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Are plasmids found in eukaryotes?
There are some who says plasmids are found in some eukaryotes but is it like scientifically proven?

Welcome to SE.biology. Please take a look around the help center on how to ask a good question. In particular, it's expected you show evidence of prior research on your question, and also include links to information you cite, rather than just 'there are some who say...'. Thank you.

These resources may help.
This book, “Plasmids of Eukaryotes”, explains that...
“The possession of plasmids was for a long time recognized only in the bacteria. It is now evident that plasmids, or replicative forms of DNA structurally and experimentally comparable to bacterial plasmids, exist in eukaryotic organisms as well. Such plasmids are in fact common among fungi and higher plants.”
Also, this website (ScienceDirect) explains that...
“Most plasmids inhabit bacteria, and indeed around 50% of bacteria found in the wild contain one or more plasmids. Plasmids are also found in higher organisms such as yeast and fungi. The 2 micron circle of yeast (discussed later) is a well-known example that has been modified for use as a cloning vector.“


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What is this plant, and should the lowermost leaves be curling up?
We've got a couple of these plants but have no idea how to look after them. Watering them regularly (every 2-3 days, or when the soil seems dry) seems to help. The pot rims are about a foot at their widest part.
However, we're concerned about the lower leaves drying up. Is this a normal part of this plants growth process and does it continue this way and produce a 'trunk' of sorts?
As a follow on question, do we need to re-pot these plants?

I think you are likely to find more knowledgeable help at Gardening.stackexchange

I may be wrong, but I believe these are two Foxtail Agaves (Agave attenuata). These resources may help you take care of them.
Foxtail Agave Care Information
And for the wilted leaves:
How to Save a Dying Agave Plant
Also, the Gardening SE may be able to help more.
Hopefully this helps!

source: Stack Exchange

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

sort: votes


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Did the jackal (wild African dog) evolve independently or with some form of human domestication?
The jackal is a wild dog species in Africa that feeds on carrion, much like the hyena.
Pop science, as it were, would make us believe every dog species emerged as a result of human domestication. Was that the case for every dog species? Or might some have evolved independently?
Another way to phrase this would be: Do wild dog species have a completely wild heritage, or did they branch off of some previously domesticated line?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, this is a site for biology questions and your references to Egyptian mythology seem irrelevant (I will delete these). ——— We also expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). The wikipedia article on jackals is one place you could start. Thanks!

This answer is just for African golden jackal evolution, but this website (sciencemag.org) explains that...
“...researchers compared genomewide DNA samples from jackals, gray wolves, and dogs. They found that African golden jackals diverged from coyotes and gray wolves some 1.3 million years ago...”.
Also, this Wikipedia article about Canis arnensis (the Arno river dog) (I know that Wikipedia is unreliable but it had related helpful information) explains that...
“The Arno River dog has been described as a small jackal-like dog. Its anatomy and morphology relate it more to the modern golden jackal (Canis aureus) than to the larger Etruscan wolf of that time. It is probably the ancestor of modern jackals.”

Interesting, "wild dog" seems to be a misnomer then. It's more of a wolf species. Thanks for the input.

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


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Narwhal tusk evolution
I was reading about whales and wondered why did only narwhals, among all other species of whales, evolve to have tusks? Is there a specific environmental reason, for example something unique about the Arctic environment that requires them to have a tusk for easier survival?
I researched a bit and found many reasons why narwhals have tusks (e.g. weapons for fighting other male narwhals to compete for mates, sensing the environment, attracting female narwhals, echolocation, stunning prey for easier hunting) but couldn’t find a reason why other whales do not have tusks.
Sources:
https://www.google.com/amp/s/api.nationalgeographic.com/distribution/public/amp/news/2017/05/drone-footage-narwhal-tusk-mystery
https://www.google.com/amp/s/ocean.si.edu/ocean-life/marine-mammals/why-tusk-real-life-unicorns-sea-and-tusks-make-them-famous%3famp=
https://oceanconservancy.org/blog/2019/03/08/exactly-narwhal-tusk/
https://scholarblogs.emory.edu/evolutionshorts/2014/04/25/the-evolutionary-significance-of-the-narwhals-tusk/

Can you tell us more about what you found out? https://www.google.com/search?channel=fs&client=ubuntu&q=narwhal+tusk+evolution  "Why not others?" would have to do with differences in selective pressures (operational sex ratios, ecological context, etc.) between ancestors of narwhals and their closest relatives ...

@BenBolker Thanks for the answer! Edited accordingly, is this better?

Unusual features in animals (and the narwhal tusk certainly must qualify) can most often be explained by advantages provided for foraging, defense against predators, adaptation to extreme environments or in connection to reproduction. It is common for the three first explanations that one will expect to see the feature in both males and females, whereas the opposite is the case when it comes to reproductive specializations. I'm sure people can come up with exceptions, but as a general rule it is useful. Hence, the most likely explanation for the (male) narwhal's tusk is that it gives them advantage in reproduction, analogous to antlers in male deer, and also the tusks seen in males of most beaked whale species. Exactly what advantage a large tusk gives a male narwhal is difficult to find out, but if they engage in head-butting, as is not uncommon among male mammals when fighting over females or territories, it seems fair to assume that early proto-narhwal males, with one or more slightly protruding tooth had an advantage, as they could injure their competitors with this tooth. Just as seen in the paired scars many male beaked whales have, which closely match the distance between the tusks in their lower jaw. Once such males with a protruding tooth were around, it is easy to see why there would be a strong selection for having the longest tusk in a head-butting competition!
Alternatively (or in combination), tusks could be a form of 'honest signal', useful for females to judge the health status and strength of the male. It must be a very large handicap for a male narwhal to have a large tusk. Not only does it make swimming (and turning) very difficult (imagine swimming with a 2 m pole stuck to your forehead), it also warns potential prey well in advance about the arrival of the whale. If a male has a large tusk, it therefore must mean that it has been able to not only survive but also grow the long tusk and therefore would be expected to have good genes.
If one wants to explain the narwhal's tusk with one of the alternative proposals, a lot of additional explanation is required. Especially important is the question of why females do not have tusks, if they are so useful to males. And yes, occasionally female narwhals do have a tusk, but they are tiny and unlikely to be functional in the same way as the males'. Because females don't have a (large) tusk, it is difficult to believe that it has a function related to the Arctic environment, or that it has an important role as a sensory organ. The walrus is a very good example of the opposite. Here the tusk are clearly useful in foraging and to make it possible for the animals to get up on the ice, which is why also females have them.
Explaining why narwhals are the only whales with a tusk is close to impossible and also less informative. Evolution does not result in the most optimal solutions to all problems. Rather, it works by the principle of improving something that already works a little bit in the right direction. This often results in many different solutions to the same problem, for example the above-mentioned tusks in beaked whales.


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Visual Quality Indicators for Soil and Plants
I would like to know what are the visual indicators that can be used to determining the quality of the soil and plants by looking at the in-situ photos?
Can the following quality indicators be determined by visual check such that a decision making can be done?

Approximate Soil Salinity
Soil pH
Soil Moisture
Soil Content (red indicates presence of iron etc)

For Plants

Presence of weeds
Presence of bug infestation (perhaps different visual patterns to
identify kind of infestation)
Plant Health (rigid looking vs hanging etc)

The above is whats there in the top of my head, can this list be expanded and upto what degree the quality indicators can be relied upon?

Note: Soil salinity might not be easily determined if the excess salt doesn't precipitate (visible white layer on the soil can help determine the excess of salt hence its not a good visual quality indicator for most of the time.

The type of plants, and their health helps decide what the soil is like, and whether overgrazing has occurred. Sorry no refs yet

@PolypipeWrangler Good point. But perhaps when we plant a seed, we might not have a visual evidence from the plant itself so a visual inspection of soil itself might be required. I am looking to see if algorithms for computer vision could be extended to assist and encourage planting.

There are numerous visual indicators for various type of plants that determine plant health. For example the rigidity of the leaves can help you determine that enough water is supplied to the plant (1). Now you can also determine the leaf shape and detect for presence of disease (2), pests (3), and plant health in general (4). This research however mentions no correlation between lamina shape and area so you would need wiser methods for your corrlelation methodology(5). Moreover, you can look at the fruit shape/sizes to determine if plants have been supplied enough nutrients(6). Another study which is worth mentioning is using chlorophyl to determine plant fitness but this cant be done insitu and you would need lab analysis (7)
All these are visual indicators for the plants itself. As far as soil is concerned is it more challenging because you can make soil and compost using various materials and methods so there is no general approach that can be used to determine the quality. So if soils is your primary concern then as @PolypipeWrangler mentioned looking at the plant fitness can help you determine soil quality.


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Why doesn't the polar side of the plasma membrane block nonpolar diffusion?
It is often stated that small molecules or nonpolar molecules can diffuse through the plasma membrane because they can pass through the middle nonpolar bit, but why don't the polar sides block these nonpolar molecules. Estrogen is nonpolar and can diffuse across the membrane right? Why don't the polar heads of the phospholipids block it? Or look at H+. H+ can't diffuse across the membrane because it's charged (it's not like nonpolar molecule have a repulsive force against it, neutral objects don't repel charged ones as far as I am aware, I don't get why we say polar and nonpolar repel each other, as I understand they just stick to themselves better than each other). Regardless, H+ a small charged molecule would be able to get past the hydrophilic heads right? Estrogen wouldn't be. Where am I going wrong here?
Thanks!

You might get the answers you're looking for on the chemistry stackexchange

Polar and nonpolar molecules don't actually "repel", it's that polar molecules attract each other much more than nonpolar molecules attract anything. Therefore, to take a polar molecule from the (polar) water on one side of the membrane and bury it in the nonpolar region in the middle of the membrane is difficult because it means breaking its relatively strong interactions with the polar water molecules without forming new strong interactions to compensate.
In the case of a nonpolar molecule passing through the membrane, it is already in water when it approaches the membrane, and transferring it past the polar head groups isn't much "worse" (there's likely a slight effect of the often charged head groups attracting ions that bridge them to one another, but this would be small). The large effect of it being nonpolar, however, is to make it less unfavorable to move it into the middle layer of the membrane where there aren't polar groups for it to interact with.


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1% water solution of deoxycholic acid. How is it prepared?
According to Sigma, the solubility of deoxycholic acid is:

0.24 g/L in water at 15C

According to the FDA, Kybella (trademark) is a 1% water solution of deoxycholic acid.
How did they do this?

Which wikipedia site are you referring to?

[link]https://en.wikipedia.org/wiki/Deoxycholic_acid

Not sure this is really a biology question.

According to the sigma document you referenced (emphasis added by me):

"The free acid is soluble at 0.24 g/L in water at 15ºC, while the sodium salt is soluble at >333 g/L in water at 15ºC. Therefore, pH control is very important to the use of this product. Aqueous solutions precipitate as the pH is lowered to 5."

According to the FDA document (emphasis added by me):

"Each 2 mL vial of KYBELLA® (deoxycholic acid) injection contains 20 mg synthetic deoxycholic acid as the active ingredient and the following inactive ingredients: benzyl alcohol(18 mg), dibasic sodium phosphate (2.84 mg), sodium chloride (8.76 mg), sodium hydroxide(2.86 mg) in water for injection, USP. Hydrochloric acid and additional sodium hydroxide are added as necessary to adjust the formulation to pH 8.3."

The solubility of 0.24 g/L in water at 15ºC is determined by dissolution of the free acid in pure water. As you dissolve an acid in pure water, the pH will get progressively lower, and since this compound is less soluble at lower pH, it limits it's own solubility in pure water.
The sodium hydroxide in the KYBELLA is a strong base, which raises the pH and, when mixed with the deoxycholic acid, forms an aqueous sodium salt and water via an acid-base reaction. The conjugate base of deoxycholic acid in aqueous solution is deoxycholate. This portion of the compound remains unchanged, regardless if it is part of a free acid or a sodium salt. The sodium phosphate is a buffering compound which helps stabilize the pH and allows for finer adjustment to control the final pH to ensure it remains soluble.


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What is the process of aging exactly?
Getting old
Hello community, I have been thinking about age, and I thought that aging is the reverse of how a biological system is able to fix itself over time. Actually, some species actually are able to reverse it completely, such as the jellyfish and lobsters for up to 400 years in the Greenland sharks. Moreover, by evolution principle, those species must've exchanged this ability over others, which is noticeable considering they're really adapted to their habitats.
What does research tell us on aging so far?

According to Britannica, aging affects many dimensions for all humans.

So, when scientists are talking about "a cure to aging", I cannot comprehend whether they're proving that those are symptoms of some biological factor (such as producing a certain gene, etc.) or whether all of them share the likelihood to appear more often over a certain age?

How can studying those species help science advance in research?

this is an awfully broad question. Can you start with https://en.wikipedia.org/wiki/Ageing#Biological_basis and narrow down your question?


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Do adult mammalian cochlear inner hair cells regenerate?
The consensus seems to be no, but I see conflicting evidence.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5361427/

Supernumerary human hair cells—signs of regeneration or impaired development? A field emission scanning electron microscopy study

The combination of scarring and proximity to the supernumerary cells suggests it is regeneration and not just misplacement.
Do adult mammalian cochlear inner hair cells regenerate?

Short answer
The current consensus is that hair cells in the cochlea of humans do not regenerate spontaneously.
Background
I took the liberty to show the linked paper to a colleague of mine. This guy has been doing histology on the inner ear for his entire professional career.
He pointed out that the consensus is that in mammals, cochlear hair cells do not regenerate. This as opposed to birds and fish where they can regenerate. In mammals, vestibular hair cells can also regenerate (Santaolalla et al., 2013).
Where do these 'supernumerary inner hair cells' (sIHCs) the authors of the paper show in their (quite stunning) EM photos come from? I wish to point you to the last lines of the Discussion of your linked paper (Rask-Anderson et al., 2017):

Taken together, it cannot be settled if the sIHC represent renewed or redundant accessory IHCs. Further molecular studies are needed to verify if the regenerative capacity of the human auditory periphery might have been underestimated.

In other words, the extra hair cells may have appeared during development in utero, or perhaps due to regenerative processes later on. Note that the inner ear in mammals is fully developed and doesn't grow anymore in size. The EM photos in the article don't allow for the identification of functionality either. Also note that sIHCs have been identified in the 1800s in other animals and that the beauty of this paper lies more in the fact that it shows that sIHCs exist in humans, rather than showing that IHCs regenerate in man (that would likely not appear in the Upsula journal of medical sciences, but in Nature or the likes). On a side note - the authors of the paper are giants in the field.
Literature
- Rask-Andersen, Ups J Med Sci (2017); 122(1): 1–19
- Santaolalla et al., Neural Regen Res (2013); 8(24): 2284–9


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Is the mRNA produced constant during time?
I am doing a statistical data analysis of a dataset of P. Furiosus cells exposed to gamma radiation.
For the samples exposed to gamma radiation, I have the values of mRNA produced over time. For the samples not exposed to gamma radiation (reference samples), I do not have the time at which the mRNA has been extracted.
Therefore, I was wondering: under normal conditions, generally, is the mRNA produced constant with respect to time? I thought that maybe the fact that is constant could be the reason for which there are not the values of time.

If your sample culture is asynchronous, meaning they're at all different stages of the cell cycle, then mRNA production should be consistent over time. However, if you use chemicals or environmental conditions to synchronize the culture, then release it, you'll see periodic production of mRNA for a while until the cells start to gradually slip out of synchrony. For your paper, I highly doubt they synchronized the cells, otherwise they would have clearly mentioned it.

thank you  @MattDMo but I do not really get the meaning of "consistent over time" ?


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Why exactly are the reflections of sunlight in this dragonfly's eye hexagonal?
I photographed a rather cooperative, large dragonfly today and after getting back to my desk and looking closer at the images I realized that the reflection of the Sun in its eyes produced large hexagonal bright spots that are:

much larger/wider than if the eye surface were smooth specular reflector
relatively uniform in brightness all the way to the edge
have very sharp edges, transition from bright to dull red is very abrupt.

I'm aware that the components of compound eyes are usually at least roughly hexagonally packed, but what is happening here is something more than that.
What is it about a dragonfly's compound eye that can account for all three of these characteristics of reflected sunlight?
Presumably this is the same red dragonfly species as is seen in Identify these two large, colorful dragonflies in Taiwan? It's the same area and time of year.

Two more taken at different angles relative to the Sun. (click for larger)

Here are high res pics if they are of assistance. I can't tell if the reflection is on the concave inside of the lenses or the convex top of the lenses, perhaps even some wall effect in the ommatidia. There are graphs of reflection in ommatidea. https://img.fotokonkurs.ru/cache/comment_image_big/comments/2013/04/26//305186.jpg and... https://www.youtube.com/watch?v=lVqO6gwcVKU

@aliential Oh, I see what you mean I'll try to read further about the lens and what's below it, maybe I can make a model of it in Blender and then try rendering. Thanks!

@aliential update: google suggested this video next, Insect Vision: Ommatidium Structure and Function You mentioned graphs of reflection in ommatidea but I don't see any in your links, was there another?

https://i.pinimg.com/originals/9d/e6/43/9de643a614510e726d3cb48810b4ab2f.jpg and https://www.ephotozine.com/photo/ommatidia-57879669 and https://simple.wikipedia.org/wiki/File:Dragonfly_compound_eyes02.jpg

Yes this can be modeled! lens: n=1.43 to 1.45, crystalline cone: n=1.34 from The properties of the visual system in the Australian desert ant Melophorus bagoti

It would be cool to model the compound eye in blender. perhaps there are some guides to building a hex lattice, that you can copy adding a lens and cone, perhaps do a flax hexagon lattics and then bend it into a hemisphere as a final step. perhaps make the lattice from flat to sphere using a maths mutation equation, in meshlab there is an equation option.

Here is the image in comments. The direction of the sun can be seen from the shadow of the left antenna. I just sketched this image to note some observations, it's the best answer that I can find at this time.

source

Yes I think this provides a lot of insight, thanks!

It's a bit of a steep optics challenge sorry it would be better to demonstrate using a 3D graph. Using blender there is probably an algorithmic option to place many components, so you'd just have to put in one ommatidea and then algoritmically copy it to a geode/spherical group. i don't know if the light comes from  the lens or the cone, although the straight edges which are shorter are giving less reflection.

I think that in Biology SE we can only go as far as identifying the anatomy/morphology. Consider adding the diagram in Figure 5 of the paper linked in this comment so readers can see the anatomy from an optical point of view? The interface between the bottom of the lens material (n=1.43 to 1.45) and the crystalline cone material (n=1.34) below it will also produce a small back-reflection, a bit like retro-reflective glass beads

ok, i'll send you the mesh if you do the light render: i'd send an occluding mesh to wall off all the lenses, and one mesh made of thousands of lenses to be rendered in transparent. I can use 250 vertices per lens and render 10k lenses, and another mesh with cones is fine too. i can render the mesh although i don't do raytrace apps only wavefront.

Thanks, and I appreciate your enthusiasm, but it's outside the scope of what I can do right now, and outside the scope of how we should use Stack Exchange. However if you't like to pursue it then you can take the information here and in the question and try  a "How to model a dragonfly's eye's optics and reproduce this photo" type question in Blender SE and there's a chance someone there will find it interesting to try! They are quite an active, creative bunch!

But it has to be "How can I..." not "Please do this...".


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What's the exact species of this African Giant Snail?
We've got an African Giant Snail a few years ago but failed to identify the exact species so far. When we got it, it's been about 20 % smaller than now, so it's probably not been an adult snail, but we don't know the exact age.
We only got this single snail, so there's no way to check for the eggs.
Here's a picture (small version, about 400 KiB) and a link to a bigger version. If you need more detailed pictures of certain parts, please let me know.

Bigger version: https://i.stack.imgur.com/S9z2x.jpg (about 2.2 MiB)
This picture shows that the apex is about 12 centimeters (4.7") in length, while the foot is about 14 centimeters (5.5").

I try to remember... but are snails not able to lay eggs without another snail?

Snails are hermaphroditic, so 2 snails will always be able to reproduce, but they aren't autogamous, like e.g. tape worms.

thank you :) then I mixed this

I am not sure how to handle this.
The answer is the content of this page, which (I guess) should not be entirely copy / pasted here for copyright reasons.
So based on the texture of the skin, you have a variety of Achatina.
If I receive advice about how to make this answer comply more with the rules of the site, I will edit my answer.

Could it be an Achatina Fulica? The sentences "Though shell coloration may be variable [...], generally it is reddish-brown with light yellowish, vertical (axial) streaks." & "There is a wide variety of shell and body polymorphism in snails, perhaps none more than Achatina fulica. This often leads to it being mistaken for less widespread species." seems to indicate this. I've never been sure of that before, since the apex of Gary not only gets brighter towards the tip, but also more red/pink.

Of course it can be, but I cannot make any informed claim, other than what I stated already.


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bunsen vs meker for best sterile field
I need one bunsen and i have a friend that sells me a bunsen-meker burner.
I see that bunsen-meker burners have more flame diameter, so should have more diameter of sterile field, but i dont know XD
Is good for sterile field? or i should buy a typical bunsen?
thanks.

Can you maybe explain what you plan to work on?

I need to prepare culture media to inoculate with spores of my mushrooms. Isolate the mycelium and inoculate liquid media for later inoculation in solid media for medium-scale production.
Until now I used a homemade still an air (SAB), with good results, but uncomfortable and unpredictable.
Now I want to buy a lighter to have a sterile field as large as possible, so I would like to know if the bunsen-meker that I have available to buy is correct or do I need a common bunsen burner, which I It would be more expensive as it is not second hand (the meker is brand new).

Bunsen was a person. Give him a capital in your title at least, even if you have an aversion to titular norms.

The difference in flame diameter between a Bunsen and Meker (or Fisher) burner really isn't that much, so I'm not sure how much larger the sterile field would be. On the other hand, Fisher burners can be tuned to be much hotter than standard Bunsen burners, so that may impact the size of the field as well. But, at the same time, they use more fuel, so you have to think of that as an additional cost.
If you're just sterilizing inoculating needles/loops, flask necks, etc., a Bunsen is perfectly fine. However, if you're trying to create a larger "sterile" field, there are too many variables to make a definitive recommendation. Are you setting up in an area with relatively little airflow, or are there cross-breezes? How large of a field do you actually need - what is the area where you'll be working with open containers of sterile media?
All in all, to be safest, you'd probably want the Fisher burner, but I don't know what the cost differential is and what your budget is. If you're careful with media manipulation and have a good still area to work in, a Bunsen should be fine, though.

thanks! This info is so useful!

@JaumeEscaleCamps glad to help. If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. If you have >= 15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.


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Meaning of 5’–3’ in relation to ORFs
I was reading a paper in the journal Molecular Basis of Disease, which stated:

The ORFs are arranged as replicase, and protease and major S, E, M,
and N proteins which follows a typical 5’—3’ order of appearance, are
considered are as considered as major drug/vaccine targets.

(Naqvi, et al., 2020)
I'd like to know what the " ' " means; if it means inch, or something else like minute. I am doing research so I don't know what units are being used.
Source
Naqvi, A. A. T. et al., 2020. Insights into SARS-CoV-2 genome, structure, evolution, pathogenesis and therapies: Structural genomics approach. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1866, p. 165878.

Inch? Imperial units were abandoned in science by the 1950s, and probably before.

I assume you are referring to the "typical 5’—3’ order of appearance".
The correct way to pronounce these is with the word "prime", that is, "Five prime to three prime". These are not units but refer to the directionality of RNA/DNA and the numbers five and three refer to specific carbon atoms arranged in the sugar molecules that make up the RNA/DNA backbone.
RNA/DNA are typically "read" (and always written) from the 5' to the 3' end of the molecule by molecular machinery in the cell, so that's usually the order we read the sequences as well. "5' to 3'" in molecular biology effectively means "beginning to end".

Thank you, and yes I was very confused normally I would have picked a physics topic but this topic of structural virology was interesting especially with whats going on. That is the topic of my paper which is why I included the citation.

In this context, that symbol is read as "prime".

"...a typical 5’—3’ order of appearance..."

would be read

"...a typical 5-prime to 3-prime order of appearance..."

In organic-chemistry, these values are used as a systematic means to denote different Carbon atoms that are part of the same compound. DNA and RNA consist of a sugar (ribose) backbone connected by phsophodiester bonds between the 3' and 5' carbon atoms (source for image).

Since these are the bond sites that link subunits of nucleic acid together into a single molecule, at either end of any given strand there will be an available bonding site, either the 5' or the 3' carbon. So, at the 5' end of a DNA strand, there is an available 5' carbon on the terminal ribose subunit. And at the 3' end, there is a free 3' carbon on the terminal ribose. This determines in which direction the DNA is read. By convention, strands are written from 5' to 3'. In some genomes (especially in viruses and bacteria), there are open reading frames (ORFs) that are found in the 3' to 5' direction, hence the statement given to clarify the nature of these specific ORFs.


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Do neurons with dopamine inside only send signals to another neuron with dopamine?
A nerve cell with dopamine receptors gets an action potential and releases dopamine to other neurons. Does this nerve cell only release to cells with dopamine inside? Because what if a neuron has a dopamine receptor but serotonin as a transmitter?

If that was true, how would the rest of the brain ever communicate with dopaminergic cells and vice versa?

No, neurons with all sorts of neurotransmitters frequently synapse onto neurons that release other types of neurotransmitters. In fact, aside from the most common neurotransmitters like glutamate and GABA, this is the rule rather than the exception. You mention specifically dopamine, and this is a perfect example--the medium spiny neurons in the striatum that are the most "famous" dopamine-receiving cells are NOT dopaminergic themselves--they are all GABAergic. The other aminergic neurons are similar; the noradrenergic locus ceruleus neurons and the serotonergic neurons of the raphe nuclei project to much of the forebrain, which contains few noradrenergic or serotonergic neurons of its own.
Neurons frequently have receptors for neurotransmitters that they do not produce, and these are commonly known as heteroreceptors, as opposed to autoreceptors, which respond to the same transmitter that the cell possessing the receptor responds to. Autoreceptors commonly exist more for the purpose of negative feedback ("I've already released enough of my transmitter, therefore I need to stop so I don't overload the cells I synapse onto") than for neurons releasing the same transmitter to activate one another.


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Are the transitions between the different brain frequencies states easy to see on an EEG?
Are the transitions between the different brain frequencies states: Gamma to Beta, Beta to Alpha, Theta to Delta, etc. easy to distinguish on an EEG? How quickly can the brain transition between any of these states?

Delta/theta/alpha/beta/gamma are not different states and so there are no changes "between" them. These are terms used to label different bands of the frequency spectrum. Every EEG has energy in all of these bands. Brain state can change/be measured by the relative changes in different bands (either relative to each other, or in absolute power change over time), but there is always some energy in every band.
Here are some example spectra from different brain states (stages of sleep and anesthesia states) across different brain regions:

(from Banks, M. I., Krause, B. M., Endemann, C. M., Campbell, D. I., Kovach, C. K., Dyken, M. E., ... & Nourski, K. V. (2020). Cortical functional connectivity indexes arousal state during sleep and anesthesia. NeuroImage, 211, 116627. Disclosure: I am an author on this paper)
WS and WA refer to "wake" in the sleep and anesthesia experiments respectively; N1, N2, and REM are stages of sleep. S refers to sedated under anesthesia - subjects can still respond to commands, and U refers to unresponsive under anesthesia. These are actually not from EEG but from electrocorticography where the electrodes are placed directly on the brain, sometimes called iEEG, but there are a lot of similarities with EEG.
You can see that in all brain states, there is energy across all the frequency bands (identified with Greek letters), but there are changes with state. For example, delta has more power during N2 sleep across the brain. A trained eye could also easily pick this up in the time-domain EEG signal, but it's much easier to convert to the frequency domain like in this figure.
You'll notice that the energy decreases with increasing frequency. This is normal, and is typical of natural frequency spectra with certain properties, see Pink Noise; it's rare to ever have less power in the delta band than any other band, for example. You will also see that for the most part the spectra are gradually changing: there are few peaks in the spectrum, and it can be a bit misleading to refer to energy in a specific band or to compare between bands when there is no peak there. Some exceptions are that there is typically a peak in the alpha band for humans, especially with eyes closed. Hippocampus tends to generate rhythms in the theta band, and rodents have very large hippocampus relative to the rest of cortex, so you'll often see a theta peak in rodents especially during locomotion.
Lastly, these EEG differences are probably not the best way to discriminate between different brain states. There are lots of other measures that seem to do better. In the rest of the paper that I've taken this figure from, my colleagues and I use a specific measure called the weighted phase lag index which does a much better job at discriminating between putative conscious and unconscious states.


text:
Can all oxygen be provided cutaneous in humans?
What partial pressure of oxygen is needed on the skin to completely replace the lungs function as oxygen receivers? Respiration has other functions too. I am only asking about oxygen intake.
Oxygenation through the skin could eventually be used against ischaemia like gangrene and covid clotting.
The skin might eventually be kept wet to improve oxygen diffusion through the skin, as this is the case with animals.
In normal conditions cutaneous respiration is 1-2% in humans. This means that with an atmosphere of close to 100 % oxygen and pressure of 10 bar, 50-100 % of a humans oxygen intake can be through cutaneous respiration.


text:
Microarray experiment validation meaning
I have a quick question: what does microarray experiment validation mean ?
I was reading a paper in which they say that the data of the experiment show that the 3 genes radB, dp1 and dp2 are co-regulated following gamma irradiation "validating our microarray experiment".
I tried to find something in Google but it is not yet clear.

I think here it means the results of their gamma irradiation experiment give the same results as the microarray experiment.  Here 'validating' means 'support'.

ok thank you @user438383


text:
Problem with epoxy silane (Random results in glass silanization). What are crucial points to look at?

I`m trying to immobilize an antibody onto the glass surface by means of GPTOMS (glycidoxypropyl trimetoxy silane). Using the same protocol (silanization in toluene or acidified ethanol (see below)) I get different results any time, what are key points to check?

Looking through literature on immobilization, I see a lot of articles where authors use APTES (aminopropyl triethoxy silane) and only a few using GPTOMS, why? Epoxy group seems so atractive...

For toluene:

Rince slides with water
Ultrasonicate them in isopropyl alcohol for 3 min, dry them
Put for 3 minutes into piranha solution
Rinse with distilled water
Treat with oxygen plasma for 3 min
Slowly put slides into 2 or 4 % silane solution in toluene, incubate for 3 min
Rince with toluene and isopropyl alcohol.
Put them on dry heater (max temp. of ours is 97 C, most protocols say 110 C), incubate an hour

For ethanol:

Rince slides with water
Ultrasonicate them in isopropyl alcohol for 3 min, dry them
Put for 3 minutes into piranha solution
Rinse with distilled water
Treat with oxygen plasma for 3 min
Put slides slowly into 2% silane in ethanol solution (silane + alcohol + acetic acid (pH 4,5-5,5)), incubate 3 minutes
Rince slides with ethanol
Put them on dry heater (max temp. of ours is 97 C, most protocols say 110 C), incubate an hour

Please [edit] your question and post the protocol you are following. We can't help if we don't know what you're doing.

please take a look


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Do prokaryotic chromosomes have centromeres?
I found this here.

Eukaryotic chromosomes are always linear. ... In contrast, prokaryotic chromosomes are either completely devoid of centromeres or carry the so-called “plasmid centromeres” which are not essential (with a few exceptions, such as Caulobacter) (57,–60).

What does it mean by prokaryotic chromosomes carry "plasmid centromers"?
Their chromosomes carry the centromeres of plasmids? Do they have centromeres or not?

Did you look up what plasmid centromeres are? What did the references say?

No, prokaryotes do not have centromeres.  They do, however, generally have a somewhat analogous structure used during cell division to partition the replicated chromosomes and plasmids between the two daughter cells. The analogous place on the chromosome or plasmid is the parS element, a DNA sequence on the chromosome or plasmid which is part of the parABS system.  This system, consisting of two proteins (parA and parB) along with parS, forms a mechanism to segregate the copies of a chromosome or plasmid for the daughter cells.
parS is usually called a "centromere-like" site, but is sometimes referred to as a "plasmid centromere”, which is why the quote uses the phrase so-called “plasmid centromeres”.

Do they have a centromere-like protein that links a pair of sister chromatids?


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Why are there different gene expressions that are refered to the same gene in microarray experiments results?
I am studying gene expression profiling considering a dataset available on NCBI website. I do not understand the following: why are there some genes that have different profile and different ID numbers but they refer to the same indentical gene ?
The dataset that I am analysing is here .
For instance, we have that ID-8938, ID-1870, ID-7323 and ID-15 refer to the same gene called RadA but the gene expression profiling is different for each ID. So I ask which is the difference between these ID if they represent the same gene ? Moreover, how can I understand which is the one that has to be chosen for the analysis ?

Why would you expect only a single profile measurement to be in the database for a gene?

@mgkrebbs because if you do the measurement of the mRNA produced in those time points for that gene, how can I obtain other measurements for the same time points ? Do they take other cellular cultures of the same organism and make the same measurements at the same time points to check if the values are consistent ?

What you are looking at there is a microarray dataset (see the description here).
Microarrays are chips that have many sequence specific probes on them and sometimes they have multiple probes for the same gene.
Readout differences between the probes of the same gene could be caused by either noise in the data or biological effects like expression differences between transcript isoforms - other reasons could be possible as well.


text:
What inhibits linkage between actin and myosin filaments
What is the mechanism behind the inhibition for cross-bridge linkage between actin and myosin filaments in the binding-tilting cycle? There are 2 possible ways that are in my mind:
a.  Tn-I (tropnin-I), binding to F-actin: when [Ca2+] falls below the threshold, Tn-C are inactivated. Therefore, Tn-I relocates and SOMEHOW this causes the cross-bridge to break (ref)
b.  ATP rebinds to the myosin head, forming ATP-myosin complex. This has a relatively low affinity towards binding the myosin-binding sites on F-actin (than myosin-ADP-Pi complex). Therefore, the cross-bridge break.
From my understanding, (a) is strange: when Tn-C is inactivated, it should cause Tn-T to change conformation so that tropomyosin covers the binding sites again. But I think I am wrong as otherwise, Tn-I is useless, but I really don't know how Tn-I exerts its inhibitory effect.
Thank you.

I am not sure if you are referring to a mechanochemical cycle of "stepping" of a myosin molecule along an actin filament, or a cycle of contraction and relaxation of a muscle cell as a whole. These take place on completely different timescales and control the binding and unbinding of the two proteins in entirely different ways.
In the mechanochemical cycle, there are no proteins directly involved other than actin and myosin themselves, and the breaking and re-formation of contacts is controlled by the nucleotide occupying the ATPase site of myosin. ATP binding leads to a low affinity (weak interaction) state and ADP binding leads to a high affinity (strong interaction) state. ATP hydrolysis and nucleotide binding/unbinding "power" this cycle.
The cycles of contraction and relaxation of the cell occurs on a much longer timescale--each contraction involves many repetitions of the actin/myosin "stepping" cycle across many actin and myosin molecules, while relaxation involves slowing or stopping this cycle. This is where calcium and the troponin I/C complex come in--they are a "switch" that allows the stepping cycle to happen or not. So when the calcium is low and the troponin complex is bound, the actin/myosin interaction is continuously disengaged, whereas when calcium is high and the troponin complex releases, the cross-bridges form and release in a cyclical manner as ATP binds to myosin and is hydrolyzed.
As an analogy, think of a person walking across a room full of chairs. As the person is walking, his feet alternately make and break contact with the ground, and this is due to the coordinated movement of the legs. If the person sits down in a chair, then his legs stop propelling him entirely for a while and are still, and this is like when calcium is low in a muscle cell.

Thank you for the detailed explanation! Can I say like this: in my question, (a) is talking about muscle relaxation, (b) is talking about where muscles are contracting (isotonic tetanus - 'stepping' of myosin heads on actin filament)?

May I ask one more question? when Ca2+ returns to the sarcoplasmic reticulum (unbind Tn-C), how actually Tn-I inhibits the cross-bridge binding? Since I thought it is Tn-T that does the job by pulling tropomyosin back to covering myosin-binding sites. Thanks!


text:
Is Panmixia very rare?
I'm reading the wikipidia page on Panmixia.

Panmixia (or panmixis) means random mating. A panmictic population is one where all individuals are potential partners. This assumes that there are no mating restrictions, neither genetic nor behavioural, upon the population and that therefore all recombination is possible. The Wahlund effect assumes that the overall population is panmictic.

In genetics, random mating[4] involves the mating of individuals regardless of any physical, genetic or social preference. In other words, the mating between two organisms is not influenced by any environmental, hereditary or social interaction. Hence, potential mates have an equal chance of being selected. Random mating is a factor assumed in the Hardy–Weinberg principle and is distinct from lack of natural selection: in viability selection for instance, selection occurs before mating.

Now, I would guess from this definition that Panmixia is a condition that almost never occurs, that in the vast majority of cases, there is some sexual selection going on which makes some pairings more likely than others.
But the way the page is written seems to suggest that this is a pretty normal condition of populations, or at lead doesn't mention that it is a "spherical cow" abstraction.
Am I missing something here?


text:
Quantifying Gene Expression
I have found that many studies use the mRNA concentration as a “proxy” for protein activity because there should be correlation between mRNA levels and proteins expression levels. How is protein activity quantified? Which quantity is used? What are protein expression levels?
I am doing some statistical data analysis using this dataset. I would like to understand why they have been interested in measuring mRNA concentration after the cells gamma irradiation (and in general it seems to me that biologists in many experiments are interested in that). I found in this site that discussion about correlation between mRNA concentration (so gene expression level)  and "protein expression level". Therefore I wanted to know what the latter is. Moreover, in the article related to my dataset is written

Very few DNA repair genes displayed significant differential expression in P. furiosus following gamma
irradiation.

And then

the data we reported here suggest that DNA repair proteins in P. furiosus and several other archaea are constitutively expressed and that they may be present in the cell at a level sufficient to maintain the integrity of the cell’s genetic material.

So putting together what the scientists conclude with what MattDMo has answered to me and what is discussed here , I think that I can conclude that "protein expression level" is a measure of the amount of protein actually translated from the mRNA, that then (in this case) will effectively act to repair DNA. Therefore, "protein expression level", as well as "protein activity", indicates the proteins translated from mRNA and that will actively act to repair DNA damages (in this case that we are talking about DNA repair proteins and DNA repair genes).
I have to say that I do not really know well what "DNA repair proteins are constitutively expressed" means, but I think that is that DNA repair proteins have already been translated from the mRNA and therefore they are "present in the cell at a level sufficient to maintain the integrity of the cell’s genetic material" (as they say soon after).
All this makes sense to me if I think about my first objective that was to understand the reason for measuring mRNA concentration. We are interested in it because there should be correlation between mRNA concentration (gene expression level) and the proteins actually translated from mRNA from that specific gene, in order to know which kind of proteins will effectively act in the DNA repair processes (in this case).
I wonder if all this interpretation is correct...

I have deleted my comments as they are now embodied in an answer. I have changed your title to be more general and for reasons I make evident in my answer.

I have now added a postscript addressing the specific circumstances of your work, which are of less general interest than main topic of my answer. (Good questions on answers on Stack Exchange should be of general interest, not a dialogue with the poster.) In summary, "all this interpretation" is not correct. Further, measuring the  mRNA concentration is done because it reflects the extent to which a gene is expressed as mRNA. The topic of interest is gene expression — of which the amount of protein produced is just a part. And the term "protein activity" is meaningless and is not to be used.

What is Protein Expression Level?
This was the original title of the post, which I edited myself because I regard the answer as trivial, but the question as more substantial. To deal with the trivial first:

‘Level’ is not a scientific unit, and can only be used unambiguously
as a scientific term in its English sense in relation to liquids, e.g. “The level of mercury in the thermometer had
fallen.”, “The land is 10 metres above sea level.”
It is used by some people in informal speech or writing to indicate an
undefined quantitation, and because of its very ambiguity is to be
strongly discouraged in scientific communication.

So neither I nor anyone else can say what ‘protein expression level’ is without finding out what the originator of the phrase intended (if indeed he knew) in any individual instance: quantity or concentration of protein, or the rate of its synthesis.
Quantitation
Let us consider some general aspects of a cellular molecule that may require quantitation: Amount, Rate of Synthesis, Rate of Degradation and, where relevant, Biological Activity.
The quantitation of molecules at its most basic is the number species,  or, more practically, their total mass (grams), where possible related to their molecular mass (i.e. moles). The rate of their synthesis or degradation is expressed in terms of the change of their amount in unit time.
In order to compare different systems a reference is needed for the quantitation. This may be per unit volume, per cell, per g cellular protein, per g DNA etc. (However for comparison of similar systems or within one system the reference is often omitted.)
The biological activity of molecules only has meaning if the molecules are, indeed, biologically active (e.g. enzymes). It is expressed in units related to that activity.
Examples of Quantitation for Proteins
The actual units used in quantitation are determined by how one is able to measure the parameter of interest.
Relative amount of protein: You might detect a protein by the intensity of staining of a band on a gel, or by the extent of precipitation using a corresponding antibody. These would have to be calibrated against standards in order to convert raw experimental measurements to g or mole protein. Typical units of relative amount are g/g total protein, g/g DNA.
Rate of synthesis or degradation of protein. You might detect the synthesis of protein by the rate of incorporation of radioactive amino acids into non-radioactive protein, and the rate of degradation by the liberation of radioactive amino acids from pre-labelled protein. Typical units of synthesis would be mg amino acid incorporated per min per mg total protein. (This can be converted to molecules synthesized or degraded per minute, if necessary.)
‘Protein Activity’: The use of this term is not recommended. In chemical terms the activity of a molecule is a measure of its “effective concentration”, and in relation to proteins would only be the concern of biophysicists and the like. Other biologists would associate the term with the biological activity a protein such as an enzyme might have, but as many proteins are structural the term ‘activity’ cannot be applied to proteins generally. Where it is of interest it would be quantified in terms of the nature of the activity, e.g. an enzyme is quantified in units related to the amount of substrate converted to product in a given time.

Quantitation of Gene Expression using Oligonucleotide Microarrays
The two extremes in quantifying gene expression are the detailed study of the expression of one particular gene encoding a protein for which information and tools are available; and general study of the expression of many genes using modern methods that allow the study of many molecules simultaneously. Such methods included mass spectrometry (for small metabolites), two-dimensional gel electrophoresis (for proteins) and microarrays or RNAseq (for mRNA). In general in the latter case one would examine the effect of some agent or condition on the whole spectrum of gene expression.
Let us examine microarray technology as that is the main concern of the poster.

Microarray technology measures the relative amounts of mRNA.

The methodology involves amplifying a mixture mRNA species by reverse transcription to cDNAs, which are labelling with a fluorescent dye. The cDNA is hybridized to immobilized oligonucleotides based on the sequences of the genes in the organism, and the strength of the fluorescence signal is assumed to be proportional to the amount of individual mRNA species in the sample. However the data supplied to the user is the relative image intensity within the experiment, rather than units that allow one to calculate the actual amount of mRNA.
How does these relative amounts of mRNA relate to gene expression?

The relative amounts of mRNA are a relative measure of the rate of synthesis of proteins (3 in dig.), if one assumes that the rate of synthesis of each protein is similarly proportional to the amount of its mRNA (a in dig.) which would be limiting. This is a reasonable assumption in most cases given mRNA is degraded more rapidly than protein. (They are not a measure of the amount of protein — b in dig.)

The relative amounts of mRNA cannot be taken as a measure of the rate of transcription of a mRNA from its gene (1 in dig.) because of the relatively greater effect of mRNA degradation (2 in dig.) on the steady state concentration of mRNAs, and the fact that different mRNAs have different half-lives.

Postscript for the Poster
I have tried to make this answer general, to be of use to more people. As the poster is not a biologist she may still have difficulty in understanding the background to the biological experiments that generated the data she is analysing.
The biological system of interest is gene expression, which encompasses the whole series of events from transcription of genes to mRNA and their translation into protein. The background to this is that there are some genes that are (almost) always expressed, irrespective of physiological circumstances because they are needed to maintain the structure and everyday functions of the cell. This is termed constitutive expression, examples being expression of the genes for cytoskeletal actins or ribosomal proteins. Other genes are expressed (‘switched on’) only when needed (and may be termed inducible). The question here would appear to be whether the genes for the enzymes involved in DNA repair are expressed all the time (constitutively) to deal with normal ‘wear and tear’ of DNA, or whether their expression only occurs in response to some insult knwn to damage DNA, such as gamma irradiation.
As I mentioned, as an experimental scientist, one approach that can be adopted here is to look at the expression of one or two well characterized proteins that are known to be involved in DNA repair. However, there may be proteins involved in this process that you are unaware of, so the modern methods of looking at the expression of all the genes in an organism (if the DNA sequence is known) — oligonucleotide microarrays or, better, RNASeq. These methods measure relative quantities of mRNA in a cell. This is not a proxy for amount of protein or rate of  its synthesis (the term ‘protein activity’ is meaningless and is not and should not be used), it is what it is, but is also a reflection of the expression of the genes that encode the mRNAs. No expression, no mRNA.
You can think of the microarray and RNASeq approaches as a fishing expeditions. If you find mRNAs that are only present after the cell receives a stimulus or an insult, expression of the mRNA has occurred (whether or not the amounts are directly proportional to the rate of synthesis). If the mRNA is synthesised you can assume it is translated into the protein it encodes. In the case of gamma irradiation you might assume any mRNA that shows a large increase in quantity encodes a protein that involved in protecting the cell from the radiation. This will be of scientific interest, especially if it is not what one anticipated.

I have a doubt about the relative amounts of mRNA: they are somehow the log10 ratio between the irradiated sample and the reference sample . So if the ratio is 0, there should be no changes in gene expression (because it is log10(1)=0); if it is greater than 0, it means that the gene expression (amount of mRNA) is increased after irradiation (up-regulation); finally, if it is lower than 0, it means that the mRNA production decreases (down-regulated gene) ?

This is what I have deduced by reading the Wikipedia explanation (indicated by you) and the comments about RadA in fig1a of the article . I think that if I have understood well this case with not irradiated samples and irradiated, I can extend this reasoning to other cases like unhealthy and healthy cells cultures.


text:
Is once per day the optimal sleep pattern for all mammals?
If a typical human body clock is 8 hours sleep, 16 hours awake, interested to know if any mammals have:

a 12 hour body clock (4 hours sleep, 8 hours awake)
a 6 hour body clock (2 hours sleep, 4 hours awake)

And very interested to know if any mammals' sleep patterns are on an "as-needed" basis - i.e. simply sleeping whenever tired, without ever establishing any particular pattern over the days/weeks

"typical human body clock is 8 hours sleep" - I recommend you to google "first sleep and second sleep" and how people used to sleep before 1800.

Dogs and cats regularly sleep for short periods during the day.  (And so do I, on occasion :-)) Then there are dolphins, which have only half of their brain sleeping at a time.

Thanks @BagiM very interesting. I did some googling as you recommend. Fascinating to read that the French used to sleep for some hours, wake around midnight for a few hours of housework or recreation, then go back to sleep for a few more hours. I'm not too sure how to verify any of these claims though. I wonder if there are scientific studies or 'go to' texts/resources that provide more rigorous evidence of sleeping patterns of humans and animals? Canonical papers preferably (but simple enough for a non-biologist to consume).

@stevec To find scientific studies on this topic search "segmented sleep" in scholar.google.com . There seem to be both studies of historical texts from various periods and antropological studies of contemporary preindustrial societies.

@stevec: Anecdotally, I do just that quite often - more in winter than summer.  I will sleep for a while, wake up and do stuff for a couple of hours, then go back to sleep.  I don't think it's at all unusual.  (I also work from home, so I don't have set working hours to force me into a perhaps unnatural pattern.)

Theres also a 4 hour cycle in humans, thats why we have meals every 4 hrs, and siesta make you live longer, i.e italy.

@aliential: Who is the "we" having meals every 4 hours?  Perhaps the British, with their afternoon tea, but it's hardly an American pattern.  More usual seems 5-6 hours between breakfast and lunch, anywhere from 5-8 between lunch and dinner, and 12 or so between dinner and breakfast.

@jamesqf "I will sleep for a while, wake up and do stuff for a couple of hours, then go back to sleep.". Would you do that for any sustained period though? As in weeks/months? I am very interested to learn of cycles that are not 24 hour cycles with one big clump of sleep (in either humans or other mammals). You could consider putting your ideas in an answer

@jamesqf i'm quoting a research publication from about 3 years ago on the subject of the discovery of a secondary body clock that accounts for meal regularity quoted as " scientists find new 4 hour body clock" thats what it sais, im french and the research made sense to me about humans having a regular rhythm every 4 hours.

@aliential: Yes, I do that biphasic sleep at least half the year.  Between roughly the fall & spring equinoxes, it is almost every night.  In the summer, with longer days, it might be about 1 night in 3 or so, and the waking period tends to be shorter.  As to making it an answer, this is just my own experience.  For an answer, I'd have to look up citations and so on.

@jamesqf a lot of references say: The circadian rhythm dips and rises at different times of the day, so adults’ strongest sleep drive generally occurs between 2:00-4:00 am and in the afternoon between 1:00-3:00 pm. Its very documented.

@aliential : Evidently none of those studies bothered to look at me :-)

So as we know that every mammal needs atleast some amount of sleep or a resting period to perform cognitive functions through out the their day, this however can vary drastically based on the mammal's habits, such as if they are herbivores or carnivores, their place in the food chain (if they are a predator or prey), their habitat, their body size etc.
Starting with humans (to set a point of reference), we ideally need 7-8 hours of sleep in a day. Getting less or more sleep than this ideal can have a lot of different consequences (ranging from feeling tired and foggy to heart conditions and even death). A study performed by a group of researchers to find out the ideal sleep duration in humans showed that just after 14 days the people getting 8 hrs of sleep showed average cognition and a healthy mind, those getting 6 hrs of sleep per day for 14 days showed a similar reaction time to a person with blood alcohol level of 0.1% (which is considered legally drunk in most places), and the group getting 4 hrs of sleep per day for 14 days were tending to fall asleep while performing basic cognitive tasks. This show exactly how important sleep actually is.
Now moving on to some other mammals.
A very commonly discussed example is that of giraffes. Giraffes generally exhibit a cycle of just 2 hrs of sleep per day, and some days they just tend to not sleep at all. A lot of factors contribute to their sleeping habits. Firstly since they are herbivores, and primarily feed on leaves, they need to eat a lot of leaves to get enough energy for their body, having a large body also contributes to this. So, they tend spend about 75% of their day just eating. Other than this since giraffes are prey and a good source of food for lions, they need to stay awake and alert at all times. Sometimes they will take little 10 min long powernaps (this is when they are the most vulnerable, so they don't do it often).
Carnivores however (like lions) sleep a lot more, due to their diets (just like us they feel sleepy after eating) and also since they are minimal risk of being attacked as they are on top of the food chain.
Next lets talk about some sea mammals, they have a hard time trying to snooze because of them being underwater.
Dolphins have very interesting sleep habits as they have to actively come to the surface to breath. Dolphins practice something called "unihemispheric slow-wave sleep", this basically means that they only rest one hemisphere(or side) of their brain at a time(so that they can be awake and asleep at the same time), this is what uni(one) hemispheric(side) means. Slow-wave sleep refers to the deepest phase of sleep, meaning when the one hemisphere is sleeping it is out like a lightbulb. This way dolphins tend to sleep a lot, they have sleep cycle of about 8 hours of sleep a day (resting each hemisphere for 2 hrs at a time). So the dolphins you saw at sea world last year could have been half asleep (literally).
Some birds also practice this uni hemispheric sleep.
I can't think of any animals that sleep "as needed" because activities like sleep and wake are rhythmic and control various hormones and metabolic reactions of the body, this is primarily why we have sleep patterns so that other activities in the body can be done in a habitual manner. This is maintained by our "biological clock", which is the term used to define the natural sleep-wake cycle in animals. The biological clock is regulated by a hormone known as  "melatonin".
So yeah, these were some examples I remembered off the top of my head. I have provided some links to why sleep is important, ideal sleep habits in humans and other mammals and some other stuff for further reading.
Hope this answer helped you understand sleep better.
Sleep: a good investment in health and safety - https://pubmed.ncbi.nlm.nih.gov/19042703/
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884988/
How Animals Sleep - https://www.sleepfoundation.org/animals-and-sleep#:~:text=Giraffes%20need%20less%20sleep%20than,of%2030%20minutes%20per%20day.
Melatonin: what you need to know - https://www.nccih.nih.gov/health/melatonin-what-you-need-to-know
This is an animated video series explaining sleep in different animals (highly recommend watching this):
Part 1 - https://www.youtube.com/watch?v=HA1EPRbMMQU
Part 2 - https://www.youtube.com/watch?v=EJzUKsJ-uhA
Part 3 - https://www.youtube.com/watch?v=S4uX2KeEifM
Rare Genetic Mutation Lets Some People Function with Less Sleep (this might also interest you) - https://www.scientificamerican.com/article/genetic-mutation-sleep-less/

The circadian is already complex. No need to further complicate it.
Melatonin and light exposure regulate the day night cycle. Because night occurs once per day, by definition, this is how it is regulated. Humans in artifical environments may adapt a different schedule but in natural sunlight it is the simplest regulatory pattern.
There are other patterns that are the opposite of this and those are anti predator adaptations.

If that were all there is to it, wouldn’t we expect to see very different sleep patterns (in humans and other creatures) toward the poles where there can be months extremely short nights / days, and literally constant sunlight/night in places extremely close to the poles ?

Not necessarily if there are atavisms. And I don't think the arctic circadian is well understood.

It may be the simplest pattern, but observational evidence shows that it is not the pattern followed by many animals (including humans).  In addition to the examples already mentioned, there are those, such as deer, that have a crepuscular pattern, being active during dawn & dusk, and presumably sleeping otherwise: https://en.wikipedia.org/wiki/Crepuscular_animal

@jamesqf It's still a 24 hr cycle, because days last 24 hr.

@Bryan Krause: But the question is asking about ONCE per day, which is very much not the case for all, or even most, mammals.

@jamesqf A day lasts 24 hours whether you sleep once, twice, three times, or never.

@Bryan Krause: Yes, that is a fact.  However, it is irrelevent to the question, which is asking about daily sleep patterns.


text:
What is the difference between a dermatome and a sensory neurone?
I read that a dermatome is an area of skin supplied by a single spinal nerve but that this is sensory information? Why do spinal nerves supply the skin? I thought it was the other way round- sensory information is carried by a sensory neurone to the spinal cord.
Please could someone explain this in simple English because I am really confused.

This is just a confusion of English.
"Supplied" is a bit of a weird term to use, I agree, due to the direction of information flow, but feel free to substitute in just "connected to". It seems pretty common to use this word, for example Wikipedia says:

A dermatome is an area of skin that is mainly supplied by afferent nerve fibres from the dorsal root of any given spinal nerve

and I see similar phrases elsewhere (not sure which is your original source). Afferent nerve fibers, as you describe, are those carrying information into the central nervous system from the periphery, so yes, the information is coming in from the skin.
If you interpret it instead as the spinal nerve providing the connection rather than information flow, then it makes a bit more sense to say "supplied". I suspect the phrasing is borrowed from blood supply since nerves and major vessels tend to develop and travel together. I also suspect the phrasing comes from anatomy, which is sometimes not particularly interested in function which can lead to some confusing results. You'll also see similar phrasing in standard English in other contexts, like roads, even when movements of goods or people are two-way. Merriam-Webster also provides a definition addressing exactly this circumstance:

to furnish (organs, tissues, or cells) with a vital element (such as blood or nerve fibers)

So yes, a given spinal nerve is "supplying a single dermatome with nerve fibers", even if the information ultimately moves the other direction.


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How is sexual selection evolutionarily stable?
It seems like in any population subject to evolutionary pressure, sexual attractiveness will inversely correlate with other kinds of reproductive fitness. If you see a peacock with a small tail feather, this is information that it is likely above average in other areas, because otherwise its genes would already have been wiped out. So intuitively, you would think that it would benefit individuals to find less conventionally attractive mates.
So far, I have encountered two possible explanations for this. One idea was that the things that make an animal attractive correlate with evolutionary fitness. I'm not an expert here, but it feels like the correlation here will diminish over time as soon as there is direct pressure to increase attractiveness.
The other, more convincing, explanation was that it is advantageous to produce attractive offspring. So, there might be a feedback loop here where if members of a population care about sexual attractiveness more, then attractiveness would confer a greater advantage, making attractive offspring more important, increasing the evolutionary pressure for individuals to choose attractive mates.
Can someone give an intuition (or better, the relevant math) for why these two latter effects dominate my original intuition? Or are there other effects at work here?

If your 3rd paragraph is true, isn't your 2nd paragraph also true?

Good point, I guess I meant that sexually attractive features (e.g. big muscles) might correlate with advantages in individual (i.e., not sexual) selection.

first off you are talking about runaway sexual selection, run away sexual selection works because attracting mates matters MORE than individual survival. An immortal survivally perfect creature that cannot mate is an evolutionary dead end and might as well not exist where its genes are concerned. A bright red neon sign on your back that draws  the attention of potential mates is an advantage as long as it attracts mates more often than it attracts predators. Coincidentally this is why so many sexual displays are things you can turn off, even a peacock can fold its tail fan down. These displays often exploit existing attention  factors, like eye shaped objects, bright contrasting colors, loud noises, ect, things organisms are already predisposed to pay attention to.  Of course once neon sign displays exist your second idea comes into play, once neon signs are in play a female is best served if her own male offspring and descendants also have neon signs, which makes attraction to the  neon signs (and thus the genes making them) an advantage.
For normal sexual selection both your ideas also come into play, likely more often. common attractive features are things like size, symmetry, health, or excess energy, direct signs of fitness.
Most of the time displays reaches a point of stability where the cost is balanced by the attractiveness, this is how most displays work.  But sometimes runaway selection can drive it past the point of no return, where the cost of reducing it is so high (lack of mates) the only winning strategy is to invest more and more, on and on until the cost is so high you never get a chance to mate.

You gave the example of a brightly colored male bird... and what about the females? The are well camouflaged and optimally fit to evade predation. So, even if 50% of males are caught and eaten due to theor bright colors, the demography stays the same.
The species as a whole is the same with or without the bright feathers.
The sexual display amplifies the pressure for fitness selection, to obtain more food, evade predators better, and invest more energy in sexual lures, horns, feathers, song.
You are right, if a predated population places sexual selection on the females, it is counter productive. Fish, birds, insects, frogs, they nearly always have super robust camouflaged females and males that fight and display their high fitness, except parrots and reef fish.
Birds are so good at evading predators and flying to food, that even the females are colorful in some species i.e. parrots, and thats a less easy example, why do female parrots risk having no camouflage? Perhaps their climate doesnt provide enough selection.
www.google.com/search?q=sexual+selection+graph+feathers+demography&tbm=isch&ved=2ahUKEwjN77n5lobsAhUPWBoKHSgGAcMQ2-cCegQIABAC&oq=sexual+selection+graph+feathers+demography


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Why is the null hypothesis of trait evolution Brownian motion?
Many models of continuous trait evolution assume that traits evolve according to Brownian motion. What is the biological or physical basis for this choice?
I realize there are models that do not assume Brownian motion, but what I am interested in asking is why the null model is so often chosen to be Brownian motion.

What else would you choose?

Please define "Brownian motion".

Brownian motion models the random motion of particles suspended in a medium. In biology it is often used to model situations where change in some system occurs via a random walk.

I asked because some people use "Brownian motion" as a synonym for Wiener process. I conclude you are not one of those people.

@RodrigodeAzevedo Thanks for pointing that out. I had believed the Wiener process was one and the same with Brownian motion. Reading the wiki page, it certainly does have the same mathematical properties. What other conception of Brownian motion did you have in mind?

Lévy flight.

I think that the simple answer to this question is that the present comparative methodology was largely established by Felsenstein 1985, American Naturalist. For mathematical convenience, he suggested Brownian motion as a null hypothesis, because "...the variance of the distribution of change of a branch is proportional to the length of time of the branch...", and then "...it is easy to see that the differences between pairs of tips... must be independent." Also: "...after one unit of time, the contrast [between a pair of tips] has expectation 0 and [easily defined] variance..."
He explicitly discusses whether Brownian motion is a reasonable model in the section "What if we lack an acceptable statistical model of character change?"
I would suggest reading that paper in more detail if you are interested in the details of Brownian motion applied to phylogenies.
A recent historical perspective on this influential paper can be found here.
For a more extensive bibliography/more details you can see here.

thank you very much for the papers! Yes, this is exactly what I was looking for. Felsenstein's a giant - I should have guessed he had something to do with it...

@jmah i feel like my main contribution to this website is as a felsenstein stan

Just came across a chapter by Felsenstein on phylogenetic inference with quantitative characters. In it, he states this biological justification for using Brownian motion:

A quantitative trait that has genetic variation controlled by a single locus will change as the gene frequencies at the locus undergo genetic drift...  Brownian motion is a reasonable approximation to change of a quantitative character by genetic drift, provided that ... [additive genetic variance] ... remains approximately constant.

Felsenstein also mentions that Cavalli-Sforza and Edwards (1967) consider that varying selection at a locus can be approximated by Brownian motion.
So I suppose that's another slant on why Brownian motion is used.


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Does "RT-PCR" denote "real-time PCR" or "reverse transcription PCR"?
I often find the term "RT-PCR" used in articles without any further qualification. Searching for the meaning of the acronym sometimes leads to "real-time polymerase chain reaction" and sometimes "reverse transcription polymerase chain reaction." I understand that reverse transcription PCR uses a reverse transcriptase to convert RNA to DNA, which is then amplified by the usual PCR method. I'm not sure I understand what real-time PCR is, but it sounds to be distinct from reverse transcription PCR. Are these distinct methods that happen to have the same abbreviation? Or do they somehow mean the same thing? What is usually meant by the acronym "RT-PCR"? Is there some context I can use to distinguish them?

Related: https://biology.stackexchange.com/questions/95268/rt-pcr-not-seeing-how-it-can-measure-mrna-expression-levels

Does this answer your question? RT-PCR: Not seeing how it can measure mRNA expression levels

I find those answers somewhat confusing. This statement for instance seems contradictory to me: "RT-qPCR refers to real-time quantitative PCR, but some organizations refrain from any reference to quantitation (because it's really only semi-quantitative), instead using the nomenclature rRT-PCR (reverse transcription real-time PCR, I guess)."

Unfortunately, there is no real and hard definition and it can mean both, depending on the context.

Real-time PCR is used to quantify a target in real time, thus is sometimes called quantitative PCR (qPCR). Basically, any mention of Ct or Cq values indicates a real-time PCR methodology. If they are quantifying a DNA target, it's likely referring to real-time PCR (aka qPCR). If they are using it to detect (not quantify) a target from RNA, it's probably reverse-transcription PCR. If they are quantifying an RNA target (like gene expression from mRNA), it's likely RT-qPCR (real time reverse transcription PCR).

PCR means (piece of DNA) amplification with 2 primers, a polymerase, free nucleotides and temperature cycling (to favor (un)hybridization and polymerization). For RNA viruses, prior to PCR there is RNA extraction and reverse transcription to DNA. In qPCR a fluorescent probe is added in the PCR reaction, when hybridizing (with the target piece of DNA) and cut by the polymerase ExoN and excited by some light the fluorescent tag emits some detectable light. An alternative is to use electrophoresis to obtain the amplification product, followed by sequencing.

@MikeyC That was the answer I was looking for: it that states the definitions in a systematic and unambiguous way. If it were an answer and not a comment, I would accept it.

FWIW, it seems like the field is coalescing around RT-PCR meaning reverse transcriptase and qPCR meaning real-time. RT-qPCR is the combination of the two. However, there are always going to be exceptions, so context is very important.

Real-time PCR is used to quantify a PCR target by measuring some indicator of target amplification in real time after each amplification cycle, thus it is sometimes(often) called quantitative PCR (qPCR). The key to distinguishing between reverse transcription PCR and real-time PCR in the context of a paper or protocol is to look at the starting material being used and the data output.
If the source material is RNA, it needs to be reverse-transcribed into cDNA before PCR amplification. And if they're showing quantification of a specific target, it's likely a real-time PCR of some sort. Quantification of a gene target from normal DNA is likely a standard real-time PCR (aka qPCR). Quantification of an RNA target (like gene expression from mRNA), is likely quantitative reverse transcription PCR (RT-qPCR). The same goes for if the starting material is cDNA (end product of an RNA reverse transcription reaction). Lastly, any mention of Ct or Cq values (or delta-Ct, or delta-delta-Ct) generally indicates a real-time quantitative methodology.
If they are citing the use of RT-PCR to simply confirm the presence or absence of a target (sometimes called endpoint PCR) or to amplify it for downstream applications like sequencing, with no mention of specific target quantification, it's likely a standard reverse-transcription PCR.
There are exceptions to some of these rules, but it should help get you through most literature with some idea of what methods are being used.
Edit: In the past few days, I've seen multiple papers using "RT-PCR" as shorthand (I guess) when they were talking about RT-qPCR or rRT-PCR. Like I said, always exceptions to the rule. But as long as you read the methods it should be simple enough to figure out.

Why was this downvoted? Is it incorrect?

An addition: real time PCR or qPCR requires a a dye which binds to dsDNA. This will give you readings of RFU (relative fluorescence units) per Cycle. In RT-qPCR the dye binds to the dsDNA from the conversion of ssRNA by RT.


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what powers power strokes
I am wondering what really powers the myosin head to undergo the power stroke to push the actin filaments towards the M-line. I have 2 thoughts:

when ATP in the myosin head gets hydrolyzed, the energy released is stored in the head. This energy powers for the power stroke.

when ATP is hydrolyzed, inorganic phosphate and ADP leave accordingly (90deg--> 50deg --> 45deg), the conformational changes of myosin head proteins cause the power stroke.

I think (2) is more plausible as the order of actions (moving actin filaments by 6.7nm + 1.3nm in order) is more 'conventional'(wiki), rather than a single action (using energy by ATP hydrolysis, a 1-step boost of energy).
However, if (2) is really correct, then may I ask what is the energy released in (1) used for in the myosin head, does it just simply fade away as heat energy?
thank you very much.


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Summation on muscles
I am learning myology and encountered 2 problems in tetanus and summation:

Unfused tetanus is just a continual summation of twitches if I am not mistaken. However, is it a MUST for summation / unfused tetanus to constantly increasing muscle tension from the photo (the graph) i.e. is this the definition?

Since we are in unfused tetanus when we hold something, and I can’t feel my biceps are constantly increasing in contraction / tension. (to my understanding, complete tetanus is when we are lifting up very heavy things only as it utilizes too much ATP)

Can I say the muscles are in tetanus during contracting (lifting), and also in tetanus during constantly contracted state (keep the thing holding up) Since tetanus is just a frequent action of sliding filaments, which is common in both actions?

Also, during tetanus, I don’t need to shorten my muscles anymore (just holding something still), but myosin heads are still power-stroking to shorten the sarcomere/muscle, may I ask how to explain this?
Thank you very much.


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Why don't cats have to pant?
I understand why dogs pant and humans transpire, namely for temperature homeostasis. So why don't cats need to do either, even after expending a lot of energy on a hot day?

Do cats ever expend a lot of energy?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site (it is not identical to SO) and [edit] your question accordingly. In particular, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). I believe you have not done this because your question is based on a false premise — google search result. Thanks!

Cats have low endurance, dogs can jog for 20 kilometers, endurance hunting. Besides, check videos of lions on hot days, they pant under a tree.

@aliential: Depending on the breed of dog, a 20 km jog might just be a gentle warmup.  Even my friends' small dogs - not much bigger than a cat - will happily go 10 km or so.  But I don't think I've ever seen a cat run even 100 m.

domestic cats do pant sometimes: https://www.timeforpaws.co.uk/s/cat-panting-should-you-be-worried

The answer to this question should be that cats do pant when overheated. It's a thermoregulation system that they do use in extreme circumstances (aside from paw sweating). Especially after exercise (zooming up and down the stairs). It could also be a sign of disease, though, it should all be taken into context when analyzing panting (or any other behavioral cue) in cats. It's not a frequent thing to see, because of their high tolerance to heat as stated in one of the answers, but only a few days ago with all this heat waves I saw one of my cats precisely panting after a good random run.

Cats are smaller and hotter than dogs and humans, with a temperature  between 100.4°F and 102.5°F (38.1°C to 39.2°C).
Smaller animals have a higher surface-to-volume ratio and so radiate excess heat more efficiently.
Being hotter, cats tolerate higher temperatures.
I could not find an accessible ref for this, please insert some if you can find some.

I've added as source for a cat's core temp. But you say 'Cats are smaller and hotter...' than what? An elephant? And the fact that they are more heat tolerant and that it's due to core temp and size is what really needs a proper source. But in itself a nice answer.

Somebody should do a study correlating the RoP (Rate of Panting - excuse the technical lingo) with dog size! I must say thinking about it - my sausage dogs do indeed pant less than my husky...

Transpiring and panting are ways to regulate body temperature. When sweat evaporates, it cools the skin, and panting releases heat through the mouth. Horses, humans and even plants transpire for this reason, while dogs and birds pant. But how do cats release heat?
In fact, cats sweat through their paws. It appears that a cat after it has been frightened may leave wet pawprints on the floor. Although it's all over the internet, I couldn't find a convincing picture and as a cat lover, I've never noticed this phenomenon. That aside, cat's paws have little surface area, and cannot provide much cooling power. Instead, felines have other, more effective strategies to adjust their core temperature. Like dogs, they often sprawl out on cool surfaces (Fig. 1), or they seek out the shade on hot days. They also tend to sleep a lot, which reduces core temperature and is preferable of being very active in hot times in terms of body temperature (Fig. 2).

Fig. 1. Sprawling cat. source: Columbian blogs

Fig. 2. Cats in the shade. source: Cat memes
Source
- Indiana Public Media

A cat on a hot tin roof is in greater trouble that I always thought! :) I'm having trouble understanding how my cat with thick fur is cooling down through it's paws at the same rate as my short hair dog panting under the same conditions. Maybe a cat's metabolism is much slower so heat buildup is less of a problem.

@HeinduPlessis as said, they keep calm :)

They sure do! I wonder if there's a paper in this?

The second paragraph of this answer is substantially copied from the source you linked to. You should make it clear through quotations when you are using someone else’s writing.

@canadianer it's not quoted though; the text has changed. I can add the source somewhere again, but it's clearly mentioned below? I guess it's fine as is.

Copying the phrasing of others, even if you change some words, is plagiarism regardless of whether you cite the source. You might consider consulting some academic guidelines on plagiarism, for example: https://integrity.mit.edu/handbook/academic-writing/avoiding-plagiarism-paraphrasing or https://www.ox.ac.uk/students/academic/guidance/skills/plagiarism

@canadianer - I'm aware of the rules, and normally I'm always really careful. I've edited the text.


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Estimate mutation rate in UVC treated cells
I am wondering how to get a coarse estimate of the number of mutation I obtain doing UVC treatment on eukaryotic cells (microalgae) starting from information such as the survival rate, genome size, number of genes or gene density... I heard about a similar estimation for EMS mutagenesis (I don't remember the exact details but it was a correlation between number of colonies surviving the treatment and the number of point mutations per kb of genome). I cannot find the source of this kind of estimate so I really appreciate any help!

Could you give us some more information about the kind of data and experiment you have please, as it will help people give you a better answer. If you have genotyped your colonies, then I would imagine it's not too hard to estimate the number of mutations which have occured.

I just did UV mutagenesis on my cells and determined a kill curve, that's all. I do not have genotyped my WT or MUT colonies (I'm not looking at a specific gene).
My question is if there is a way to have a very very rough idea of how many changes I introduced in the genome by just correlating the survival at a specific dose to the genome size / number of essential genes or similar ( I know this requres lots of assuptions but that will be fine).


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How can cane sugar sucrose be different from beet sugar in regard to carbon-13 content?
According to an article in SCIENZA IN CUCINA, by Dario Bressanini, le Scienze Blog content of $^{13}C$ differs in sucrose in beet sugar compared to cane sugar. What is this due to? Are there any similar examples?
Is the difference in synthesis enough to explain the difference?
One could guess that the weight of the carbon molecule is more critical in one of the synthesis chains.

@user438383 That looks like an answer, but you've posted it as a comment.

@user1136 I just asked another user to not answer in the comments, why are you now doing the same?

Hi, I don't think anyone is critiquing your question. Two different people have posted comments (now deleted) that started to answer your question, instead of answers, which is against policy at https://biology.stackexchange.com/help/privileges/comment . We're just asking them to move that to the Answer box instead, I think your question is good as is.

The differential uptake of different isotopes of carbon is covered well at:
https://en.m.wikipedia.org/wiki/Fractionation_of_carbon_isotopes_in_oxygenic_photosynthesis
Plants have a lower proportion of C-13 than atmospheric CO2.
The two mechanisms that cause this are the reduced diffusion speed of the heavier C-13, and an energetic difference in the chemical reactions that favours C-12.
In sugar cane (C4 photosynthesis) the carbon dioxide is captured in an additional step compared with sugar beet (C3 plant).
This capture step in C4 plants (using phosphoenolpyruvate carboxylase) is less exclusive toward C-13, so the carbon in these plants has detectably more C-13 than C3 plants.
This subsequently affects the isotopic proportion of all the carbon in the plant


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Understanding muscle tone
I am relatively new to Physiology, and I've just learnt about muscle tone.
I however find it difficult to understand the electrical changes that initiate (and/or accompany) muscle tone in smooth muscles .
To be specific, I know that action potentials(AP) cause muscle contraction (just like they cause nerve impulse propagation), and I also know that smooth muscle tone is a result of irregular contractions of the muscles at rest.
How then can these muscles contract when no AP is generated at rest?
PS: This question has been edited to achieve more clarity.

Action potentials usually maintain muscle tone in skeletal muscles, but muscle cells are affected by other influences that can affect their contraction and thus the tone of the muscle.
Smooth muscle occurs in the walls of hollow organs, most notably the blood vessels and the GI tract, and in a few other places.  Contraction of smooth muscle is generally involuntary and can be stimulated by the APs from the autonomic nervous system, but often for the slow maintenance of muscle tone contraction is controlled by hormones, other external molecules, or external pressure.  The mechanisms that cause this contraction generally involve the phosphorylation of myosin light chains. (1) (2)

If action potentials can at all maintain muscle tone, why is muscle tone spoken of as passive contraction? (https://en.m.wikipedia.org/wiki/Muscle_tone). As much as I know, passive processes don't involve ionic changes seen in active ones (such as action potentials). If I am wrong about this can you point out the misconception?

Disclaimer: it has passed some time since my studies in muscle physiology.
Muscle have stretch receptors to monitor the change in length. These are connected to the central nervous system, where information is properly processed and the response triggered. This response, as far as I know, propagates through action potential (AP) across neurons, which activate the muscle (transverse tubules, AP, Ca2+). In summary, muscle tone should be regulated by APs and I am not aware of another mechanism of muscle contraction in this case.
Do you have some references where they discuss another mechanism of non-AP muscle tone? I am very curious to know more.
/Emilio

My several days of research on the mechanism has turned out futile. But this is the statement which prompted my question: "...smooth muscles of some visceral organs maintain a state of partial  contraction  called  tonus  or  tone.  It is due  to the tonic contraction  of the muscle  that occurs without any action potential or  any stimulus...". It is from the text: essentials of Medical Physiology by K Sembulingam

@Chemo-Mike Pretty important to indicate you are talking about smooth muscle in your question if that's the case.


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NCBI blast for exact match of short sequence
I'm trying to Blast for exact matches to the sequence: 'ATTGNNNNGCAAACCA' in the human transcriptome using NCBI Blast on its 'refseq_rna' database. However, when I do a basic query I get "No significant similarity found."
Note the N's in the middle of the sequence, if I get rid of those N's, yielding the sequence 'AGCGGATTGCAAAGCAAACCA', I get a match in the 3' UTR of the human MeCP2 gene (which is correct). I don't understand why adding the N's here make it not work.
I looked at the help section and I believe this may be due to shorter sequences being less "statistically significant". Statistical significance of output is completely irrelevant to me, so I set 'Expect Value' to 100000000000000. However, I still get the same result.
I also tried to modify the HTML of the page to allow me to submit a word size of 4 to the form. This went through, but I still got "No significant similarity found".
Could someone help me out with this? I feel like searching for a short sequence shouldn't be this hard.

You are asking a question about a piece of software which is extremely well documented. What does the documentation say about searches with wild cards?

it says absolutely nothing

Well you might email their help desk. They are quite good about replying to queries in my experience, although my own have been of a different sort.

The second sequence is not the first sequence with the N's removed, should it be?

no it's with the N's replaced with 4 bases to make it the MeCP2 sequence

This was answered in the bioinformatics StackExchange: https://bioinformatics.stackexchange.com/questions/14423/ncbi-blast-for-exact-match-of-a-short-sequence

@MikeFlynn Please tell Maximilian Press that 4^4 = 256

You don't usually use BLAST for exact matches. I would rather suggest that you simply do a regex match using any programming language you like. Since this question has already been answered in [bioinformatics.se], I won't elaborate further.

I’m voting to close this question because it is cross posted (and answered) in [bioinformatics.se]. (https://bioinformatics.stackexchange.com/questions/14423/ncbi-blast-for-exact-match-of-a-short-sequence)


text:
Question on thick filaments

In this photo, I know that the arrows pointing towards the M-line of sarcomere on actin filaments are due to the power strokes of myosin heads. However, what I don't understand are the arrows on the myosin filaments pointing away from the M-line.
Are they the reaction forces (action-reaction pair, where the action force is power stroke)? Also, will this force (pointing away from M-line) 'tear apart' the myosin filaments on M-line? If not, how can the filament withstand this force?

Yes, they are action-reaction pair.( Newton’s third law).
No, it won’t tear under normal circumstances. The filament withstands all that force because the attractive force between its constituents is far more than the force generated by myosin actin cycle.

Thank a lot. For (2), for the attractive force, do you mean the force between the myosin filament and the M-disc?

@234ff yes. That’s it.