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Why can all animals swim in water without learning to swim but humans cannot?
I had a question since I was a child. I was always curious about the fact that all animals can swim in water. They don't need any training or to learn swimming. But humans need to learn to swim. Why ?
I am a technical person and not in biology after my 10th year in school. Can anybody please shed some light on this question?

Can you back up the assertion that all mammals can swim without being taught?

i think it's reasonable to say that a new born porpoise or otter needs very little instruction compared to a human baby to learn to swim.  Human learning is an unusual process, even though some animals have the capacity to learn it takes years and hardly ever goes past the abilities of 5 year old, say.

I found a website that claims "Most animals are good swimmers. In fact, they can swim from the time they’re born. But some animals have to be taught how to swim. This group includes people, gorillas and chimpanzees."

Wow .. Thank you all for the quick responses . I thought only humans cannot swim without learning. But some animals also have the same case.

possible duplicate of Can all mammals swim?

@fileunderwater Though the question is a duplicate, this post seems to have better answers or atleast offers a different perspective. I am not sure if it is right to close the post as a duplicate. I am nonetheless VTC this question because the other one is more detailed and better researched.

@WYSIWYG Maybe a candidate for merging by the moderators?

@fileunderwater can posts be merged?

@WYSIWYG I've read that it is possible, but I haven't seen it in practice at BioSE yet. See e.g. http://meta.stackexchange.com/questions/16437/when-merging-questions-leave-the-duplicate-one-as-a-placeholder and http://stackoverflow.com/questions/20674300/how-to-compare-%CE%BC-and-%C2%B5-in-c-sharp/20674425#20674425 (labelled as "merged" below the Q).

While I am not sure I buy your assertion that all mammals know how to swim, I would say that humans are at least as good as dogs when swimming. If you drop a human in water we will instinctively flap around and try too keep our head out of the water in about as elegant a way as a dog. The main problem for humans is panicking. Someone who does not know how to swim is likely to panic and not manage to keep their head out of the water. Remember that humans float in water, if you keep calm you should be able to keep your head above the water line easily enough.
Dogs can't swim as such, they simply do the same motions in the water as they do on land. There is no different action happening, they don't instinctively do a breast stroke.
In addition, human infants actually have a couple of instincts that make them "swim" (source):

The Diving Reflex
The diving reflex, or bradycardic response, means that infants whose heads are submerged in water will naturally hold their breath. Their heart rate will also slow down while they are underwater. This reflex disappears after about six months of age.
The Swimming Reflex
Newborns placed stomach-side down in water will move their arms and
legs in a repetitive "swimming" motion. This is known as the swimming
reflex. This reflex, too, begins to fade at about the six-month mark.

That is no better and no worse than any other non-aquatic mammal can do. Try dropping a cat in water* and telling me she is a graceful swimmer :).
* Don't, that's not nice.

I know cats hate water :)

It is almost funny to see a cat in the water though :) ...If you're lucky enough to see it before they come flying back out XD

Unlike Terdon I think that you are generally correct in your assertion that animals can swim whereas humans can't (although I'm sure there are exceptions). However, I think his answer contains the real answer:

Dogs can't swim as such, they simply do the same motions in the water as they do on land. There is no different action happening, they don't instinctively do a breast stroke.

Try making walking motions underwater, see how well they work for you. Whereas for a four legged animal their land based motions function as a passable swimming motion and the shape and weight distribution of their body means they can keep breathing simply by holding their heads up, humans need to learn a new skill in order to swim.
I'd note, however, that a human who has learnt to swim is much better at it than the natural swimming ability of a quadruped.


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What's the difference between Ki and IC50?
I have just read this post at researchgate: "How to calculate experimental binding free energy from the IC50 value"
I am not be very sure about what the difference is between Ki and IC50. Could anybody explain?

In biochemistry the Ki is the dissociation constant of a complex and molecules bound to it. It is a measure for the  functional strength of the inhibitor. This can for example be an enzyme and its substrate, the Ki defines the stability of the complex.
The IC50 on the other hand is the halfmaximal inhibitory concentration of a substance on a biochemical process. This can be an inhibitor of an enzyme.
See this figure (from the Wikipedia article on the IC50):

The Ki plays an important role in the calculation of the IC50, as it defines the strength of the enzyme-inhibitor complex.

I don't know if I'd call the Ki a measure of functional strength, I think it measures binding. It might be possible for a ligand to bind a protein tightly, giving it a low Ki, but not inhibit it, giving it a high IC50. But this situation probably only exists with allosteric binding sites, where a ligand can bind in a location separate from the active site.

source: Stack Exchange

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How does extracellular potassium ion concentration and calcium ion concentration affect the excitability of a cell?
When extracellular $K^+$ concentration increase by a certain amount, excitability of cells is higher because the resting potential shifts toward a higher equilibrium potential of $K^+$, therefore causing depolarization. However, when there concentration of extracellular $Ca^{2+}$ increases, excitability of cells decreases. If $Ca^{2+}$ and $K^+$ are both positively charged ions, what is the cause behind their opposite physiological effects?
I'm not a biology student, so detailed answers would be kindly appreciated. Thank you!

Hyperkalaemia (high potassium levels) actually paradoxically decreases the excitability of cells due to increased channel inactivation

If extracellular $Ca^{2+}$ concentration increased, it makes the extracellular membrane more positive then it used to be, then it would take the membrane potential to lower level then the excitability of the cells will be decreased
if extracellular $K^+$ increased more than the concentration inside the cell than it will make the $K^+$ on extracellular space move inside the call down the concentration gradient, it would take the potential membrane to higher state make it easier to reach the threshold (easier to be excitable)

Well, the answer which explains the difference between calcium and potassium is quite simple. Do we agree that charge separation (between the two sides of the membrane) is the thing which creates the potential? meaning, if the charge concentrations at the two sides were the same, then the membrane potential was zero. right?
So here is the thing. You have much more Ca outside the cell than inside and you have much more potassium inside than outside. So now, if you add Ca outside, you increase the difference between the two sides (the separation of Calcium ions) so that Ca will be in a greater state of unrest, the system will be less stable and the potential will be higher. On the other hand, when you add K outside, you narrow the gap between its two concentrations on the two sides (decrease its gradient), so now it'll experience less tension, less unrest, hence contribute less potential to the membrane.
Remember that in our cells, the ion pumps are the ones which serve as the battery that keeps the potential fixed. When do you think the pumps will have to work harder and to do more work (voltage times charge is work), when you add more K outside, or when it's the Ca which is being added?

Welcome to Biology SE! Can you add more sources to this answer.

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Why is knowledge of bacterial pathogenesis important?
Why is knowledge of pathogenesis increased more and more for common bacterial pathogens? Most of these studies lack a near application in disease control such as vaccines or antibiotics.
Examples:

Studies on the interactions of Haemophilus parasuis with porcine
epithelial tracheal cells: Limited role of LOS in apoptosis and
pro-inflammatory cytokine release
Sialic acid in the lipopolysaccharide of Haemophilus influenzae:
strain distribution, influence on serum resistance and structural
characterization

Because it is also important to do basic research. It has no goal besides solving questions and is the basis for applied research.

@Chris You should convert that to an answer :) Also it is important to note that these small contributions make it possible to improve the applied part of science.

Because it is first important to understand a mechanism before you can think about using it for drugs. Take melanoma for example: A large subset of melanoma has a mutated and constitutive active BRAF kinase which permanently signals towards the nucleus and thus deregulates gene expression. Once this mutation was found it was possible to design inhibitors which only work on this specific mutation, which are available in the clinic today.
The same is true for example for activity of antibiotic on bacteria and the fight against resistance. Once it was known that the enzyme beta lactamase inhibits beta lactam antibiotice (penicillin or ampicillin for example) it was possible to find an inhibitor of the enzyme. The clavulanic acid works as a specific inhibitor and has been added to beta lactam antibiotics subsequently to overcome resistance. The same is true for changing antibiotic molecules chemically so they evade the established resistance mechanisms.
The contributions of basic research is the basis for applied research and drug design. Without them, this wouldn't work. Besides that it is also the curiosity of humans which drives science - without having any particular application in mind. These often come much later.


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Were early human beings (about 100 - 200 K years ago) far more promiscuous than we are now?
I found that many friends of mine are quite easy in sexual relationship. Ex, I knew a lot of girls went to the night club & met a stranger & brought home to sleep  with him even she had never known his name. The next morning, the guy left her & she starts to do the same way to get another guy maybe in 3 days or so.
So that triggered my thought. I wonder "Are early human beings (about 100 - 200 K years ago) far more promiscuous than we are now?"
My hypothesis is "Yes", that is "Early human beings are far more promiscuous than we are now". So how i came up this? Cos Human came from Chimpanzee right?, so if we want to know early human, then we could study Chimpanzee. The early human & Chimpanzee could have some similarities.
There is a research saying that "Chimpanzees are far more promiscuous than humans" http://www.nature.com/news/specials/chimpgenome/interactive/chimp_interactive_graphic_pf.html
So, that proved my hypothesis.
Also, when human evolved, they started to realized that promiscuousness wss not healthy & not good for society so they started to develop some regional/society (ex,  monogamous relationship) codes to prevent that.
Do you approve my hypothesis?

i'd be surprised if there weren't some time when sex was not socially regulated in the way it was and then the typical human would have more partners than they do on the average (though modernity has definitely increased the maximum number of partners someone can have).  people did not live very long though and sizes of human groups were small on the other hand..

Your question is interesting but I just want to make some comments about basic stuff that sounds weird in your question. The article you found is not a prove neither an evidence for your hypothesis. But it is an interesting fact that should be considered in the discussion. Humans does come from chimpanzee but they both share a common ancestor. If you observe two different phenotypic trait in two sister lineages you cannot quite know which of the two trait had the common ancestor.

My hypothesis is "Yes", that is "Early human beings are far more
  promiscuous than we are now". So how i came up this? Cos Human came
  from Chimpanzee right?

No.

Also, when human evolved, they started to realized that
  promiscuousness wss not healthy & not good for society

I'm sorry, what ancient society are you claiming cracked down on male promiscuity?

I guess you meant that chimps are not human ancestors, because the claim regarding human promiscuity is much harder to disprove. 2. Jewish?

Well, your logic is flawed because it is not proven that humans evolved from chimpanzees. not trying to start another debate with the whole evolution, but even if I did believe in evolution I would suggest before making up your hypothesis of researching a lot more than monkeys. Research things like: ancient brothels, traditional marriage views/ cohabitation views, {things that humans practiced and accepted back in the day} and you will have much more evidence.

Humans did not evolve from chimpanzees. Both evolved from a common ancestor some 5 Mio years ago (which is an important difference).

even if I did believe in evolution?? So you don't now??

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How is the diploid chromosome number maintained at mitosis?
A normal human cell is diploid that contains 46 chromosomes in 23 pairs. Thus, when the cell undergoes mitosis, the cells still has the full chromosome with the two sister chromatids. What is it doing in interphase when it produces the other chromosomes?
I thought that the sister chromatids were pulled apart and, in interphase, the single sister chromatid grew another one. How is this possible if a human diploid cell contains 23 pairs of 2 chromosomes each?

No division takes place in interphase.

The terminology of "chromosome" during this process is confusing, but here it is:

There are 46 chromosomes in the cell (23 pairs)
Before division, each chromosome has two sister chromatids, joined in the middle (92 chromatids in total)
During division, the chromosomes split and each daughter cell gets 46 chromatids, one from each chromosome
These chromatids are now known as chromosomes
Each one of these new chromosomes only has one "chromatid"
During interphase, the new chromosomes replicate and now they have two chromatids each, joined in the middle

So whether a chromosome has one or two chromatids it is still called a chromosome. I hope this helps.
The following link contains a more complete explanation of mitosis. The first picture explains this point quite succintly: http://biology.tutorvista.com/cell/mitosis.html

Joe-can you add some references to your answer... it will strengthen the answer and allow other individuals to read more about the question/answer. I know it may seem silly when questions have a very easy answer that is based on common knowledge of those in the field, but we do have users as young as high school students (and potentially younger) that benefit from cited references. Thanks for your contribution!

Thanks for the advice, I've added a link to a more complete explanation with figures.

In a diploid cell the two sets of chromosomes are called homologous chromosomes (except in the case of XY pair) and not sister chromatids. Sister chromatids refer to the exact duplicate daughter chromosomes produced after DNA replication during mitosis.
After mitosis each cell receives a copy of all the pairs of homologous chromosomes.
I hope your doubt is clear now.


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How can I accurately measure glucose concentration in culture media?
I am trying to identify the best way to measure glucose concentration in culture media with E. coli. Now, I imagine I can use those glucose meters that diabetic people use, but unfortunately can't find any papers as background.
Any ideas would be appreciated.

you definitely cannot measure media glucose concentration with a blood glucose analyzer - see this link for more information on that... http://biology.stackexchange.com/q/20325/16299

there are a number of colorimetric assays that are commercially available - we routinely measure plasma and other fluid glucose concentrations using a single reagent method and a standard curve - you just need a UV/Vis reader and some reagent which is inexpensive

Thank you Vance for taking the time to reply. As you can probably tell, it's my first day here!

@VanceLAlbaugh,  It think it's possible to measure glucose concentrations in pretty much any solution with a blood glucose analyzer. But you need to recalibrate the signal since the typical assumption of the instrument are no longer valid. Just do a standard curve of known glucose concentrations in medium. We have done this before with blood glucose analyzer and I think it works well. These analyzer are just a glucose oxidase kit in miniature, they are no better or worse than other enzymatic methods in my experience.

The most common method of measuring glucose concentrations (in pretty much any sample) is an enzymatic assay based on the glucose oxidase enzyme. This method is reliable because the enzyme is known to be quite specific for glucose; it does not oxidize fructose, galactose, or any of the other common hexose sugars which can contaminate many other measurement methods. The enzyme can be coupled to other reactions so that the amount of glucose oxidized can be read out by a standard spectrophotometer. There are many kits commercially available based on this principle, like this one. A review of glucose oxidase from the glucose measurement perspective is found here.
Blood glucose analyzers are also based on glucose oxidase. Typically, they have disposable slips that contain glucose oxidase along with some electron-carrying chemicals that convert enzyme activity into an electrical current sensed by the device. It is possible to measure glucose in pretty much any solution with such insruments, but as mentioned in comments, you need to make a calibration curve for glucose in your solution of interest (culture medium, or whatever), as you cannot trust the readings from the instrument directly when measuring under different conditions. We have previously used this approach to measure glucose in mammalian cell culture medium, and it works fine in our hands.
It is also possible to quantify glucose by mass spectrometry or nucleic magnetic resonance methods, but unless you have such a facility and expert help, I guess that is not an option in this case.


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What happens to the brain during sleep versus unconsciousness?
How does being unconsciousness differ from being asleep and whether it causes breaks in consciousness?

I'd recommend you to formulate the question on the basis of the mechanisms stopping the brain to control the body during dreams.

sounds like a great question for an anesthesiologist


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Reptile identification - Is this a green iguana?
At first instance it looks like an iguana and since this photo was taken near the coast of Pernambuco, Brazil it could only be the green iguana, but as you can see from the photo the reptile is black. Perhaps green iguanas can be black under strict circumstances, but I could not find any instances concerning that from a reputable source, only from some dubious pet blogs and it was due to the lighting, temperature and overall cage conditions. It's worth noting that there were multiple animals and they were all black. In response to tyersome comment, the picture was taken in summer so I'm gonna assume it was hot at the time, regarding the size it seems to have almost 2 meters. This has to definitely be from the Iguanidae family and it appears to share similarities with the green iguana but the color is off.

Welcome to Biology.SE. You've done a good job of providing information, but it would be helpful if you could add: 1) an estimate of the iguana's size; and 2) as much environmental, habitat and behavioral information you can. In particular, was it cool/cold when the picture was taken?

Okay thanks for the heads up. I've updated the post. Also added another photo that I've found.

Could be a hybrid or simply a melanistic green iguana.

Never heard of this melanistic phenomenon before, very interesting. That might be it, many thanks.

You might find the following interesting as it discusses the phylogenetics / splitting of I. iguana and descriptions of melanistic iguanas in/around S. America: https://zookeys.pensoft.net/article/48679/

This is a Green Iguana (Iguana iguana) of the genus Typical Iguanas (Iguana)

The green iguana (Iguana iguana), also known as the American iguana or the common green iguana, is a large, arboreal, mostly herbivorous species of lizard of the genus Iguana. Usually, this animal is simply called the iguana. The green iguana ranges over a large geographic area; it is native from southern Brazil and Paraguay as far north as Mexico.
Source: https://en.wikipedia.org/wiki/Green_iguana

How to identify
The iguana is of the genus Iguana due to its defining characteristics:

Iguanas are large lizards that can range from 1.2 to 2.0 m (4 to 6.5 ft) in length, including their tails. They possess a dewlap and a row of elongated scales running from the midline of their necks down to their tails.  Source: https://en.wikipedia.org/wiki/Iguana

After identifying the genus, the rest is straightforward. There are two iguanas that live in Brazil: The Brazilian Steppe Iguana (Urostrophus vautieri) and the Green Iguana (Iguana iguana). The species is easily determined as not being Urostrophus vautieri because the Steppe Iguana has a distinguishing stripped pattern along its back. Therefore this must be Iguana iguana.
The Reason for the Black Color
The black coloration on the Green Iguana is not at all unusual, in fact the US Fish and Wildlife service describes the lizard as:

large, typically green lizards, though they can sometimes be brown or almost black in color. Some adults can take on an orange or pink coloration during certain times of the year. Hatchling and young green iguanas usually have bright green coloration.

And this wikipedia article notes that green iguanas are often found in many different varying shades of colors:

Despite their name, green iguanas occur in different colours and types. In southern countries of their range, such as Peru, green iguanas appear bluish in colour, with bold blue markings. On islands such as Bonaire, Curaçao, Aruba, and Grenada, a green iguana's colour may vary from green to lavender, black, and even reddish brown. Green iguanas from the western region of Costa Rica are red, and animals of the northern ranges, such as Mexico, appear orange.Juvenile green iguanas from El Salvador are often bright blue, but lose this color as they get older.

So what is the reason for this color change? This scientific article on iguanas provides the answer. Stating that:

Body colour of the green iguana changes depending on its mood
and is a good form of visual communication. Highly aroused green iguanas usually lighten their
typical brownish green hue, within five minutes of arousal. Males who have been ousted from
their territory during mating season also display a visual form of defeat in the form of a colour
change from the reddish orange colour displayed during mating season to a dull brown.

The speed of the color change is quite remarkable, taking place within hours:

This colour change can take place in a matter of hours and the iguana remains this way until it regains control of its territory

The color of the iguana will also change during the mating season:

Mating season for the green iguana occurs just before the start of the
rainy season in the tropics. Males usually experience intensification of colour at the start of the mating season with larger males changing colour to bright red or golden hues of orange along with this change in colour was an increase in the number of displays occurred with males becoming well spaced apart and conspicuous. This reduced the number of incidences of males meeting each other and reduced the occurrence of antagonistic encounters

The reason for the black color is more normal. The green iguana turns color with age, becoming black or brown as it becomes older:

The adults become more uniform in color with age, whereas the young may appear more blotchy or banded between green and brown. Color of an individual may also vary based upon its mood, temperature, health, or social status.  Source: https://animaldiversity.org/accounts/Iguana_iguana/

Examples of the green iguana (Iguana iguana):

First Image Reference: https://www.inaturalist.org/photos/21169473, Photo 21169473, (c) Andrés Mauricio Forero Cano, all rights reserved, uploaded by Andrés Mauricio Forero Cano
Second Image Reference: https://www.inaturalist.org/photos/187564945, Photo 187564945, (c) Luiz Carlos Ramassotti, all rights reserved, uploaded by Luiz Carlos Ramassotti

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What is this Patagonian biome?
This image was taken in Patagonia, near the Torres Del Paine National Park.
What type of biome this is? There are trees and other vegetation, but they seem mostly dried. I think this is either a semi-arid region or some type of transition zone to a forest, but I'm looking for a more concrete answer.

Certainly some kind of heathland. Looks too moist and shrubby to be Patagonian steppe. I'd guess a Magellanic subpolar forest type of ecoregion. Coloration appears to be due to it being autumn. I know that there has been a long history of grazing in this region with recent efforts of conservation returning steppe to shrubbier habitats. Hard to see details on my phone. I'll try to draft up an answer when I get a chance

Welcome to Biology.SE! It would probably be helpful if you provided more precise location information (altitude might also be informative) — Patagonia isn't a small area and I suspect it contains multiple biomes. If you could provide identifications for any of the plants in the picture that would also be helpful. Thanks!

@tyersome Unfortunately I have no information about the plants, but I did found out some more information about the photo, I'll add it.

A visual search (Bing) turned up several similarly stunning photographs at Culture Trip.  I think that the mountains are recognizable in at least one - with suspicion this photo may have been reversed.

If as @MikeSerfas has suggested this is not an image you produced it is important that you include a source and copyright information (you should not be reposting other people's work without acknowledgement and permission). Thanks!

I didn't mean to suggest any such thing - I only wanted to help understand the beautiful location.  The main thing that seems out of place about the photo above is that the animal in the foreground is not a unicorn. :)  But looking at the Wikipedia article I noticed great similarity of the mountain (not the photo!) to their lake image of Cuernos Del Paine from the Lago del Toro (but reversed), which should help to identify the biome.  Also see https://www.google.com/maps/@-51.144369,-72.6814447,14993m/data=!3m1!1e3 though it isn't as helpful as I'd hoped.

@MikeSerfas Yes, the photo was most likely reversed, already put the original, thanks!

Based on my experience, the answer to this question my further be complicated by grazing in the area. We have a horse in the image, and the ground vegetation looks like it has been grazed quite heavily (if this is a grassy type ecosystem). If this is a heathland then we seem to be missing many of the heath shrub species we would expect (Genus Ericaceae) unless they are quite small.


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Contrast Fluids in MRI: Which tissues "glow" first?
I am a bioinformatic and data scientist in progress, working on my Master Thesis about prostate cancer. Now I am at that point, I have a strong guessing, that contrast fluids in magnetic resonance images (of the prostate region) will first show their effect in blood vessels, and later in other tissues by a specific ranking/order/timing. But I can not find any good (scientific) source to flesh out this hypothesis.
I found some equations about relaxation times, but this seem to be more about "wavelength" then "when after injection will it start". Also I found a lot of equations for different transportation between cells and from blood to cell. But this is to specific.
My wish would be some kind of table, stating "after injection of contrast fluid, first blood vessels will be visible, then tissues nearby, then tissues with very active metabolism (like cancer), then tissues without fat, then tissues with i do not know..."
In which scientific source I can find some characteristics, in which order (in question of time) contrast fluid is transported into tissues in the prostate region?
Edit: In case it is as simple as the comments state, that I may need other terms for search, for example I tried: "tissue fluid transport"; "contrast fluid which tissue gets it first"; "how fast react tissues to contrast fluid"; "relaxation rate of different tissues" and combinations, more and less words, and so on.

This is possibly interesting, but I was readily able to find some relevant references  by googling ('"contrast fluid" penetration prostate'), e.g. table 1 here. I'd suggest putting a little more effort into your search.

@MaximilianPress Thank you! I did not have "penetration" as term in my search. Sometimes it is that simple, with the right words :) (I do not know, if this is because I am not full biologist, or not native english...) Would you make an answer out of it?

@MaximilianPress I had a closer look into this source, and it is not helpful for me. The times noted in the table are connected with the different contrast fluids and their different dosage. And it gives times for "when is the structure (ie whole liver, whole prostate gland) completely visible". I also tried the search term you suggested, and your link was the only one, matching in general my goals. The other results are about prostate infections or general health of male organs.

This isn't really my field, but I think you're not finding anything because what you're describing isn't how contrast is used. Contrast is used to differentiate tissues at a single point in time, it's not as if things light up one after another. You might look at search terms like "time course gadolinium" to find information about when certain tissue contrasts are most prominent, but that's not going to be because some tissue "got it first", these are smooth differential equations.

@BryanKrause Thank you for the help in search terms. I have a time series of MR images, so it is not one single point in time in my case.


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Can restriction enzymes (Type II) displace single-stranded binding proteins (SSB)?
Many type II restriction enzymes have been shown to be able to cut ssDNA.
If single-stranded binding proteins are bound to single-stranded DNA (ssDNA), does this prevent restriction enzymes which cut ssDNA from scanning the ssDNA and interacting with the target cut site?
The NEB website says that using SSB's improve restriction enzyme digestion, so it doesn't seem to be the case that SSBs inhibit target site recognition. But it is unclear to me how a restriction enzyme could recognize the target sequence unless it can also displace SSB's while scanning.
edit: specified REs that cut ssDNA

I'm curious as to why you are trying to add SSBs to ssDNA endonuclease digestions, is this some in house protocol you are trying?

I was thinking about how ssDNA endonucleases would work in vivo, where there are other proteins like SSB that could potentially interact with the ssDNA and interfere with cutting.

Please update your question to indicate why you think type II restriction enzymes (that cut  double-stranded DNA) would need to displace a single-stranded DNA binding protein.

I was thinking about type II restriction enzymes that were capable of cutting ssDNA.

Do you have some reason to think that this is a normal activity of type II REs? If so, please [edit] your post to include a summary of that evidence with supporting references. In the absence of that evidence your question doesn't appear to make sense.

Sorry, I just added a paper that supports the idea that there are some type II REs that can cut ssDNA.

That is talking about cleavage happening while the ssDNA forms dsDNA regions.  Why would you expect such regions to be bound by SSB proteins? Is there any evidence for this?

I did not read carefully, apologies. I did find a paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC432807/)  which describes the cutting of ssDNA by an endonuclease, but it is not a type II RE. I can either delete this question, or rephrase it.

Since you've got an answer, I would recommend rephrasing so that it fits the answer you got as well as possible. Thanks!

This is an interesting point. In the case of typical restriction enzyme digestion, it is double stranded DNA that is being digested. So in this case the SSBs are presumably binding to the sticky ends after digestion, so there is no competition with the restriction enzyme.
If you are interested in a specific case where you are digesting ssDNA, and have decided to add in single strand binding proteins, the binding strength (rate constants) of the SSB and restriction enzyme would influence how much the enzyme can displace the binding protein.
Here's a paragraph from the NEB/T4 gene 32 page indicating many similar applications involving reverse transcriptases, polymerase etc.

"Recently, it has been shown to improve restriction enzyme digestion
(6), improve the yield and efficiency of reverse transcription (RT)
reactions during RT-PCR (7-9), enhance T4 DNA polymerase activity
(10-11), as well as increase the yield of PCR products (12)."

EDIT: Although the reference (6) cited by NEB does not have any evidence that proves the enhancement of restriction digestion with single strand binding protein 32. This chapter might be helpful? - Kowalczykowski et al., "21 single-stranded DNA binding proteins." The enzymes. Vol. 14. Academic Press, 1981. 373-444.
From their abstract, it looks like the mechanism of enhancement could be through prevention of ssDNA hairpins so that the endunuclease can access it's recognition site (I haven't read the full chapter). Another fact supporting this is that ref(6) mentions that other interacting enzymes can work alongside SSBs only when SSB's are not saturating all the DNA in the in-vitro reaction. In an in-vivo context, the chapter abstract states that intracellular SSBs are sufficiently abundant to saturate all ssDNA intermediates formed inside cells (I presume they are talking about E. coli)
Below is the supporting text from reference (6) mentioned by NEB - bolding is mine, for emphasis : Bittner, M., R. L. Burke, and B. M. Alberts. "Purification of the T4 gene 32 protein free from detectable deoxyribonuclease activities." Journal of Biological Chemistry 254.19 (1979): 9565-9572.

Nuclease Assays-The presence of both exo- and endo- deoxyribonuclease contaminants in the 32 protein fractions has been monitored carefully throughout these purification schemes. The results of exonuclease assays are presented in Table III, and the results of sensitive endonuclease assays are presented in Table IV. Note that, when such assays are designed to detect nuclease activities on single-stranded DNA, it is important to test 32 protein at subsaturating, rather than only at saturating, protein to DNA ratios. Otherwise, an activity which hydrolyzes only free (non-32 protein-com- plexed) single-stranded DNA will escape detection.

Thanks for the response, that makes sense about dsDNA. I was mainly interested in the case of RE's cutting ssDNA, and how SSB's might interfere or not there. I looked at the paper  in that is referenced in your quotation, but don't see the data that would point to the same conclusion. I assume it must be something in Table IV?

Oh yes. I couldn't find anything relevant in that paper, NEB might have cited it in error. I edited my answer with another potential reference

I looked near both table III and IV

Please do not post text as images. Copy and paste the text into your post. Images are not searchable, and can not be interpreted by screen readers for those with visual impairments. Use the [edit] link to modify your answer. See this for more information. Thanks!

Ah, that makes sense. Thanks for pointing that out. I was lazy because it was an ancient PDF that wasn't copying well. I fixed it now :)


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Homework: Diffrentiate between 2 toads

How to differentiate between 2 toads one of them result of artificial parthenogenesis and the other from renucleation?

I answered that the toad resulting from artificial parthenogensis is identical to the mother
While the other toad which result from renucleation is identical to that which the nucleus was taken from
My answer is so unrealistic and I can't find any other answer so I though I could use some help.

Welcome to Biology.SE. What data do you have access to make the differentiation? What frog species? If you could explain what's your interest behind the question, it may help.

I recommend looking at the tags again

Oh indeed.... Is it the entire homework question exactly as phrased, or is there more information around it? I don't want to be pedantic but make sure to quote correctly. You can highlight a quote is a quote by starting the line with >

Sorry I am new  .The question is exactly as its phrased

No worries. It is part of being new to Biology.SE to have its post reviewed, corrected, clarified and sometimes closed. I edited you post. Please note that homework questions are allowed on Biology.SE only if the OP is displaying its attempt at answering the question. So, in its current form your post should get closed. Can you please add your thoughts about this question? On top of protecting the site from "do my job" type of question, it also allow us to understand what level of understanding the OP have and what is unclear for the OP.

Going to edit it now . Thx


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Why won't birds move an inch in total darkness?
One day, a bird flew inside my house. I locked the door. It landed on my TV and then I turned off the light. Then I touched the bird and it didn't even to try to fly or move.
Then I went to the kitchen and turn on the light,  and suddenly it flew into the kitchen.
Why won't birds move an inch in total darkness?

The bird could have walked on the TV but it didn't know where the edge was, and walking would have made it easier to see for a predator. If it had flown, there is no way it could have seen safely where it was landing. Walking and landing at flying speeds are different things. Turn the lights off on a bird, you give it an sensory sequence of events that it's ancestors hadn't experienced from 100 million years, other than flying in a cave perhaps.

@com.prehensible I made some changes to my question.

in a birds mind is a very weird place, very many weird scenarios exist. perhaps it's ability to panic is overridden if it's in the dark. also perhaps birds don't have any night time predators. he perhaps instantly switched to night mode and felt safe.

Most birds are diurnal and have vision adapted for daylight. Vision is among the most important senses for most birds, so much so their eyes have evolved to be quite large -- much larger than human eyes, proportionally to body size. In order to have excellent daytime vision, many birds also sacrifice some of the cells in the retina that allow for dim lighting conditions. (These photoreceptor cells are called rods and cones; cones are responsible for color perception while rods are more sensitive in dim lighting. Diurnal birds can have a lower percentage of rods than other animals adapted for nocturnal activity.)
Falconers have been exploiting this trait for millennia, by using a hood, diurnal birds of prey calm down in darkness.

Owls are a great example of a bird that can see in very dim lighting conditions, though they can't necessarily see in total darkness. They also rely on acute asymmetrical hearing in order to pinpoint prey in extremely dark conditions.
Your avian visitor likely can't see in dim conditions in which you can still see. To avoid injury, birds will hold still and wait for light.


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Why does a frog's oxygen intake through the skin and lungs vary throughout the year?

Why does a frogs oxygen intake through the skin and lungs vary throughout the year?  And why does the intake through the skin vary slightly while through the lungs dramatically? (Blue line = oxygen intake through lungs and orange line = through skin.) Thanks.

Cutaneous respiration is based, as every type of respiration, on diffusion of gases from a higher concentration (in water or air) to a lower one (in capillaries).
Citing from Johnson, Peter H. Raven, George B. (2002). "Respiration". Biology (6th ed.). Boston: McGraw-Hill. pp. 1053–1070:
In general, the rate of diffusion between two regions is governed by a relationship known as Fick’s Law of Diffusion:
R = D - A x ∆p/d

In this equation,

R = the rate of diffusion; the amount of oxygen or carbon dioxide diffusing per unit of time;
D = the diffusion constant;
A = the area over which diffusion takes place;
∆p = the difference in concentration (for gases, the difference in their partial pressures) between the interior of the organism and the external environment; and
d = the distance across which diffusion takes place.

As you can see, the rate of diffusion R can be increased:

By increasing A, the diffusion area;
By increasing ∆p, the difference in concentration;
By decreasing d, the diffusion distance.

In cutaneous respiration, nr.2 is not really an option; yes, capillaries can be optimised to bring blood rich in carbon dioxide and poor in oxygen really close to skin surface (which brings us to nr.3), but it's a lot less efficient than, for instance, lungs that can exhale air filled with carbon dioxide and replace it with fresh air. While the intake of oxygen of the skin remains more or less the same even with different metabolic demand, lungs can quickly adjust the breathing rate depending on the metabolic demand of the moment.
So, the answer to the question

why does the intake through the skin vary slightly while through the lungs dramatically?

is that skin cannot regulate its gas exchange rate, while lungs can. This brings us to your first question:

Why does a frogs oxygen intake through the skin and lungs vary throughout the year?

The answer lies in the biological cycle of the frog throughout the year: during cold months, frogs hibernate. In winter, frogs slow dramatically their metabolism and they don't need so much oxygen; thus, in this season they are able to rely only on cutaneous respiration. In other seasons they are active, and they have to breathe actively through their lungs to supply their blood with the necessary quantity of oxygen.

Thank you for the in depth clarification and helpful information, highly appreciated!

Another factor contributing to these results may be that some of the most of the most common species of frogs such as the  leopard frog(Rana pipiens) and the American bullfrog (Rana catesbeiana) both hibernate.


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What kind of bug is in this photo
Wondering what kind of bug this is found outside

I'm no expert, but it looks like a potato beetle to me: https://en.wikipedia.org/wiki/Colorado_potato_beetle Might be helpful to list location and other info to help people orient to what the possibilities could be.

Yes, it is robust like a Colorado potato beetle (Chrysomelidae), but its antennae give it away as a scarab.

That is a Ten-lined June Beetle, (Polyphylla decemlineata) in the family Scarabeidae. You can tell its a scarab by its lamellate antennae. The stripes indicate the species.
https://en.wikipedia.org/wiki/Ten-lined_June_beetle

Agreed as to genus; the species may be in error (we need a location to be sure); see here for a list of North American possibilities.

Yes, I may have been premature.


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Is it possible to fuse DNA from two sperms into one sperm?
Is it possible to fuse the DNA of two genetically different sperms into one singular sperm? In theory, half of the number of chromosomes in a normal sperm would come from one sperm and the other half could come from a separate sperm. In return, the fused sperm could fuse with a healthy egg cell for fertilization.

It would be theoretically possible to engineer such a cell, but something very similar can occur in nature, two sperm cells can fertilise a single egg cell, resulting in a fetus with DNA from both. See here

Awesome, thank you! If it were to happen by engineering the cell, what process or pathway would theoretically be used to fuse the two sperms together?


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Trying to understand reduction of color dimension in colorblind case
I understand that dichromats have one of their cone missing/not functioning. And as for Monochromats, 2 or all of their 3 cones are missing/not functioning. And I read from Wikipedia - Color Blindness :

Dichromacy occurs when one of the cone pigments is missing and color is reduced to two dimensions.

and

Monochromacy occurs when two or all three of the cone pigments are missing and color and lightness vision is reduced to one dimension.

Since in the description they relate the cones with Red, Blue, Green (RGB) a lot, eventhough I'm fully aware that relation of cones and RGB is most likely for historical reason . I'd like to assume in this reduction from 3-dimensional into less dimensional colorspace dimension written in Wikipedia based on RGB colorspace.
This is original RGB colorspace in 3-Dimension

Question 1 : How exactly reduction from 3-dimensional to 2-dimensional or even 1-dimensional in colorblind case happen ? For example in Protanopia, would they lose the Red axis ? So only Blue and Green axis left ? (Any reference will be appreciated).
I also read this question If people with colorblindness lack one type of cone cells, shouldn't they be unable to recognize one particular color?. And it's written that Dichromats can match any color they see with some mixture of just two primary colors. Cones do not literally interpret colors. The three cones work together to encode a signal.
Question 2 : If cones don't really interpret any color in human color vision system. Is it wise that losing cone means reduce from 3-dimensional color into 2-dimensional by completely erase the corresponding color axis to the cone ?
[UPDATE]
For Question 1 :
Taken from the book Visual Transduction and Non-Visual Light Perception (p308),
Univariance, Monochromacy, Dichromacy, and Trichromacy

If only one photoreceptor type operates, vision is monochromatic or reduced to a single dimension

If only two cone photoreceptors operate, vision is dichromatic or reduced to two dimensions

and

Most observers
  with normal color vision have three classes of cone photoreceptor and are therefore trichromatic.

So, I'm sure in my Question 1, they really refer to Young–Helmholtz Trichromatic theory. A theory when human color vision possess 3 types of cones thus they have three dimensions of color vision.
However, I still need some opinion related to Question 2. Any comments will be appreciated.

Let's start with a quick overview of the different types of dichromats in man:

Protanopes have no functional red cones. Red appears as black. Certain shades of orange, yellow, and green all appear as yellow.
Deuteranopes have no functional green cones. They tend to see reds as brownish-yellow and greens as beige.
Tritanopes have blue-yellow color blindness and lack blue cone cells. Blue appears green and yellow appears violet or light grey.

Now color vision can be modeled with the Hering model, where there are two opponent channels, namely red-green and blue-yellow. These opponent channels determine color vision. Because of these two limbs, color space is often represented as triangles, rather than cubes as in your post. Fig. 1 shows the color space in trichromats. In Fig. 2 the same is shown, alongside the three types of dichromatic deficiencies.

Fig. 1. Color space in trichromats. source: Lighting Analysis

Fig. 2. Triangles in trichromatic and dichromatic vision. source: Chartlr.

Thanks! I'm aware of this triangle 2D representation. I believe this is adaptation of colorblindness taken from CIE 1931 color space. I believe color vision can also be represented by Helmholtz trichromatic theory which has 3 primary color, exactly like RGB. What I want to confirm is the reduction of 3-dimensional space into 2 (or 1) dimensional space in colorblind. I'm open to any possibility that the RGB 3D diagram above is wrong. I'm not sure is it RGB or which other 'color dimension' they meant, since it's not exactly written there.

It depends on the definition of dimension, but yes, you could say you loose one.


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Shortest route for a Nitrogen atom from fossil fuel to a protein in your body?

Millions of years ago fossil fuels originated from plants. A nitrogen
  atom from fossil fuel is now inside in a protein molecule in your
  body. What is the shortest path that the nitrogen atom could have
  taken starting with plants that lived millions of years ago, until the
  protein molecule in your body. Use those points:

consumers
producers
reducers
fossil fuels
$NO_x$

I guess the route could be producers -> reducers -> fossil fuels -> consumers -> $NO_x$
But this could be wrong, because NO does not have to be produced by consumers.

producers-reducers-fossil fuels-NO-producers-consumers.

fossil fuel is out of question.. it is a byproduct not a precursor for a metabolite.. atmospheric nitrogen can be fixed to nitrate by physicochemical or biochemical processes

Fossil fuel -combustion-> NOx -deposition-> plant -> person


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which signalling pathway is involved in cancer?
Columnar epithelial cells from the colonic mucosa are studied to identify abnormalities in cell signaling pathways. Abnormal epithelial cells from colonic adenocarcinoma are shown to have a mutation that blocks hydrolysis of GTP-bound active RAS. Normal columnar cells have active RAS protein that undergoes hydrolysis to the inactive GDP-bound form. Which of the following signaling pathways is most likely abnormally stimulated in the carcinoma cells?
a. Jak-Stat Pathway
  b. MAP kinase pathway
  c. p53
  d. Both a & b
I think its MAP kinase pathway because RAS is part of MAP kinase pathway that ultimately leads to transcription and expression of genes but if GTP is not hydrolyzed then RAS will be constantly activated leading to continued gene expression that may lead to cancer but I am not completely sure about it because p53 is also a tumor suppressor gene.

Is this a homework/test question? It looks a lot like one.

Homework questions are off-topic unless you show some effort of solving them yourself. What are your thoughts about it?

Hi, this very much sounds like a homework question! It will be great if you show some evidence of what you think the likely answer is and why so that any input would be constructive!

I think it is MAP kinase pathway because if GTP is not hydrolyzed then it will lead to constant activation of RAS as RAS is in MAP kinase pathway..so what is your opinion..?

Perhaps also take a look at Jak-stat and see what pathways influences it! and as correctly mentioned p53 is an inhibitor so it can't be the right answer!

The answer is b, as the mutation constantly activates the RAS protein. RAS is part of the MAP-Kinase pathway, constant signaling of it permanently activates this pathway and leads to changes in gene expression. See the image below:

If you are interested in more details, have a look at these papers:

RAS oncogenes: weaving a tumorigenic web
RAS mutations and oncogenesis: not all RAS mutations are created
equally

Whoever downvoted my answer, what is your problem with it? I can (and will) improve it, when you can tell what you think is wrong with it.

yeah you are right that both are involved in cancer but in question a specific condition is mentioned that is "mutation in RAS" and it is constantly activated that leads to cancer so its only MAP kinase pathway...as no RAS in JAK-STAT pathway..by the way I didn't downvote your answer..

@emi Yes, you are right. I missed that point somehow. Adapted the answer.


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How many blood types are there?
In total how many blood types are there?
And why do people normally know only 8 of them? (A+, B+ , AB+ and O+ and Rh- counterparts)

As I remember from my physiology studies that there are more systems. So you're interested in the ABO system only or the other ones as well? check this: http://en.wikipedia.org/wiki/Human_blood_group_systems#Blood_group_systems

@zeller Thank you, anyway I cannot understand why normally we know only ABO system and I cannot understand if each system is only a different "convention" of if it denotes a somewhat different blood system.

Unfortunately I can't answer that, as I haven't studied immunology, but based on my recent readings (on wikipedia...), most of them check different antigenes/ligands/whatevers.

Adding insults to the question will not help to reopen it. Working on the content will. Comments should be added into the comment field.

@Chris insults? What's not clear in "This question has been asked before and already has an answer."? I repeat: the time line goes from left to right, from lower numbers to higher numbers. It's pretty easy.

@HAL9000 The question is not whether ur query was answered first or not.. In general it has been answered. Shouldn't you just be glad that you have been pointed to the answer. Just ask a new question for any further clarifications


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How do you increase eumelanin but not pheomelanin?
Are Scientists currently looking into this?

Where do you want to increase eumelanin, in the skin? And why would you do so?

I read that it is more efficient in protecting against skin cancer. I have also read that you usually cant increase Eumelanin without increasing Pheomelanin. Is there a way?

Please edit your question to include those details (where, why,...) for future readers , as they will then be more likely to attempt an answer.

I doubt that this will be really successful, since the synthesis is rather complex and can be influenced (positively and negatively) in many ways. First, the synthesis pathways looks roughly like this:

The first step is identical for both melanin forms, it is the conversion of the amino acid tyrosine into dopaquinone by the enzyme tyrosinase. The next steps are different for each process and only one of the possibilities can happen at any given time. The decision is done by the availibility of the necessary components. When the cysteine concentration in the cell is high, the pathway goes exclusively into the direction of pheomelanin, only when the cyteine concentration is lower than 0,76µM eumelanin is made (see here and here for details).
But this is not the only influence on the reaction. The availibility of dopaquinone is critical, and the activity of the tyrosinase can be influenced by the pH of the melanosome (the compartiment in which the pigment production takes place). The tyrosinase activity for people with dark skin is about 10 times higher than for people with pale skin (see here and here for details). The difference here is mainly the pH, which is neutral for dark skinned people and acidic for pale.
Then there is of course the availibity of tyrosine (which is less of a problem, as this amino acid is not essential) and also the availibity and activity of downstream enzymes for the eumelanin production as tyrosinase-related protein 1 and dopachrome tautomerase.

Thank you Chris, very interesting. I am guessing that there isn't a way to naturally reduce the amount of Cysteine (to increase the chance of producing Eumelanin) or influencing the pH to neutral?

I don't think so.

Is this a "no goer" on any level then? Surely if we can increase Eumelanin we can increase the efficiency against skin cancers.

Is there a way to take an Eumelanin supplement?

I wouldn't say it is completely impossible, but it will be difficult. And the question is, if it is wise to do so. You have to mess around in some pretty fine balanced pathways and nobody knows what side effects this could have. Using sun protection and/or avoid to short clothes in the sun works as well and is non-interventive. If you supplement melanin with the food it will most likely be metabolized.


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What this shape name? (concave laterally and straight medially, cross section shape of crayfish rostrum)
What is a shape name for upper surface (colored black) of the cross-sectional shape in the attached image? It is a cross-section through a crayfish rostrum. It is horizontal and linear medially, but concave laterally. By shape name, I'm thinking of words along the lines of emarginate, cuspidate, etc:

In what way is this a biology question?

This is a shape I see in a crayfish rostrum.  It would be nice to describe it succinctly if possible.

Then please edit the question and include this information in it, possibly with an image.

@crayman9 it would help if you could label the parts of the image or even use a drawing tool to make a better drawing. For instance are the 2 left and 2 right asterisks parts of the body or the claws? Is the line the ventrum of the animal? Which part of the animal was the section through.

Ok, I added a drawing.  I didn't realize it was as simple as drag and drop.

Laggingly/tardily concave is the best I could think of. Imagine it takes time to become concave.


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How is bio electricity modulated experimentally?
In the research performed by Micheal Levin et al, the morphological changes induced by changes in bio electricity are well demonstrated, most strikingly in his experiments in planarian worms.
Yet while doing a comprehensive review of his work, I either did not understand well or overlooked it entirely, but I could not find how he and his team were able to rigorously and meticulously regulate the bioelectricity.
I will be using the following article as a basis Endogenous Bioelectric Signaling Networks: Exploiting Voltage Gradients for Control of Growth and Form
In “Control of Growth and Form” there is mention of “specific ionophores and molecules” as well as changing the the electric fields within cells, but there is no specificity regarding the nature of the compounds and methodology here apart from a generalized overview. So I am unclear how the ion channels are selectively changed with such high degree of precision.
I imagine they are changing the quantities and frequency of certain neurotransmitters but there is only so much I can extrapolate.
My background is solely on chemical synthesis so many of the mechanism and jargon might go over my head and I understand this is a emerging and complicated topic, but any help or re-direction regarding this question/topic would appreciated.

The article you shared is a review article so methods will not be described in detail. You can try cheking the method section of some papers in the reference section to get an idea of keywords to search for.

Ionosphere is a rare or confused term to use in biology, Ion channels make sense... Ionospheres are 99.9% atmospheric, so it makes the term confused to employ in biology. Why not ask chat.openai.com questions like "explain in advanced academic language how bioelectricity is used on a biochemical level to influence growth and development of body structures. " ... OK it's experimental, like asking a confused professor who makes erroneous statements, but it can help you to understand the different areas of the field, then you can look at videos on ion fluxes / electrochemical gradient of cells.

By the way, if you are studying the biochemistry of form development, you should research signalling biochemistry used to decide cell orientation, distance, size and development, because there are chemicals that exist in both arms and legs to make them exactly the same length, and those chemicals also decide thousands of other cellular arrangements. studies have been done on fruit flies, and they have electrical potential so they are in common with the field.

You are correct. I typed ionophore and ionosphere, as I do research on both. I did ask ChatGPT but it gave contradictory and null results.

I would strongly recommend against using chatGPT or any other language model to learn things. These models don't know anything, and if you aren't familiar with a field you won't know when it stumbles into correct or incorrect combinations of words.

I briefly glanced through the paper you link to... It covers a lot but it seems like a reasonable starting point. It's not reasonable, though, to make your question "please explain all of this to me". This would take multiple textbooks. You'll really need to narrow down and focus a bit. Maybe grab an undergraduate neuroscience textbook to start? Purves or Kandel are popular.

Thanks Bryan. Yeah Chat isn’t my first option, I always use it to give it a glance. I’ll absolutely do what you suggest once I can access academic journals again. Out of my university and having problems accessing online research. I’ll edit my question once my knowledge has expanded but thanks  for the advice on Purves and Kandel


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Are SNPs or SSR copy number variation mutations more prominent?
I'm trying to get a sense of the dominant way that mutations occur.  I have seen various numbers which seem at least at first glance to conflict, and I was curious if anyone had clarification on this.
According to Shastry, "SNP alleles in human disease and evolution" (Journal of Human Genetics 47:561–566, 2002),

In two randomly selected human genomes, 99.9% of the DNA sequence is identical. The remaining 0.1% of DNA contains sequence variations. The most common type of such variation is called a single-nucleotide polymorphism, or SNP.

However, according to Nevo, "Genetic Diversity" (Encyclopedia of Biodiversity, 2001),

Significantly, SSRs experience mutation at notably higher rates than do nonrepetitive sequences: $10^{-2}$ to $10^{-3}$ per locus, per gamete, per generation, which leads to their high polymorphism.

Additionally, according to Kashi and King, "Simple Sequence Repeats as Advantageous Mutators in Evolution", (TRENDS in Genetics 22(5):257),

Mutations that alter repeat number typically occur at rates orders of magnitude greater than single-nucleotide point mutations.

So, if variations in organisms is mostly due to SSRs, and this is mostly copy number variation, then would it be correct to say that copy number variants in SSRs is the dominant form of variation, or am I missing something?  Which one is correct, or which source is more authoritative, or is there a more up-to-date review I should be consulting?

NOTE - I added the word "mutations" to the question title to be more clear what I'm asking about.

I like @mgkrebbs answer, I think that it hits most of the high points, but I wrote a review on this subject a couple of years ago where we specifically put together estimates on the mutational load of different mutation classes (see Table 1).
Yaniv Erlich's group directly addressed the question that you are trying to answer, and they estimated that microsatellites contribute slightly more mutations per generation than substitutions:

These predictions indicate that the load of de novo STR [SSR] mutations is at least 75 mutations per generation, rivaling the load of all other known variant types.

Most estimates of diploid overall substitution mutation rates are ~50/generation, for comparison.
However, if you are interested in overall variant number you will also need to take into account an incredibly complex architecture of structural variants in basically any genome, including also plasmids, viruses, and transposons. So when you talk about the "dominant form of variation", you really do need to be a bit more specific. On a per locus or even per mutation class basis, STRs/SSRs probably are "dominant", but it's hard to argue that e.g. 1 STR mutation is more important than one transposon hop or one chromosome aneuploidy or one centromeric satellite contraction.
I'd recommend reading the papers linked for a little more context.

It's not really clear to me what you're after when you ask about how prominent or dominant these two kinds of variations are. But let's look deeper.
Guichoux et al. (1) say:

There are two main differences between SSRs and SNPs. First, SNPs are more numerous than SSRs in the genome of most species. On average, in the human genome, there is one SNP every 100–300 bp (Thorisson et al. 2005), com-pared to one SSR locus every 2–30 kb (Webster et al. 2002), depending on how SSRs are defined (Kelkar et al. 2010).This can be important for genome-wide association studies but not necessarily for other applications. Second, the mutation rate per generation differs drastically between the two marker types. SSRs have mutation rates ranging from $10^3$ to $10^4$ per locus per generation (Ellegren 2000), compared to about $10^9$ for SNPs, i.e. several orders of magnitude lower. As a consequence, SNPs are typically diallelic: In humans, < 0.1% of SNPs are triallelic (Lai 2001).In contrast, SSR loci generally have high allelic richness, often in excess of 10 alleles.

Based on these numbers, SNPs occur perhaps 80 times as often as SSRs.  Is that more prominent?
An SSR is larger than an SNP, covering perhaps one hundred to several hundred bases versus one base (by definition).  An SSR locus also occurs in multiple variants, e.g. having a copy number from a wide range, versus only two possible variants that usually occur for an SNP locus.
The mutation rates are substantially different, apparently typically 5 orders of magnitude more frequent for SSRs than for SNPs.  Note, though, that mutation rate does not directly affect the frequency of variants seen in the genomes of extant organisms: the variants present are a result of the filtering of mutations by the forces of selection.
Note also that all bases are subject to mutation, thereby producing an SNP, but SSR mutations only occur where a repetitive sequence already exists.  (Also, the likelihood of mutation becomes significant only when the existing sequence has more than a few repeats, as the mechanism of mutation depends on this.)
A main question, though, is what is the significance of the variation?  Are you interested in variation just because they mark individual genomes within a population, or are you interested in the variation of the phenotypes of individuals?  Some genetic loci are irrelevant to phenotype and some can affect the phenotype to lesser or greater degree.  SNPs can occur anywhere so can be presumed to have a "fair" chance of affecting phenotype.  On the other hand SSRs can occur where only where repetitive sequences can occur (and persist where they survive selective forces). With SSRs, varying copy number in some contexts such as protein coding sequences, may have larger phenotype effects than an SNP, and thus be subject to stronger selection forces.
My view is that both SSRs and SNPs are important and it's not terribly productive to worry about general prominence or dominance of one over the other.
Reference:
(1) Guichoux, Erwan & Lagache, Lelia & Wagner, Stefanie & Chaumeil, Philippe & Léger, Patrick & Lepais, Olivier & Lepoittevin, Camille & Malausa, Thibaut & Revardel, Emmanuelle & Salin, Franck & Petit, Rémy. (2011). Current trends in microsatellite genotyping. Molecular ecology resources. 11. 591-611. 10.1111/j.1755-0998.2011.03014.x.

The reason I'm interested is that I think that the nature and pacing of evolution is tied to the mechanism of mutation.  I think there is relevance to modeling in population genetics.  If I understand correctly, you are saying that there are far more SNPs in existence than copy-number variants of SSRs.  On a per-base-pair basis, SSRs predominate, but, since they are fewer and further between, this might not mean more actual SSR mutation instances per generation,but it sounds like it it might favor SSRs by about an order of magnitude(4 orders of magnitude less in genome vs 5 orders more likely)


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What accounts for size variation in breeds of dogs?
My assumption is that dogs vary so much in size because of artificial selection pressures coming from human breeders, but are there genetic loci that roughly determine approximate size?  Do other feral species of animals exhibit such a wide range in sizes or is this something that only occurs when breeders intervene?

Shigeta did a great job summarizing what we know about genotypes and dog size variations, does anyone know whether there are wild species that also very so dramatically in size?

This is a fascinating bit of genetics.
Dogs are especially variable in size and many appearance, behavioral and temperamental phenotypes.  It was long expected that variations in developmental genes were the reason that dog breeds were responsible for the amazing flexibility of dog sizes.  One early locus found was IGF1 (insulin like Growth Factor 1).
This 2011 PLOS paper actually review the specific genotypes of dog breeds and identifying loci that are strongly associated with breed phenotype supports this idea.

... (we scanned) the genome for signatures of selective sweeps in single breeds, characterized by long regions of reduced heterozygosity and fixation of extended haplotypes. These scans identify hundreds of regions, including 22 blocks of homozygosity longer than one megabase in certain breeds. Candidate selection loci are strongly enriched for developmental genes. We chose one highly differentiated region, associated with body size and ear morphology, and characterized it using high-throughput sequencing to provide a list of variants that may directly affect these traits.

Emphasis added.
This theory has an intuitive appeal as well - no dog breeds (I think) are larger than the wolf, the stock from which all dog breeds are descended.  All such breeds being derived from earlier developmental stages of the wolf makes an intuitive, if imprecise description of the effect here.
Regardless, dogs remain an important model organism for so many traits because relatively few genomic regions can cause so many important phenotypes, including size, but also behavioral and morphological variations.
In the below figure you can see how few genomic regions are responsible for the 46 breeds Vaysee et al. examined.


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What's the recommended maximum passage number for mammalian cells (NCI-H441)?
Is there a generally accepted maximum number of times you should split and reseed mammalian culture cells before restarting cultures from new stock?

I only know the maxime to keep the passage number as low as possible. Especially in immortalized cell lines funny things can happen, we once found a cell line in the lab (I think it was 293T) that was hexaploid for some chromosomes...So split cell lines in early passage numbers and make stocks. The problem you have with cells from other labs is that you often don't know how long the line has been in culture...

Yeah, unfortunately this was the first time I had done any mammalian tissue culturing, by the time I had grown enough to make a sufficiently large stock of frozen cells, I had already hit passage number 6. I was thinking I would draw from frozen stock each time my current line hits passage number 10. Does that seem reasonable or should I buy new cells? We sourced our current cells directly from the American Type Culture Collection.

How long does it take to do six passages?

About 9 weeks. :/ I made a lot of dumb errors at the start.

If your cells come from ATCC they shouldn't be in culture for ages, since they are one of the good cell banks. I would still use this cell stocks and I would also test, how long you can keep them in culture without noticing changes in behavious and/or shape. What does ATCC recommend here?

This is a very good question and it highlights a very frequent misconception about cell culture and it is using the passage numbers as an indication of how well a cell is behaving. Although this can be a good barometer but it is misleading. Passaging can stress the cells if performed very frequently, although again that depends on how fast the cells are dividing.
You should not think of passage (and cell culture in general) in terms of the procedure itself but in terms of population doubling (PD) which can be calculated using the formula provided here (http://www.sciencellonline.com/site/techsupport.php). I personally use [Log10(harvesting cell No/seeding cell No)/Log10(2)]. This should allow you to characterise your cellular behaviour between every passage and allows you to draw a cumulative PD graph. Once the cumulative PD versus time becomes non-linear, then you would know that the cells have changed behaviour and it might be best to use a fresh stock.
The main advantage of this method is that you are not relying on guess work and deal with solid numbers and allows you to predict when you should expect to start a fresh batch for passage. Although passage numbers can do the same job if you assume per passage, the cells have done a certain PD but this is more of a guess work and you can not track how well your cells are doing at a given time point. For example one of the main problems with using a passage as a measure is that you can passage the cells at 98% confluence to a fresh flask and although that counts as a passage but it is pretty uninformative in terms of cell behaviour and gives you no solid numbers and you can do this many many times and although you would have done high number of passages but your cells would appear ok. Although such an exercise is pointless and will probably stress the cells but it is just to make the point that passage numbers are not necessarily a very informative and quantifiable measure of how well the cells are doing or behaving hence PD and cumulative PD should be used. Another advantage is that since you are dealing with actual cell numbers, if you changed your cell culture flask size from lets say T-75 to T-25, you don't have to be worried about changes to your frequency of passage or having to make further guess work on how that has effected your cell behaviour.
My main advice is that you should keep you frequency of passage the same at least in the beginning (although keep an eye on the cell density as you don't perhaps want to let cells to be too over-confluent or unconfluent when passaging, depending on your specific methodology and what has been established in your lab), but count your seeding and harvesting density (cell No) and calculate the PD and cumulative PD and draw a cumulative PD vs time graph and monitor the behaviour of cells. This should give you a good indication of you cellular behaviour under the conditions you are working with them since guidelines are just that, guides and they can never substitute experimental characterisation of your cells under your conditions and handling method!


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Does a blood transfusion cure disease?
Does transferring blood between two people also transfer all the white blood cells?
Why can't AIDS victims with low t-cell count just get blood transfusions till they have more t-cells? Why can't someone who's over a cold give blood to someone with a cold to cure them? I know this is silly, but I really want to know why this won't work.

Don't know if this qualifies as a disease, but have you heard of the experiment that supposedly slowed down ageing by transfusing blood from young to old mice?
It was a normal transfusion, consisting just of RBCs as described by @Amory, and apparently, there was something in the young blood that decreased in concentration as the mice aged.
See here and here for more info.

Wow, that's some sci fi stuff. I assume it will lead to a dystopian future where everyone is Elizabeth Bathory - https://en.wikipedia.org/wiki/Elizabeth_B%C3%A1thory

t-cells do not last forever, the victims would need constant transfusion.

Not really no.  Most blood transfusions we think about are red blood cells or platelets, which don't have the immune function you're asking for.  That's a good thing.  Usually, if there are white blood cells in the transfused blood, the host's immune system will recognize them as foreign and destroy them.  Remember, your cells all look like foreign invaders to my cells; blood transfusions of red blood cells are carefully matched to limit negative reactions.  There is also a process called transfusion-associated graft versus host disease in which the donor white blood cells will attack the host cells; this mainly occurs in immune-compromised individuals, but GvHD is definitely something to avoid.  Blood transfusions are usually filtered and irradiated to remove, among other things, white blood cells.
That being said, people are beginning to use white blood cells as treatment.  A new therapy being studied heavily for all sorts of diseases, from cancer to HIV, is to take the hosts own white blood cells and grow them up in the lab to select for the strongest and most effective cells.  The researchers then wipe out the individual's immune system and give them a dose of their own, super-powered white blood cells, hoping that works.
Sometimes it kind of does.  They've also been trying a new system, similar to what you propose, using bone marrow.  They had a huge success with an HIV-positive individual now referred to as "the Berlin patient."  They gave him a marrow transfusion which would produce HIV-immune white blood cells and replaced his immune system.  He was and is effectively cured of HIV/AIDS.

Wow interesting! But why do they have to wipe out the host's immune system before injecting the "super white blood cells" that they grew?
Also why can parts of the body be transplanted without (usually) being destroyed like the white blood cells? Are blood cells more scrutinized by the native white ones?

@CornSmith To answer your first question, it's usually a numbers game.  No matter how many cells the researchers can grow your body is probably producing more.  A virus like HIV, for example, infects T-cells, so if 5% are super-charged but 95% are still susceptible...

As for your second question, all transplants are hugely scrutinized, far more than red blood cells.  We distinguish our own tissues from foreign ones using the MHC antigens, and they're very difficult to match perfectly; siblings, for example, have only a one-in-four chance of matching up.  If there's any difference, there will be an immune reaction.  In most cases, there will be some attack, which is why people can reject transplants (in the worst cases) and why almost everyone receiving a donation takes immune-suppressors.  It's better to have a liver.


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How different are tissue-specific fibroblasts from each other?
I am planning to utilize a new system in our lab, in which I will co-culture cancer cells from different tissues with fibroblasts.
I have the option to receive skin-derived primary fibroblasts. I have been told the normal fibroblasts are very similar all over the body. Is this really true? I assume that fibroblasts secrete factors, for example, that are tissue specific. The question is, how quickly do they adapt to a new environment? For example if I take these skin-derived fibroblasts and co-culture them with breast cancer cells, how long will it take the fibroblasts, if any, to become more like fibroblasts derived from the breast?

I have been told the normal fibroblasts are very similar all over the body. Is this really true?

No.

Strong evidence indicates that fibroblasts in different parts of the body are intrinsically different, and there may be differences between them even in a single region [3].

They have morphological similarities, but they act differently (at least in cultures):

Examination of skin and lung fibroblasts derived from the same human fetuses revealed significant in vitro differences. Fetal lung cultures had faster cell replication rates, greater [$^3H$]thymidine incorporation into DNA, higher cell numbers at confluency, smaller cell volumes, decreased cellular RNA and protein contents and lengthened in vitro life spans when compared with fetal skin cultures. In addition, these cell cultures had different responses to the addition of hydrocortisone to culture media [1].

They hardly adapt to a different serum (in vitro) [2]. Yet they have a great capacity to differentiate (in vivo):

[...] fibroblasts also seem to be the most versatile of connective-tissue cells, displaying a remarkable capacity to differentiate into other members of the family. [...] “Mature” fibroblasts with a lesser capacity for transformation may, for example, exist side by side with “immature” fibroblasts (often called mesenchymal cells) that can develop into a variety of mature cell types [3].

References:

E.L. Schneider, Y. Mitsui, K.S. Au, S. Stuart Shorr. Tissue-specific differences in cultured human diploid fibroblasts. Experimental Cell Research. Volume 108, Issue 1, August 1977, Pages 1–6. DOI 10.1016/S0014-4827(77)80002-5
Zamansky, GLEN B., et al. "Adaptation of human diploid fibroblasts in vitro to serum from different sources." Journal of cell science 61.1 (1983): 289-297.
Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Fibroblasts and Their Transformations: The Connective-Tissue Cell Family. Available from: http://www.ncbi.nlm.nih.gov/books/NBK26889/


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Ticks hitching a ride on a fly?
Recently, my brother has been bothered by some particularly aggressive houseflies.
According to him, when these flies are squished, there is often a clacking noise, and then small arachnids come crawling off or out of the body (it's unclear which).
He recently managed to take pictures (see hereunder) where two of the things are in view, and I tentatively recognized them as ticks.

Apparently the clacking noise is produced when the arachnids are squished.
Are these actually ticks ? And is this normal behaviour ? I haven't managed to find anything about ticks hitching a ride on flies, but I don't have any other ideas.
If it helps, he lives in Brittany, in western France.
Edit : For scale, the fly in the pictures was a little below 1cm long

Viewer discretion advised: The image above contains blood and violence ;) Jokes aside, I haven't heard of ticks riding on flies, but I read that they can carry parasites such as pinworms, roundworms, hookworms and tapeworms.. Here is some more info

There are mites that ride on bumble bees.  https://www.bumblebeeconservation.org/bee-faqs/bumblebee-mites/

Do you have a scale on how big those are? Most mites are <1 mm across.

@bob1 the fly was a bit under 1cm, i'll edit the question to add this

@NinDjak - great, that makes these <1 mm, so they are likely to be mites.

What about seed ticks? They are very tiny as well. I am thinking flies can carry them.

These are not ticks. They're parasitic mites

Without a close up examination of the subjects, which would require microscope images or a decent macro image it is impossible to identify these creatures with any certainty to the level of species. With that in mind I will give an attempt at an answer.
These creatures are not ticks, they are almost certainly mites. Mites are of the subclass Acari within the Arachnida (spiders and scorpions also belong to this class). Ticks also belong in the Acari, so they are closely related to mites and quite similar morpholgically.
Mites are quite diverse, but generally less than 1 mm (0.039 inches) in length and are very diverse in what they feed on, ranging from being decomposers in the soil, to grazing algae in water, to feeding on plants and parasitising animals. As humans we have a particularly odd one (to me at least) called Demodex that lives in hair follicles, eating the sebaceous (oily) secretions and dead skin cells from around the hair.
For insects I believe (with no certainty, experts please weigh in) that the majority of mites are parasitic, feeding on the insects hemolymph (blood equivalent for insects) by puncturing the seals at the joints in the exoskeleton. Incidentally, you can see some mites feeding on the legs of the crane-fly in this SE Biology post.
In the case of the OP we are likely looking at a parasitic mite of the common house fly (Musca domestica, which have left the now dead insect as their food source is no longer supplying food.
Flies do have a common mite species Macrocheles muscaedomesticae, which is a mite that feeds on the eggs, and to some extent the larvae of the house fly and several other species of fly, and may also be associated with a range of other insects (see Biology Ecology sections here). The mite is found world-wide and is believed to be distributed on the adult flies. It is uncertain if the mite actually attaches to the adult fly while it is being carried.
There are several species in the Macrocheles genus, which all parasitise in a similar manner to M muscaedomesticae. There are also a few other species of mites that seem to parasitise house flies, including Poecilochirus species, but these are less species-specific as far as I can tell.

A very thorough answer, thank you ! Since your mention of mites in the comments i've also found references to mites being used for house fly control in livestock farms , so this definitely checks out.
I doubt there's much more to add, and the question's been open for a few days, so I'll mark this as accepted answer.


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dilutions in bacterial culture
In overnight bacterial culture, why do we put bacteria in a small flask to culture before moving it to a larger flask? Why not just put the sample in a large flask to begin with? This is in reference to growing e. coli to produce proteins in a 125mL flask overnight first, then over a liter after that. For recombinant protein expression.

Not sure, but it may have to do with equalizing/standardizing the size of the initial innoculum for the large culture.  Normally you want to harvest the large flask while it is still growing in log phase or otherwise appropriate condition. If your initial innoculum varies widely in number of cells, time to harvest of the large flask can also vary substantially. It might also have to do with maintaining selection for a plasmid, as partially permissive culture conditions under many generations can lead to selection for faster growth/loss/deletion of plasmid.

@Val Can you please give a specific example of a protocol you're working with? With what you've written right now, there's too much unknown to be able to answer your question clearly.

While this is old and therefore unlikely to be marked as answered, it can be easily answered.
The comments have it correct; it is to standardize the inoculum so that you get your culture to the correct density after a set time of incubation. It also helps eliminate problems associated with not selecting the correct colony and ending up with nothing growing.
In culture of E. coli, assuming ideal growth conditions, the cells reach a maximum density of greater than 109 colony forming units per milliliter1.
For your protein expression culture ideally you want the culture growing vigorously as this is the point where the most proteins are being produced and you want the culture to be at a high density too, so that you maximize the amount of protein produced. Typically this is done by inoculating using your overnight culture at 0.5-1% of final medium volume (e.g. 5-10 ml overnight culture into 1 litre protein production medium) and then growing to mid-log phase growth at optical densities (600 nm; OD600) between 0.6 and 0.9. See flow chart at Figure 2 from this publication2.
You can, of course, inoculate with a much lower volume or even from a colony picked off a plate, however, this results in a very long incubation time before you reach the log-phase growth you are targeting, often extending the incubation time from a couple of hours to 8 or more, which is not ideal for a working day and you'll spend much of your day monitoring the culture for growth hoping to not overshoot the point wanted. The difference in incubation time between 0.6 and 0.9 can be as little as about 30-40 min, so you don't want to miss this after having incubated for 8 hours - better to do it with the short incubation.
Growth in a large volume from single or even a few colonies also leaves you prone to time wasting in the form of selecting colonies that don't contain your target protein; they've lost the plasmid somehow. A quick overnight culture allows you to be sure that you have something growing before inoculation.
References:

Tuttle AR, Trahan ND, Son MS. Growth and Maintenance of Escherichia coli Laboratory Strains. Curr Protoc. 2021 Jan;1(1):e20. doi: 10.1002/cpz1.20. Erratum in: Curr Protoc. 2022 Aug;2(8):e552. Erratum in: Curr Protoc. 2022 Aug;2(8):e551. PMID: 33484484; PMCID: PMC8006063.

Francis DM, Page R. Strategies to optimize protein expression in E. coli. Curr Protoc Protein Sci. 2010 Aug;Chapter 5(1):5.24.1-5.24.29. doi: 10.1002/0471140864.ps0524s61. PMID: 20814932; PMCID: PMC7162232.


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Unknown Issue with qPCR Standard
I am currently doing the ground work for a SELEX experiment and I am attempting to verify my standards for the starting library. I ran a reaction with samples containing 50, 5, 0.5, and 0.05ng of my starting library and the samples for the 5, 0.5, and 0.05 appear to amplify as expected, but whenever I run a sample containing 50ng of my starter library, the curves start around -2000 RFU and peak at 0 RFU. Has anyone seen this behavior before?
EDIT: Added annotated graph
Method: SYBR Green
System: Bio-rad CFX384
Software: Bro-rad CFX Manager

Can you please label your curves to make it clear which is which? Also, how are you computing RFU? Getting negative fluorescence usually indicates a process failure of some sort.

@jakebeal My apologies, I should have annotated it from the start. I've updated the post to include the annotated graph and more information. I am reading RFU with SYBR Green on a Bio-Rad CFX384. I've performed this assay several times with fresh dilutions of library DNA and the results seem to be the same each time.

I'm not too familiar with SELEX, but just looking at the curves, it seems like a baseline normalization issue. The Bio-Rad software that I use automatically normalizes amplification curves to a baseline average from the first few cycles. Since your 50ng wells were hot from the start, it looks like it took the saturated endpoint fluorescence as baseline, and normalized the rest of the curve to that. You can turn normalization off in the software, but probably still won't be able to get a good Cq value for the 50ng curves.

@MikeyC This does seem like the most likely explanation. The only thing that might make a difference in this regard is that I did run a no-template control which was stable at 0 throughout the run. It is not pictured here because it covered up a portion of the 50ng sample curve. I am new to this system so I am not totally sure how it goes about calculating a baseline. Thank you for your input.

@jakebeal The no-template control doesn't factor in. The software determines a different baseline for each well, which it subtracts from that well's fluorescence readings throughout the run so they can all lineup at 0 for the first few cycles. It's just not getting a usable baseline from those wells, so it's subtracting the saturated fluorescence instead. You can disable baseline subtraction under the Settings menu in your CFX manager software. Only problem is, you can't set a threshold for Cq determination without baseline subtraction.

@MikeyC If you're right, then yes, definitely a process failure --- and yet another example of why I never let instrument software handle calibration processes. Can you please turn your comments into an answer so that they can be voted up?


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Spider identification North-West Italy
I would like to know what kind of spider is the one I killed and if it is somehow dangerous.

Location: city in North-West Italy.
Dimensions: ~1.5 cm, with legs opened.
Time of day: around midday, but the external jalousie of my window was closed, so it was dark when I found it.

It seemed to have some sort of marking on its abdomen, but colors were very dark, so it was difficult to view it properly.
Edit: The marking was some sort of symmetrical shape covering quite all the abdomen. Colors were very dark and it was difficult to distinguish it properly from the rest of the abdomen.

Unfortunately I didn't photograph it when was alive, and intact, because I found it out of my window and I didn't want to lose its tracks while getting my phone.
For what I know, the most dangerous spider that can be found here is the Loxosceles rufescens (Mediterranean recluse spider); it seems different, but obviously I'm not an expert.
Thank you very much!

Welcome to Biology.SE. You've done a good job on supplying the information needed for ids, but I'm not sure what you mean by a "form on its abdomen". Do you mean a marking and if so is it a different color, texture, or something else? Any additional information you can [edit] into your post will increase the chances of getting an accurate id.

Here is a gallery of species observed and submitted to the iNaturalist website... filtered the species by limiting the search to 'typical spiders' (excludes tarantulas or other weird things) and limiting the search to NW Italy. Sorted by most-commonly observed first. You can click on the "N Observations" to see the submitted photos that are currently IDed to that species (not necessarily a correct ID) https://inaturalist.ca/observations?nelat=46&nelng=13&place_id=any&subview=map&swlat=42&swlng=4.5&taxon_id=120474&view=species


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Do Colorblind People Have Stronger Sensitivity in Their Other Remaining Cones?
I came across this paper Color defect and color theory. The paper explained about how unilateral color blind (people who color blind only in 1 eye) actually see less bright in their color-blind eye (in graph : filled bullet) compared to the normal eye (in graph : white bullet). Especially to the scene that corresponds to the missing cone (in this paper, Deuteranopes. Missing cones = green)

I have 2 questions regarding this brightness loss in color blind people.

Green cones response are near the red cones response, and they are overlapping. How is it possible that Deuteranopes loss brightness in Green and Blue (which will make more sense if they also loss brightness in Red, thus loss brightness in the whole spectrum) but instead, still achieve the same amount of brightness in Red ? Despite Red and Green color-blind have the same color combination possibility (gamut mapping) that they can perceive ?
Could it be that color-blind people have stronger sensitivity in other cones (for example : stronger in red) and then this red opsin actually replace / fill the missing cones stimuli in retina, so their retina still able to perceive the same amount of brightness on that excessive cones ?

Kudos for Delta-S in Reddit for enlighten me. Original post is here.
The answer is no, color blind people don't have stronger sensitivity in their other remaining cones. This goes back to the Photopic Sensitivity Graph below.
As you can see, human vision are most sensitive to green. All responses of green cone are within the photopic sensitivity as well as most response of the red cones. And despite few responses of red cones are outside the Photopic sensitivity, the peak sensitivity of red cones is very close to the peak of Photopic sensitivity (560nm and 555nm).

Peak Photopic Sensitivity: 555nm
S cones peak  : 420nm
M cones peak  : 530nm
L cones peak  : 560nm

So, in case of Deuteranopic, depending on which wavelength is loss (defected) from their eye, if it closer to the red response then they will likely to experience luminance loss as well. However, if the green cone that is defected is far from the red response, the red cones still have possibility to maintain the luminance they can achieve.
Unfortunately in the paper, it's not mentioned which sensitivity wavelength was defected from the unilateral participant. It is only mentioned "result indicate that she was deuteranopic".