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Does low gravity exposure to early stages of human fetus have potential to unloc unused genetic information from earlier stages of evolution?
The title seems quite self explanatory but let me elaborate.
New mutations do take a very long time and many generations to occure in the genetic code. But our genetic code already holds all the information gathered trough evolution process...even information that are older than mammals.
In case of start of pregnency in zero g or gravity of Mars (0,38 g)... there are many replications from the single cell egg to fetus couple month old...
Can gravity in this case has potentional to "open new variant" of genetic information gathered in our cells? Does diferent gravity has impact on metabolic processes on cellual level?

It seems like the question here is, "Does a reduction in gravity affect the way that biological macromolecules interact with one another in cells?" Specifically, does low gravity affect gene expression and metabolism? Is that what you're asking?

Yes. That is exactly it. Sorry if it was was not so clear. So is there any study about impact of different gravity?

I mean I do not expect that anyone know how exectly the gene expression and metabolism changes on cellual level due to long time in low gravity....I just wanted to understand the potencial of possible changes that can occure. What is the scale of potentional changes we might be able to observe during space clolonization.

No
The question itself does not even make sense, we do not hold onto much unused information, there is nothing to unlock. Unused genes mutate and get co opted for other purposes. We have about a hundred new mutation per generation. Much of so called junk DNA is actually just used for other purposes besides coding for proteins.
Will a colony evolve differently sure, any isolated population evolves along its own lines but it will happen at evolutionary speeds.

It has been known for some time that there are physiological changes associated with spaceflight- bone and muscle mass decrease, and the distribution of fluids in the body changes as well, all in response to the decrease in gravity. This is why astronauts ride exercise bikes when they are in space.
Perhaps the most accessible (and trustworthy) resources I have been able to find about the effects of low gravity on the molecular behavior of cells is from the NASA Twins Study, where one twin of an identical twin pair was sent into space for one year, while his brother remained on Earth. Before and after the year in space, the brothers were sampled and tested in all kinds of ways and interesting changes in gene expression and metabolism were found. For example, many genes changed expression levels in the brother who went to space, but they quickly returned to baseline after return to earth. However, a small number of genes remain at changed levels of expression, suggesting that long-term exposure to low gravity does change patterns of gene expression. It is important to note that these changes are not at the genome level; rather, they are attributed to changes in epigenetic regulation of the genome. You can see a summary of these results here.
My knowledge of evolutionary biology is too thin to comment fully on the part of your question that asks about unused genetic information from earlier stages of evolution, but I would expect that if gene expression and cell behavior changes in low gravity, that several generations of humans living entirely in zero or reduced gravity would be trending toward genetic difference from Earth-bound humans. You wouldn't necessarily see changes in an individual, but over time they could accumulate and cause different regions of the genome to be expressed in ways that humans on Earth do not experience.


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Shape of the first leaves of a plant
I am quite unfamiliar with everything that is in the slightest related to biology,
so I am very sorry if this question does not meet your standards and is too basic.
Lately I am quite enjoying growing some plants from seed and watching them grow.
Doing this I noticed that, at least for apples and tomatoes, the first 'pair of leaves' looks quite like different from the leaves following. Especially for the apple,
the first two leaves look like from a completely different plant.
So just out of curiosity, is this a general phenomenon and how can it be explained, i.e.
why do these plants do it?
Thank you in advance for any reference/ hint/ answer!

They are referred to as cotyledons (seed-leaves).
Apples as specified in the question are dicotyledons, they have two seed-leaves. Some other plants are monocotyledonous, i.e. just have a single seed leaf, thus:

User: Pengo, via Wikipedia CC BY-SA 3.0 2022.
The cotyledons are a part of the embryonic plant and whilst inside the seed capsule store energy in the form of starch (e.g. in oats and barley) and or fats/oils (e.g. in nuts). They are a distinct form from the mature leaves which grow as the plant matures.
They are also present in the seed prior to fertilisation, as distinct from true leaves which develop later after germination.

source: Stack Exchange

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

sort: votes


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Seeds of fruits
Some fruits  ( like watermelon , pomegranate,  etc ) have their seeds spread out throughout their bulk . Also , there are fruits which have seeds at their centre of symmetry ( like apples ) .
Is there any theory or mechanism which explains that why and which type of fruits possesses the type of arrangements of seeds inside their bulk ?

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

In addition, biology is rarely (at least at this stage of knowledge) a matter of distilling rules — to make this an answerable question (for this site) I think you should focus on a single type of fruit and start by figuring out the botanical name for that type (e.g. pome). You can then use search terms like "development fruit pome" to learn more and then ask a clear, focused question based on what you've learned if and when you get stuck.

I looked up and worked on it by asking to my teachers . They told that this may be due to weather , climate and geographical factors.

Sorry I missed your reply — your teachers's answers don't really seem at all helpful to me. Please note that asking good questions is a skill that one needs to work at. If you lack the time for or interest in improving this question (see previous comments for details), please delete it. This will prevent you from losing reputation (and can lead to loss of the privilege of asking questions) due to downvotes and closure.

@tyersome Hello , what I want was an answer not reputation. However , don't close it please.

Ultimately the decision of whether to close is up to the community. If you improve the question then it will be left open and is more likely to receive an answer ...

@tyersome Then please suggest me that how can I improve . What shall I omit and add to my question to improve it?

I already did that in my first two comments ...

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


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Could water soluble dyes be directly absorbed by a plant's / tree's xylem?
Amateur woodworker / hobbyist here, I enjoy using colorful or exotic wood species, the issue is that many of these species are rare, expensive, endangered, hard to grow, or otherwise difficult to obtain.
What I'm wondering is... is it possible to directly introduce dyes or color to a young tree slowly over time, either through directly exposing the internal rings to some kind of dyed water while its growing, or by somehow getting around the root's natural filters? (People have tried to grow plants in just dyed water, but the roots are able to filter most of it out)
It would be interesting to have a plank dyed with a more saturated color than is naturally possible, without treating it and introducing dyes after the wood has been felled.
Often times treating wood can damage specific properties of it, some dyes and treatments can make the planks virtually useless for sanding or staining, and reintroducing water or other fluids can cause warping and other damage to the wood.
If a natural, water soluble dye existed within the wood from the start, it might be possible to get around some or all of those issues.
I'm just wondering if this is even possible, and if so, how it could be done without killing a tree..
This is more of an idea then an experiment, but it would be interesting to try.

You could try using a small weed or hydrophilic species like willow and hydroponics. For bigger trees it would be possible using some obscure metholodology and highly cumbersome.

I don't believe it's possible; the roots have selective permeability. Try this: add food dye to water (darker is better), use it to water a cut stem and a rooted plant. The cut stem will take it up. The rooted plant will not.


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Can crossing over between X and Y chromosome of sex chromosomes take place?
Can it? If no, what would happen if it did?

What effort have you put in yourself to try to answer this question? Failure to show your own effort will result in your post being voted down and closed. Please update!

Yes, it can, but it is rare, and typically only in the pseudoautosomal region, meaning those sections on the X and Y chromosome that have homologous genes.
The reason it's rare and more difficult is that the DNA does not match as well, so the chromosomes have trouble interacting along the length of the chromosome.  Furthermore, there are less recombinant zones available.

Sources:

Kauppi, Liisa, Marco Barchi, Frédéric Baudat, Peter J. Romanienko, Scott Keeney, and Maria Jasin. 2011. Distinct properties of the XY pseudoautosomal region crucial for male meiosis. Science 331 (6019): 916-20.
Hinch, AG, N. Altemose, N. Noor, P. Donnelly, and SR Myers. 2014. Recombination in the human pseudoautosomal region PAR1. Plos Genetics 10 (7): e1004503.

So even if it does, there won't be any effect? The offspring will be as normal as any other child?

Typically, yes.

Yes, I believe it can, however, crossing over between non-autosomal chromosomes can occur. I think it depends upon what regions came to cross over, in terms of how it would affect an individual, as the y-chromosomes surpisingly has few sex related genes, and individuals only use one (X), male or female, I do not think that it would produce a really mutated individual.


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Which statements are true regarding an energy pyramid?
The number of producers is greater than the number of primary consumers.
The amount of energy at the primary consumer level is greater than the amount of energy at the secondary consumer level.
The number of primary consumers is less than the number of secondary consumers.
The amount of energy at the producer level is less than the amount of energy at the primary consumer level.

Sorry, we're not here to do your homework for you.


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If an ethnic group holds nearly 100% of a particular haplogroup, does it means that people who have this haplogroup are their descendants?
Let me give you a hypothetical example. If the Egyptians were 100% E3b1, and the Levantines 50%, and the Anatolians 25%. Does this indicate that the Levantines and Anatolians are descended from Egyptians?
But what if instead of Egyptians, it was a distant people like Vietnamites who were 100% E3b1?

Short answer:
No.
If populations A and B share a haplogroup it does not imply that population A is B's ancestor, or population B is A's ancestor. No present-day population is the descendant of any present-day population, though both populations may share common ancestors. The common haplogroup is probably inherited from common ancestors.
Long answer:
No.
When you say "Egyptians" or "Vietnamese", in genomic studies you generally mean present-day people. People living in present-day Egypt or Vietnam may be related to each other, but they cannot as groups be each others' descendants. It is more likely that there is some ancestral population that is the common ancestor of both groups that carried the genetic variant. The only exception I can imagine is a VERY recent colonization (assuming there were no indigenous people in the colonized country, which is effectively never the case).
To take this specific example, it would be most likely that at some point in ancient human history the expanding human population (from e.g. out of Africa) had people carrying a haplogroup that settled Egypt, Anatolia, and Vietnam in independent events.
Therefore none of those groups would be descended from one another. Each population was founded by the people who stayed in that region, not the related people who left and colonized other regions.
Sampling of ancient DNA makes the question more interesting, if you for example found 20,000 year old bones sharing the haplogroup. Maybe that is a descendant of one or both populations. But again the relationship of that ancient individual to present-day geopolitical borders would still be fairly meaningless without a lot of supporting data.
It is additionally possible that the haplogroup arose independently in two different populations. This is sometimes called parallel evolution or convergent evolution. In this case there is actually no relationship at all between the populations. While this is much less likely than common descent, it is nonetheless a hypothesis that you need to reject before you claim that one group are the descendants of another group.
I hope that this helps!


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Is brewer's yeast a good source of protein for humans?
I read that brewer's yeast protein is not a "real protein" and is not usable by non-ruminants. Is that true?
If yes, how can I know what kind of protein is good for humans (especially athletes)

brewers yeast is generally used as a  niacin (vitamin B3) supplement not protein. it prevents pellagra.

Please state the source. What is a “real protein”? Why would ruminants be any different from other animals? And this site is the wrong place for dietary advice.

Thank you for taking the [tour], but please also go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular it would be helpful if you were to include where you read about this and what you have done to check whether that information was true. Also note that almost all foods contain protein, but it isn't accurate to say that any of them are protein. Thanks!


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Can fructose take multiple forms ? Which of these structures of fructose is correct?
When I look up the structure of fructose I get various different structures
Which of them is correct ?
Are these all just isomers of fructose ?

The two structures on the left are correct; the one on the upper left is the alpha-D-fructofuranose form, while the one on the lower left is the beta-D-fructofuranose form.
Fructose is a ketohexose (a six-carbon sugar with its carbonyl group present as a ketone group in the molecule's open-chain form); the carbonyl carbon (the 2-carbon, to be precise) is optically inactive in open-chain fructose, as the oxygen and two carbons bonded to it adopt a flat trigonal planar geometry, but, when the carbonyl group is attacked by the 5-carbon's hydroxyl group to form the cyclic fructofuranose (fructose in a five-membered ring) configuration, the 2-carbon changes from being part of a (trigonal planar) carbonyl to being part of a (tetrahedral) hemiketal, introducing an additional stereogenic center that wasn't present in the linear form.  The arrangement of the substituents around this new stereogenic center is essentially a random crapshoot, with half of the new fructofuranoses having the hydroxyl pointing in direction 1 and the hydroxymethyl pointing in direction 2 (the alpha form), and the other half having the hydroxymethyl pointing in direction 1 and the hydroxyl pointing in direction 2 (the beta form).
There are, by the way, eight other configurations that fructose can take; three of them (plus the two you've already drawn) are for D-fructose (the naturally-occurring-in-the-vast-majority-of-naturally-occurring-fructoses form), while the remaining five are for L-fructose (which occurs only very rarely in nature and is essentially useless for most living organisms), which has the hydroxyls on the 3-, 4-, and 5-carbons pointing in the opposite direction.1

The alpha-D-fructopyranose and beta-D-fructopyranose forms have a six-membered pyranose ring, rather than the five-membered furanose ring; these are formed when the hydroxyl group attacking the carbonyl is that attached to the 6-carbon, rather than the 5-carbon, and are actually energetically much more favourable than the fructofuranose forms, making up essentially 100% of crystalline fructose and 70% of fructose in aqueous solution.
The open-chain D-fructose form is acyclic, with the 2-carbon actually being part of a carbonyl group rather than a hemiketal.  It is present in only minuscule concentrations in aqueous solution, but serves as the intermediate between all of the various cyclic forms of D-fructose.
L-fructose can adopt the alpha-L-fructofuranose, beta-L-fructofuranose, alpha-L-fructopyranose, beta-L-fructopyranose, or open-chain L-fructose forms, which are essentially equivalent to their D-fructose equivalents apart from their opposite chirality.

1: In the L-fructofuranose configurations, this takes the form of the hydroxymethyl group hanging off the 5-carbon pointing down rather than up.


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When is voltage generated across a membrane?
I'm very confused so bear with me please.
Electrogenic pumps are carrier proteins that generate voltage through the movement of ions, right ?
When is a voltage generated ? When there's a net movement of ions ?
Doesn't that mean that when any ion passes through a channel protein, voltage is generated ? And energy is released ? Doesn't that make them electrogenic too ?
We need energy to move ions against their concentration gradient but if energy is released when ions move then why do we need energy ?
Is it that a voltage is generated when an ion moves towards the env with the same charge ? So when the movement enhances the overall seperation of charge , a voltage is generated ? And energy is released ?
In other words, the movement of Na+ through the Na+ channel protein down a concentration gradient doesn't release energy because the Na+ is moving towards the -ve environment but it being pumped outside does ? See that doesn't make sense either, because we need energy to pump and ion.
I'm very very confused

The main thing the sodium/potassium pump does is to move sodium and potassium ions, Na+ and K+. It technically generates a bit of charge separation in doing this, but you can ignore it for now.
What is important is that because of the operation of this pump, you now have two sides of membrane with different ion concentrations. One side is high in sodium ions (outside the cell), the other side is high in potassium ions (inside the cell).
So far, that doesn't really do anything electrical, but it does take a lot of energy to get this arrangement: the whole time, the pump is moving sodium ions to where sodium ions are high, and moving potassium ions to where potassium ions are high. Moving things against their concentration gradient costs energy. The sodium/potassium pump gets this energy from ATP.
Now, imagine you open some pores in the membrane (we call them leak channels), that are a particular size that only lets potassium ions through. The sodium ions can't move, but the potassium ions can. A few potassium ions move over to the high sodium side, down the concentration gradient for potassium. This doesn't take any energy, it just happens passively. It also doesn't involve very many ions, just a few, so the concentrations don't change much.
However, potassium ions have charge! These are positive charges, flowing out of the cell: that makes the inside more negative.
Also, because they are positively charged, potassium ions would tend to move towards more negatively charged spaces. So, as the inside of the cell gets more negative, potassium won't leave as quickly. There is an equilibrium, where the forces pulling potassium ions out to where potassium concentration is low equals the forces pulling potassium ions in to where the voltage is negative.
The voltage where this equilibrium occurs is called the resting membrane potential, and for many cells is somewhere between -100 and -40 millivolts: that's the voltage generated across the membrane, indirectly, by the sodium/potassium pump.
Purves' Neuroscience is a good general reference textbook for this sort of thing. The Goldman equation is a mathematical way to figure out what the voltage will be if you know the concentrations and permeability.

I think I understand but 1 more thing, my book says "A solute that exists in different concentrations across a membrane can do work as it moves across that membrane by diffusion down its concentration gradient". Doesn't that mean that whenever passive diffusion occurs, energy is released ?

@Jaca Creating a concentration gradient costs energy. Much of that energy is converted into potential energy, similar to how carrying water up a hill. When water flows down the hill or ions flow down their concentration gradient, that potential energy can be used to do other things.

So, your answer ,in short, is yes ? I get the water example, but I have a question, is this potential energy ( the result of movement against concentration gradients ) electrical when the movement of ions is also down their electrical gradient ?

@Jaca They both apply. In the example I described from potassium above, the potassium ions aren't really available to do any work. They have both a concentration gradient and an electrical gradient, and at equilibrium (for the single ion case) these are equal and in opposite directions. If you want to stretch the water example a bit, you could imagine the electrical gradient as a constant vacuum keeping the water at the top of the hill. The vacuum pulls water up, gravity is pulling down, but when they are in equilibrium the water doesn't go anywhere and can't do work.

@Jaca Also, if you follow the steps in my answer, you could interpret the movement of potassium down its concentration gradient as converting the potential energy of the concentration gradient into electrical potential energy. In biology, either or both can be used to do subsequent work. Sodium would be high outside the cell and also the inside of the cell is negative, so there are both electrical and concentration gradients by which sodium can do work.

So you're saying that when Na+ moves from outside to the inside it is releasing both, potential energy due to conc gradient and electrical potential energy due to electrical gradient ? Then why did you say that the K+ ions weren't available to do work if they're moving down their electrical gradient ? Isn't that supposed to release electrical potential energy ? Sorry for constantly asking but I'm trying to understand

@Jaca High potassium inside the cell, negative voltage inside the cell. Potassium is a positively charged ion. When a potassium ion leaves, it is going down its concentration gradient but against its electrical gradient. Therefore there is no energy left to do work: the concentration energy and the electrical energy sum to zero. Sodium is also a positively charged ion, but it is high outside the cell. For a sodium ion moving into the cell, it is moving down both its concentration gradient and it's electrical gradient, so the potential energy sums to a larger value and can do work.

Oh my god I think I get it, so, to sum up, generally, when an ion moves down both its concentration gradient and its electrical gradient it is available to do work but when it moves down one of these gradients it is most likely not available to do work ?

@Jaca "when an ion moves down both its concentration gradient and its electrical gradient it is available to do work" - Yes, always. "when it moves down one of these gradients it is most likely not available to do work" - Only if it is in equilibrium with the other gradient. You could easily have a concentration gradient that does work without any electrical gradient at all, for example. Really what you should consider is the net electrical+concentration gradient.

Voltage is not generated through the charge movement as such, it the magnetic field that is generated directly through movement of charges, although such movement contributes to voltage generation.
Voltage by definition is a potential to do work (to move charges), it always involves 2 points the difference in electric potential between which is voltage. If you want to measure voltage in a selected area, you always measure it relative to another reference area (like, there always is a "reference electrode"), because you measure the difference in electric potential between these 2 areas.
So, voltage is generated through separation of opposite charges. Like, a negative -80-60 mV resting potential inside a cell is maintained relative to an area of positive charges outside.
"The Na+/K+-ATPase enzyme is active (i.e. it uses energy from ATP). For every ATP molecule that the pump uses, three sodium ions are exported and two potassium ions are imported; there is hence a net export of a single positive charge per pump cycle." (wiki) Thus it can be supposed that energy is consumed by Na+/K+ ion propagation, though the definition of "energy" varies by context, voltage means potential energy.

My book says " A transport protein that generates voltage across a membrane is called an electrogenic pump. The sodium-potassium pump appears to be the major
electrogenic pump of animal cells. ." If that's the case then Na K pumps generate a voltage aka release energy then why do they need energy  ? Also, do Na + protein channels generate a voltage ? Or is that because the motion is from a +ve environment to a -ve environment no seperation of charge is enhanced and no voltage is produced ? Sorry if it's a dumb q I'm only 17 and taking this for the 1st time

"Generate a voltage" is not equal "release energy". If you take a smartphone battery out and measure voltage, it will display a manufacturer's preset voltage, so the voltage would already be generated. But there will not be any "release of energy" unless the battery is (generally) plugged into a conductive circuit, where the potential energy provided by voltage will be transformed into any type of energy used by circuit elements - kinetic, light, mechanical, etc.


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

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


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Why are additional classification levels necessary?
When I was in school I learned that all organisms can be classified using the seven levels kingdom, phylum, class, order, family, genus, species.  In the course of teaching my own children now, and in looking up information about animals with them, I find that there are additional levels like superorder and infraorder.
Is there a scientific reason why these levels were added?  Are the seven levels i learned insufficient?
I learned then with a lovely mnemonic, would be a shame to have to dispense with King Phillip and what he allegedly came over for...

What if you want to describe a group of organisms in between some of these arbitrary levels?

Relevant question on the usefulness of these designations: https://biology.stackexchange.com/a/55667/27148

It’s been my experience that these additional levels pop up when the more typical rankings are huge. For example, the family Asteraceae has so many genera that to even begin to work on the phylogeny of such genera without repeatedly listing dozens of names requires prior subgrouping of the family into subfamilies and tribes.


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How quickly could mice evolve to avoid mousetraps through artificial selection?
So, we have a mouse problem in our attic.  I set traps routinely to keep the population down.  We have taken pains to exclude them by sealing cracks and holes, etc., but they still manage to find their way in somehow.  Alas.
In any case, I find myself wondering this.  More and more frequently, I find the traps disturbed, the bait taken, evidence of mouse activity, but no dead mice.  Clearly some mice are able to take the food without getting snapped, or they have learned how to set off the traps and then take the food.  It seems to be happening more and more, which makes it seem like they are getting smarter.
I'm curious about this.  Could I make the case that the mice who successfully steal sunflower seeds and peanut butter from me are more likely to successfully mate, and this forms a process of artificial selection?  There are quite a few uncontrolled variables, of course.  Here are just 3:

Surviving in the woods all summer long until fall, when they come indoors is probably a greater effect.
There are other houses around, all bordering the same large woodland area, and so plenty of other and different opportunities to get food.
I am probably not setting the traps exactly the same way each time, nor are all the traps equally sensitive.

BUT if there were to be a controlled experiment with a specific population of mice, calibrated traps, etc., how many generations would it take for "mousetrap-aware" mice to evolve?
NB - I am not suggesting that anyone undertake this study, as I'm sure it would violate many ethical boundaries!
-

I think evolutionary pressure in urban environments is a truly fascinating area of research. Nonetheless I am afraid the current question is open for discussion and won't fit in too well on this site I reckon. Adding your own research efforts so far can help focus the question and shape it into a more answerable format.

I have not attempted any research on this, lacking both the scientific background and the ability to control the experiment

You need to distinguish between evolving and learning. The traits to evade traps would not be lost if there was a single generation of rats not exposed to traps, but any learning would be lost (unless mice did something like explicitly pass on knowledge like humans do). In the same way human did not evolve from being able to ride horses to being able to drive cars.

Have you considered the possibility that something else is removing the food? In addition to rodent pests, leaving food out in the open could be attracting insect pests, like ants. I've personally witnessed ants clean the peanut butter off mousetraps, and it doesn't take long once they've discovered it.


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What are the differences and relationships between online plant taxonomy databases (POWO, WFO, WCSP, WCVP), and is one considered the most reliable?
Each of these databases has their own summary of their aims and process - but they rarely seem to mention each other in comparison. It's hard to figure out what differences or relationships exist between them. It seems like some of them use data from others, but not exclusively.
Should one of these be considered the primary or central source for botanical taxonomy? Are each of these databases reinventing the wheel independently, or are they just presenting the same data with different interfaces? Is any of them considered the most reliable or complete?

World Checklist for Selected Plant Families (WCSP)
World Checklist for Vascular Plants (WCVP)
Plants of the World Online (POWO)
World Flora Online (WFO)

Please check this open access article : https://nph.onlinelibrary.wiley.com/doi/full/10.1111/nph.18961# It proposes a comparison of WFO, WCSP, LCVP and WorldPlants and explain why and how they differ. WCVP, POWO and WCSP are the same basically.


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Hardy Weinberg Clarification
So I am taking an introductory Biology Course and I was recently introduced to the idea of Hardy Weinberg Equilibrium. I wanted to find out why exactly we calculate the frequencies of alleles in the next population using the law of multiplication.
For example,
In a hypothetical population of let's say 300 civets, 20% of the gene pool codes for blue eye color and the remaining 80% codes for black eye color. It is given that blue eye color is recessive.
300 civets = 600 alleles total
80% code for black eye color = 480 alleles
 20% code for blue eye color = 120 alleles
When we calculate the frequencies of the next population we basically say what is the probability a given offspring will this pair of alleles. Following the example above, I would argue that the probability an offspring has two blue eye color alleles is (120/600) * (119/600). However, my textbook says that it is (120/600) * (120/600) = 0.04 but doesn't that assume replacement of alleles! My only rationale is that as the population tends towards infinity the difference becomes negligible.
Am I right?

What do you mean by "replacement of alleles"? I posted an answer guessing what you meant. If I misunderstood could you elaborate on what you mean by it and why you think it is not possible?

the population tends towards infinity

Well yes, Hardy–Weinberg principle is based on several assumptions one of them being "population size is very(infinitely) large". Another being "Mating is random".
However, even if the population is small your version of calculation does not make much sense biologically.
If we talk about civets (gonochorists) the probability an offspring has two blue eye color alleles is
(probability mother gives him blue eye allele copy)*(probability father gives him blue eye allele copy).
The two probabilities are not connected. What allele individual gets from mother has no influence over which allele they get from father. This is assured by "Mating is random" assumption.
To calculate the probability we should calculate:
(allele proportion in all possible mothers)*(allele proportion in all possible fathers)
In your example there is no information about sex of individuals, so the best approximation we have for allele proportion in females/males is the overall allele proportion in the whole population (20%) therefore the best calculation is 20%*20% = 0.04

but doesn't that assume replacement of alleles!

It seems you think that there is some rule that each parent allele copy is used only once in next generation. This is not true. Under random mating some parents can produce many children and some have none. Some allele copies get replicated several times some don't get replicated at all. In large populations the resulting random changes to allele frequency even out. In small populations allele frequency drifts.


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Why are tardigrades so rare?
If tardigrades are so resilient and nearly immortal, why are they so rare when looking at samples of a pond or lake, where tardigrades should thrive?
I've met people who've been studying protozoa and metazoa in nature all their life and have only seen tardigrades once or twice!

They're not, they're ubiquitous.

From wikipedia > tardigrade

[Tardigrades are] considered cosmopolitan and can be located in regions all over the world.
Tardigrades are often found on lichens and mosses. Other environments are dunes, beaches, soil, and marine or freshwater sediments, where they may occur quite frequently (up to 25,000 animals per litre). Tardigrades, in the case of Echiniscoides wyethi,[20] may be found on barnacles.[21] Tardigrades can be often found by soaking a piece of moss in water.

Tardigrades are, in fact, very common. See the simple video how to observe tardigrades. If the people you've met have rarely seen tardigrades, it is probably because they are not looking for them.

"If the people you've met have rarely seen tardigrades, it is probably because they are not looking for them" [+]


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Which aspects of evolutionary biology are most relevant to medical practice?
I'm not pretty much sure if this question suites this forum. But I think its important.
In what aspects evolutionary biology can be seen to be very helpful in medical curricula?
Clearly infection and drug resistance seems to be relevant, also pointed are Cancer evolution.
Are there some interesting output on Neurology in particular?

wikipedia > Evolutionary medicine

ah thanks, I never heard of this term in all of my medical life. I see that there is a whole discipline addressing this question, that is actually never even been mentioned in medical schools unfortunately.

I see that there is evolutionary neuroscience as well. Good!

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


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Are there known chains of beneficial mutations?
Are there known examples of chains of beneficial mutations?
What I mean by that is a mutation that leads to a series of mutations occurring after each other over a relatively short period of time and all of those being beneficial for the organism. And I mean also that there is some etiological impact of the prior mutations on the subsequent ones, that is any mutation in the chain will increase significantly the likelihood of occurrence of the next mutation in the chain. And if there are such chains then would those be considered as a mechanism for speeding up evolution?

The answer will strongly depend on how you define "relatively short" (minutes? months? millennia? generations? and if so how many?) — please clarify this in your question. ——— Note that in general this will be very difficult to know since you would need genomic sequences from many generations of organisms and I would guess from many individuals in each generation to have any hope of seeing this happening. The best candidate I know of for finding such evidence is an ongoing long-term evolution experiment in E. coli.

Adaptive radiation

In evolutionary biology, adaptive radiation is a process in which organisms diversify rapidly from an ancestral species into a multitude of new forms, particularly when a change in the environment makes new resources available, creates new challenges, or opens new environmental niches.

The key-innovation that can lead a species to go through rapid adaptive evolution might well be an initial beneficial mutation. You might want to rad about these key-innovations at Salzburger et al. (2005).
As an example, much of the diversification in ciclid fishes is thought to be driven by jaw morphology driven by a few key genes (a ligand; bmp4, a receptor; bmpr1b and an antagonist; nog2; Brawand et al., 2014). While I don't know the literature well on the topic, it sounds plausible to me that a key mutation may have allowed for the diversity of jaw morphology to diversify (which lead lineages to diversify).
Note, I am aware, I focused my answer on diversification and not on single lineage adaptation per se but I do not know better examples (or a better concept) of a single mutation that could lead to a "chain of beneficial mutations".


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What's the plant name? It is climber or creeper plant..like money plant...help me finding its name...it has seven to five lobes

It is climber or creeper plant..like money plant...help me finding its name.

Please add the location where you found it (country, state or city), and something on the habitat (forest, garden, wasteland in a city etc.). Only a leave is a bit difficult... Might be Bryonia

To add to @RHA's comment, when you add to the question, do it with an [edit] rather than in the comments. It may be useful to review the tag information at [tag:species-identification].


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Have there been new discoveries concerning the perception of taste for the last 10 years?
What are the last discoveries concerning the perception of taste for the last 10 years?
We discovered the 5th flavour: umami.
Also the 6th and 7th: oleogustus and starchy.
Anything else?
Maybe in genetics, as we all have genetic predisposition?
Or concerning the creation of the systems in charge of the perception of taste during the embryo-genesis?

We welcome new users to SE Biology, but ask that they bear in mind that this is "a question and answer site", not a discussion site. "Focus on questions about an actual problem you have faced. Include details about what you have tried and exactly what you are trying to do." This question does not fall into that category, but is a broad question about a field, inviting subjective answers. Furthermore, you provide no evidence of having searched the literature for reviews on this topic. Sorry, but I have voted to close.

The field of chemosensation is an active field of research. The answer to all your questions is yes. So, so much has been discovered in the last decade, both regarding detection by sensory neurons, genetics, behavior, the (embryological) development of these systems, and the coding of tastes and odors in the brain. What's more, there are many model organisms used to study this (insects [flies, moths, locusts, mosquitoes, etc.], worms, mice, zebrafish as well as in vitro methods (e.g. electrophysiology) currently in use.  Sadly you'll have to narrow down your questions to get concrete answers.

I'm not quite clear on exactly what you're interested in, but the short answer is yes, there have been discoveries related to the perception within the last 10 years.
The example that comes to mind is the role of the cannabinoid 1 receptor in the sense of taste of lipids.  The full text of a good article is available online here.

Source:
Brissard L et al. 2018. Orosensory Detection of Dietary Fatty Acids Is Altered in CB1R−/− Mice. Nutrients 10(10): 1347.


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How do astronauts eat in space?
If there is no gravity in space how does the food enter the stomach?
My guess is that it is due to the movement of the esophagus.Am I correct?

swallowing does not require gravity. you can test it by yourself if you stand on your head and eat something

Have you ever eaten lying down? What did you notice (or not notice?) This is very easily answered with a simple google search. They even have videos of astronauts eating in space.

swallowing of food or water from mouth to stomach is done with the help of peristalsis action of esophagus
Then rhythmic, unidirectional waves of contractions will work to rapidly force the food into the stomach. This process works in one direction only and its sole purpose is to move food from the mouth into the stomach.
In earth it also happens but it is assisted with gravity but in space Peristalsis action is the only process by which food or water is taken to stomach .

Welcome. In this community we require answers to be accompanied by suitable sources, preferably journal papers.


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Can muscles work as brakes?
When I walk downhill I lose potential energy.  If I descend 100m in, say, 10 minutes I lose potential energy at a rate of about 114J/s (114W).  Where does the energy go?  Not into kinetic energy provided I don't run or fall, not into heat, for there is little friction to create such heat.  My leg muscles appear to be acting as very efficient brakes, absorbing the potential energy but turning it into what? Chemical energy?

Yes, muscles do work as brakes; it's a process called eccentric contraction.
The energy balance of an eccentric contraction is a pretty difficult question. Some fairly recent research (Linari et al., 2003) found that a low velocities more energy is consumed (i.e. released as heat) even during eccentric contraction, while at high velocities, the muscle does store some energy from the eccentric motion. In frog muscles, at least.

So muscles do work a regenerative brake... in some conditions.
It's an active research topic where exactly this (non-heat) energy gets stored. Current models (in the previously cited paper) cannot account for all of what's measured experimentally; only 34% of it could be explained.


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In my DNA sequence for one sampling site there're W's; Y's; R's and K's?
I also just experienced the same thing with my DNA sequences, there are w's, Y', R', s' and k'. This is the very first time I've seen this. I am used to N but not these ones. Please kindly assist with knowing what might have caused these. Thanks in advance.

These are the so called "DNA ambiguity codes", when the sequencing result allows to bases at the position but it cannot be decided which. This can happen for example when you sequence genomic DNA and you have two different alleles present.
The code is the following (taken from this website):

Thank you so much. I was really confused and now you've given me some light. Thanks a million!

@AudreyVanya You're welcome. What is easy for one person, is not necessarily for the next. That's why we have this community.


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Origin of different brainwaves
I'm creating a project in which I can measure brainwaves (more or less like EEG). Since I'm not a medical student im having a problem finding the origin or most prominent regions for measurements of alpha and beta waves. I have researched on the internet but can't find a definite solution. So can  someone please tell me the exact origin or the most prominent region (active region) of our brain where  the alpha and beta waves can be measured reliably??( Like ocipital region or frontal temporal etc)

This is probably not off-topic here but I personally think this is an excellent question for the psychology & neuroscience SE. Also, the first search engine link I stumble on states that alpha waves mainly "originate from the occipital lobe during wakeful relaxation with closed eyes" and beta waves are "general over the whole cortex and occur during normal wakefulness". I think this checks out but I'm not entirely confident this answer is as satisfactory as one you could get from a cognitive neuroscientist.

If I ask the question now on nueroscience then it will be marked as  duplicate right??

It wouldn't. It's a completely separate stack exchange. Please try to search whether an answer already exists there. Also, put in a little effort using a search engine, I'm sure this information may exist already on online educational pages. If you are still lost, feel free to ask there!

@infottie Does this answer your question? https://psychology.stackexchange.com/questions/20075/why-do-brains-oscillate-within-specific-frequency-ranges/20086

No it doesn't..it doesn't say which wave is most prominent in which part of the Brain..

Alpha and beta brainwaves are just two of several arbitrary, named frequency ranges for a brain-wide phenomenon. See Types of Brain waves. These so-called brainwaves are big electrical events that sweep across the entire brain.
My recommendation for electrode placement is based on my engineering experience. Pick any location on the scalp. You could start with the temples. Take your measurements. Then move the electrodes to a different location and repeat the measurement. Continue this experimentation until you discover by observation which location yields the best results. When you have finished with the experiment, you can post your experimental results on SE Biology and answer your own question.
I suspect that electrode type and method of contact (dry versus conductive gel) will be more significant than actual placement on the head.


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How many palindromic sequences in human genome?
I'm writing an article on palindromes (the words) and I wanted to mention the existence of palindromic gene sequences. Roughly how many palindromes exist in the human genome? I understand the number will vary from person to person. All I want to know is the order of magnitude. Is it 10^2, 10^3, 10^6?

Note that a DNA palindromic sequence does not really match the usual meaning of palindrome. .For instance, GAATTC is a palindromic sequence, but does not match its reverse, CTTAAG.  Instead it matches the reverse of its complement, which is a useful biological property. ('C' is the complement of 'G', 'T' of 'A', etc.)

@mgkrebbs. Thanks for the detail. I understand it is not exactly the same, but the principle is analogous, which is fine for my purpose.

The human genome contains approximately 1.25*10^7 palindromes longer than 6 bp (that is 8 bp or longer). Some interesting facts are also known about their distribution.

We found that 24 palindrome-abundant intervals are mostly located on G-bands, which condense early, replicate late, and are relatively A+T rich. In general, palindromes are overrepresented in introns but underrepresented in exons. Upstream region has enriched palindrome distribution, where palindromes can serve as transcription factor binding sites. We created a Human DNA Palindrome Database (HPALDB) which is accessible at http://vhp.ntu.edu.sg/hpaldb . It contains 12,556,994 entries covering all palindromes in the human genome longer than 6 bp.

And no, the number of shorter ones (shorter than 8 bp) isn't mentioned in the paper because they are considered unimportant, biologically.


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Where to search for which sequence of SNPs belong to specific Alleles
I'm trying to find more information about a specific Allele, namely the "A1 allele of the DRD2 gene". How can I find more information about this allele, and which SNPs are part of this Allele?

I doubt this is enough information. Most SNPs have systematic identifiers starting with rs. This should be available via the 23andme interface, either as raw data download or browser (I don't have it these days so I can't check web, but it's definitely in the raw data). Once you have that number it should be extremely easy to find studies for which that variant is relevant, along with any phenotypic associations of the variant.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

The systematic ID of this allele is rs1800497.
You can use this information to learn a lot about it. Here is one such resource, here is NCBI on it, there is a lot more via google.
Those links should have everything you ever wanted to know about this variant.


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Is there are theoretical limit to the number of proteins possible and their respective structure?
I saw an article saying that DeepMinds AI has catatogued every protein known to science. I guess "known to science" and what is the theoretical limit is not exactly the same thing but the only way one can claim "known to science" at least as I can figure out is to have some idea what the highest value can be in the first place.
On the other hand it may be all the proteins known from every living object on the planet but I don't see how anyone could claim that when most species on the planet are not even know.
So that is why I ask is there is some theoretical limit.
As for example there is a theoretical limit for the highest possible element past the transuranics based on nuclear chemistry. I believe at some point the number of protons would not be able to stay bound long enough to get past the electrostatic repulsion. I think the number is 200 something. But that is an example and not my question. In this question I am interested in knowing how a computer algorithm could predict all protein structures if there was not a theoretical limit imposed in the first place.
I have never posted here before so if the question is inappropriate for this stackexchange my apologies

They just mean known proteins, the simplest interpretation of the statement.

yes amazing still but that would solve my problem. You are probably right on. Thank you

Not even all known proteins! There are many proteins that exist in multiple isoforms, and they used only one isoform per protein coding gene. For a reddit q/a on this, see here.

All depends what you mean by protein - basically take a single amino acid and add another .... on to very high number. Largest known is titin I think, at about 35,000 residues, but no reason that there couldn't be 35,001 or 70,000 or 100,000 etc.

You can certainly estimate a theoretical limit, given some assumptions.
Let's say you do not care about any post-transcriptional modifications, you are interested only in the primary sequence. There are (more or less) 20 proteinogenic amino acids, so there are $20^N$ possible proteins (amino acid sequences) with length $N$.
An "average" protein has about 400 amino acids. Therefore, there are theoretically $20^{400} \approx 2.6\times 10^{520}$ possible proteins with 400 amino acids.
But proteins can also be larger. Let's enumerate all possible protein sequences up to length 1000:
$$ \sum_{N=1}^{1000} 20^N \approx 10^{1301}. $$
All of this is only a lower limit. We did not take into account any non-standard amino acids, none of the post-transcriptional modifications, or the ability of proteins to have multiple different stable conformations.

Note that there are only about $10^{82}$ atoms in the visible universe.


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What is a crypt in a histopathological image?
I am doing a science fair project on using histopathological images for cancer diagnosis, and I came across something that says a characteristic is exemplified by superficial serrated architecture and elongated crypts, I was wondering what that meant.

What tissue? Could you give more information on the sample, "cancer" is incredibly broad.

You should give more details and information to this question as we don't know what tissue/cancer you're referring to.
If I'm just taking a guess I'd say you might mean intestinal glands which form tube-like glands called crypts found in the lining of the gastrointestinal system (i.e., digestive tract). Cancerous tissue including the crypts can be colorectal carcinoma for example. Superficial serrated architecture most likely refers to sessile serrated polyps or colorectal serrated lesions.

Colorectal carcinoma: Pathologic aspects
Superficially serrated adenoma: a proposal for a novel subtype of colorectal serrated lesion
Sessile Serrated Polyps: Detection, Eradication, and Prevention of the Evil Twin


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Growing peaches from (supermarket) bought seeds
As a hobby I like to grow stuff from the seeds of fruits (or bascially everything) that I buy in grocery stores.
I have heared often that if the trees will eventually grow own fruits, they will not taste well, or maybe they do not even grow fruits.
What is the reason for this?
I know that normally the trees are 'grafted', but I do not see the reason why this causes bad taste by seed grown trees.
Can you explain?

Not sure about peaches but in apples the part you eat is made from the genes of the only the mother plant, but apples breed easier with very different strains of apples, and breeding is required to make fruit , so the fruit body  may be say honeycrisp but the seeds will be a hybrid of honeycrips and crab apple.

Having done this for peaches, the fruit was not as large it still good. This is usual.

@John Thank you for this comment. I didnt know this. Very interesting.

@PolypipeWrangler Thank you!

I'll admit I'm not super familiar with peaches specifically, but many agricultural strains are carefully selected hybrids of true-breeding plants.
That means that you take two breeding stocks that are crossed with themselves extensively to the point that we can consider them homozygous at all alleles, and then you breed two of those plants together. The resulting F1 generation is your primary agricultural production strain.
You can get more seeds by continuing to successively inbreed and cross-breed the parental strains, or by making grafts (clones) of the hybrid strain. Importantly, the F1 generation of two inbred strains will be genetically consistent.
Not every F1 generation is going to be the perfect plant, but if you carefully test and try out different parent strains, you can find combinations that give you a great offspring.
If you breed the F1 generation, you don't get a constant offspring but rather a whole mix of possible phenotypes. Some might be great, some not, but they're going to be much more unreliable.
See also https://en.wikipedia.org/wiki/Seedless_fruit

Very insightful. Thank you.


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Simultaneous activation of myosin kinase (MLCK) and myosin phosphatase (MLCP)
Reading about smooth muscle cells, I stumbled upon this sentence in Guyton & Hall, Textbook of Medical Physiology (14th ed):

When the myosin kinase and myosin phosphatase enzymes are both strongly activated, the cycling frequency of the myosin heads and the velocity of contraction are great. Then, as activation of the enzymes decreases, the cycling frequency decreases but, at the same time, the deactivation of these enzymes allows the myosin heads to remain attached to the actin filament for a longer and longer proportion of the cycling period.

I'm having trouble reconciling this with myosin phosphatase's role. Elsewhere in the book it is stated that myosin phosphatase plays a role in smooth muscle contraction cessation, and that phosphorylated myosin (i.e. the product of myosin kinase) can, by itself, repeatedly attach to and detach from the thin filament and perform the cross-bridge cycles. As in, detachment of the myosin head from the actin filament does NOT require its dephosphorylation (via myosin phosphatase); and rather, the dephosphorylation only occurs when the cycling should stop altogether so that muscle relaxation occurs.
If this is true, then why would myosin phosphatase need to be 'strongly activated' (as per the quote above) so that the cycling frequency and velocity of contraction increases? Would that not actually reduce the cycling frequency? It seems to me that myosin kinase should be strongly activated and myosin phosphatase be strongly inhibited if the cycling frequency is to increase, but I'm probably misunderstanding something.
How does myosin phosphatase activation (or as the quoted part says, strong activation of both myosin kinase and myosin phosphatase) actually increase the cycling frequency?

Simply cutting the calcium level will not revert the mechanism in case of Vascular Smooth Muscles. Due to absence of Troponin in their sarcomere.
For the reaction to go forward as well as backward we are dependent on MLCK and MLCP both respectively and to shorten the time period(increase frequency) we need to raise the concentration of both.
Citation & Explanation
Unlike skeletal muscle, smooth muscle is phosphorylated during its activation, which creates a potential difficulty in that simply reducing calcium levels will not produce muscle relaxation.(Section:Mechanism Paragraph 3rd).
Citation: https://www.ncbi.nlm.nih.gov/books/NBK526125/
This is due to absence of troponin which is present in Cardiac Smooth Muscles and Skeletal Muscles but not in vascular smooth muscles.
Citation:https://pubmed.ncbi.nlm.nih.gov/12665242/
Citation:https://cvphysiology.com/Blood%20Pressure/BP026 (check paragraph 1 and the Image shown on the page)
Thank You

For the reaction to go forward as well as backward we are dependent on MLCK and MLCP both What is this 'reaction' that needs to go backwards? I don't understand what muscle relaxation has to do with the cycling frequency. Doesn't relaxation (via MLCP) happen AFTER the cycling is done? I'm asking about how increased MLCP activity is needed for the contraction itself (i.e. the cross-bridge power-stroke cycles that occur during the contraction), not why MLCP is required for contraction (and the entire cycling mechanism) to stop.

https://pubmed.ncbi.nlm.nih.gov/9887960/ this is the paper which you'll probably find the answer, i will post my updated answer after reading it.


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Sensory-motor pathway from visceral organs
Does anyone know is which nerves carries the transmission of sensory-motor impulses from the visceral organs? Is it splanchnic nerves?
There is conflicting evidence in the literature. On the one hand, many sources told that splanchnic nerves belong to the sympathetic nervous system. On the other hand, there is information that sensory-motor impulses from the visceral organs travel along the splanchnic nerves. And there is a slight contradiction, because sensory-motor impulses usually go not in to to the sympathetic trunk, but to the dorsal ganglia. But the splanchic nerves connect just with the sympathetic trunk, and not with the dorsal ganglia.
For example, in this study:
https://www.ncbi.nlm.nih.gov/pubmed/22209656
sensory transmission pathways have been found to go to the spinal cord through the dorsal ganglia, which, to my knowledge, are not associated with splanchic nerves.


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Could something akin to Cyanobacteria evolve on earth today or are all available niches taken for different kind of life to come to be?
The most basic form of my question would have to be: could new life form from molecules as happened with the first life on earth, here on earth? If not why not?

Are you asking about abiogenesis? There are many similar questions here, check the 'related' list or the tag [tag:abiogenesis]

It seems that this Question answers my question.


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Photosynthesis: Can light directly excite the reaction center instead of going through the antenna complex?
The reaction centers that I am interested in are P680(photosystem II) and P700 (photosystem I)
Here is what I think:
If pigments such as chlorophyll a and b capture light in the antenna complex, and
if the reaction center contains chlorophyll a,
then the reaction center should be able to directly capture photons and transfer their electron to an electron acceptor.
Or do reaction centers use energy from both the sun and antenna complex?
Also, a side question, I thought chlorophyll a were also efficient at absorbing light in the 400nm to 400nm range, but then why are reaction centers called based on their absorption of 680nm and 700nm light?
Thanks!


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Placebo Effect Reactions
Why do some people actually experience measureable effects when given a placebo(fake drugs) versus the actual drug?  Is is the power of suggestion, belief, or something else?

Few examples in which placebo looks effective even if it isn't (Wikipedia):

The condition, for example, common cold heals on its own in participants who received a real drug and in those who receieved a placebo.
In psychological and other conditions in which the participants are asked only how they feel after the treatment, some of them may just think that they feel better.
Sometimes neither the real drug nor the placebo work, but the condition has a naturally fluctuating course, so it looks that they both work.


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Evolution versus Creationism
If nature, or any aspects of it, are intelligently designed, how could we tell? How would we be able to test that hypothesis?

Consider this: if a potter makes a pot, does it make sense to search the pot for direct evidence of his/her existence, or would doing so only possibly imply that someone made it? Does lack of finding the potter in this instance mean (s)he doesn't exist? In the same vein, if the Christian God created all the universe and reality that we know, would lack of finding direct evidence for such a God inside that universe mean that God does not exist?? (by the way, we have a lot more universe to explore anyway).

The scientific process could provide evidence supporting the potter's existence, but one could never prove the existence of the potter unless one expanded his/her viewpoint beyond the pot. Similarly, the scientific process could potentially provide evidence supporting God's existence or his resulting created design, but it can never prove that a god does not exist because of the endless possibility for searching. In other words, "science" cannot prove existence (or lack thereof) of a God.

To answer your question: verly likely not. The world and universe is an amazingly complex and beautiful existence, but we have no objective way of demonstrating definitively where it all came from. In science, hypotheses have to be testable and falsifiable, but in your case, we do not know what intelligent design should look like, so we have no truly objective test to perform...

By the way, I think your post will be closed as being primarily opinion based (i.e., potential answers will likely only be based on opinion). You could try to rewrite to avoid having your post closed. Unfortunately, no matter how much you edit, this community typically reacts quite negatively toward religious-slanted posts, so get ready for copious downvoting

lots of natural things are intelligently designed, they are called artifacts or tools and they tend to stick out. If you mean nature a s a whole that's not biology that would be physics.

While we can't disprove design, we can certainly test the hypothesis of INTELLIGENT design, by finding any number of things - the human lower back comes immediately to mind - that no intelligent designer would have designed that way.

Visit Physics.SE. During the 1st 10$^{-43}$ seconds everything was smaller than anything thereafter. All of the universe was compressed smaller than a molecule of DNA. For a considerable period of time after that there were not atoms (from which we are made). It took billions of years for chance to happen, and the earliest form of self-replicating chemicals (RNA) came into existence. Modern science does not praise the ingeniousness of the design, but notes it's flaws; those early chemicals we came from were not life, that came ltr.

I am voting to close because the question ask for testable hypothesis for a fundamentally non-scientific concept.

You would work through the millions of examples of evolution processes and proofs, DNA, morphology, geographical, etc, which show that volcanoes, meteorites, weather, and evolution are all equally based on chaos... are the pebbles rolling around on a beach intelligently arranged individually for a plan or chaos, you decide.

Only someone who believes in intelligent design can answer that question for you and that answer will most likely be unscientific (therefore not fit for this site). The reason is because intelligent design is a claim that is not based on observable reality rather divine revelation so it is impossible test any hypothesis regarding it.
Evolution on the other hand is based on two observable, testable facts: (1) all living things on Earth inherit their traits from their parents and (2) those traits are not always copied and passed on with perfect fidelity. With these two facts we can theorize on what other observable facts lead to the variation in life that we see today i.e. evolution by natural selection.

I have never read any testable hypothesis from the Intelligent Design (ID) community. As such ID is not wrong or right, it is just not testable.
To be fair, ID contains a lot of logical fallacies. Not only does it not offer any testable hypotheses but it often just does not make much sense anyway!

Your whale hypothesis is non-sense too. 1) Whales are big but they aren't that numerous. If you combine all krills together you'd get a mas much higher than all whales together. The same would be true for termites, ants, humans and many other things. 2) Also, the mass of whales is so, soooo negligible compared to the quantity of carbon in the world. 3) The hypothesis is not testable as it would it so full of much stronger confounding variables (evolution and demographic changes of other life forms)

As you said, showing a correlation or another would not in anyway prove any intention anyway. If whales were to stuck a lot of carbon, nothing would suggest that someone "created" whales for that purpose.

Yep. Going up to suggest that bananas easiness to eat are evidence of god forgetting what wild bananas looked like before being selected by us (here).

Saying that almost all animals have eyes could imply there is a common cause. But creationists affirm, I think, humans are the last step, there will be nothing after (implying we will destroy everything ?) ? Or is it humanism ?


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Base pair and amino acid weights?
How does a base pair weigh approx. 650 Da (which is two paired nucleotides) but an amino acid (3 nucleotides) weighs only approx. 110 Da ?

There seems to be a  misconception: amino acids do not consist of nucleotides, but are coded by them. Please look up the structures of amino acids and nucleotides and read about the process of biological translation. If the question remains, please edit your post  and add your prior research on that topic.

Welcome to SE Biology. Please take the time to take the Tour and consult the Help on asking questions. You will see that you are expected to do some research before posting. Try looking up amino acid on Wikipedia etc. You will discover what an amino acid is. It is not a trinucleotide.

In short: base pairs are not composed of amino acids but nucleotides. Base pairs are parts of the DNA, while chains of amino acids forms proteins.
Certain parts of the DNA (called genes) are transcribed to messenger RNAs (mRNA) which are sequentially translated to amino acids and the chains become proteins. 3 bases (called a codon) code for 1 amino acid.
Please look up the Central dogma, DNA, mRNA, protein and translation for further information


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What is the ball of jelly on the left eye of this mantis?

This mantis was seen in the wild in north Israel.
It would be great if the Mantis species can be identified too.


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What is this mushroom in Illinois?
I live in the Northwest suburbs of Illinois and we moved into this house last year. I noticed these mushrooms popping up in one corner of my yard and I’ve never seen this type before. They don’t seem to grow a typical stalk and cap shape and stay rather low to the ground. I’ve had to dig down under them a decent amount to get them out of the ground. We’re approaching Fall now so colder nights and hot humid days.

oh cool I also had one on my toe last week.

I might have figured it out. It looks to be a ganoderma sessile type fungi which is often associated with declining trees. It just so happens that this area of my yard is right next to a tree that isn’t doing too well from poor drainage. There were times where if I dug deep enough I’d end up hitting a tree root, so that tracks well.

It's possible to click "Accept" on your own answer (if you're not bothered about waiting for other responses), so that the question appears as "answered" in the list.


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Is it possible to change the DNA of all the cells of an adult human
The process of making and transferring changes is pretty straightforward relatively speaking in an embroyo. You change the DNA of one cell and all the cells now inherit this change.
But let's say that after x amount of years from now on we are capable of creating perfect changes to the DNA of a person.
What could the process of transferring this change be for an adult human being? Given that there are about approx. One trillion cells in our body, is it even possible to change it?
I think that using a designed virus could be one way, T4 bacteriophages do a pretty good job of taking over the nuclear material of the bacteria. But I don't think it can be too effective given that most of the viral activity is restricted to the blood. Also I don't think the blood brain barrier let's the viruses across.
Highly speculative topic but I would appreciate any insights on this.

What has your research told you?

@BryanKrause He's given a decent rundown of his research.  I think it's reasonable that he's posing the question to the community now.  It's a speculative topic (as he said) but I think interesting to some people here.

I agree with @sterid. That being said, I would consider the question "Is it possible to change the DNA of all the cells of an adult human" to be on-topic but the question "Assuming it will be possible to change the DNA of all the cells of an adult human in the future, what are the possible ways for this to happen" to be border line off-topic and should maybe rather be asked on worldbuilding.SE. I am not sure which question the OP is asking.

I apologize for the confusion. The latter isn't my question, it's an assumption necessary to make to pave way for the question that whether or not is it possible to implement the change made in the DNA of one cell to be implemented in now a trillion cells. By "what are the possible ways for this to happen?" I am not referring to the ways of changing the DNA but to implement the change presumably made.

@sterid OP is speculating that maybe a virus could be used, and the question doesn't mention anything to suggest they have considered existing approaches to use viruses to change adult human DNA.

Is it possible to change the DNA of all the cells of an adult human?

In development? Yes.
Changes in the DNA prior to S-phase in the zygote will result in all the cells inheriting the changed DNA. Before or during the 1-cell stage in embryology, any changes will be ubiquitous in the developing adult and all their cells.
In the adult? No.
No technologies for this exist. None are on the horizon either, to my knowledge. The closest concepts are in targeted gene therapy. There are plenty of workable ideas, but they are all restricted to specific targets.
In the future? Most probably not.
In all cells, in all tissues, in a controlled manner? I very much doubt it, it's an extremely complex undertaking, and (all) the laws of statistics and chemistry are against you. We can speculate all we want but all in all, it's smarter to make the changes in specified locations (see answer two), or at the right time (see answer one).

As an addendum: think of it this way... You can achieve interior design in many ways. You can move your couch around to achieve an aesthetic, or you can draw a plan before you furnish a room to save the trouble of experimenting. Similarly, here too we can speculate about whether it's possible to detonate dynamite in your living room as a way to rearrange your furniture in a pleasing manner. It's probably not going to be a method of approach in the future, simply because the alternatives are a hell of a lot easier, and likelier to bring more tangible results.

But the question wasn't "is it possible now?" but "could we in the future". And your answer is the subjective "probably not". The question is off-topic and best ignored until there are enough votes for close. You certainly haven't answered it.

@David I don't think anyone can actually answer this question cause apparently we just don't know enough about epigenetics and gene expression yet.

@SPr I don't agree with this not being a preferred method of approach in the future. Let's say a human is born on earth but it turns out that he will have to spend a significant portion of his life in space for whatever reasons. He probably won't want to be stuck with a body that isn't adapted to space. The window of changing the DNA before birth is very small and it does not contain the consent of the actual person. So given that everyone wants their DNA changed when they are adults, won't the next question be that how to sync the DNA of all the cells with this newer version.

@Arkilo Do you think research in the future will aim to change DNA in every single cell in the adult body? I will pay you the compliment of assuming you understand how stupefyingly unlikely that is to work. Restricting to small areas or subtypes of cells (e.g. progenitors) is already in development though. I'm also sure we can agree it's easier to make a spaceship hospitable and build spacesuits to protect from radiation, rather than mutating DNA comprehensively, precisely and confidently enough to make us radiation or lack-of-oxygen tolerant. Even our pedant David would probably agree!


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Formula for Oxygen Consumption for Atlantic Salmon (Mathematical) - insecurities regarding variable

The oxygen is calculated in mg per kg per something, so what does $h^{-1}$ stand for? hours maybe?

The formula given below is an estimation of oxygen consumption for Atlantic salmon

\begin{equation}
        V_{O_{2}} (mg \cdot kg^{-1} \cdot h^{-1}) = 61.6(\pm6.6) BW^{-0.33(\pm0.11)} \cdot 1.03(\pm0.10)^{T} \cdot 1.79(\pm(0.10))^{U}
    \label{eq:salmonoxygenconsumption}
\end{equation}

Here is a link containing the scientific article describing the formula - ScienceDirect

Yeah, it's hours.
Further down in the paper, you can read,

The mass exponent was estimated to be −0.33 (b in Eq. (4)) for the specific metabolic rate \begin{equation} V_{O_{2}} (mg\space {O_{2}} \cdot kg^{-1} \cdot h^{-1}) \end{equation}

Rate by very definition implies an extent of time; since mg refers to oxygen and kg refers to water, the only variable left is h, which evidently refers to hours. Hours also jives well with the experimental design.

Source:

Grøttum JA, Sigholt T. 1998. A model for oxygen consumption of atlantic salmon (salmo salar) based on measurements of individual fish in a tunnel respirometer. Aquacultural Engineering 17(4): 241-251.

Thank you very much for your answer @rotaredom, very helpful!


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In touchdown PCR, should the extension temperature match the annealing temperature in phase 1?
For TD PCR, it's recommended that the annealing temperature (T_a) be 10°C higher than the normal cycling T_a for the first 10 cycles or so, dropping 0.5 to 1.0°C/cycle. Should the extension temperature (T_ext) match this pattern to prevent miss-annealing? It seems that if the initial T_a was 75°C, then T_ext was set to 72°C (or whatever is optimal for the polymerase), the purpose of the high T_a would be lost.
Instead, should T_ext match T_a with an increased extension time until the optimal T_ext is reached?

Your initial annealing temperature 75°C would mean nomal cycling annealing temperature 65°C. That is really high. Is there a reason why you did not design your primers with Tm ~60°C (normal annealing ~55°C)?

I do not if I understand correct the question. But I write you an example. For example for the amplification of the gene nirS, I used a touchdown PCR. The Tm of the primer is 60°C. I created a touchdown from 65°C and each cycle decrease of one degree (total cycle of the touchdown is 5). The thermoprofile is the following:
94°C for 3 min; 5 cycles of 94°C for 15 sec, 65°C (touchdown -1°C) for 30 sec, 72°C for 30 sec; 34 cycles of 94°C for 15 sec, 60°C for 30 sec, 72°C for 30 sec; followed for 72°C for 10 min.
Is better that in total your PCR do not make more than 40 cycles.
I hope that this help you
Jo


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PCR in different cell line
I developed a PCR cycle to amplify a 5.5 kb genomic DNA region in HEK cell line. When I tried to use the same protocol in A375 cell line I had no results but only smear. Can you help me?
Thanks in advance

Are you running a housekeeping gene? how does that look like?

No, it's an intron of a gene upregulated in this cell line

And in this intron there is an enhancer region

Do you have a positive control run with your sample?

I use HEK gDNA as positive control

@Annalaura Your positive control should be some region that would be amplified in both samples. A test of whether the gDNA prep is good.

@WYSIWYG Yes, i have amplified 2 smaller amplicon using this gDna sample


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How do enhancers induce transcription?
DNA response elements are DNA sequences that are could be found upstream, downstream of genes that regulate gene expression at the transcriptional level.
One type -Enhancers- bind specific transcription factors called activators, this binding leads to the bending of DNA, bringing the otherwise distal enhancer near the promoter region of the gene, leading to induced transcription.

My question is:

How and by what mechanism do enhancers induce and increase transcription rates? i.e how does the interaction between the activators and the transcription complex, increase transcription rates?

The activators are proteins that bind to specific DNA sequences in the enhancer region. These activators also bind to the RNA polymerase and other associated members of the transcription complex, which makes it more likely for an RNA polymerase to hang around the promoter sequence of the region it enhances.
This in turn increases the chance of the gene being transcribed.
It's basically a little magnet that sucks in the RNA polymerase and then nudges it towards the promoter.

If the RNA polymerase is already near the promoter, why would it need an activator to bind to it?

This way if the RNA polymerase is near the promoter it binds to it, but if it's near the enhancer and the activators it also binds to the promoter. It extends the reach of the promoter, like how a magnet can help you grab things from further away, even though you can still grab them by yourself if they're within arm's reach.

Thanks, can you please provide refrences that propose this mechanism.

There's a pretty good review here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6795546/?report=classic

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Does children have a gender?
I heard that a male is a human which produces smaller gametes and a female produces bigger gametes (Hanna Kokko and Katja Bargum: Kutistuva turska ja muita evoluution ihmeitä, a Finnish nonfiction book). But if a child does not produce any gametes, does children have gender at all?

Gender? I think you may be confusing biological sex and gender.

Children do not produce gametes, not does a postmenopausal female. Of course they still have a gender.

A grand majority of all mammals have 2 sexes (with notable but rare exceptions with very particular considerations): male and female. Humans are mammals and the same applies to humans. Sex is determined pretty much in the zygote, immediately following fertilization and gamete fusion, and rarely escapes 'fixation' beyond this point.
Gender refers to the range of characteristics pertaining to someone's idiosyncratic (personal) ideas of femininity and masculinity. You may be aware that these terms are politicized.
Since you ask a biological question, we ought to limit ourselves to the term sex and acknowledge that sex(ual dimorphism) is a broad concept, genetically, developmentally, behaviorally, morphologically, etc. We can talk about sex-linked genes, which we associate with X and Y chromosomes, and not genital morphology or even gamete size. We can talk about gametes (sperm and eggs) without speaking about menstruation. We can talk about maternal inheritance of mitochondrial DNA without considering one's endocrinology. We can talk about motherliness or breastfeeding without considering X-inactivation.
You can also imagine real world scenarios that complicate our simple 2-category grouping, at some scale of consideration. For example:

Sex hormone insensitivity (just as diabetics can be insulin-insensitive, one can suffer testosterone or any other hormone insensitivity).
Chromosomal disorders such as trisomies (e.g. Klinefelter syndrome, characterized by an additional X chromosome, producing a karyotype of XXY for the sex chromosomes).
A lack of traits commonly associated with feminine or masculine groupings (e.g. secondary characteristics such as hair growth, genitals, behaviors such as courting and mate choice, etc.).

The list goes on. Sex is a broad concept, and the adjectives we have for it are simplified categorizations; nuances are crucial or insignificant depending on context. Sexual dimorphism exists on a spectrum and determinedly male organisms can be female-like and vice versa.
From a biological point of view, it's practical to use this simplification, especially because many animal lineages continue and tend to depend entirely on the fact that two disparate gametes undergo fusion. Not because the gametes are sized just so, or because  of genes that exist only on one sex chromosome, or another.
We can overthink a strict definition of what constitutes sex, but I think the crucial point - directly addressing your question - is that infertility of any kind does not re-classify one's sex, generally speaking. It may remove you from the sexual pool from an evolutionary point of view. But that's too unreasonably specific. If all the nucleated cells in your body lack a Y chromosome, and you are of genotype XX, you are sexually female by most accounts and considerations, and pragmatically one would refer to you as female, just like a nurse can "diagnose" one's sex at birth by glancing at the genitals. Karyotyping, or a nurse's glance, are not meaningless efforts to make distinctions. If you were to suddenly stop producing gametes, stop ovulating, or make a decision to never have children in your life, that would not automatically strip you of a sex designation. Sex designation is important for reasons other than offspring production - e.g. social or medical reasons; often related or associated or 'co-morbid' with sex.
Sex designation also has no bearing on one's self-perception or self-identification, or social perceptions of one's social roles. These are additional layers beyond the scope of a biology Q&A site.

See also https://biology.stackexchange.com/a/89513/25523

To be fair, "gender" used to be mainly used as a politer-sounding word for "sex" until fairly recently.  (And still appears as that in some dictionaries).  It's only since the idea of "gender identity" distinct from biological sex has become well-known that the idea of using "sex" and "gender" to mean different things has become widespread.  So it's an understandable mistake.  It does seem pretty usual now, though.  ( https://www.etymonline.com/word/gender , https://en.wikipedia.org/wiki/Gender#Etymology_and_usage  )


text:
What type of bug is this? Found under a blanket
I'm a bit worried as we found a few of these bugs under a blanket in a spare bedroom. It was very small (3-3.5 mm) and rust/brown in color with a tubular/long shape. There seemed to be a nymph next to it (looked like a small worm). I live in France and autumn is approaching. I could only decipher shape when zoomed in with a photo. Looks really small with the naked eye. I really hope this isn't a bed bug as I have been doing LOTS of global travel in the last 6 months.
Thanks for your expertise. I also found one crawling on the ceiling in the same room. Thank you for your expertise.

@ commenters. Comments are not for answers. They cannot be downvoted if incorrect, which is especially problematic on species ID posts and even more so when most of the above comments are wrong. This is not a black beetle, is not a weevil, and is not a Cardinal beetle. It's more likely a pest (likely some type of grain beetle or related) that I would recommend the OP worry about.

Also, FYI: See Insect identification - Is this a bedbug? for some images of bed bugs.

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


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Triangulation Number of Icosahedral Capsids: Formula Variable Definitions
I'm trying to understand the definition of the Triangulation Number for Icosahedral Virus Capsids: In Alan J. Cann's "Principles of Molecular Virology 5th Edition", it is defined as

$T=f^2\times P$ where $f$ is the number of subdivisions of each side of
the triangular face, and $f^2$ is the number of subtriangles on each
face; $P=h^2+hk+k^2$, where $h$ and $k$ are any distinct, nonnegative
integers

I have also seen the Triangulation Number defined as

The number of structural units that creates each [triangular] side

in Chapter 2 of Jennifer Louten's "Essential Human Virology". I have redrawn part of a diagram I am confused about:

Only one face shows the relevant subdivision, with sides drawn in yellow. Blue marks edge subdivision points, and red marks triangular face subdivisions. To my eye, the $T=1$ icosahedron has 1 edge subdivision per side, again marked by the blue dots. If $h$ and $k$ are $1$ and $0$, then it makes sense as to how that icosahedron has $T=1$, and similarly there is only one shape repeated 3 times comprising the triangular face, so Louten's stipulation makes sense to me so far (I don't understand where the 1 subtriangle for $f^2$ is, maybe its considering the whole face as a subtriangle). For the $T=3$ icosahedron though, it appears to me that there are two subdivisions per edge, and there's no $h$ and $k$ such that $3=4\times P$. Further, in "Principles of Molecular Virology", the $h$ and $k$ for $T=3$ are listed as $(1, 1)$, unless I'm misreading; How are those values distinct per the original definition?
My raw questions coalesce to this list:

What is being counted in the "number of subdivisions of each side of the triangular face"?
What does "distinct" mean when referring to $h$ and $k$?
How is a "structural subunit" defined? For example, in "Essential Human Virology" Figure 2.8, why is the (A) $T=1$ tiling considered a single structural subunit while the $T=4$ tiling is not? The distinction of what is and is not a "structural subunit" seems nebulous to me. I could see it being the largest average number of non-overlapping triangular units excluding non-triangular subfaces, but I can't tell if that's just me grasping at straws

I don't have Cann's virology on hand here, can you provide their figure that shows subdivisions? Or another redraw for that one? I suspect their use of the the terms "subunit" and "subdivision" is at least slightly different from Louten's.

The above diagrams are from Cann's, I can redraw the other capsid on the diagram too if that's what you're referring to (I think its T=4), in the originals the subdivisions are drawn on every triangular face but in my redraw I only drew the subdivision for the face facing the observer, to reduce visual clutter and because I am lazy; They repeat on each face in Cann's. I'd post the diagram itself but I'm worried about copyright. I can do another redraw once I'm back home at my drawing tablet, I just want to ensure I'm including the parts you're mentioning.

I'm not familiar with the $T = f^2 * P$ formulation. In Caspar + Klug (1962) $T$ itself is equal to $h^2+h*k+k^2$, so I guess $f$ is assumed to always =1. So I don't really know the answer to your first two points.
As for the last point, "structural subunit" basically means an individual copy of the protein that makes up the viral shell. Icosahedral symmetry means there must be 60 identical "asymmetric units", regardless of the $T$ number. In these diagrams its usually presented as the 20 faces of an icosahedron, which are equilateral triangles and therefore can be divided into 3 identical parts, so $3 * 20 = 60$. (I find it more helpful to focus on the 12 vertices, where 5 faces come together, so $12 * 5 = 60$) The $T$ number for a particular icosahedral virus tells you how many copies of its protein are needed for its asymmetric unit. So in fig. 2.8 of Essential Human Virology, the structural subunits are the trapezoids, not the tiling of three of them in a face.
One of the important results from this theory is that only certain T numbers can exist. For example, you can't make an icosahedral shell out of 120 subunits ($T=2$).

Thanks for your answer! Could you wager a guess as to why the T=3 Cann diagram splits the face into 4 unequal parts instead of 3 identical parts then? And defined like that can't you just take the average number of proteins on a face and divide it by 3 to get the triangulation number instead of the whole $T=f^2×P$ formulation?

Yes, the large hexagon in the center of the T=3 diagram should be composed of 6 triangles identical to the ones at the corners. so 9 identical parts.

Generally you can't tell where one protein ends and another begins until you have a very good 3D reconstruction of a virus, while general symmetry features like T number can be determined from very low-resolution data. I assume the T=f^2×P formulation is useful in some situations, but I don't know what those are.


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Why Can't Muscles Push When They Return To Their Original Length?
I understand that muscles can only contract and shorten and thus can only pull, but why can't a muscle push when it relaxes and returns to its initial length?

Try to push something with a piece of string :-)  To push with something, it needs to be rigid.  Muscles aren't.

In effect, the "Push" does happen automatically when the muscle relaxes.
The muscle itself does not push and cannot push, but it sets off the connected bones from the adjoining joint/s after its contraction.
It's the same as firing a gun or a catapult or a rubber band - create big tension in the contraction or pull, and let go suddenly, and there is the Push, achieved on relaxation.

You are now answering a lot of old (and sometimes downvoted) questions. There is nothing bad on this per se, but please do not use the answer box to simply write a small comment below the question. If you have to add something, please add it but write real answer which explain something and add references. Since you are a new user, I also recommend you take a look into the help section on what is expected from answers here.This avoids deletion of your answers.


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Does The Sympathetic Nervous System Increase or Decrease Urination?
According to my book:

Sympathetic nervous system stimulation, leads to the release of Norepinephrine(Noradrenaline), priming the body for the "Fight or Flight" response.

It is also stated that:

The effect of sympathetic stimulation is to maintain urinary continence.

But if sympathetic stimulation results in urinary continence, why do we urinate more when afraid or nervous?

I've read this quesion, but the accepted answer states that adernaline(epinephrine) is released (not norepinephrine) and doesn't provide evidence to support why does adernaline result in more urination.

Are you sure that we urinate more when we are nervous?

I think that is what is common, you urinate when you are afraid.. @user438383


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How are the images of both eyes combined to form one image?
When you see an object by one eye, ex.right eye, you see it from the right direction and the opposite if you see it by your left eye, but when you open both eyes, the image appears somehow centric in between.

How does the brain combine both images to form the final image?

You might also ask "how does the image on the retina become inverted ?"

@blacksmith37 - that is a very different question, and for that matter a question based on an invalid premise, assuming the image gets flipped back again in the brain; it is not, as there is no retinotopic ground truth necessary in the brain. The merging of two retinal projections, however, is the very basis of the most important cue for depth vision, i,e., retinal disparity.

well to start the brain does not form an image, there is no homunculus.

The visual system contain several stages in which the information from both eyes is progressively mixed and analyzed, starting in the lateral geniculate nucleus.
Even if you feel seeing just one merged object with both eyes, your brain is using both images to calculate the 3D position of that object.
One fun fact: The image that you feel centric, it is actually bias towards one of your eyes, the called "dominant eye". You can check what is yours by a simple experiment