are moved closer to the surface by the act of digging, which then means they are now able to germinate and grow.

In addition to the geotropism mentioned in the other answers, experiments on the ISS have shown that plants will grow oriented in a manner such that “upward” (i.e. the stem, leaves, etc.) is toward a light source, even in the absence of gravity. Of course, this depends on the plant being able to determine which way is toward the light source. Although I have no source for this, I imagine something like a thermal gradient could be used before the plant breaks the surface.

Interesting. Do you know if there were any experiments where plants were grown on the ISS with an equal distribution of light and heat? Ex: either completely dark or completely light from all directions.

Not to my knowledge, but it’s certainly possible.

@Aaron Check out the last site I have just now included in my answer concerning zero gravity and growing plants on the ISS.  I hope I've sent enough sites to support what I am trying to say...

@alex_d  I meant to make sure I pinged you as well.  Thanks!

@stormy and alex_d: note also that I have since asked a question about this on space.SE here: https://space.stackexchange.com/questions/31762/have-there-been-experiments-in-space-to-determine-how-plants-grow-without-any-gr

Gravity sure contributes to this behavior (that is to the growth vector being "up"), but none of the other answers mention moisture gradient, which is also a major contributor to the seed growth vector.

It is probably because the plants which did this were more successful in catching light with their chlorophyll than the ones which did not do this.
More successful in growing and maturing and sprouting flowers: bigger chance of more baby plants next generation et.c.
Consider the converse: a plant that grows deeper into ground. It will clearly need some other way to get energy than by photosynthesis to survive and thrive underground. As far as I know this is not at all as common among plants.

Sorry I don't have any sources. I am just Darwinguessing.

Note added; Gravity is but one factor in a 'sea' of complex factors that have effected everything living in this thin blue line on Earth.  Atmospheric pressure, temperature, humidity, the medium's porosity, the Earth's spin counterbalances the gravity and a myriad of things I didn't list or was able to mention a myriad of things we humans just do not understand about life, gravity. I am trying to say that there is no ONE thing controlling the direction of the cotyledon nor the root growth.  Roots do not grow and grow towards the earth's core.  Roots stay within the top 4 to6" of topsoil for a reason and gravity has nothing to do with it other than gravity is part and parcel of all the systems that put pressure on an organism to make it adapt to its environment and file that information away in the seed of a plant, within every living cell. As DNA.  It is weird we share 99% of the DNA messages with all animals all plants all life.  What does that tell us?
Geotropism isn't quite right because it certainly is not the only factor plants have taken into consideration.  Again, roots grow horizontally to the force of gravity, not vertically.  The fact that gravity is a constant tells us that there has to be many forces that shaped the physiology plants display. We animals are able to run and jump against and with gravity forces.
This question is a very good one because it causes us to pause, step back to think about the larger picture, a picture we humans have just begun to imagine.Geotropism seems to be a pretty minuscule reason plants grow upwards and roots grow outwards.  No one thing could ever be pointed to as the reason a life form as evolved to survive with or against. If seeds are planted too deeply (more than 3X the widest diameter of the seed) that seed will more than likely damp off with fungus and decompose. Animals are the same, we sit still too long in one place and we start decomposing, grins!
I have a feeling that people think plants are dumb like rocks.  In fact, they were here first, before animals.  Lots more time to perfect their survival abilities.
If it was up to gravity, the roots would grow and grow and grow downwards.  That is not at all what happens.  95% of all plant roots are within the top 6" of soil. The reason is water doesn't infiltrate the subsoil well at all.  Plants 'know' this fact.  Roots grow where there is air and moisture and temperature stability. There is absolutely no reason to grow any deeper roots with the exception of a few plants that need find deep water sources, chemistry for photosynthesis and/or need support. AT the same time in the desert environment, cactus don't waste any energy on deep roots!  They instead, figured out how to store water.  They keep their roots very shallow and very small. Deep roots would be a waste of energy and resources. They can live to 150 years, 50 feet high but their root system is just enough to keep the 2 to 10 ton plant from falling over in a wind.
There are a few plants that are programmed to have tap roots that are for support and scouting that do grow very deep. 1000's of feet deep and 1000's of feet horizontally.  They don't have the ability to store water.
The cotyledons grow upward against gravity.  They don't even need light to be persuaded.  Plants have had more time than us animals to evolve.  Gravity is like a 'positive' stressor, makes plants and animals more 'sturdy'.  But gravity certainly isn't at all the main director of plant direction of growth.
It is said that animals share 99% of DNA with plants.  That number has qualifications but what does that tell us?  Other than plants were here first, DNA or the blueprint for life started earlier plants. Before that DNA was in virus and bacteria. Plants may be stationary but they are by no means dumb as rocks.  There is life in rocks that never sees light, O2 or any organic matter; bacterium and worms.  They eat rock.  They procreate once every 1000 years.
Dr. David Attenborough stated in a documentary called "The Earth's Core" that 50% of all life is below the surface of the soil, in the crust and mantel of the earth.  I have a hard time with that statement, but heck, David Attenborough? I filed that away to deal with later.  I am thinking 'numbers' of individual lives, not biomass?
Plant DNA guides them via experience of billions of years. As long as this planet hasn't stopped spinning, lost its oceans or heaven forbid is below 150 ppm atmospheric (manmade or not) CO2, or have temperatures too low for too long, plants will thrive.  Our current CO2 at 400 ppm is getting too low.  2000 ppm was dandy.
Plants even communicate.  Via chemistry.  Some amazing instances of plants getting together for survival, such as when an animal population gets too large?  Plants that evolved to handle some grazing by those animals as a mutually beneficial symbiosis, will become toxic to those same animals.  Herds have mysteriously died within days. Then it was discovered the plants had communicated and all switched their DNA to temporarily be toxic to the animals in their environment.
Plants are not at all dumb as rocks. They are just not as well understood as animals. Cotyledons grow upward in pure darkness.  When a light is turned on off to the side, that plant will grow towards the light.  If that light is turned off and another turned on that same plant will easily change directions.  Trying to get at light necessary for further growth and survival of that plant.
There are some incredible documentaries on the life of plants. If aliens show up they will be hard pressed to decide who is smarter; humans, other animals or the plant kingdom!
plants are smart
Also watch; "The Mind of Plants", a documentary I thought was excellent.
David Attenborough's documentary, "The Earth's Core" is a must.
Plants grow just fine in zero gravity

This answer doesn't address the OP's question. They asked why seeds grow upwards, and you have pointed out that indeed they do grow upwards. You talk about plants being 'intelligent', but don't explain any of the mechanisms involved in plant growth. You've also contradicted yourself (perhaps it's a typo?), you said "cotyledons grow upward against gravity", but then "gravity certainly isn't at all involved in plant direction of growth". Finally, I would like to see some citations for the "animals share 99% of DNA with plants" claim as well as the other anecdotes.

Some of this is right, some of it is wrong ("But gravity certainly isn't at all involved in plant direction of growth." is wrong), and some of it is confusingly nonsensical ("Then it was discovered the plants had communicated and all switched their DNA"). Please clarify this!

Gravity is part of the information all around us that of course affects all of life.  But it is only information.  Gravity does not tell plants HOW or where to grow.  We walk upright because we 'know' the best direction is perpendicular to the force of gravity.  Plants have been grown in zero G and that changes nothing for the growth of the roots and the growth of the photosynthetic part of the plant.

@wizzwizz4  Plants have DNA that like ours has 'switches'.  For instance, when animals find themselves in an overpopulated by their own species environment, there are 'switches' in the DNA that respond to the additional stress to tell an organism in utero to become a homosexual.  This is step one to reduce population.  DNA is more mutable or malleable than we imagine.  I think this was about a Mesquite type shrub/tree in Africa.  The plants, in response to this antelope type animal overpopulated and was decimating these trees.  All trees in the area had their DNA switched to become toxic.

I'll try to find that specific documentary; there are a few out there that talk about this very topic.  Sorry it sounds nonsensical, I'll keep trying to make sense of it for others.

@stormy The DNA doesn't change... Those "switches" aren't actual switches. Imagine DNA as a kind of set of instructions, which are followed depending on what's going on in the environment. The genes might've been "enabled", but the actual DNA wasn't changed.

@stormy Never ever try to summarise those documentaries; you'll just sound like an idiot. They already simplify it enough, even when it doesn't need "simplification" (wrongification) so without the inherent credibility of being a documentary you'll just be embarrassingly wrong. I speak from experience, if you're wondering; it took a while for people to stop teasing me about my "explanation of E=mc^2, the black hole theorem". What you're saying kind of sounds like an approximation of correct, but it's already explained by lots of other people.

Let us continue this discussion in chat.

"But gravity certainly isn't at all involved in plant direction of growth" - this sentence is totally incorrect.

Another error here is the statement that "water doesn't infiltrate the subsoil well at all".  That's true for some soils, but by no means all.  For instance, in spring or stream-fed meadows, the water may be coming up from the subsoil, or plants may grow deep roots to access subsurface water.

I am an expert where plants are concerned, including soil science.  Water does not infiltrate compacted sub soils well...the horizons below topsoil.  Water coming up from the subsoil would mean wet lands, marsh.  Plants will not grow deep roots unless they are genetically predisposed to HAVE large root systems.  Such as cool season grass mixes for lawns.  One can 'train' the root systems to grow deeper by deep watering and then allowing the soil to dry out from the top down.  Poa annua for instance, a weed grass with shallow root systems used a lot on golf courses will not grow deep roots...

This question demonstrates the need to back up and fill in a bit of logical science.  My goodness the nit picking.  Please substantiate WHY such and such is in error.  I am talking on a scale of what is important and what is not.  Yeah, let's just go with 'geotropism'...nice scientific sounding label that is black and white and works. Grins.

@Ben I need to learn to be more PC.  Gravity of course is involved in plant growth but as I've shown?? is a minuscule force.  But it most certainly is there and I was in error saying the words "is not at all involved" in plant direction of growth.

@jamesqf water tables are independent of soils,  High water tables will cause even genetically disposed plants with deep roots to grow shallow roots.  I am sorry I didn't word that comment better.  I doubt one would find in a natural ecosystem plants with large root systems growing where there is a high water table, a marsh, a bog.  Roots not adapted to aquatic situations would simply not flourish and not be found where there are high water tables or influence by surface water systems.  Roots grown in water are different than roots meant to grow in soil. Wet land habitats are not the norm.

stormy: late last week I asked a question related to this on space.SE about ISS experiments on this topic, and I got a good answer: https://space.stackexchange.com/questions/31762/have-there-been-experiments-in-space-to-determine-how-plants-grow-without-any-gr

Also, I want to +1 your answer but I do not know enough personally, and the other comments have dissuaded me from doing so. However, I'm not going to vote it down either. If it is any consolation, I thank you for providing more information, and that is the most important thing.

@Aaron I love your honesty.  I am glad you think enough of my line of thought to not mark me down.  I've got plenty of points to lose and not at all afraid to lose them.  We humans have a tough time thinking, linking information to other information to make information more credible.  Part of that is this negative feedback towards thinkers like myself.  I know you brought up ISS and that is why I sent this rather pronounced site everyone could have looked up and read to support my words and your assertions!  It is not much fun being the rebel.  I will never 'mimic' someone else's thoughts.

I am not merely nit-picking when I say that it is wrong that plants are not affected by gravity. It has a very significant effect on plant growth. Not that gravity forces the direction in which the plant grows - rather plants use gravity to detect and respond to their orientation, with some parts of the plant having mechanisms which direct their growth towards or away from the earth. This is the meaning of the word "geotropism" - which can be positive or negative - towards or away from the earth. While this is not the only thing plants detect, it is an important factor.

@Ben  We humans have problems in zero gravity, they, the scientists don't think we humans will be able to procreate in zero gravity.  But we shall go through the motions just fine.  if gravity were such a big deal to plants, why would they be able to grow in zero g?  My answers are just getting longer and longer trying to explain how I understand a problem or question.  I need a serious course on conciseness....when discussing live organisms, I have a hard time with short answers.   Again, how do plants deal with zero gravity so well?

@stormy The question that Aaron links answers this very clearly: https://space.stackexchange.com/questions/31762/have-there-been-experiments-in-space-to-determine-how-plants-grow-without-any-gr The stem has to come out in some direction; if there is no gravity, it just keeps growing in roughly that direction, because it doesn't have the cue (gravity) to tell it which way to go. They don't actually deal with zero gravity so well, as that answer also discusses.

I read all of those excerpts from Dr. Sheldon.  The point is plants are programmed to grow in the gravity in which they evolved.  But, they most certainly can grow in zero gravity.  Not well, but they can still adapt in zero gravity to a certain extent.  Of course gravity and normal conditions one has evolved with will ensure more success but zero or minimal gravity is not a 'deal breaker'.  To say gravity is direly important is just...just...not quite right.  The seed has programing to tell the photosynthetic part to grow 'away' from the roots which has been shown.

Plants can grow in 0g because they have many mechanisms for orientation, I never said geotropism was the only mechanism, or even an essential mechanism. I would be happy to edit your answer for conciseness, if you like, but I fear you might not like the result.

@Ben, knock yourself out.  Edit away.  If I don't like it I shall re edit what you edited.  Ugh, I made an error saying gravity isn't important, when of course it is.  I have tried to mitigate that statement but I don't think throwing the baby out with the bath water is necessary?

I have tried an edit - but I'm afraid it may be rather too drastic. I did try to keep most of your points, and not add any additional information, but I am not sure if it is still true to your original intent.

ummmm @Ben how do I check out your edit?  Thank you for editing by the way!  I'll get to understand you better!  I'll go and try to find this edit or is this edit already showing as my answer?  No problem.  and thanks!

Sorry, I don't know where my edit is, I don't have a lot of rep on this stack, so I got a message that it was being "peer reviewed"

Peer reviewed, huh?  They should be happy you took the time, Ben!  I'll watch for your edit.  I might just remove my answer, that usually makes everyone happy, grins!  Thank you again.


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What makes/breaks the hydrogen bonds between DNA and RNA during transcription?
So I know that RNA polymerase catalyzes the phosphodiester bonds that hold the sugar backbones of a growing mRNA molecule together during transcription. However, I'm less sure about the hydrogen bonds between the nitrogenous bases of the forming RNA and the template DNA strands.
I do assume that hydrogen bonds are forming, but they must be short-lived.
Their existence are confirmed here:

ribonucleotides containing 3 phosphate groups hydrogen bond through the process of complementary base pairing with the exposed deoxyribonucleotides on the unwound strand that is to be transcribed

and represented in this gif:

Is RNA polymerase responsible for creating the hydrogen bonds between DNA and RNA? Is it, then -- I assume -- also responsible for breaking these bonds? Are the breaking bonds driven by chemical reactions or more due to the physical movement of the polymerase along the DNA template?
This site mentions the transient H-bonds formed by holoenzyme at promoter sites, but I haven't been ale to fnd a reputable source discussing the transient H-bonds between nucleic acid strands.
I'd appreciate if someone can provide a clearer molecular description of what's going on here. Pictures/animations are a plus!

Be careful with animations. The one you present indicates an unwound stretch of DNA with RNApol (not shown) somehow moving along it. Misleading at the very least if RNApol is causing the DNA to unwind. I'd remove it. The formation of a transient heteroduplex of at least one bp is fundamental. It seems to me that the crux of your question should be 1. How does RNApol melt the dsDNA, 2. How does it process along the DNA duplex, and 3. What causes the transient heteroduplex of the growing RNA chain to dissociate?  The answer is presumably to be found in a recent review paper.

David, thanks for the comment. I think you're right that all those components are an important part of the process, but I am most interested in the construction/breakdown of the H bonds themselves. I'd welcome an answer that addresses the H-bonds in the context you indicate. Do you have a citation or title for the review paper you have in mind? I'll allow your comment to provide the caution regarding the unwound nature of my animation, but I think I'll leave it as part of my "evidence" that H-bonding occurs and as a quick indication of the H-bond to which I'm referring. Thanks!

I am away with just my phone at the moment which is not really the thing for literature searches etc. If nobody else has done so by next week I'll either do a Papers search for reviews and/or look at recent PDB entries for RNApol. However remember that hydrogen bond formation is driven by thermodynamic considerations at a rate that is governed by kinetic factors.  If RNApol makes additional interactions with the rNTP and binds it so it is in the right position and configuration to base pair with the DNA this will allow it to speed up the kinetics — catalyse the reaction.

Finally done it. Perhaps a bit over the top for a non-chemical biologist (as I assume from your bio) or for teaching at certain levels (as you mentioned previously). However as you have made frequent contributions to SE Biology your question deserves a thorough answer.

I wouldn't really say RNA polymerase is "creating" the hydrogen bonds so much as it's thermodynamics that creates them. When we talk about an enzyme "creating" a bond, what we're generally referring to is an enzyme facilitating a reaction by lowering its activation energy so that it can proceed.
However, in the hydrogen bonding between base pairs, there's not really much activation energy to overcome. Before the formation, the nucleotide is just floating around in the cell (solvated by water), and forming a base pair is more energetically stable than not being paired. When a ribonucleotide happens to diffuse into contact with the unpaired DNA strand, the hydrogen bond will spontaneously form because it's energetically favorable. The thing about hydrogen bonds, though, is they're fairly weak, so there's an equilibrium between formation and breaking. When a mismatched nucleotide diffuses into that space, the hydrogen bonding isn't as strong, and it might be in an improper orientation, so it'll diffuse out again. When the correct nucleotide enters, the hydrogen bonds will form spontaneously, hold it there longer, and orientate it properly. This properly places the phosphates for backbone formation, which allows RNA polymerase to proceed with making the backbone.
As for the breaking of the hydrogen bonds, it's the energy released from the phosphodiester bond formation that causes the bonds to break at the other end of the RNA-DNA hybrid. To simplify things a lot, it's kind of like a zipper, where forward translocation of RNA polymerase along the DNA strand is driven by phosphodiester bond formation, which breaks the hydrogen bonds of the RNA-DNA hybrid somewhat mechanically, as the nascent RNA strand leaves through a different channel than the DNA does.
References:
Structural Model of RNA Polymerase II Elongation Complex with Complete Transcription Bubble Reveals NTP Entry Route
Transcription elongation: Heterogeneous tracking of RNA polymerase and its biological implications

Although the answer provided by @StephenB is essentially correct, I’d like to supplement this with more visual illustrations — including a link to an animation which the poster requested — as well as reiterating the important points he makes about enzymes. This is a question about enzymology and structural biology and is essentially chemical in nature.
Enzymes and Chemistry
To answer the specific question posed:

No. Enzymes are not responsible for creating any sort of bond.

The creation of bonds — including the hydrogen bonds of base-pairs — is governed by the thermodynamics. Enzymes are catalysts and only affect the speed of reactions that are thermodynamically favourable. In brief:
1. Reactions only occur which result in a decrease in Gibbs free energy.
We are always comparing two alternative situations. In the case of nucleic acid hybridization, for example,  we may at different stages of transcription have to consider ssDNA v. dsDNA, ssDNA and ssRNA v. RNA-DNA heteroduplex, DNA-DNA homoduplex v. RNA-DNA heteroduplex. The problem with transcription is not why rNTPs bind to DNA, but why different hydrogen-bonded structures, of necessity, occur at different stages in the cycle.
2. Reactions involve an equilibrium between the forward and reverse direction.
Unless a reaction product is removed, there is generally no conceptual difficulty about the reaction also occurring in the reverse direction. The extent to which this happens will depend on the position of the equilibrium. For transcription such reversal is important because stretches of RNA, initially hydrogen-bonded to DNA, need to be released from it, and stretches of DNA have to alternate between being double-stranded and single-stranded.
3. Enzymes speed up reactions (in both forward and reverse direction). They have no effect on whether or not a reaction is thermodynamically favourable.
As @StephenB mentioned, enzymes speed up reactions by affecting the activation energy — generally raising the ground state or lowering the activation energy by facilitating an alternative reaction sequence. In the case of the binding of the an rNTP we know from chemistry that the strength of a hydrogen bond depends on its directionality. Hence many random collisions will be unproductive. Without knowing anything about the real situation, we can speculate that weak bonds to residues on the rNTP binding-site of RNA polymerase may facilitate a reorientation to the optimal position for base pairing.
This material is covered more fully in textbooks of biochemistry, e.g. Berg et al. Ch. 8.
Transcription — The Movie
In a Cell Perspectives article in 2012, Cheung and Cramer described a movie of mRNA transcription by RNA polymerase II and other factors based on published structures of various intermediates. Although this was produced by interpolating between static ‘snapshots’ of structures, it is a comprehensive attempt using three-dimensional structures to address different stages of transcription — melting of the dsDNA, movement relative to the DNA duplex, and dissociation of the transient heteroduplex. This is illustrated in a figure from the paper:

I have  constructed my own composite of screen shots of that section of the movie (from about 3.00 min) that deals with binding of rNTPs. In  contrast to the figure above, it shows only a small section of RNA polymerase in order to focus on the dynamic changes that occur in two sections of this protein on binding the substrate (another feature of many enzymes).

The rNTP-binding step
The depiction of rNTP-binding in the movie is summarized as:

…an NTP substrate first binds to an open active center conformation, adopting a preinsertion state…. The NTP then moves slightly to occupy the insertion site as the trigger loop folds to close the active center…. Closure of the active site around the NTP generates contacts that are required for correct NTP selection and leads to catalytic nucleotide incorporation and RNA extension ….

This is based on the work of Vassylyev et al. who describe the molecular interactions in more detail. I quote an extract from their paper to illustrate that the supposition about interaction of the substrate with residues on the enzyme is borne out, but also that the complexity of the interactions is such that it is not possible to make a simple summary:

In the ttEC/AMPcPP complex, AMPcPP forms a Watson–Crick base pair with the acceptor template sandwiched between the 39 end of the RNA/DNA hybrid on one side and the protein residues from the TH and BH on the other. Met b91238 (TH) and Thr b91088 (BH), which stack directly on the substrate and template bases, respectively, seem essential for the positioning and selection of the substrate (Fig. 2); the corresponding RNAPII residues Leu 1081 and Thr 831 seem to have similar functions in the yeast EC13. In agreement with modelling and biochemical studies1,4,15, Asn b9737 forms hydrogen bonds with both O39 and O29 of the substrate ribose, thereby permitting discrimination against the non-cognate dNTPs lacking either or both of these atoms (Fig. 2b, c).

The interested reader will need to study the paper himself. I restrict myself to reminding him that the structures of enzymes are dynamic because there may be an equilibrium between different possible structures and the position of this equilibrium can be changed by the binding of other molecules to the enzyme. It’s still chemistry — not magic!
Coda — Why no straight answer?
The reader accustomed to having reaction mechanisms of enzymes presented in dogmatic form may wonder why there are so many ifs and buts and molecular dynamics involved in working out how the rNTP gets to the correct conformation to bind to the DNA template. The answer is that although the structure of the binding site (actually there appear to be two alternatives) is known in detail, the successive positions of the rNTP are not, because there is no way of ‘freezing’ it at these different stages. Generally one captures intermediates in a reaction by making derivatives of them that will bind but not react, for example. So it is relatively easy to get structures for the rNTP bound and hydrogen-bonded, but not on its way in. A 2017 paper in the Journal of Biophysics indicates that mathematical methods are still being used as the basis of arguments about the detailed binding mechanism.


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What's the difference between a lymphocyte and a plasma cell?
According to my understanding, lymphocytes is the broad terminology for both T lymphocytes as well as B lymphocytes, while plasma cells refers to mature B cells which produce antibodies. But then why are they mentioned separately, doesn't a plasma cell come under category of lymphocyte?

But then why are they mentioned separately, where are they mentioned separately? If you are referring to a specific text or quote that raises this question, it would be best to include that reference here. right now your question is a bit confusing.

Yes, in Robbin's Basic Pathology, while describing inflammatory process of several diseases, it is mentioned that there is presence of both plasma cells as well as lymphocytes in the affected tissue. So that raises the question, why are plasma cells and lymphocytes mentioned separately? Why not just mention that there was infiltrate of lymphocytes (assuming that plasma cells come under a category of lymphocytes)?


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Why is there low hepcidin levels in hemochromatosis?
If hemochromatosis is iron overload and there is excess iron in the blood, why does the liver reduce hepcidin secretion (which increases the iron uptake) furthering the worsening of hemochromatosis?

From what I remember it all depends on which type of hemochromatosis we are talking about. There are several types depending on the cause and some of those like the hemojuvelin gene mutation-related have low levels of hepcidin as the CAUSE of the hemochromatosis (since like you mentioned, seeing it as a consequence wouldn't make much sense)
The first 4 pages of this paper should clear things up a little bit https://www.aasld.org/sites/default/files/guideline_documents/Hemochromatosis2011.pdf


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use of antibiotics in selection of good plasmids
I have not understood the role of antibiotic medium in filtering the bacteria containing the recombinant plasmids with the ones having normal plasmids. Since all the plasmids of a certain bacterial species have a antibiotic resistance gene regardless if its recombinant or not , shouldnt there be no effect of the antibiotic on the colony?

Please tell us what you have read about this topic with reference to your text or web pages and more detail about what you understand. Also search for other questions on recombinant selection on this list. We expect you to show a little more evidence of having tried to solve the problem yourself.

Short answer: selection protocols are designed to work
When choosing a selectable marker for a plasmid, one chooses a gene that is known to be absent in the host organism of interest. For example, standard lab strains of E. coli are free from extragenomic plasmids and are susceptible to the antibiotic ampicillin. As such, plasmids that confer resistance to ampicillin are commonly used to maintain plasmids in E. coli lab strains.
Other things worth noting:
1. Antibiotic resistance genes are not universal.
That is, a bacterial strain that has a gene imparting resistance to one antibiotic may still be susceptible to many other antibiotics.
2. Not all plasmids carry antibiotic resistance genes.
Many naturally occurring plasmids are selected for in the wild because they carry genes that enable the bacteria to perform new metabolic functions, or impart virulence genes that enable bacteria infect a host organism: (https://en.wikipedia.org/wiki/Plasmid#Properties_and_characteristics).
This is also true of recombinant plasmids. Many commonly used yeast plasmids are selected for by enabling the host strain to produce a necessary nutrient that is absent in the growth medium.


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Chance of cancer as a function of smoking frequency
I was wondering if there is some kind of known relation between the chance of getting cancer and the frequency of smoking cigarettes. A quick Google search did not yield results. Would any of you perchance know of a relation?

There is an approximately linear relationship between the total number of cigarettes a person smokes in their lifetime and the risk of getting lung cancer.
That is, each cigarette someone smokes increases their chance of getting cancer by about the same amount, whether it's their first cigarette or they've been smoking for 40 years.
Pack-years are a way of quantifying someone's total cigarette exposure; it's calculated by the number of packs someone smokes per day times the number of years they've smoked for. So someone who has smoked half a pack per day for 20 years would have a pack-year history of 0.5 * 20 = 10 pack-years.
The following graphs show the linear relationship between the odds of getting lung cancer (relative to non-smokers) versus pack-years smoked.

Source: Lubin and Caporaso (2006), "Cigarette Smoking and Lung Cancer: Modeling Total Exposure and Intensity"


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why finger of hands and feet become wrinkled due to to water?
Mostly due to bathing or washing clothes our finger become wrinkled what was the reason behind it??

There are a few hypothesis around it, but it is known that its associated with the function of distal nerves of the hands and feet. I suggest reading this short case for a glimpse at this - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2464382/
Also another tip I can give is that professional swimming athletes for example, eventually experiment an adaptation process in which this wrinkling reaction diminishes due to being exposed to the same stimuli repeatedly and for long periods of time.

I am not talking about swimming, it it different thing I am simply asked about how to prevent this?

Mmm I thought you wanted to understand the biological  behind it :(

@Anum In your question you do not mention about this. And therefore it will be closed as a duplicate.


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Are the seeds in a single capsicum fruit genetically identical?
Hopefully not a too-basic question for the venue. I'm a chile pepper growing hobbyist and have spent some time searching around and reading up on pepper (angiosperm) reproduction, but I'm not getting a clear picture of the details.
It seems like flowers have multiple ovules and it seems like one pollen-grain landing on the stigma leads to fertilization of a single ovule. And it seems like that process produces a single seed.
But that fertilization also prompts fruit growth and flower death and capsicum fruits have many seeds, never just one (that I've ever seen).
So, does each seed have a potentially different father? Or are the multiple seeds generated through a reproductive/cloning process that I'm not seeing written about? Or something else?

No, the seeds are not genetically identical.  Each seed come from the fertilization of an ovum with a sperm from a separate pollen grain.  Since each pollen grain can come from a different plant, the seeds will generally differ from one another.
Additionally, even ova from a single plant will not usually be genetically identical to one another.  This is because the process that creates the ova (meiosis) shuffles the genes of the parent plant on then places only half into the ovum.  The same kind of shuffling goes on in the creation of pollen grains.
In the chili pepper genus (Capsicum), plants are predominantly self-pollinating. This means the majority of the pollen for the seeds in a fruit will come from the very same plant.  This generally reduces the amount of variation seen in the offspring compared to complete cross-plant pollination. Some cross-pollination can nevertheless occur if there are other varieties in the neighborhood.  The fruit will not show the effects of the new genetic combinations present in its seed, but only a plant grown from the seed will make the differences evident.

Thanks! So, it sounds like if I grew a plant in perfect isolation, removed all but one flower, and removed the anthers from that flower, and then brought in a single grain of pollen, I'd expect to see a fruit develop with a single seed?

No more than one seed since the single grain might not be successful.  (Also, the fruit might not develop due to not enough seeds being present.)


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Identifying a mushroom. (Pyrenees near Gavarnie, France)
Can anyone help me identify this mushroom? (a still frame from video taken in the Pyrenees near Gavarnie in France). Also is it edible or poisonous?

This is almost certainly the parasol mushroom, Macrolepiota procera. The parasol mushroom is edible, but many other often resembling mushrooms are not. Never eat a wild mushroom unless you're an expert or consulted one.
 https://en.m.wikipedia.org/wiki/Macrolepiota_procera

Very helpful. Thank-you very much....and also for the note of caution. :0)

@OrbitRob If you think your question has been answered, please check the checkmark next to the answer.


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Is evolution of gametangia in land plants and charophyceae convergent?
Is the presence of gametangia in both land plants and charophyceae a result of convergent evolution or are they of the same origin (and have been lost in other types of algea)?


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Is dandelion a sporophyte or gametophyte?
My text book claims all land plants undergo alternation of generation. However, I don't see how it could be with dandelion. The flower head gets pollinated and then turn back on itself. After a while it opens back as a seed head ready to blow seed in the wind. What would be the spores then? And the gametophyte organism? All seeds are a result of sperm and ovula so it would mean the dandelion flower is a sporophyte?

See Alternation of generations - Life cycles of different plant groups

Dandelions are sporothytes. In Wikipedia you can read (Alternation of generations):

"In the spermatophytes, the seed plants, the sporophyte is the
  dominant multicellular phase; the gametophytes are strongly reduced in
  size and very different in morphology. The entire gametophyte
  generation, with the sole exception of pollen grains
  (microgametophytes), is contained within the sporophyte. The life
  cycle of a dioecious flowering plant (angiosperm), the willow, has
  been outlined in some detail in an earlier section (A complex life
  cycle). The life cycle of a gymnosperm is similar. However, flowering
  plants have in addition a phenomenon called 'double fertilization'.
  Two sperm nuclei from a pollen grain (the microgametophyte), rather
  than a single sperm, enter the archegonium of the megagametophyte; one
  fuses with the egg nucleus to form the zygote, the other fuses with
  two other nuclei of the gametophyte to form 'endosperm', which
  nourishes the developing embryo. For further information, see Double
  fertilization"

Hi @Olga. Welcome, and thanks for contributing to Bio.SE! Generally, we ask that answers don't simply include large quoted blocks of text, and instead we hope that those that answer expand upon the resources (quotes, pictures, links) that they provide with additional context, backround, etc. Your post will likely garner more positive attention if you expand upon it further. Additionally, if you reference or quote something specifically, please provide a direct link to where the quote arises so interested users may explore the topic further. Thanks!

Hey! Thank you for constructive comments (my English is not very well and that's why I decided to take such a long quote). For the future I will try to try harder :-). Have a nice day..


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research on brain-eating amoeba
Are there any alternative treatments for brain-eating amoeba?
I've spent about 6 hours trying to find information about this and haven't had any success.

Sorry, this is a science list. We don't do "alternative medicine", nor can we recommend research projects to students. This is a site for questions about biological processes.

I'm voting to close this question as off-topic because it is asking for recommendations for research topics, and not about biology.

This is off-topic indeed but to foster interest, intravenous amphotericin B and rifampicin was used with varying success. Miltefosine has shown efficacy. In almost all cases the infections are fatal without intervention or luck, however.

Naegleria fowleri & other protozoa like Acanthamoeba castellani are sometimes referred to as "brain-eating" amoebas. The latter due to the severity of the disease they can cause and the remarkable inefficiency of the treatments administered at the moment of diagnosis. If you wanna know more about this I would suggest reading this paper
https://aac.asm.org/content/aac/59/11/6677.full.pdf
Although if you are a beginner in the field of microbiology you will probably have trouble understanding a paper like that. If this is the case I would suggest reading the introductory chapters of a general medical microbiology book first. The one I started with was Murray's Medical Microbiology from elsevier saunders; I know there is a spanish edition (which is what I read) as well if you happen to prefer that instead of english.


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What kind of fish is on the picture?
I saw these fish in a video at an art exhibition, I'd like to find out what kind they are.

This is an Atlantic wolffish (Anarhichas lupus). It's a very characteristic fish, with the teeth, the long dorsal fin and the small back fin.

https://en.m.wikipedia.org/wiki/Atlantic_wolffish


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How does carbon dioxide diffuse into red blood cells?

Carbon dioxide diffuses out of the tissues and into the blood, where it is dissolved in the plasma. While some of the carbon dioxide remains dissolved in the plasma, most carbon dioxide diffuses into our red blood cells. In the red blood cell, some carbon dioxide binds to hemoglobin, forming what we call carbaminohemoglobin.

Do any other gases also diffuse into the red blood cells. If not, why does only carbon dioxide get into the red blood cells?

The red cell membrane is highly permeable to gases because the molecules of gases are small, uncharged, and soluble in lipids, such as those of a bilayer.The effect of 4,4′-diisothiocyanato-stilbene-2,2′-disulfonate on CO2 permeability of the red blood cell membrane Remember red blood cells are  cells like any other cells only that they have hemoglobin and no nucleus. Because they have an ordinary cell membrane, it follows that the laws of diffusion which apply in gases and other cells will also apply with gases and RBCs. Oxygen is the major gas which gets into RBCs, so is carbon monoxide and others

Hi welcome to Bio.SE, and thanks for contributing an answer! We generally like to see answers contain citations or other indication of sources of support for answers. Links, pictures, etc. also enhance posts. We're trying our hardest to be better than low-quality sites like Yahoo Answers and Quora, so any effort you can make to shift your post from looking like an "unfounded" personal opinion to a well-supported claim would garner you more upvotes and reputation on our site. Please take a moment to use the "edit" button below your post to indicate research effort and some citations. Thanks!!

@Moyo Freeman , can you just explain me the paper  in brief.

@Dhruva, the paper involves inhibiting trans-membrane transport proteins (Band III or capnophorin) in RBCs and then checking if they have an effect on the movement/transport of gases across the membrane.


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Can some colours be processed faster/more accurately than others?
Is the human visual / motor system able to track, and move in response to, objects of certain colours more quickly and reliably than for others?  By more reliably, I mean with greater accuracy in judging position and velocity, and with greater accuracy when moving in response.
Which colours are "most visible" in that sense, as a function of background and illumination?
This interests me specifically in the context of juggling: I like to juggle, and I wonder whether there's a difference in my response time and accuracy with different colours of balls/clubs.  Usually I'm indoors, and ceilings are usually white, sometimes black or brown, with strip lighting.  My only personal observations are rather obvious: dark colours can be hard to see against dark backgrounds, and white can be hard to see against white.

The answer is yes and yes. Firstly, motion cannot be processed at equiluminance. In other words if you have clubs that are equally as bright as their background you will not be able to see them move even though they are clearly visible because of a different color. It's a remarkable effect (demo link below), as you become in effect motion-blind. Obviously you notice after a while that things moved, but you don't see them move smoothly as you are used to. This is similar to what people with akinetopsia experience (had lesions to brain areas involved in motion processing). So have clubs that have clear luminance contrast to the background (very dark, or very bright).
Then there are known difference in processing latencies for different colors. More specifically yellow is processed faster than blue. And black is processed faster than white (if you consider them colors). These effect are massive, a few hundreds msec in some cases which is very long. There is also a known relationship between stimulus intensity (here color contrast) and response time, called Piéron's law. However that effect saturates at fairly low contrast so as long as you can see the clubs clearly it's unlikely there will be a difference in response time for more contrasted colors.
Finally there are discrimination differences for colors. For example yellow and orange are more easily discriminable than blue. But that's only true if you have to perceive a low contrast color difference (a yellow club on a yellow background). Here again as long as you see your clubs very clearly, it's unlikely the specific color of the clubs will make a difference.
So overall I would recommend to use clubs as contrasted as possible to the background (which is common sense). Then prefers darks to lights colors, and prefers yellows to blues. The ideal color is brown, which is in facts a dark yellow.
http://visionlab.harvard.edu/Members/Patrick/Demos/index.html
http://www.michaelbach.de/ot/col-flicker/index.html
Komban, S. J., Alonso, J. M., & Zaidi, Q. (2011). Darks are processed faster than lights. Journal of Neuroscience, 31(23), 8654-8658.
Wool, L. E., Komban, S. J., Kremkow, J., Jansen, M., Li, X., Alonso, J. M., & Zaidi, Q. (2015). Salience of unique hues and implications for color theory. Journal of vision, 15(2), 10-10.
Witzel, C., & Gegenfurtner, K. R. (2013). Categorical sensitivity to color differences. Journal of vision, 13(7), 1-1.

I know I'm not supposed to leave comments like this, but this is a really fascinating answer!  Thank you!  Just to make as if I'm adding some content here: having likely only one set of props at a time, I guess orange seems like a more general-purpose choice than brown, because it won't be too far from optimal whether the ceiling is white, brown or black?  And if one were going all-out for optimality with two sets of props, I suppose dark brown and bright yellow?

...or I suppose for props that are multi-coloured, you could go for bright yellow AND dark brown, all in a single club/ball :-)

You may want to mention that the reason for this is because the dorsal stream (which processes motion) is fully colorblind, and the ventral stream (which can distinguish colors at equiluminance) is incapable of processing motion efficiently. I think this is also why edges become harder to see in the linked video when motion also appears to stop (either that, or it's the fault of the crappy ancient QuickTime codec it uses).


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Why is gel used in electrophoresis?
In analysing amino acids content in a protein through gel electrophoresis, What's the purpose of the gel? Wouldn't putting the amino acid in the gel prohibit the amino acid from dissolving into the buffer solution (which its pH controls the protonation and de-protonation of the amino acid)?

Just to be sure: You ask why the gel matrix is used to analyse proteins?

What research have you done to answer this question yourself? A Google search for gel electrophoresis of amino acids will give ample results. But your question is based on a complete misapprehension about the physical nature of the system. The gel is an inert and insoluble matrix which the buffer and amino acid solution permeates.

In gel electrophoresis, the gel is the mechanism by which macromolecules of different sizes are separated. By loading the gel with amino acids (or proteins or DNA), you start all of the samples equally, and then push them through a gel using a salty buffer solution that is electrified.
The gel has a certain concentration of a polymer (commonly agarose or polyacrylamide) that acts as a mesh that slows your macromolecules down. So, after running a gel for a certain amount of time, molecules of different sizes will have traveled different distances. This can be visualized by different methods (ethidium bromide for DNA and antibodies for proteins, commonly) after further preparation.
So, the amino acids in question should not be dissolved in buffer, as this would result in loss of sample.
Edit:
Regarding the last point: when loading samples on a gel, they must first be dissolved in some loading buffer that will help the sample settle into the well and not diffuse out. I took your mention of "buffer" in the original question to be the running buffer for electrophoresis, which you should not dissolve your sample in. I am also unfamiliar with analyzing amino acids by electrophoresis, and I do not know if there is a specialized loading buffer that kind of analysis would require. A quick look didn't uncover anything, but you might be in a better position to answer the loading buffer issue.

I'll take this point by point: i) thanks for pointing that out, it's been a couple of years since I've had to think about conformational changes during electrophoresis. ii) Antibody staining would indeed require a Western, I should have been more precise there. iii) My last sentence was an attempt to tie the answer back to OP's question, where they were assuming that the amino acids should be dissolved in buffer. I assumed they meant the running buffer for the electrophoresis process, but they could easily be referring to loading buffer, too. I'll edit my answer to reflect this.


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What does the acronym ‘PIN’ stand for referring to PIN proteins in plants?
There are so called PIN proteins, or PIN-formed proteins, in plants. What does this acronym mean?
Wikipedia briefly explains the function of the protein but not the origin of the name.  It's not explained even in the link-linked review paper, if I'm not missing something.

Like many genes and gene products, PIN proteins were named for a mutant phenotype and PIN is not actually an acronym; the source in your link does actually explain this (emphasis mine):

The significance and function of AtPIN1 was discovered through the phenotype generated by the loss-of-function mutation in the gene: mutant plants fail to develop floral organs properly and generate naked, pin-like inflorescences, which gave the name PIN-FORMED (PIN) to the family

Křeček, P., Skůpa, P., Libus, J., Naramoto, S., Tejos, R., Friml, J., & Zažímalová, E. (2009). The PIN-FORMED (PIN) protein family of auxin transporters. Genome biology, 10(12), 249.

Thanks. So it is explained there… (I was lazy to read more than the summary, then I've did just /\<[Pp][a-z]+(\s|-)[Ii][a-z]+(\s|-)[Nn][a-z]+/ regexp search).

It begs the question: why was “PIN” all-caps at all? When something is all-caps, it makes people think it’s an acronym. I’m not a geneticist, or even a biologist, by training. So please enlighten me if there’s some rule in the field that justifies all-caps.

Explaining what actually is a “pin-like inflorescence” would be very helpful.

It is not an acronym; it is an abbreviation of pinnulate (or pinnulated), which means having the pinnulae of a pinnate leaf properly developed.
Gene symbols written in all caps indicate the wild-type condition of the organism: If a gene is referred to as PIN1, it means its product (an auxin transporter) permits normal branching (or at lest does not contribute to malformations); when it is written in lower case, pin1, it indicates the gene has a variant associated with a mutant (non-pinnate) phenotype.
PIN1: nothing is broken
pin1: a single stalk without pinnulae (in the case of Arabidopsis)
If the mutant looks like a pin, it is a co-incidence (probably a mnemonic suggested by a English-speaking teacher). The original meaning derives from pinna, which refers to the normal appearance of leaves and flowers.

Welcome and thanks for your answer. Can you add sources to support your claims and allow folks to background read on your answer?

Hearsay. That's the explanation I heard from folks in my orbit. Here's one example:
https://youtu.be/jFiqj9NKQfc?t=1452
Apparently, while functionally accurate, it is incorrect as a matter of origin. The discovereres of PIN genes named them pin-forming.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC160035/pdf/030677.pdf
They do write gene names in lower case, so that's not where the confusion originated.
There are pictures in the paper illustrating the mutant phenotypes.


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Programming Languages for Bioinformatics
Good day everyone,
I am very much interested in math, biology, and programming; ideally I would like to study bioinformatics and, as such, was wondering what languages are typically used by bioinformaticians? Particularly for fields of bioinformatics relevant to biochemistry, virology, and immunology, what are the most useful programming languages to know, as well as their strengths and limitations? (i.e. in what setting would it be better to program in C++ than Python, is R good to know and if so why, etc.)
Thank you in advance.

I believe many relevant pointers can be found over at https://biology.stackexchange.com/questions/15292/basic-programming-and-bioinformatics. In short: If you're expecting to do data analysis and visualisation, R. Anything else where you work on the biology itself, Python. Everything else is unpredictable; you might end up doing modelling in Mathematica or C++, or developing plugins for FIJI in Java.

Hi welcome to Bio.SE! This question is unfortunately off-topic here, and likely will be closed. However, in addition to the already linked post, a related discussion exists on our Meta site that might also interest you: What program(s) do biologists use for statistics?

The languages currently popular for bioinformatics work are Python, Java, R, Perl, and BASH, though the use of Perl is gradually declining. Note that Python has become the most popular language in a general context, so it's natural that it's the most popular in bioinformatics too. Of course 'most popular' doesn't mean 'best'. Pick a computer language and I'll point you to some publication that uses that language in a bioinformatics context (perhaps excepting COBOL, and RPG).
Some bioinformaticists spend most of their time performing analyses using existing software, perhaps using a scripting language like Python or BASH to 'glue' together existing programs or to control the submission of jobs to a computational cluster. Scripts and packages using the R language are often used in these analysis pipelines to perform sophisticated statistical analysis and visualizations.
Other bioinformaticists are developing new algorthims. In these cases computational speed can be very important, so languages like C, C++, or Java are often used. However, newer languages like Go, Julia, and Rust are also used, according to the taste of the researcher. New machine learning tools are often prototyped using MATLAB.
If your interest is primarily biology (biochemistry, virology, and immunology) then you'll want to focus on learning the biology, and supplement it with Python, BASH, and R. If your interest is primarily in developing new algorithms, then focus on statistics, and computer science. You'll still want to learn Python, BASH, and R, but you'll also want to add something like C++ or Java. The good news is that once you've learned 2 or 3 computer languages, you can pick up additional languages much more easily.

Good resources for getting started: https://www.biostarhandbook.com/ and https://software.broadinstitute.org/gatk/best-practices/ . I very much recommend biostar handbook as they have you work with manageable datasets in a class-like format.


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How does DNA determine all of our hereditary traits?
It's my understanding that DNA codes only for protein synthesis. Does that mean that hereditary traits, like the shape of our nose, are determined only by the proportions in which various proteins are synthesised in various parts of our body ?

DNA does not only code for proteins. Other products (e.g. non-messenger RNAs like microRNAs or ribosomal or transfer RNAs) exist. Also, DNA has further functions aside from protein-coding. Many DNA regions are regulatory, bind transcription factors, affect the topology of chromatin, host modifications, and much more. Lastly, it's important to be aware that hereditary traits can also be non-DNA-based. There is a very active field of research called epigenetics. Worth reading about!

"only for protein synthesis". those are bold words for someone built from proteins ;-)

Sure, but I am wondering what makes my nose stick out one way more than an other, when the instruction manual only indicates the local proportions of various proteins I am made of.

Does that mean that hereditary traits, like the shape of our nose, are determined only by the proportions in which various proteins are synthesised in various parts of our body ?

Yes, more or less!
A trait that is called heritable is a trait which variance in the population is in part at least explained by genetic variance. Most of these heritable traits, however, are also affected by environmental variation (and other sources of variance). For more information, please have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?
So when you say

[..] are determined only by the proportions in which various proteins [..]

The term "only" is a bit misleading. Other sources of variance exist that will affect the variance for this trait. However, it is a pretty good approximation to say that the heritable information is conveyed via the transmission of DNA and the phenotypic expression of this DNA is mediated via proteins.
We refer to the DNA -> RNA -> protein having some phenotypic impact relationship by the term central dogma of molecular biology. You might want to read more about it or maybe have a look at an online course such as this one from Khan academy for example. You will want to know the terms translation and transcription.
Now, in reality DNA can affect an individual's phenotype by means other than proteins (or polypeptides to keep it more general) that are synthesized from it. Indeed, many loci (locus=position on a chromosome) affect the expression of other proteins, others are translated into RNA but not transcribed into proteins (e.g. rRNA, tRNA, RNAi, ...) but yet still have an important action on a cell's physiology.


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Does every protein encoding gene necessarily have a transcription factor?
For instance, transcription factor gene A is responsible for activating gene B that encodes protein 1.
However, it is possible for genes like gene B to encode proteins without having transcription factors to activate them?
(Otherwise said, can protein encoding genes have no transcription factors)?


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How is CO2 and O2 separated in our body during gas exchange?
https://www.msdmanuals.com/home/lung-and-airway-disorders/biology-of-the-lungs-and-airways/exchanging-oxygen-and-carbon-dioxide
The image in the above link shows that CO2 and O2 both pass through the same membrane but still CO2 is exhaled and O2 is taken in the body.
Why doesn't the CO2 mix with O2 and stay in the blood ?
Why is only CO2 passed out through the membrane?

You actually inhale and exhale both CO2 and O2, what changes is the relative amounts of each.
Besides tiny percentages of various gases and non-gas particles, air contains primarily nitrogen (78%) and oxygen (21%). Carbon dioxide makes up roughly 0.04% of the air you inhale.
By the time you exhale, that air now contains about the same amount of nitrogen, but the amount of oxygen has decreased to around 15% and the amount of carbon dixoide has increased by about a hundred times to around 4%.
On the level of individual cells, both gases pass through the membranes in both directions, what matters is how much passes in each direction. As @porkchop explains, that depends on the relative concentrations. When it reaches the lungs, blood has relatively high CO2 and relatively low O2, compared to the outside air that you inhale. As long as the air stays inside, the two will equilibrate. There will be some molecules going each direction - some CO2 molecules will go into the blood, but many more will leave it and go into the air, and some O2 molecules will go into the air, but many more will come from the air into the blood. As a result, the net flow is CO2 going out of the blood, and O2 into the blood. Diagrams usually only illustrate the net flow.

But if the CO2 attains equilibrium shouldn't there be 5 % of CO2 also stay in the blood and shouldn't the concentration increase with time?

5% isn't an appropriate way of describing it because blood isn't a gas, it's a liquid with CO2 solved in it. But yes blood leaving the lungs should have about the same "CO2 content" as exhaled air, and as it runs through the body it accumulates more CO2. There can be conditions under which more CO2 accumulates throughout the body than the blood can get rid of in the lungs (i.e. suffocation), and we also have a programmed responses to that condition (gasping).

But we don't suffocate frequently, right? But still CO2 is accumulating in the blood.

Blood is never completely devoid of CO2, but that doesn't mean the baseline increases over time. How much CO2 is left in the blood when it leaves the lungs depends on the concentration of CO2 in the inhaled air. As long as that's constant, the blood will always end up at the same baseline CO2 content after undergoing gas exchange.

@poin yes. But CO2 in blood is also being converted to carbonic acid and eventually bicarbonate, so the chemistry is a bit more complicated

@Poin Don't forget about the breathing part: blood and lung gas match in the lungs, then you breathe out the lung gas and bring in new gas that matches the outside air, then diffusion happens again until they match and so on. If you stop breathing yes, CO2 continues to accumulate in the blood and lungs and you asphyxiate.

It all comes down to concentration gradients. In deoxygenated blood, which is what enters the lungs, the O2 concentration is relatively low and the CO2 concentration is higher than that of ambient air. On the flip side, the air that we breathe in has a higher concentration of O2 than deoxygenated blood. The alveolar membrane is thin enough that the gases can diffuse across this gradient almost instantly. And just like that, you have oxygenation of blood, and removal of CO2.


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What does this graph explain?

I find this graph incredibly confusing. Is it saying that when there is a decreased affinity (of hemoglobin to oxygen, I think?), the partial pressure of oxygen increases with the same percent saturation of hemoglobin? What does that even mean if that's the case?

is there text around graph? can you add source link

A graph is generally meant to be interpreted as y being a response to a change in x. This graph highlights that as the partial pressure of oxygen $P_{O2}$ increases, so does the percentage of hemoglobin that are saturated in oxygen. The relationship is not linear (unlike you seem to suggest) but is logistic.
The graph also highlights how three different level of affinity would affect the relationship between $P_{O2}$ and the fraction of hemoglobin that is saturated and highlights side consequences of such affinity variation.
Finally, with vertical dotted lines, the graph indicates what the $P_{O2}$ is in the lungs and in the other tissues.

why a decreased affinity is a shift to the right and an increased affinity is a shift to the left?

Consider a single point in the x axis such as $P_{O2} = 40$ for example. If affinity is increased you would expect that the percent saturation of Hb would increase, right? This causes a shift of the left.

That all makes sense, I guess I should've been more specific. The only thing I'm really confused about is why a decreased affinity is a shift to the right and an increased affinity is a shift to the left?

@AliceD X and Y are rarely arbitrary choices. In no way do I mean that correlation implies causation but a person makes a graph as to imply a causality of X on Y. Also, when statistical analysis is involved as in any linear model (incl. GLM, ANOVA, ...) one of the variable is considered as a response to the other variable variation.

@AliceD Of course, thinking everything as causation can be very misleading but this is still what is portrait through graphic representation. Google what goes in x axis what goes in y axis for more info. Note that following your comment, I corrected my first sentence from "always" to "generally", which is much more correct. Thanks!

@PatrickSalas Pease, see edit in my answer

I don't see how a shift to the left shows that the percent saturation of Hb has increased. It is only shifting in the x direction, so it seems like it's saying an increased affinity results in the same saturation for a smaller partial pressure of oxygen. Is that the case?

At $P_{O2} = 40$, the "baseline" affinity curve indicate a Y value of about 75. The increased affinity curve (the left shifted one) indicates a Y value of about 95. So, yes shifting a curve toward the left here lead to matching a greater perceneage of Hb saturated for a given $P_{O2}$ which is what you would expect from a case where affinity is increased. Btw, your issue has nothing to do with biology. It is about basic of mathematics and how to interpret a graph.

This answer is exactly correct. @AliceD correlation does imply causation, but does not prove causation. Here, either of those statements are nonsensical. This isn't a cohort study, it's a fact about physiology. With a healthy Hb molecule, when $P_{O_2}$ goes up, $O_2$ saturation goes up, with exactly this pattern, every single time.

You're right- there is a lot going on in this graph and it is hard to understand it at a glance.
Let's take the lines one at a time. The middle line is the curve that represents the relationship between PO2 dissolved in blood and percent hemoglobin saturation under physiological (essentially, healthy) conditions. We can see that percent Hb saturation is very low when the PO2 is between 0 and 20 mmHg, that Hb saturation sharply increases between approximately 20mmHg and 50mmHg, and that Hb saturation reaches near-maximal levels after the PO2 reaches approximately 50 or 60mmHg. From just looking at the middle line, we can learn that coming out of the lung, Hb will be about 100% saturated, while in tissue, at a much lower PO2, the Hb saturation is still around 75%.
Now, let's look at the dashed line, to the left of the middle line. This line represents the shift in hemoglobin saturation that occurs when PCO2 drops, when pH raises (blood becomes more basic, which could also occur as a result of inappropriately low PCO2), or when temperature decreases. This results in an increased affinity of Hb for O2, so Hb saturation stays much higher at a much lower PO2, when compared to the middle line. Therefore, at a PO2 that is very close to what tissue might see, Hb is still very close to maximally saturated. This becomes a problem for O2 delivery to tissue, since O2 is less likely to leave Hb to oxygenate the surrounding tissue.
Last, let's look at the rightmost line. This line represents the converse of the dashed line- here, PCO2 has increased, pH has decreased (blood is now more acidic), or temperature has increased. This causes a decrease in Hb affinity for O2, meaning that even at a high PO2, Hb will, on average, be carrying less oxygen. So, when blood leaves the lung, Hb might be almost maximally saturated, but by the time PO2 reaches tissue levels, Hb is actually closer to minimal saturation under these conditions. This causes issues with O2 delivery since there is just less O2 to be delivered once the PO2 reaches the level it might be in tissue.
Hope this helps- LMK if more questions.


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about lipid oxidation, does acid fatty transforms in glucose?
Lipid oxidation generates fatty acid and glycerol going into the bloodstream.
Can they be converted into glucose by gluconeogenesis or are they turnd into ketone bodies?

Welcome to SE Biology. Please take the tour and read how to ask questions before posting.  You will see that you are required to demonstrate the attempt you have made to answer the question yourself. This question has been asked and answered before on this list and generally on the internet.

My english is very bad. Can't you give me the article?


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What is the difference between cytokine and chemokine?
I often see these terms being used in inflammation, and I'd like to know, are they synonymous with each other or do they mean different things? Also could someone provide an example of each?


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plant dormancy in different locations
Say plant x has a dormancy period of y in location z, for instance in Sweden. We bring this plant to another location z', say France. Are there any results with respect to if/how the dormancy period would change? (I would assume such observations would be of interest to understand how plants adapt to/can cope with climate change.)

Not really clear what you want.  Do you mean dormancy of seeds, of bulbs &c, of the kinds of perennials that die back to the ground, or trees & shrubs that lose their leaves but keep the aboveground parts?  It's also a quite complex question.  There's more going on than just winter dormancy, e.g. plants of mediterranean-type climates that go dormant in the hot, dry summer.

My question was more in the direction took by the answer of @Jonathan Moore; that is, i was missing the notion of "vernalisation". With this, i found an article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532801/ which answers even more my question.

It might depend on the signal that the seed uses to end dormancy. Some seeds require 'vernalisation', that is a prolonged period of low temperatures, for them to germinate successfully.  If they don't have the cold period, they don't germinate because they 'think' that they haven't had winter yet.
Dormancy can also depend on the conditions that the parent plant lived under, so it is quite possible that if two plants were grown in different environments, their seeds would have differences in dormancy. This study looked at that effect in the 'model plant' Arabidopsis thaliana:
Donohue K., Dorn L., Griffith C., Kim E., Aguilera A., Polisetty C. R., Schmitt J. Environmental and genetic influences on the germination of Arabidopsis thaliana in the field. Evolution. 2005;596(1):740–757.
This paper gives a good review of Seed Dormancy and Germination in Arabidopsis from a few years ago:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243337/#i1543-8120-70-1-1-b60


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What happens in a nerve cell when a thought is generated?
I know basic nerve physiology of impulse conduction and transmission, but I don't know what actually happens in a nerve cell when a thought is generated. When a external stimulus (like tactile stimulation, injury causing tissue damage) leads to stimulation of respective Na+Channels and action potential is generated. But what is the stimulus in the neurons of the Central Nervous System when we think about something? What exactly is the stimulus that cause the neuron to generate action potential and then following it, it is transmitted to different circuits and then we react accordingly?

This is a recurring question that many people are bothered with. I read an interesting answer on Quora. Basically, the author says that there is always on-going activity in the brain. Each thought is triggered by something, let it be conscious or unconscious. The brain is never silent, even in your deepest sleep with only slow-wave synchronized activity, there is still activity. Even when it seems that a certain thought pops up totally randomly, it is still triggered by certain inputs, let they be sensory or internal. Note that action potentials can be triggered either by signals from the outside world (sensory receptor neurons), or by signals from other cells in the brain and body.
Also note that most, if not all neurons show background activity ('neuronal noise'); they never stop firing even without inputs. When one or more of those background potentials impinge on a postsynaptic neuron, that neuron may be activated an fire an action potential. This may also explain some random events in the nervous system.


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Why is inhibition of inhibition (reciprocal inhibition) such a common motif in cell signalling?
In transcriptional regulation, you often find that positive signals proceed by inhibiting or destroying a protein that is in turn inhibiting or destroying the effector protein. This can be seen in the retinoblastoma - E2F signalling pathway, and many others. I was wondering if there was any direct biological utility, and if so what this utility was.

You might be interested in reading Uri Alon's take on network motifs: https://doi.org/10.1038/nrg2102

This reminds me, somehow, of the Dining Philosophers Problem, which is about avoiding deadlock in distributed systems.

This feels like a my philosophical question...
Direct regulation of proteins would have to have biological utility - such a gene has to be driven by positive selection to adapt that ability.  The question is more about learning what might be driving its role.
I would hazard that protein deactivation and degradation would be important to make sure that these inhibitors could be down-regulated fast enough - if they were left to degrade via a general pathway, the specific signal would not be available for too long a time.


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Has any scientist elaborated on the "selfish neuron" hypothesis?
Daniel Dennett references a talk by Sebastian Seung, where the latter speaks about "selfish neurons". I've been trying to learn more about this hypothesis, but cannot seem to find anyone who has elaborated on this line of thinking. Could someone point me to some resources, or this an idea whose time has not yet come?

I would argue that the "selfish neurons" idea is a lot less interesting in terms of biological implications than the similarly-named "selfish gene" hypothesis.
It's basically proposing a bottom-up understanding of neuronal circuits where the developmental design feature is that neurons are individually optimizing their input-output relationships in some way. There isn't really any biological controversy about this suggestion.
Dennett (and probably others) goes a little crazy with it and turns it into a discussion of the agency of individual neurons, etc, but from a biological perspective I would argue that this is a pretty boring type of agency, at least in so far as using this definition pretty much all cells in a biological organism would be argued to have agency, because they are on some level "making decisions," but that's all biology is: organic systems of machines that respond in some way to their environment, and which are subject to selection pressures by which the systems of machines that reproduce best come to predominate.
Where this argument is useful, and Dennett uses this approach as well, is in contrasting biological systems with silicon computers. However, all of today's machine learning algorithms are really based on "selfish" nodes according to Dennett's description.
In summary, the selfish neuron hypothesis is just a philosophical approach to what we already know about biological neurons. It's meant as a way especially for people from a more algorithmic/computational background to think about how biological neural networks differ from algorithms structured from logical first principles. It doesn't make strong hypotheses for biology beyond what is already understood and agreed upon. I think this is probably why you don't see much more study about it.

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


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Are fruiting bodies, basidiocarps, heterokaryotic?
In that, if we have a mycelium with genetically compatible hyphae, will the fruiting body created by this mycelium be heterokaryotic, or will it just contain one dikaryotic organism's genetic material?


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Average width of the male body
I've been looking for the average width (at widest point) of the average American male body but couldn't find it anywhere so far.
When I say "widest point", I mean that if you draw a rectangle (that gives X for width and Y for height) around the whole body, all of it should fit inside the rectangle, whether the shoulders are wider than the hips or vice-versa. I'm looking for the average value of X (arms against body).
If the hips are the widest point inside the rectangle, the width should contain the width of the hands that are against them.

Do you have (or know where I can find) that information?

I am so wondering now whether in the USA the average widest point would be the shoulder or the belly. Did you mean the point for which the average is the widest or the average widest point (consider the the widest point might be should for one person, belly for another and butt for yet another person)?

@Remi.b i meant at widest point

Let me re-ask my question. Do you mean measuring size at shoulder, belly and butt and then each of them and consider the largest number or do you mean taking for each individual the largest of these three values and then average those max values? Note that even once this is clarified, I am not sure anyone will be willing to really look and analyse such data for you.

why exactly are you asking that? What will you do with that information? If you explain a bit about your real problem, maybe we can help with it. Right now it looks like XY problem http://xyproblem.info/ For example, for health studies people use waist circumference. Caskets come in 28 inch wide or 31 inch wide options (quick google)

In addition to the other comments, I don't see any interesting Biology here as defined for this stack.

Widest as seen from the front, or from the side?  And if from the front, do you measure at the shoulders, or include the arms?  And if the arms, how are they held?  (That is, some people with a good deal of chest muscle have their arms out at an angle.)

hi. thanks for clarification. You might get some answers, but i urge you to describe your problem fully, not just request for X.

@maashatheytaz won't this mostly just covary with weight? More overweight people will have on average wider bodies. This seems a curious variable to attempt to measure.

I think it's a perfectly valid question, but highly doubt that anyone has an empirical answer because the information indeed isn't biologically relevant (and hence nobody has it). I could imagine it being interesting for game or furniture design, or architecture. As @aaaaaa said, it does sound like an XY problem and you should probably go back to the X and figure out which Stack Exchange site can provide you with information that might solve your problem.

@NatWH that's why I am asking for an average. They are anatomy statistics made out there, so if we a range, we can extract an average.

@maasha theytaz: I don't think an average is going to be all that useful, because there are distinct body types (mesomorph, ectomorph, &c).  Add on the effect of either obesity or weight training, and it seems like few people would actually be close to the average.


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Does freezer burn affect only the cells on the surface of food?
Suppose i submerge a banana halfway through in a tray with water. Part of the banana is submerged in water, part of it is on the outside. The water and banana in the tray is being put in the freezer and freeze. Since part of the banana is exposed to air freezer burn is going to take place. How deep does it affect the tissue?
Not a homework question.


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How does acetylcholine (aCh) cause erection?
I have read this article on physiology of erection :

Activation of cholinergic receptors on the endothelial cell by acetylcholine or stretching of the endothelial cells as a result of increased blood flow may elicit underlying smooth muscle relaxation through the release of NO.

I know erection is caused by parasympathetic outflow; but how come the cholinergic receptors on the endothelial cells are activated by aCh because there are no parasympathetic neuronal endings on endothelium, as from what I've learned and there could not be aCh freely released in penile arteries because butrylcholinesterase in blood would inactivate the aCh?
I understand that the corpora cavernosa are relaxed to help sinusoids accumulate blood and corpora spongiosum are contracted to prevent venous outflow of the blood to maintain the erection.

ACh is released onto blood vessels and affects receptors on smooth muscle and endothelium. Can you cite your assertion that this doesn't occur?

You may be confused because most peripheral blood vessels do not have direct parasympathetic innervation. The pelvic region is unique here (pelvic blood vessels do have direct parasympathetic innervation)

@DeNovo Maybe not quite unique, but "special" perhaps?

@BryanKrause yes, you're right. Lets go with special.

@DeNovo I've got my answer then.


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Are small peppers inside others twins?
This happens frequently enough that we've probably all seen it at some point - you buy a pepper, and when you cut it open you find another small pepper inside it. There's plenty of pictures out there if you don't know what I mean.
The other pepper obviously didn't grow from a seed; a sprouting seed would generate a plant and not a fruit.
My first guess is that it's a twin. But seeds should be the equivalent of a fertilised animal zygote, so "monzygotic twins" would be split-seeds, not fruit-inside-fruits.
The only reliable-sounding information I was able to find online is this 8 year old blog post: https://www.csmonitor.com/The-Culture/Gardening/diggin-it/2010/0401/Have-you-ever-found-a-pepper-inside-a-pepper which concludes that it's unknown what these mini-peppers are.
Is that still accurate or has anyone figured out what exactly peppers inside peppers are?