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Is that true that plant stem cells can be used in humans?
I was reading an article (which seems very fake to me) on sensitive topics, but there was one astonishing statement:

Stem cells are obtained from certain plants that grow all over the world. Once the stem cells have been obtained, the doctor will inject them on the target organ...

I want to ask specialists if this particular statement can be true. If yes, does it imply nucleus replacement in stem cells, or anything like that?
Sorry guys, for the stupid question.

They very likely can't be used. The number of chromosomes won't match and most likely the immune system will mount a response against the plant cells

Absolutely not, plants do not have the same signal pathways and have very different cell biology.

Of course, the stem cells must be obtained from the plant stems ;-)

I’m voting to close this question because it is very poor quality and under researched.

@tyersome, poor quality? It's readable - yes. Under researched? You wish to answer only clever and obvious school-test grade questions? If everyone had the knowledge, no questions would be needed. Don't like this question - don't spend your time here.

https://stemcells.nih.gov/info/basics/6.htm
...
Viruses are currently used to introduce the reprogramming factors into adult cells, and this process must be carefully controlled and tested before the technique can lead to useful treatment for humans. In animal studies, the virus used to introduce the stem cell factors sometimes causes cancers. Researchers are currently investigating non-viral delivery strategies. In any case, this breakthrough discovery has created a powerful new way to "de-differentiate" cells whose developmental fates had been previously assumed to be determined. In addition, tissues derived from iPSCs will be a nearly identical match to the cell donor and thus probably avoid rejection by the immune system. The iPSC strategy creates pluripotent stem cells that, together with studies of other types of pluripotent stem cells, will help researchers learn how to reprogram cells to repair damaged tissues in the human body.
So as that all points out, no, the genetics of it will cause a plant stem cell to be genetically not a match, where it might do something for a little while, but upon that cells first interactions, it will stimulate the immune system to get rid of it, rather than incorporate it.
Anymore, I want to know about how Bone Morphinogenic Proteins (BMP-4 or above) can be injected into an organ, and if that will help stem cells for reviving an organ at all.


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Is transition more common than transversion during the evolution of duplicated genes?
Transitions are base mutations of purine to purine (A <-> G) or pyrimidine to pyrimidine (C <-> T). Transversions are purine to pyrimidine or vice versa (A <-> C, A <-> T, G <-> C, G <-> T). And it is well-known that transitions are more common than transversions in the populations.
So what is the condition in the evolution of duplicated genes? Suppose a gene A is duplicated with two copies A1 and A2 in the same genome (not two alleles in different sets of chromosomes, or the same gene in two different cells/organisms). At first A1 and A2 had the same sequence, but then they went through an evolution process and each got some mutations. Now let's check the sequence of A1 and A2 again, are the differences between A1 and A2 mainly transitions instead of transversions?
Although I think it would not be surprising to find that transitions are more common in this condition, I've searched some papers focusing on the evolution of duplicated genes to look for some support. However, they mainly discuss what happened to their functions instead of sequences.

If we consider that the biochemical impact of transitions vs transversions is constant across the two scenarios, then the only discrepancy can be due to the level of purifying selection, or the level of positive diversifying selection, or both, between the two duplicates.
By far the most common fate to one duplicate copy is for purifying selection to be relaxed, leading to accruing deleterious mutations and eventually loss. This means that fixation of non-synonymous mutations are more common, and as transversions are more likely to be non-synonymous, this implies that the rate of fixation for transversions would increase.
Similarly, one might expect functional change leading to positive diversifying selection, which implies a greater rate of fixation of non-synonymous mutations and, following the same logic as above, a greater rate of transversions.
Whether or not this contributing increase to the rate of fixation of transversions mean that transversions actually outnumber transitions, or instead merely decreases the ratio of transition:transversion, will be dependent on the particular gene and selective scenario.
As a final note, while the first cause I identified (biochemical)  actually changes the rate of mutation, the selection-specific factors are changes to rate of fixation, which is a population-level process. So while the relative rates of transition and transversion may stay the same, the fixation rates of these two categories of mutation between the two duplicate copies are the important difference.

source: Stack Exchange

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

sort: votes


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Why swordfish aren't put in the same family as Marlins?
Why Swordfish (Xiphias gladius), which are very similar to Marlins, do not belong to the same family as Marlin - Istiophoridae?
Both has long bill or a sword in the upper jaw, both has (at least in some stage of life) a long sail along the back, both are predators and fast swimmers and both are of similar overall shape and size.

Moreover, as cladistics is prevailing over Linnean taxonomy, the ranks of family or superfamily are not essentially different, can we say that swordfish and marlins belong to the same clade which includes the two families Xiphiidae and Istiophoridae?

Why Swordfish (Xiphias gladius), which are very similar to Marlins, do not belong to the same family as Marlin - Istiophoridae?

The decision about what we call an order vs a family is very subjective. Someone decided that Istiophoriformes was an order containing the families Xiphiidae and Istiophoridae but someone else could have decided to call Istiophoriformes a family (although the name would have ended in -idae, then) and Xiphiidae and Istiophoridae subfamilies.

[C]an we say that swordfish and marlins belong to the same clade which includes the two families Xiphiidae and Istiophoridae[?]

Yes, you can. This clade is the order of Istiophoriformes. You can hence say that swordfish and marlins are both Istiophoriformes. Or if you prefer, you can say that swordfish and marlins both belong to the order of Istiophoriformes.

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


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False positives in TAP - MS experiments
Is anyone aware of a website where they show common false positives often found when doing a TAP-MS experiment to find protein-protein interaction experiments?
Particularly the Acs1 protein (Acetyl-CoA synthetase) seems to be a protein I often see in a TAP-MS experiment so I am starting to think it is a false positives but I can't seem to find a good paper or website where it is mentioned as a commonly found false positive interacting protein.
Any insights will be helpful.
Thanks.

The common repository for affinity purification (CRAPome) contains the results from many tandem affinity experiments and scores them based on their presence in control purifications.
The database can be found here. I did a very quick and dirty comparison of the frequency that human ACSL_1 (Uniprot ID; P33121) and GAPDH were detected in control purifications. The graphs shows that ACSL_1 is not a frequent contaminant (detected in less than 5% of GFP control purifications) whereas GAPDH is frequently detected in control affinity purifications.

You can submit your tandem affinity experiments to the CRAPome and it will  provide quality scores for your hits. It's very well thought out and not difficult to use. You might want to try it if you're still .


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why do we tighten out muscles against cold?
When I'm in shower and I want to open the cold water on myself suddenly I make my muscles so tight before I open the water and that helps so much in being able to handle the shock. Why does tightening of muscles help in handling the shock.

This question could be improved by rewording it to be more focused on the general human actions, this may be confused for a personal medical question.

@John I don't really know how to reword it in more than one small sentence to be more general. I don't know if other people do this in shower or before an impending cold shock so I can't say we humans instead of I there.. anyway, if you have any good way of making this general please edit. I will accept:)

Consider most animals instinctively recoil from unpleasant sensations. Resisting this often involves tightening the muscles. Think about the last time you had to get a shot or pull a splinter out of the skin, you often tighten the muscles in an attempt to resist your own instinctual reaction. Even non-physical reactions like resisting fear or disgust often have similar responses, the mind and body do affect each other. Physical actions can effect mental states. Tensing muscles has been shown to have a direct effect on our willpower.

Your question can be answered by focusing on both 1) physical, and 2) psychological changes that occur when you tighten up your muscle. Of the two, psychological changes

Muscle contraction generates some heat which may account for a very small sensation of heat; however this heat can't be so much to actually prevent cold sensation. Moreover, muscle contraction can insulate the visceral organs (imclitsong the blood vessels)  to lose heat due to conduction. Again, this is not very effective for your situation.
Mammals tend to curl up when the ambient temperature is low. This will prevent heat lose from the core. By contracting the muscles, you feel good and sense warmth as this behavior is associated with warming up. Therefore, you won't feel the cold as you get exposed to cold water.


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What is the chance a given gene will end up in a given gamete?
Let us say a germ cell had a desired allele. This germ cell was replicated during interphase so that it had two of the desired allele. It then underwent meiosis.
My question then is, what is the chance a given allele will end up in a given gamete that will be involved in conception?
Firstly, there is a 50% chance a chromosome will be assigned to a given daughter cell. This is because of independent assortment. In addition, cross over occurs at chiasmata. Lets assume then that there was a 50% chance that an allele will be crossed over (although this probability may be far from true)
The process during meiosis is that cross-over occurs first. We have two desired alleles, each on one of two pairs of chromatid attached to each other. There is 50% chance for a given allele to cross over. For example, the chance for both desired alleles to cross over is 1/4 (1/2 x 1/2), the chance only one will cross over is 2/4 (since either of the two desired alleles can cross over).
Then there is the first independent assortment during meiosis I which produces the desired daughter cell. In this case there is a 50% chance that a given chromatid pair (containing the desired allele) will be assigned to the desired daughter cell. However, in the case where a desired allele is found in both homologs (2/4 of a chance), then the chance that at least one desired allele will be in the daughter cell is 100%.
Finally, during meiosis II, another independent assortment occurs which produces the desired gamete. The same rule applies with a 50% chance a given allele will be assigned to a given cell (in this case the gamete). However, if the desired daughter cell contains two of the desired alleles, then there is a 100% chance that the cell will have the desired allele.
In conclusion, the chance I estimated that the gamete will have at least one desired allele is 50%. Although, I'm not sure if this is correct. Anyone mind confirming this.

"Let us say a somatic cell... then underwent meiosis"  Somatic cells don't undergo meiosis.

Gametes do not undergo meiosis (at least under normal circumstances). Since you seem to be having ongoing trouble with basic concepts and terminology in genetics I strongly encourage you to take advantage of the many online resources available for making sure you have the background required for understanding this field. Suggestions to follow ...

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

A cell contains two haplotypes (or two set of all chromosomes). One haplotype inherited from the mother, one from the father. A haploid cell, resulting from meiosis, will receive either the maternal (or grandmother if you prefer) or paternal (or grandfather if you prefer) haplotype. It cannot receive anything else. Hence the probably must be 0.5 (or 50%).
Note that you are using the term "gene" incorrectly. You should use the term "allele" instead. And while you are improving your genetic vocabulary you should also check the term "locus". Also, the term "desired gene" is never used. We talk about "beneficial allele" or "detrimental allele".

I think "desired gene" is to mean "allele of interest" for purpose of calculations.

You are making this too complicated.  There is a 50% of any particular allele ending up in a gamete.  The end.


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What kind of longhorn beetle is this?
I live in Europe and found this interesting longhorn beetle I think and I was curious what species it is or what's it's name!
Thanks to anyone who identifies it!

Rosalia alpina (common name: Rosalia longicorn)
See here: Rosalia longicorn
The link I added shows a picture of an identical Alpine Longhorn Beetle. This longhorn beetle occurs mainly in the European Alps and the neighboring countries (e.g. Germany, Hungary, and France). Minimum height is around 700m above sea level. The adults are active from June to September. The color varies between blue and grey, the head is characterized by one spine on each side of the head. The number of black dots on the elytra varies.

Welcome and thanks for your answer. For species ID answers we expect users to post an identifying picture and additional evidence that it is indeed the beetle in question, for example by mentioning geographical distribution and check whether that matches OP's location.

Thank you for your comment. The link I added shows a picture of an identical Alpine Longhorn Beetle. This longhorn beetle occurs mainly in the European Alps and the neighboring countries (e.g. Germany, Hungary, and France). Minimum height is around 700m above sea level. The adults are active from June to September. The color varies between blue and grey, the head is characterized by one spine on each side of the head. The number of black dots on the elytra varies.

Also see https://commons.m.wikimedia.org/wiki/Rosalia alpina for further pictures

You can edit the question to add this information to your answer. I think the downvotes are harsh when you appear to have the correct ID but those leaving them may reverse them following an edit.


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Can you tell the name of this spider?
This image has been posted on the Wikimedia Commons

This spider is about 3~4cm long. It was found in the middle of tomatoes plants in a garden, in the center of France, Clermont-Ferrand. Photo taken in the early days of August. It would be interesting to specify the species on Wikimedia Commons.
Please let me know if you need other information.

Apparently, Americans aren't the only ones to use their currency as unit of length $\ddot \smile$. I changed the unit from "2 € coin" to "cm". I edited a few other things. I am not sure what you meant by specify the species on Commons though, so I left it unchanged.

Thanks. You're right. Commons refers to the Wikimedia fundation site where the image is hosted. These images are often used as illustrations on the different Wikipedias so that adding the specie in the description would be a great added value.

This is a wasp spider (Agriope bruennichi)
See here: Wasp spider
The link leads to a German Website showing the belly side of a wasp spider
Or see here: Wasp spider II


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Can Anyone Tell Me , Which Insect or I think Moth Is This

Region : Asia ( India ) , Size is about : 4 cm . Since yesterday this Insect is in the same place . I don't know any other info , I was just curious to know about this Insect.

This is not a fly! Can you give more information about this individual? Where (what region, what country, what type of ecosystem) did you find it? What is the approximate size? Any behaviour to notice? Did you get a picture where we can see its butt? Any other info?

But it is deffinitly look interesting.

Region : Asia ( India ) , Size is about : 4 cm , Since yesterday this Insect is in the same place . I don't know any other info , I was just curious to know about this Insect.


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Can the face bones be "compressed" or forced together? What would happen?
Say someone doesn't like that their maxilla bone is too long because the height of the maxilla affects the placement, position and angle of the mandible relatively.
If one were to apply mechanical force from the mandible underneath the hand (pushing up) while countering the force either with the neck and/or pulling the head forward and down for prolonged periods of time, steadily and consistently, will the maxilla literally move upwards?

Simply put, as I understand it, bones remodeled due to consistent mechanical tension and stress placed on them lifelong as part of osteoblastic/osteoclastic activity and bone metabolism. My question is, assuming my line of thinking here is right, would the maxilla actually move upwards and the mandible will rotate too? How far up can it go before it would affect facial structure in a negative and/or potentially dangerous way, and how long would this take to do if done 1-2 hours per day, 7 days a week with about 1-4 lbs. of consistent, balanced and equalized force?

What's with the premaxilla? What do you think will happen to your teeth? And with you sinuses? And your nasals? 1-2 hours a day won't help anything... This won't act like plastic surgery...

Time under tension has to make some physical changes given enough duration. Doubting that would be doubting the science surrounding bone re-absorption and Wolff's Law.

Yes, there will be some effects... But not the ones you are looking for.. Or are you looking for terrible tooth ache and a missing occlusion? I don't doubt the effects... I work with biomechanics. There's something called the phenomenon of the blind billard player... He only sees the cue ball but isn't aware of the effects on the other balls when he hits the cue ball with the billard cue.

Please don't encourage this kind of question. This is a personal medical question, common among people who frequent incel forums.

It's a serious question and not personal/medical. What does its relation to incel forums have to do with anything? It's a fairly legitimate question about bones/biology/biomechanics/etc.

Bones are remodelled,it's correct but there is a limit too in this remodelling and specially when are doing it manually. Moreover it is very important  to keep your jaws in proper occlusion otherwise this improper way of pressuring and tension creation in your maxilla and mandible will lead to more severe problems in your temperomandibular joint, leading you further to the cranial disorders. Such activities on a daily basis are quite harmful and these definitely don't work like plastic surgery. So, it's better not to perform these or it may lead you to become a regular patient to your dentist. If you are really willing to have such changes then you should consult a cosmetic surgeon.

I get your point, but this is more of a "what will happen" kind of question. Cosmetic surgeons charge money -- this experiment is 100% free so there's an advantage there.

For whom? The dentist?


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Why are there no multicellular prokaryotes
Why don't complex multicellular prokaryotes exist and also what makes eukaryotes multicellular?

Prokaryotes are called so because they are unicellular. If they were multicellular, they would be called eukaryotes. Similarly, if unicellular, it would be a prokaryote. That is just how these cells have been named.

@TheLastWord "If they were multicellular they would be called eukaryotes" - this is false. The more specific definition of prokaryote vs eukaryote has to do with the presence of membrane-bound organelles in eukaryotes. There are many many single-celled eukaryotes.

@BryanKrause Yes, I got that from the answer. I did not think about single celled eukaryotes.

@TheLastWord True, just don't want a misleading comment to confuse future users that come here, there is no way to downvote a comment, and someone already upvoted yours.

@BryanKrause Yes, I noticed the error much earlier but let it stay so that someone  else does not make the same error.

If you consider mitochondria and chloroplasts, in a way they have.

Why are there no multicellular prokaryotes?

From a Molecular Cell Biology introduction course web resource from the University of Illinios, which explains the general sentiment in microbiology over this question:
There are lots of unicellular eukaryotes, including amoebas, paramecium, yeast, and so on. As to whether there are multicellular prokaryotes, the standard answer is No, but there is a lot of evidence that some bacterial species can aggregate together and divide labor so that the "colony" is working more efficiently. This is characteristic of any traditional multicellular organism, but there's still a lot of resistance to the idea of calling these prokaryotes "multicellular."
Here's a Scientific American article on the subject, which is good for the layman and will add to your understanding. Note that the most complex 'multicellular prokaryotes' known do not form comparably large or complicated structures when contrasted with eukaryotes. Even though prokaryotes have more biochemical tools available to them, their largest multicellular specimen pales in comparison to our small multicellular eukaryotes, let alone out large eukaryotes like the Armillaria ostoyae fungus in Oregon (nicknamed "the largest organism on Earth"), giant sequoia trees, the dinosaurs, or blue whales. But I digress! Total organism size is not a requisite for multicellularity, which is why some bacteria can be termed so.
Here is a paper I found in the literature on the first reported 'true' multicellular prokaryote, from 2004. Similar organisms have been observed since. See Pubmed link.
The same question has also been answered extensively by specialists on Quora and on ResearchGate.

What made eukaryotes to become multicellular?

Your question implies external influence. Biological evolution does not proceed teleologically, with an end goal in mind. Instead, traits gradually accumulate if they are not detrimental to the replication of the genes. The evolution of multicellularity is a complex and active field of research but there is no reason behind this major switch in cellularity other than that it works as a strategy for the replicating organism and its genes. Multicellular organisms survive. That's all.

Why don't multicellular prokaryotes survive?


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Does evolution produce organisms perfectly adapted to their environment?
I have this biology assignment with this chosen topic. I have no idea where to start researching. I have studied the mechanisms and theories of evolution. I just don't know which relates to the topic. The task is to persuade an audience of one side, either yes evolution produces perfectly adapted organisms or no evolution does not produce perfectly adapted organisms. I have started research on the blind spot of the vertebrate eye and that might be case scenario for the topic. If you have anything to add at all that would help me complete this project. It is much appreciated. Thank you in advance!

Hello and welcome to Biology.SE! Take the tour to learn about this site and earn yourself your first badge.

I'm voting to close this question as off-topic because it is not about Biology in the terms of SE Biology.

You should most definitely have a look at a very introductory course to evolutionary biology such as evo101 for example.

Does evolution produce organisms perfectly adapted to their environment?

There is a lot to say about this question. The question is very broad and cannot be fully answered in a single post. The very very short answer is "no". I will very briefly develop this "no" below.
Concept of perfection
There are semantic (and hence philosophical) issues of the concept of perfection in this question but I shall not go into these issues. Typically, in the fact of sexual selection (and other arms race), the concept of "perfection" becomes very unclear (see S Pr's answer).
There is variation in populations
Evolution is all about genetic variance in populations. The fact that variance exists makes that necessarily there is no notion of perfectly adapted for a population (or for a species) as not all individuals are the same!
"Drivers" of evolution
Evolution is a change in allele frequency over time. There are a number of drivers of such changes, including natural selection, genetic drift and mutations.
While natural selection is a deterministic process, genetic drift and mutations aren't. There is hence constantly departure from a "hypothetical perfect" caused by genetic drift and mutations.
Mutations, while being a "random process" (see Are mutations random?), most mutations are deleterious, hence constantly inputting "imperfection" into populations.

Hi Remi. I see what you're doing ;) You're stiff competition, friend!

Sorry, I failed to refer to your answer. Obviously, I added a note inspired by your answer and I should have linked to your answer. Done, now! That being said.... Wow you've been fast at detecting it!

No problem, just joshing. I wanted to say hi because I see your answers quite frequently and I'm more-or-less a new person here. Hello!

Another factor here is that natural selection pressure is asymptotic.  Even if we could provide a constant environment, and define what is perfect adaptation to it, the closer individuals get to that perfect adaptation, the less pressure there is to improve.  Reaching perfection would take infinite time, so evolution generally settles for "good enough".

@jamesqf Interesting point. While it is true that selection pressure decreases with decreases additive genetic variance and hence with increased allele frequency (past a certain frequency threshold that depends upon the dominance coefficients), a statement like "the more fit an individual is, the less likely it is for a new mutation to be very beneficial" would be true depending upon the mutational effect model considered. It is standard to use a geometric model and empirical estimates appear to be quite supportive of this model.

Perhaps an angle which hasn't been covered yet, which can be used as an argument against the vague question "does evolution produce adaptations to better suit an organism's environment":
Sexual selection contributes to the acquisition of traits which are favorable in mate choice or competition for mating. For instance, ornaments such as antlers are considered attractive for others in the species (female mate choice); they also aid in male-male competition (resource-defense or female-defense mating systems)
Here is an excerpt from an essay I wrote many years ago:

Sexual selection in particular has the peculiar tendency to exaggerate
  traits even beyond their ecological optimums. [...] Megaloceros giganteus, the Irish elk, is an extreme example of
  a recently extinct animal (estimated to have disappeared 10,600BP)
  whose antlers and body size were grossly unfit for the increasingly
  distressing requirements of its woodland habitat. It stood at 210cm at
  the shoulders and its antlers spanned a width up to 365cm, weighing as
  much as 40kg. It is conjectured that extinction came as a result
  of the inability to further sustain the exaggerated trait, which
  required calcium and phosphorus replenishment as well as repletion of
  fat reserves from a rapidly shrinking high-quality forage density as a
  result of climate and eventual environmental change.

Of course, there are hundreds of examples of this. I just like the Irish elk. It was imposing, to say the least.

I must also stress that your original question betrays ignorance on the topic. Evolution is not teleological, it has no end goal. Also, very crucially, the environment is ever-changing - abiotic factors such as temperature, as well as various pressures from other cohabitants in the ecosystem, are always changing. Perfection implies an end, stable state. A 'perfectly' healthy, immune individuals will eventually become vulnerable to a pathogen or parasite. Perfection is also subjective, and means nothing in biology. In photosynthesis, the theoretical maximum efficiency of solar energy conversion is approximately 11%. Yet plants are ubiquitous. Birds have light, hollow bones to aid in flight; the eyes of eagles are better suited for visual feats not shared by humans; cats have great night vision; bats have an expanded range of hearing due to their use of echolocation; insects have well-developed and highly sensitive olfactory systems, etc. None are perfect, and can always be improved upon, theoretically speaking. And what use is night vision if there is no night? What use are exceptionally light bones if you are a flightless bird such as an ostrich?
My answer to your question is this: evolution never produces perfect adaptations, it may only sometimes produce traits which, to humans, are impressively advantageous. Biology is full of imperfections; evolution can only work with pre-existing structures so it does not explore all possible solutions, where you could likely find something resembling perfection. Evolution produces organisms with traits which are or once may have been capable of allowing the organism to survive. Nothing more.


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Why do frogs and toads only appear when it is dark outside?
I noticed outdoors how frogs and toads only appear when it is dark or cloudy. Such as only after it rains or during night time. Why is this?

The premise is false.  Frogs and toads don't only appear when it's cloudy (personal observation, easily repeated in most rural areas).  Most amphibians prefer cool, humid environments, as their moist skin serves as a secondary respiratory organ: https://en.wikipedia.org/wiki/Amphibian#Skin

I understand.. Do you think I should I reword my question?

I think it needs to be almost a completely different question, something like "why do amphibians prefer humid environments?".  Because at least in temperate areas, any small pond is likely to have frogs &c active during the day.  For instance, there's a medium-sized pond near me where during the season when tadpoles become frogs, you can hardly walk along the edge without stepping on small ones - and this is on the edge of the semi-desert Great Basin.

I see them,( or their ripples after they jump into the water ) during the day; I have 2 small ponds in the yard. I see tree frogs in my patio plants during the day but they are sleeping. The frogs/toads certainly make more noise when it rains ,has rained, or is going to rain. even during the day. They are certainly more active at night . I expect more bugs around then . I only see the geckos at night ,near the lights.

This sounds nice . maybe they need to conserve their energy during the day . maybe they are attracted to the water in your ponds!

Yes, the pond are a big draw. The neighborhood is very quiet at night , except within a hundred yards of the ponds. People on the phone have asked my wife the noise in the background. My son made the frog noise the ring tone for his phone.


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What is the difference between spidroin-1 and spidroin-2?
So I'm doing a research project for my school and I'm trying to decide on the exact nature of the project. My current plan is to try to genetically engineer E. coli or Yeast to produce spider silk protiens. However when trying to find an appropriate gene for my project I learned that the common house spider's silk has two different spidroin protiens. Just by a simple google search I can't tell the difference. So, what is the difference between spidroin-1 and spidroin-2

I've looked into literature on this. Wow, there is a lot of research on this. Here's a quick summary:
Functionally they are very similar. Both are fibrous proteins. Together they constitute spider silk. Sp-1 and Sp-2 are two different genes, often present in multiple copies in the genome, depending on which spider species you consider. They differ in amino acid content and are post-translationally modified differently. Sp-2, for instance, is heavily modified. There also exist different transcriptional isoforms of these proteins. It seems quite complex.
There are also different types of silk. You may be referring to major ampullate silk, which is only one of six different types of silk fibres spun by the spiders of the genus Nephila. Only this one contains major ampullate spidroin-1 (MaSp1) and major ampullate spidroin-2 (MaSp2).
Excerpt from one paper on the subject, which lists some differences:

MaSp1 and MaSp2 are large proteins of about 250 to 350 kDa that share
  a general domain architecture. Both proteins contain a large, central, repetitive domain that
  consists of approximately 100 tandem copies of a 30 to 40 amino acid
  repeat sequence. The consensus repeat sequences for both MaSp1 and
  MaSp2 are glycine-rich and end in poly-alanine motifs (usually four to
  seven residues long). For MaSp1, the consensus repeat includes (GGX)n
  motifs (where X = A, L, Q, or Y) and very low proline content. In
  contrast, the MaSp2 consensus repeat has significant proline content
  and characteristic motifs such as GPG and QQ.
  The repetitive domains of different spidroins display a relatively
  high level of amino acid sequence variation that has been implicated
  in providing the elasticity and toughness that is characteristic of
  the different fibers.

It is possible that different amounts of Sp-1 and Sp-2 are combined to tune the elasticity and toughness of the silk. I have no idea whether the mechanical properties of silk are changed by the spider to suit the context (e.g. elasticity in windy conditions, or whether the content changes seasonally in response to temperature differences). That would make for a cool research hypothesis.

Wow that was much more intense than I was expecting. I'd make my project about the mechanical differences but I don't have access to the appropriate machines.


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Can someone identify this odd looking spider?
I found this spider crawling on my tile floor. We live in rural central Virginia.  I’ve found spider species with similar looks but nothing exactly like this. Its size was less than 1 inch. Can anyone identify it?

Some sort of jumping spider (Family: Salticidae)

Could be Thiodina sylvana... But I'm not sure. Thiodina occurs in Virginia. Take a look at this picture: https://www.flickr.com/photos/52450054@N04/6304831786 but be careful, it shows a male. Females tend to be more brownish

I agree with JulPal's comment from August.  It looks very much like a male Thiodina (now renamed Colonus) sylvanus.  As with many Salticids, the females look rather different, and it turns out that there is apparently a similar species of Colonus in the area, which can be distinguished in the field by the fact that the white mark on the carapace is not a block so much as a thick longitudinal line.
I attach an image from Tree of Life, with the link below:

http://www.tolweb.org/Thiodina_sylvana/5911

It is Tarantula which comprise a group of large and often hairy arachnids belonging to the Theraphosidae family of spiders

It would be good to explain how you know it is a tarantula. Maybe based on on the position of the chelicerae? I am surprised that there are tarantula as far North as Virginia.

It doesn’t look at all like a Tarantula to me. It’s size was less than 1 inch.

@Penni You should be mentioning that in the question. From this zoom, I would have guessed that it was much bigger.

Yes, I should have.. my bad. This is my first post, ever, so I’m a newbie. Thanks for your help, @TheLastWord.

It is not a Mygalomorph - the eyes are in the front of the head,  with two large ones right on the forward 'face', like a Jumping Spider, rather than clustered in a turret atop the round, flat carapace; the abdomen is long and teardrop-shaped, like a Jumping Spider, rather than large and bulky, with two obvious 'exhaust-pipe' spinnerets at the back; and the legs are short and stocky, like a Jumping Spider, rather than long and thick and very hairy.

It's pretty obvious that it's a jumping spider. Tarantulas look nothing even remotely close to that.


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Is it unusual for a child to be diagnosed with diabetes?
Recently, I came to know that a boy in my town who is 6 years old is diabetic and many people were shocked from this news.

Short Answer
Type 1 diabetes is commonly diagnosed in children; type 2 diabetes is more common overall and is much less likely to be diagnosed in children, though possible.
Longer Answer
Type 1 diabetes is caused by damage to the pancreas and depends on environmental and genetic causes, most often leading to autoimmune loss of the insulin-producing beta cells in the pancreas. Type 1 diabetes occurs because insulin levels themselves are low. It commonly begins in childhood, and is also sometimes referred to as "juvenile diabetes" although it lasts life-long. Type 1 diabetics often take insulin to replace the insulin they are not producing.
Type 2 diabetes, by contrast, is caused by reduced insulin sensitivity and develops over time (lack of insulin can also eventually occur). Obesity and other lifestyle factors are strong influences on the development of type 2 diabetes, though genetics can also play a role. Type 2 diabetes is most often diagnosed in adults (and is also referred to as adult-onset diabetes, though it is also possible to occur in children), increases with age, and is overall more prevalent than type 1 diabetes, so this is likely where your community's surprise comes from.

Your overall answer is correct, but I'd add that type 2 diabetes runs in families, while type 1 does not. There are MHC associations with type 1 because it is autoimmune in origin, but clinically, we don't think of type 1 diabetes as a genetic disease.

I focused on the first phrase (type 1 diabetes is caused by genetic factors), but on looking again, you should probably correct the rest of the sentence. The specific cause of type 1 diabetes is usually known. It is autoimmune destruction of islet cells. I'd have to look it up again to be sure, but I believe anti islet cell antibodies are identified in almost all cases.

If you are going to edit, I recommend directly answering the question instead of posting information for the asker to infer from.

@DeNovo My understanding is that type 1 diabetes has quite a high heritability, and concurrence in families is rare only because the disease itself is rare, i.e., the heritable factors are a risk rather than a clear cause. I can certainly try to reference better if this is unclear or controversial, I wasn't realizing that it was.

@Cell If you are referring to my edit of the question title, I did so due to the body of the question which in my experience is usually a better marker for what new question-askers are going for here at biology.SE. I've added a more clear direct answer, however.

That's just the way it was taught in medical school (though that was a while ago)-- family history is more important for type 2 than type 1, so it was jarring for me to see type 1 described as a genetic (rather than autoimmune) disease, with the heritable component of type 2 downplayed. I'd appreciate some better sourcing if you want to contrast them in this way. Though I'm not sure you need it for the answer. Genetic doesn't necessarily mean "appears in childhood", as I'm sure you understand.

A quick search brought me to this review on type 2 and this one on type 1. They're both highly heritable, but when you compare apples to apples, it looks like what I was taught in medical school still holds. Type 2 is more heritable than type 1.

@DeNovo The twin concordance is higher in type 2 because prevalence is higher, but it doesn't really look like type 2 is more heritable biologically, at best they are similar. That review on type 2 also says that a lot of the type 2 heritability is explained by heritability of obesity. I don't disagree that what you learned clinically is relevant clinically, though.

If obesity mediates the heritability of T2DM, it doesn't make T2DM less heritable. Obesity isn't just associated with T2DM, it is on the causal pathway. This means obesity isn't a confounder.  You say T1DM is caused by genetic factors and T2DM is caused by environmental factors, though genetics can also play a role. I don't see any support for that contrast, and it is in conflict with standard teaching on the pathogenesis of the two diseases. If you want to make that argument (which you don't need to do in order to answer the question), I think you should include some non wikipedia sources.

@DeNovo As you point out, since it isn't necessary to answer the question, I can make the contrast less obvious.


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Do different microscopes and attached cameras differ in crop factor between each other?
I analyzed a bunch of microphotographs recently and used "% of image area" to describe the area of structures (chorionic villi, had to show their density in placenta). However my professor suggested I should have used mm2. There is no problem in conversion, but I suspect different microscopes may have different areas of field of view for the same scale. Thus the conversion will make the results just more difficult to interpret.
So does the absolute area of microphotographs of the same scale and size differ between microscopes/cameras? Or is it somehow standartized?

Thus the conversion will make the results just more difficult to interpret.

I'm not personally familiar with this specific measurement, but in general, unless there is a specific convention in how to report a measurement, an absolute measurement should make the results easier to interpret, not more difficult (vs. % of image area). From a quick search, it seems like absolute measures of area, volume, and density are typically used when reporting chorionic villi measurements, so there isn't a convention to do it another way.


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İrreversible dopamine antagonist vs. Dopamine agonist
Can a dopamine agonist reverse the effects of an irreversible dopamine antagonist?

What do you mean by reverse?  Do you mean withdrawal?  The brain is altered by medications which would do not always understand.

İ mean unblock.

Can you clarify whether you're talking about an inverse agonist or an irreversible antagonist? Your question title says inverse antagonist, which isn't a typical term. The body says irreversible antagonist.

William so they both block dopamine receptots then ?

No. Irreversible antagonism is, by definition, inhibition that cannot be reversed by the agonist. Let me summarize the basics. You can read about this in Goodman and Gillman's The Pharmacological Basis of Therapeutics, Chapter 3, but there are many basic biochemistry textbooks that will cover the same ground.
When an interaction between a ligand and a receptor is said to be reversible, it means that it can associate to form a ligand receptor complex, and then dissociate, leaving the system with free ligand and free receptor. In the most general case, when the ligand is bound, it changes the conformation and activity of the receptor, and when it dissociates, the receptor returns to its original conformation and activity. The effect of the ligand in the biological system is related to the proportion of bound receptors.
Irreversible ligands typically involve covalent bonding (e.g., aspirin, alkylating agents). When the ligand interacts with the receptor, it irreversibly alters the conformation and function of the receptor. Cell or tissue function is only returned to the free receptor state when the particular receptors that have had a ligand receptor interaction have been degraded and replaced by a new receptor.
One of the ways to test whether an interaction is reversible is to try to reverse it. Let's look at how you would do this.
Start by looking at the effect when an agonist binds. The agonist is reversible. When you add it to an assay that contains the receptor, it associates and dissociates from the receptor, but at any moment, some proportion of receptors is bound to agonist. This binding produces an effect you can measure. The effect is related to the overall proportion of receptors bound to agonist at any given time, which is related to the concentration of the agonist. When you increase the concentration of an agonist, more agonist binds and you can measure a greater effect. In this figure from Goodman & Gillman Chapter 3, you can see the log concentration of the agonist on the x axis and the effect measured in an assay on the y axis:

Now consider the effect of an agonist in the presence of an antagonist. Classically, a competitive reversible antagonist binds the same site as an agonist. When the antagonist is bound, it doesn't allow the agonist to bind. So run the same experiment as you did above (by increasing the concentration of the agonist and measuring the effect), but start with a solution that contains some fixed concentration of antagonist. Because an antagonist is competing for those same binding sites, there will be fewer receptors available for agonist binding, fewer receptor/agonist complexes, and a smaller effect.
If the antagonist is reversible, though, you can still get the same effect you got in the first experiment. You just have to increase the concentration of the agonist until it binds the same proportion of receptors. Since both agonist and antagonist are constantly associating and dissociating with the receptor, increasing the concentration of one of them will out compete the other.  In this figure (same source), you can see that in the presence of an antagonist (here, i, for inhibitor), it requires more agonist to get the same effect, but the maximum effect is still the same.

If the antagonist is irreversible you can't get the same effect you got in the first experiment, even by increasing the concentration of the agonist. The receptors have been permanently altered by the presence of the antagonist, and whatever portion of them had some interaction with the antagonist will either not bind the agonist, or will not produce an effect when bound. What you see in the assay here is that increasing the agonist concentration in the assay may increase the measured response, but you are unable to reach the same maximum response. Note here, the figure describes a pseudo-irreversible inhibitor (antagonist). This is just a term for an irreversible inhibitor that doesn't covalently bind the receptor, but has a strong enough affinity for the binding site that, based on the measurements, it looks like it covalently binds. Effectively, the inhibitor is going to sit there on the binding site until the receptor is degraded and will not be outcompeted by the agonist.

Thank you. Do you know how long it would take for receptors blocked by a irreversible dopamine antagonist to degrade?

@user57928 You're welcome! Your other question about how long it takes for receptors to degrade, asked here is a lot more complicated than it may seem. Try editing it, though, as suggested by my comment there, and we'll see if we can't get some answers.

@user57928 As far as this question is concerned, take a look at the help page for someone answers. If  this answered your question about irreversible antagonists, you should mark it the answer by clicking the gray check mark next to it. Once you have the upvote privilege, you should upvote useful answers as well.

But in practice I have yet to find any irreversible dopamine antagonists on any commonly prescribed drugs today(if Wikipedia is a valid source).

There's Haldol off course.


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Are RNA cleavage sites always polyadenylated?
During RNA processing (including both mRNA and non-coding RNAs), is the end of 3'UTR always polyadenylated after cleavage?
I could not find the answer to my question in the Wikipedia entry for polyadenylation.
If a recent reference could be provided, that will be great. I've done quite a bit search and hasn't found a good source yet.
Some background to this question: we are developing bioinformatics tools to predict potential cleavage sites, we need to understand this problem better in order to design a suitable algorithm

I'm not sure what you mean by "mRNA processing, including both coding and non-coding" or why you need to qualify this. Surely all you are interesting is that part of the mRNA processing that recognizes the cleavage signal AAUAAA (or variants). I have edited your question, but left this for the moment. I suggest you delete "including both coding and non-coding" unless you can clarify it.

What sort of cleavage are you talking about? Do you transcription termination?

@David, sorry for being confusing. I meant both coding and non-coding RNAs.

@Nicolai, not really, after pre-mRNA is transcribed, it will be cleaved somewhere towards the 3' end.

Then I messed your question up. I'll correct it.

This answer attempts to cover only the question of mRNA processing. It does not address the polyadenylation of non-coding RNAs.
As far as I can see from the recent review by Neve et al. (2017) cleavage and polyadenylation are tightly coupled. It is interesting, in this regard, that histones mRNAs which lack polyA tails, have a different structure, lacking the canonical AAUAAA, at their 3ʹ ends (see review by Marzluff et al.).
As distinct enzyme activities are involved in cleavage and polyadenylation, it would, I imagine, be possible (either genetically or chemically) to disrupt the protein complex responsible for polyadenylation and hence prevent it occurring (this has probably been done). However this would not be physiologically relevant.
There is an earlier review by Tian and Graber (2007) of the sequence requirements of the cleavage site which makes no distinction between cleavage and polyadenylation.
However this is not my field, so others may have additional information I have missed.

@zyxue — I think you are having trouble or typos with your negatives again. Surely you mean "It DOES seem… most are polyadenylated". Agreed.

Quote from Neve et al. (2017): "With the exception of replication-dependent histone genes, metazoan protein encoding mRNAs contain a uniform 30 end consisting of a stretch of adenosines." It does seem, at least for protein-coding mRNAs, except for histone genes, most are polyadenylated.

Thanks for the catch, @David. Do you have any lead on non-coding mRNAs, please?

Based on Table 1 from this Review paper, Strategies to Annotate and Characterize Long Noncoding RNAs: Advantages and Pitfalls
Author links open overlay panel, 2018, for non-coding RNAs, they are more often non-polyadenylated than polyadenylated.


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Are there humans which the brain sends signals to the limbs faster than the average?
I have done some researches on the time taken by the brain to send signals, but I didn't find whether that time is the same amongst all humans or there are some differences, and I have based my question on an article which mentioned that Messi(one of the best players in soccer history)'s brain send signals to the limbs faster than the normal human (https://www.ncbi.nlm.nih.gov/pubmed/27010676), so is this possible to happen.

Hello and welcome to Biology.SE! Take the tour to learn about this site and earn yourself your first badge. You surely did find an amusing paper! Good luck with your question!

Your question would be improved if you explained who "Messi" is.

helpful paper https://www.researchgate.net/figure/Experimentally-determined-conduction-velocity-of-a-nerve-impulse-in-a-mammalian_fig12_321016169

Assuming that the time it takes for a signal to travel from the brain to the limbs follows a normal distribution (which is reasonable), then certainly there are people who fall at the upper and lower ends of the distribution. In fact, it's relatively improbable that someone would fall right at the mean.
Consider the normal distribution below. If the mean for all humans is at the center of the distribution, then almost all fall above or below that mean. Whether Messi falls in the lower tail is a separate question.


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What bee do I have nesting in my front yard
Can someone help identify this bee? Its living in a hole between a boulder and a retaining wall. Our tree that is above it is now bleeding sap so I'm worried about the tree. Pest control wont come because they think it's a honeybee but I doubt that's what it is. I don't hear buzzing and one bee leaves at a time. They are not aggressive. The abdomen is black with yellow stripes.

Hello and welcome to Biology.SE! Take the tour to learn about this site and earn yourself your first badge. Also, can you specify where are you located in the world, what tree is that and the size of the bee?

I wouldn't worry about the bee with regards to the health of your tree.


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Young family members to learn genetics - Amino Labs?
I'm an engineer but want to learn about biology with a niece and nephew who are early teens. I saw Amino Labs (https://amino.bio/) and thought because I work a lot with my hands, doing hands on exercises would be a good way to learn. I don't like text books and don't think my niece and nephew will appreciate a text book. Has anyone used Amino Labs? Any suggestions?


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Glucose Carrier Proteins in Cell Membranes
I'm using Campbell's Biology textbook, and it states that certain carrier proteins transport glucose across the cell membrane much faster than would occur normally. It states that the "glucose transporter" is an extremely selective protein, which doesn't accept even fructose, which is an isomer of glucose. However, another hexose, galactose, appears to me to be even more similar to glucose- it's just that one of the H-OH pairs is flipped. In comparison, though fructose is indeed an isomer, it's a ketose, but glucose and galactose are both aldoses. Given this, I'm pretty sure galactose is more similar to fructose.
My question is: is the carrier protein specific enough to carry only glucose and not even galactose? If it isn't and it's able to carry galactose, what would happen if galactose was transported into the cell in greater quantities?
Note: I'm a bio beginner, so please have some patience if my questions are nonsensical or my facts are incorrect, any corrections would be welcome.

First thing's first: there are many different kinds of glucose transporters (genes), even within the same organism. These genes share partial sequence identity in mammals, and are part of the SLC2A, or "GLUT" gene family. In yeast, there exist glucose- and galactose-specific transporters.
Often, not always, a glucose transporter type may be tissue specific. GLUT3 is expressed in neurons, in the placenta, and elsewhere. Compare this to the expression of GLUT1, found in red blood cells, and GLUT4, found in adipose and skeletal muscle tissue.
Each kind of transporter has various affinities for glucose (or other sugars for that matter), and various levels of permeability for similar molecules. This is what is called the specificity of the transporter. The rate at which sugars can pass through the pore of the transporter is called the frequency. Together, these properties define the function of a hexose transporter, and hence why there are different kinds with site-specific expression across the body.
In terms of regulation: GLUT1 is dynamically regulated based on available glucose (up-regulated during shortage and down-regulated during excess). This is not the case with GLUT4; instead, GLUT4 is insulin-regulated, so that muscles and fat tissues can uptake glucose for storage, which is a hormone-controlled process.
Here is a great webpage to help you understand the characteristics of hexose transporters, especially with regard to galactose, fructose and glucose.


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Dihybrid cross question
An experiment is set up to study two genes. The two genes assort independently and for each gene the expression of alleles involves complete dominance. In the genetic cross RrTt x RrTt, a number of different phenotypes are seen. What is the difference between this number of phenotypes and the number of phenotypes seen when the cross RrTt x rrtt is carried out?

Welcome to SE Biology. This question appears to be from an exam or quiz. Please read the guidelines for homework questions. You need to show you've made an effort to answer it yourself.

Have a look through this presentation. Let's focus on the last slide:

First, let's understand what the letters mean:
R = red allele
r = white allele

T = tall allele
t = short allele

There are two of each because the organism is presumably diploid, i.e. contains two alleles for each genetic locus, one from the father and one from the mother. In the case of RRTT or rrtt, it means the mother and father alleles are identical and the organism can be said to be homozygous ("same alleles") for these traits. In the case of RrTt, or rRtT, or rRTt, or RrtT (they are all the same, basically), the organism can be said to be heterozygous ("different alleles") for both genes.

The two genes assort independently and for each gene the expression of alleles involves complete dominance.

So we are told the alleles are completely dominant. By convention, we use capital letters to indicate dominant traits. That means that if a capital letter is present, the organism's trait will be determined by the dominant allele. A few examples of possible genotypes (left) and their phenotypes (right), to help you understand:
RRTT -> RED & TALL

RrTt -> RED & TALL

rrTt -> white & TALL

rRtt -> RED & short

rrtt -> white & short

You first make your Punnett squares, as in the picture above. In your case, one for RrTt x RrTt and one for RrTt x rrtt. You fill both in. You will know all possible genotypes to result from the cross. Now - count how many phenotypes each cross will produce! You'll be able to say which cross will produce more, equal or fewer red, white, tall and short offspring. There's your answer!
Personal tip: Always visualize to make sense of the steps. When you see the cross RrTt x rrtt, imagine a red, tall individual carrying both red/white and tall/short alleles mating with a white, short indivual carrying only white and short alleles. When you make a Punnett square, you are simply predicting all the possible different babies to come from this cross. The amazing thing is that you can predict the ratio of traits among the babies. This was a big leap in genetics!
Keep in mind you are making a few assumptions. Every time you make a Punnett square, you are assuming the laws of Mendelian inheritance apply. You are assuming that the genes assort independently (which is not always true, especially for genes which are close to each other in the genome; they could travel together when they are being mixed), are not sex-linked (e.g. "only males can become red"), that the phenotype is determined solely by one gene ("monogenic"), and that your theoretical prediction will match reality. In practice, some alleles may confer a competitive advantage (and seem over-represented when you check the offspring), or may be lethal (expected offspring would be dead and you wouldn't even see them - they would be under-represented).


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What could explain discrepancies between dates provided by the fossil record vs. the molecular clock?
I am studying a mud snail genus called Ecrobia. For the Caspian species (Ecrobia grimmi), there is a discrepancy between dates provided by the fossil record and the molecular clock:

First appearance of Ecrobia grimmi in the fossil record: Middle and Upper Miocene (15.97 to 5.33 million years ago)
Age of Ecrobia grimmi as suggested by the molecular clock: 0.58 to 2.04 million years. The molecular clock was calibrated using an external marker-specific clock rate, and the climax of a geological event.

What could explain this discrepancy?

Could you give the sources for both dates? It would make finding the answer easier because afaik there are many different things that could account for discrepancies between molecular clock dates and fossil dates. For one thing, what was the molecular clock measuring exactly? Divergence from closest relative, and if so what relative was it? Age of common ancestor of extant individuals?

As @Oosaka said, there are many reasons that molecular dates can be discordant with fossil dates. Without actually knowing what methods you've used to generate the molecular date, we can't be much help. For example, it could be due to lineage-specific rate heterogeneity, if you have used a method which assumes a strict clock.

The source for the fossil record is Asnafi 2010, the source for the molecular clock is my own ongoing study.
The molecular clock was measuring the divergence from closest relatives; all Ecrobia spp. were included.
The age of the common ancestor is ca. 15 Ma.
The molecular-clock analyses were run with *BEAST.
The results of the strict- and relaxed-clock analyses were similar.

First, the example you give is unusual in that molecular dating analysis should be calibrated with fossils to set minimum ages. If Ecrobia grimmi exists in the fossil record, then no proper molecular analysis would estimate them to be younger than those fossils. There are two main causes of discrepancies between fossil and molecular dating.
For fossils you never find the oldest example of a species. If a species diverged 100 million years ago, you might not find a fossil of that lineage for millions of years, meaning that fossil estimates are almost always underestimates, but they do form a baseline upon which to calibrate molecular data. The problem with molecular data is that there is no "molecular clock". Lineages, genes and individual nucleotides all change at different rates. The best you can do is plug in fossil and/or geological dates into a model that is based on other lineages. Hopefully you have calibrated dates for closely related species, and the same genes. Even then, you do not know that the lineage you are working with will follow the same rates as the model predicts. At a minimum, you need to set a minimum possible age in BEAST to 5-16 mya.

I cannot use fossils to calibrate the molecular clock because Ecrobia spp. are cryptic (i.e. they are morphologically indistinguishable). Therefore, I thought the discrepancies between fossil and molecular dating might be due to a misidentification of the fossils: fossils identified as Ecrobia grimmi could actually be of a different Ecrobia sp., or alternatively, of an ancestral species. What do you think about that?

Fossils are the gold standard. But if you cannot trust their identity, then you were right to exclude them. But without a reliable calibration, I don't think molecular dating is worth doing at all. Better to not know at all than to "know" something that is wrong.

What do you think about using external marker-specific clock rate and/or geological events to calibrate the molecular clock?

@JustineVandendorpe I think they are OK, but need to be pretty solid. For example, the formation of the isthmus of Panama is well established. Is Ecrobia marine or freshwater?

Ecrobia is a brackish genus (from 6‰ to 38‰).


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Reversal form of endosymbiotic theory?
Cell's organelles give us evidence that they might have been independent organisms on their own.
Are there any single-cell microorganisms known to have gone so to say this way back as well, i.e. having some evidence to have their past as part of a larger organism?

In the life-cycle of myxobacteria, there are uni- and multi-cellular stages.

It's not exactly what I've asked.. Slime molds same do not qualify. Still, good to know.

An organelle who did not come from an endosymbiosis does not contain DNA. It cannot just go away and leave on its own without hereditary material. A piece of DNA can however eventually leave a genome and become its own thing!

Endosymbiosis leads to an irreversible loss of independence of the endosymbiont and the host.
For example, all members of the insect superfamily Aphidoidea (aphids) have an obligatory association with bacteria, commonly called primary endosymbionts (Munson et al., 1991; emphasis mine):

The primary endosymbionts are found in specialized organs, the
mycetomes, which consist of cells (mycetocytes) containing the
endosymbionts. The endosymbionts are enclosed within vesicles which
are derived from the cell membranes of the mycetocytes.
None of the [primary] endosymbionts has been successfully cultivated in
bacteriological media or in tissue culture. [These] organisms are essential
for the life of the aphids since the removal of the endosymbionts by
antibiotics leads to aphid sterility.
The endosymbionts are  maternally transmitted, and
there are complex mechanisms which assure that the progeny are
infected.

Munson et al. (1991) Buchnera gen. nov. and Buchnera aphidicola sp. nov., a taxon consisting of the mycetocyte-associated, primary endosymbionts of aphids. Int J Syst Bacteriol 41: 566--568.

At SE we're looking for answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Otherwise how can the poster or anyone else know whether or not you are correct? See the Help for "how do I write a good answer?".


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What are the classical adaptations of amphibians?
My question is about amphibians in humid or underwater environments. What biological adaptations can found in them, further what purposes do they serve?

"Amphibian" literally means "living both in water and on land" (see here)

Imagine asking "Why do fish prefer water over land?" Well... because they are adapted to water life but not land life. What kind of answer are you looking for exactly for amphibians? Do you want us to list adaptations of amphibians such as the eyes that are positionned to poke out of the water, the ears that don't let any water gets in, the skin who is thin and allow direct gazeous and water exchange or the webbed paws to move into water. Note that you will find many of these classical adaptations by just googling "amphibian adaptation".

@Remi.b: Indeed, if I were to try to answer this question from anything more than general knowledge, I'd simply copy parts of the Wikipedia page: https://en.wikipedia.org/wiki/Amphibian

@jamesqf Indeed. The OP changed the post without me noticing. I think the current post can basically be answered by my second comment. I'll post it as an answer.

"Amphibian" means "living both in water and on land" (see here). Here is a small list of classic adaptations in amphibians:

Eyes and nostril are positioned to poke out of the water while the rest of the body is immersed
Ears don't let any water gets in
Skin is very thin and allow direct gazeous and water exchange
Paws are webbed to move into water
Larvae of most amphibian species start their life in the water


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Bipolar disorder genetics
My understanding is that bipolar disorder is polygenic.
1) Does one need to have all the genes for bipolar disorder in order to have the disease?
2) Is it possible for a person to have all the genes for bipolar disorder and still not have the disease?

Does one need to have all the genes for bipolar disorder in order to have the disease?

No. In genome-wide association studies (GWAS) of psychiatric conditions, it is a constant finding that the associated variants each influence the probability/risk. The effects of all known variants can then be summed up to a polygenic score (PGS). A person with higher PGS is more likely than someone with a low PGS. But some people with low PGS (i.e. people who don't have "all the genes") still get the condition, it is just not as frequent as people with high PGS.
Another reason why we can say 'no' to this question is through findings of quantitative genetics studies. These estimate the heritability of certain traits. For the answer to be 'yes', the heritability would have to be one ($h^2 = 1$). However, as far as I know, there are no known psychiatric conditions that have heritabilities of one. Some high (e.g. $h^2\approx 0.8$), yes, but not one.
It's also worth mentioning that there is probably no sharp line between having bipolar disorder and not having it. It's a medical diagnosis that is useful but rough. Most likely, all of us have a little "bipolar" in us. I think it's probably most useful to view it as a spectrum.

Is it possible for a person to have all the genes for bipolar disorder and still not have the disease?

This is not known and it may not even be a well-defined question. We don't know all the variants that affect the risk of bipolar disorder (or most other polygenic disorders). So we cannot say for sure.
Some 'omnigenetic' hypotheses propose that all genetic variants have some effect on all traits. Some effects are just smaller and some larger. In this case, the expression 'all the genes for X' may be technically meaningless.


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Can people be bred for tameness in a similar way to Russian foxes?
Russian foxes were selectively bred for tameness. Can a similar process happen to humans, under the right conditions — say, extreme political pressure to obey ?

Do you understand how the process works for a fox (or anything else for any other trait, for that matter)? Think about what the prerequisites are and what the process is.

Cages and a basic test for friendliness. I know this has dark resonances for humans and their history - I'm not advocating it, I'm asking if it is a process that happens already. I should maybe change the question to "Have" instead of "Can".

If a trait is genetically influenced, has variation, and affects production of progeny, it can be selected on, naturally or artificially. So if there is variation in human tameness with a genetic cause (unlikely to have been studied specifically as 'tameness'), and people who are not tame are killed or otherwise prevented from reproducing, then yes, you would select for tameness. You won't be able to get a rigorous result for the more specific questions your question seems to imply or that you've mentioned in a comment.

OK so thinking about the selection within societies I suppose we're looking back at the beginning of social stratification and law - favouring obedience and punishing disobedience. Sometimes this is highly ruthless and lethal - the USSR would be one example of this. But the activities of Stalin & co were quite brief. But do the selection processes of dictators select for tameness or aggression ? Dictatorships seem to reward both the aggression (on the government side) and obedience (on the citizenry side) simultaneously. OK good thanks you've prompted me to reconsider on this.

Harpending wrote about it.

define tameness in respect to a human. Less likely to get violent, already is being selected for.

OK how to define it. Good question. In foxes it is friendliness to another species. That wouldn't count for human-human tameness. It's also submission to authority and control - for the foxes that is to the species which cages it. So I would call human tameness a propensity to obey, be friendly towards, rule makers. The law or ruling class.
I read that Russian foxes become tame in six generations. Call a human generation 25 years, and make a huge assumption (probably not true) that humans adapt as quickly, then that would be about 150 years. Some social systems and religions are much older.

@JimmyWiddle If you're using your actual name, be careful, for you're getting close to verboten ideas. Religion civilizing people is indeed an old phenomenon that seems foreign to moderns. Of course, this implies that if Alice's ancestors and Bob's ancestors spent centuries under different religions, then Alice and Bob may be very, very incompatible. Forcing Alice and Bob to live under the same laws and under the same social norms may be a fool's errand.

I hadn't thought of that, but I see what you mean. Yeah that could be a hot potato !
I think the foxes are tame to humans generally, not just Russian humans with a certain language, appearance and smell. Would it be different for humans ? I expect this has been considered already, given the authoritarian political regime under which the fox experiments were started, and maybe the reason it was conducted on the quiet out in the sticks.

@JimmyWiddle In humans, tameness to humans in general and tameness to humans of the same family / clan / tribe / race would be an interesting distinction. If I recall correctly, Dmitry Belyayev was working at the Institute of Cytology and Genetics in Akademgorodok — the Soviet version of Los Alamos.

@JimmyWiddle You may want to read this.

Quote from Slavoj Zizek, would seem to imply that the search for human tameness genes is ongoing. "I visited China five years ago I got in a conversation with some big shot from their Academy of Biogenetics. I mean biogenetic department of their Academy of Sciences. And he gave me the program of goals of biogenetics in China. A kind of a programmatic text which pretty much terrified me. It opens up the text with something like the goal of biogenetics in the People’s Republic of China is to regulate the physical and the psychic welfare of Chinese people. My God, what does that mean?"

@JimmyWiddle Einstein himself had some naughty thoughts.

Setting aside the eugenic implications of what are you suggesting (short answer: yes it is theoretically possible, but no it is practically impossible), a more interesting observation is that evolutionary anthropologists think that humans might have "self-domesticated" during our evolutionary history.
There is a wide literature on this topic, but a recent paper summarizes the main ideas and addresses the question from a genomic point of view. Theofanopoulou and coauthors find credible genomic evidence for similar patterns of genetic evolution in humans and other domesticated animals.

Good yes I was wondering about the natural neotony of humans over time. But the eugenics - I was wondering if it already happened unconsciously, for instance through the communist era in Russia and various other times and places where people have been selected by political or religious systems.
As I understand it the foxes showed signs of change in about 10 generations. In human terms that's somewhere around 250 years I think. Whether there is an equivalence between human and fox generations is part of my question, really.

@kmm What do you mean with practically impossible?

@Marzipanherz From an implementation (practical) perspective, breeding humans will not work. If there is heritable variation, it can be selected on. Actually doing that selection on humans is impossible.

@kmm I was thinking, whether something like this might have happend (unintentionally) already: Think of an isolated culture (an island, for example) that prevents non-tame people from getting children (via prison or death penalty). If such a culture has been/is stable for enough generations and assuming that tameness in human was heritable....

@kmm There are practical ways that artificial selection can be done in humans (This is a different question from whether it should be done). A country which is a welfare society could, for example, make IVF with embryo selection free and legal. When some portion of the variation of trait X is understood genetically (such as from GWAS), then you can select directly at the embryo level. For example, a procedure could be that a couple made 10 fertilized eggs, and then you can select the egg that has the highest probability of high/low X.


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How does transcription end?
In rho-dependent termination in prokaryotes, how does RNA polymerase “know” that it has reached the end of a gene and that it has to stop so that the rho-factor can bind mRNA’s rut site? Is there a termination sequence on the template DNA that “signals” the end of a gene?
And consequently, how does the rho-factor “know” when to bind to mRNA?... how does rho-factor recognize that the RNA polymerase has stopped so it can start its ATPase activity to dissociate the transcription complex from DNA and release the mRNA?

You ask about stop codon?

The stop codon ends translation of mRNA to polypeptide, not transcription of DNA to mRNA (which is what I’m asking about).

There's a corresponding stop codon on the DNA

Doesn’t the stop codon end amino acid elongation during translation? So... is the stop codon also the terminator sequence during transcription?

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

This question is very similar and has a pretty good answer.

Termination  of  the synthesis of  the RNA molecule in bacteria is also signaled by  a sequence in the template  strand of the DNA molecule.
This sequence of nucleotide in the template strand is the RNA polymerase pause site. When the RNAP continues its transcription it reaches this site and pauses it's transcription activity over here. The longevity of this pause can also be affected by various factors like high $Mg^{2+}$ ions in some cases.
Meanwhile, rho factor which after binding to rut-site, continues it's translocation along the mRNA (supposing mRNA is synthesized here) in 5'-3' direction using its ATPase activity. The rho factor utilises this opportunity when RNAP has paused it's transcription activity at the RNAP pause site to reach this ternary transcription elongation complex. When it had reached this complex it starts it's ATP dependent helicase activity which separates the RNA-DNA hybrid helix, causing the release of the mRNA.

In prokaryotes you have transcription and translation happen almost simultaneously. Downstream of the translational stop codon, there exists a C rich site on the mRNA called the rho-utilisation-site (rut) and another site called transcription-stop-point (tsp).
Rho-dependent Termination of Transcription Is Governed Primarily by the Upstream Rho Utilization (rut) Sequences of a Terminator
How does RNA polymerase know it has reached the end?
RNA polymerase pauses at the tsp site during transcription. The rut site functions as an mRNA loading site and it also works to activate the rho-factor. The activated rho-factor travels down the mRNA while still attached to the rut site and catches up with the paused RNA polymerase. Contact with  the RNA polymerase leads to RNA polymerase to dissociate from the transcriptional complex You can read about the dissociation here, the article is behind a paywall though.
I think I answered the "when does rho know?" too. Read the wikipedia article on this as well


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What does "dissipated" mean here?
This is the context:

You know cardiac muscle cells are small cells relative to skeletal muscle cells, but unlike skeletal muscle cells that are arranged in parallel and their contraction is dissipated onto a tendon to bring about movement at a joint , cardiac muscle cells aligned end-to-end.

I've googled it, but it didn't make sense

Dissipate
to (cause to) gradually disappear or waste

● Can anyone change it into an easier text?
● What does dissipated mean?
● What does end-to-end mean?
● I wonder whether skeletal muscle contraction is disappeared onto a tendon or not.
● Is there an another scientific word for dissipated?

& apparently, I think end-to-end here means that cardiac muscle cells  join strongly to each other, but actually this is not a specific definition, I suppose.

Source:  Cardiac Muscle: Function & Main Parts – Histology | Lecturio.

Have you made any attempt to understand these words with tools you would use to learn english outside of science? Dictionaries, translation tools, finding other contexts, etc? We expect some effort from askers before we answer questions here.

@Bryan Krause Yes, of course, but it didn't make sense at all.

What does dissipate mean?

It's a word from a thermodynamic context. Heat can dissipate. Doing work causes energy to be lost in the form of heat, which is called dissipation. It means to spread out your energy, as in, a hot object - like a cup of boiling water - dissipates heat to its environment. The cup cools while the environment gets warmer. Likewise, a concentrated force (like tension across a skeletal cell within a muscle) can spread over lengthwise to connected tendons, and the energy is transferred to the bones that move.
It's really not the most precise use of the term, but it's understandable and gets the point across. To waste or to disappear is the colloquial meaning of the word. To dissipate, scientifically, means to spread out energy which was once concentrated relative to its environment. The energy can take the form of heat or work (mechanical work, in our case).

What does end-to-end mean?

End to end means in series, as in, not parallel.
Cardiac cells arrange end-to-end:
beginning -- CARDIAC CELL -- CARDIAC CELL -- CARDIAC CELL -- end

Skeletal cells arrange like so to form a muscle:
beginning ---------------- SKELETAL CELL ------------------- end
beginning ---------------- SKELETAL CELL ------------------- end


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Humans have Cannabinoid receptors. Does that mean we're meant to consume cannabis?
I know the answer is no. But what then explains the name of these receptors being specific to Cannabinoid found in cannabis? Aren't Cannabinoid receptors exclusive to Cannabinoid? Why are they named like that, if not?

This is a case where the receptors were discovered while researching cannabinoids, but before they had discovered the endogenous chemicals that bind to the receptors. Once those were found, they were named the endocannabinoids.

You also have ammonia receptors. Are we also meant to smell it?

Receptors
Any drug or compound with specific effects has a receptor. You can read about this general concept in Goodman and Gillman's The Pharmacological Basis of Therapeutics. Chapter 1 introduces the concept, chapters 3 and 5 expand further. As far as the history of this concept is concerned, receptors mediating the specificity of action was first clearly articulated by Paul Ehrlich (in the context of dyes and toxins), and further developed by John Langley (and Ehrlich again in response). Cannabis and cannabinoids are not unique in this regard. Illicit and therapeutic drugs of all kinds have a target binding sites (receptors). In almost all cases, these receptors are bound by endogenous compounds as well.
Does having a receptor mean we should consume something?
There was a case to be made that having a great number of receptors that bind psychoactive compounds in cannabis means there is a physiologic role for some cannabinoid (especially given the pattern of expression) and suggested the existence of an endogenous cannabinoid before it was discovered. This was discussed in the nature paper that first identified the receptor and its functional expression and in the science paper that reported the discovery of endocannabinoids. Generally, it doesn't suggest that we are "meant to consume cannabis". Toxins and poisons also have receptors, and we certainly don't want to consume those.
As far as the name is concerned, the comment by @user137 is correct. Receptors are sometimes named by exogenous drugs that activate them, in particular when these compounds are discovered and studied before an endogenous ligand is found. Opioid receptors are another example.

So I think I had the misconception that cannabinoid receptors allow only cannabinoid to bind with it. Can you confirm that multiple ligands can bind to a single substrate? (So there's no exclusive lock and key mechanism)

@yathish that's correct. Cannabinoid is an entire class of compounds. Many different specific cannabinoids bind cannabinoid receptors, with varying affinities. The lock and key model is useful, but not entirely accurate. For most (possibly all) receptors, more than one ligand can bind.

In addition to De Novo's excellent answer, I would like to add that sometimes, the fact that we have receptors for something is precisely a sign that we should not consume that thing.
When it comes to taste and smell in particular, many receptors are evolutionarily conserved precisely because their physiological role is to warn us of a danger. For example, diamines such as putrescine and cadaverine smell well, terrible, as their names suggest. And we are very good at detecting these smells, because these molecules are produced during organic matter putrefaction; in other words, we have receptors (recently identified) designed specifically to tell us that certain foods are not suitable for consumption.
The same principle applies to olfactory receptors for volatile molecules harboring sulfhydryl (-SH) groups, that often smell like rotten eggs or feces - for the same reason. Mercaptan is even used to give natural gas its distinctive smell (it's initially odorless), making sure that we can detect any gas leak that could cause an accident - because we have really good receptors for it.

Cannabinoid receptors are a part of the endocannabinoid system, which encompasses native to our body ligands such as Anandamide, 2-Arachidonoylglycerol, Palmitoylethanolamide, and a few others.
The reason they are named after the cannabis plant is because of the role cannabinoids played in identifying and characterizing those receptors, a pattern that you'll see in biochemistry a lot, e.g. AMPAr and NMDAr receptors named because AMPA/NMDA are their selective ligands, even though both are glutamatergic receptors, nicotinic/muscarinic acetylcholine receptors, or CART(Cocaine- and Amphetamine-Regulated Transcript) named for the fact that cocaine and amphetamine regulate its transcription levels.
For what it's worth, not all cannabinoid system proteins are named after cannabis, such as the more recently characterized NAGly, GPR55, and GPR119 receptors.


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How does latency in carcinogenisis differ from the effect of chance?
Most chemically induced cancers seem to have a long latency between exposure to the carcinogen and expression of the disease. Mesothelioma typically 30-40 years, bladder cancer about 20 years, for example.
Most carcinogens also seem to have a dose-response relationship, with both tumour formation andlatency.
The only way I've ever heard latency explained, however, is the number of cell activities in the presence of the mutagen which are required to give reasonable accumulation of errors, but this seems like the same level of variation as dose. The higher the dose the more likely an error so the fewer iterations required before such an error might reasonably occur.
Yet this doesn't seem to be how latency manifests in epidemiology at all. For a start it seem an absolute value - no one no matter how unlucky, gets cancer five minutes after exposure to the carcinogen, it's seems to take some absolute length of time no matter what. Also, whilst latency is dose dependent it seems much less so. Risk can vary between 1 in a few hundred at high exposures, to 1 in a few million at low exposures, yet latency varies hardly at all despite massive variation in dose.
So basically, what causes latency in carcinogenisis, what is happening in the body for those decades, and how does this differ from the randomness of simple dose-response carcinogenicity?

I am not sure if I understand your question. To clarify, are you asking why doesn't a higher dose of the mutagen lead to a faster initiation of a tumor. Also, many times, as I understand, these cancers are due to a prolonged exposure to the carcinogen. Take smoking as an example.  Correct me if I am wrong, but that what I understand...


text:
Is there a family equivalent to "congener"?
Is there an equivalent word to "congener" but for species in the same family (family in the sense of the taxonomic rank)?
"confamer"? "confamiler"???
I know I can just say "species X and other taxa in the same family" but I thought a nice one-worder would be better if anybody uses such a word.

Confamilial is the term for same family, it has even been used in print.

Congenerics were twice as likely to fight as conspecifics, and confamilial competitors were three times as likely to fight as conspecifics.

I just found "confamilial" as well in a different paper.


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B cell clones and affinity maturation
As B-cells undergo affinity maturation, their BCR sequences change. Are they still considered to be part of the same clone?
I couldn't find a clear answer in response to this very similar question:
What is meant by clones of B-cells?

There are different opinions on this, since it's about usage. You could make an argument that, if you're talking about a B-cell clone, it is the product of a specific VDJ recombination (a mature, but naive B-cell), and refers to B-cells that produce antibody to one antigen. However, the term was originally proposed in this context:

...the expendable cells of the body can be regarded as belonging to clones which have arisen as a result of somatic mutation or conceivably other inheritable changes. Each such clone will have some individual characteristic and in a special sense will be subject to an evolutionary process of selective survival within the internal environment of the body.

In this case, I'd argue that, when the BCR sequence changes in progeny from that original naive B-cell (as in affinity maturation), you end up with different clones.
You do have to be careful, though, because people use this term differently.


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Consensus symbols in multiple sequence alignment
I was using multAlin for multiple aligning a set of sequences. The output I and came across included the following documentation (English corrected):

Consensus symbols:  ! is any of IV  $ is any of LM
  % is any of FY  # is any of NDQEBZ

I understand what it says but I don't know how to interpret it further. What impact does this have on the sequence alignment?

I find your post incomprehensible and am voting to close. However if you are having a problem with a software program I suggest you consult the documentation, the website or the support community.

Hi, this is the description:
! is anyone of IV
$ is anyone of LM
% is anyone of FY
is anyone of NDQEBZ
I have emailed them for help, and even follow up on that email, but i did not get a reply at all. I really hope some bioinformatics expert can help me here. Thank you

I have edited your question in a readable manner, which I would recommend if you post here again — the clearer you explain your problem, the more likely you are to get an answer. I have also answered your question, including sample output, that you would have done well to include in your question.

The use of these symbols in output of the type shown below is purely presentational, to help you inspect the alignment and identify regions of partial conservation.

                  51                                                 100
          CCPC50  SEEGFK.YGE GILEVAEKNP DLTWTEADLI EYVTDPKPWL VKMTDDKGAK
          CCRF2C  TYPEFK.YKD SIVALGASG. .FAWTEEDIA TYVKDPGAFL KEKLDDKKAK
          CCRF2S  TQADFKGYGE GMKEAGAKG. .LAWDEEHFV QYVQDPTKFL KEYTGDAKAK
          CCQF2R  HKDNYA.YSE SYTEMKAKG. .LTWTEANLA AYVKNPKAFV LEKSGDPKAK
          CCQF2P  TFAGYS.YSP GYTVMGQKG. .HTWDDNALK AYLLDPKGYV QAKSGDPKAN
       Consensus  t...%k.Y.e g..e.gakg. .ltWt#..l. .Yv.#Pk.fl .ek.gD.kAk

This is quite independent of the logic (algorithm) of the program, which is indicated by the documentational comments:

Symbol comparison table: blosum62
  Gap weight: 12
  Gap length weight: 2

This also gives a reference to the original paper you should read to find more information about the program.
You would also be advised to read the Wikipedia entry on Multiple Sequence Alignment and on Sequence Alignment in general. I would mention that this is an old method (as the appearance of the site also indicates). If it gives useful results, fine. Otherwise you might try the more popular and more frequently updated Clustal, which is available online or as a standalone program.


text:
Which kind of drugs get absorbed through epidermis?
Some drugs such as nicotine can be administered through skin. I thought the layers of skin are designed to prevent in-flow of any chemical/germs. Not all drugs get absorbed in this fashion. So do drugs like nicotine have any specialities(such as a special chemical group) that fool the sentries of skin? A link to an article/site would be very helpful, or even a book recommendation.

Looks like size is the largest factor: https://en.wikipedia.org/wiki/Transdermal_patch

"...that fool the sentries of skin..." The skin doesn't have sentries. It doesn't know anything, much less possess the ability to recognize drugs and let them in or keep them out. Finally, bacteria are much, much, much larger than the molecules that comprise the drugs.

According to a review (Prausnitz2004), marketed drugs with a dermal route of administration tend to fulfil the following criteria :

Small molecular size (< 500 Da)
High lipophilicity
Small required dose (up to ~milligram)

This is a consequence of the structure of the skin (with a lipophilic stratum corneum, and low diffusion speed) and practical concerns (everything else equal, a higher dose would need more surface area).
Beyond "pure" diffusion, there has been much work on improving drug delivery through other means : chemical enhancers (ethanol or DMSO being classical member of this class), medical devices (microneedle patch, ultrasonic device), and other more exotic methods mentionned in the paper.
These criteria are also mentionned in (GoodmanGillman2006, chapter 26), with emphasis on concentration gradient being the driving force behind diffusion across the skin. This chapter also contain a list of commonly used transdermal/dermatological drug, and their use.


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Could the Immune Gene HLA-B27 be gentically altered, snipped, switched off, replaced, edited within the body
Could the Immune Gene HLA-B27 be genetically altered, snipped, switched off, replaced, edited within the body.?
Thousands upon thousands suffer immune disease as do I from this highly implicated gene.
Is their a gene manipulation mechanism that 'could' work for this gene from within the body ?


text:
what snake is that in northern italy

About 75 cm long. Thin tail. Camping site near Grado, Italy, northern Adriatic sea.
It climbed a tree in the rough bark and i followed it to take these photos.

It might be a better idea to embed the images in your question instead of just putting their links.

Excellent quality photos and good views of important parts for identification.

It looks like a whip snake, either a Balkan whip snake or a green whip snake. They are both present in the very north of Italy, close to Slovenia. They both vary in color, but the coloration of this one seems to be more similar to the Balkan whip snake.

See also this discussion.

Thanks. I first compared it with natrix natrix, but the pattern didn't really match. There are also many small lizards on the camping ground, a common prey of whip snakes. My snake made jerky movements with its head when it was in the low bushes on the ground, I didn't see that in the videos. I'll accept your answer, but I'm open for other suggestions (or confirmations).


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Why is the macromolecular composition of a human cell seemingly hard to find?
I am trying to find a 3D rendering or list of molecules by volume in a cell (originally I was searching for human, but I'll take any at this point!). I understand the open-endedness of the question: what type of cell? During which phase? Under what conditions? etc.
What I am looking for, if such a thing exists, is as accurate-as-can-be list of structures/particles/macromolecules/ions/etc by volume in the protoplasm.
"Inside a living cell" by DS Goodsell is a step in the right direction but nearly 20 years old at this point.
"Diffusion, Crowding & Protein Stability in a Dynamic Molecular Model of the Bacterial Cytoplasm" is another step in the right direction.
Anything related to this query would be appreciated!
Thanks for your help!

For some components, you can find it here: http://bionumbers.hms.harvard.edu

Your title and question seem to be different. Your title would be off-topic as it is not about biology per se, but as it seems to be a concern I shall comment on it. The reason, I would think, is that modern biology — especially cellular and molecular biology — is not about classification. It is about understanding how things work. So why would any modern biologist do such a thing? Presumably you have a reason for wanting such a list, but I can't imagine why you would want the comparative volumes of all proteins, for example, even if this were known. Perhaps you could explain.

The various data related to dimensions and volumes of structures\organelles\macromolecules and cells themselves could be obtained from BioNumbers. For example, please see in the table below the information on volumes of COS-7 (monkey kidney tissue):

The details can be got at Applying systems-level spectral imaging and analysis to reveal the organelle interactome, by Valm A.M. et al


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Test question regarding botany
I'm having a hard time understanding what exactly those letters and numbers in the task in the photo below represent, also the task says "Is the blossom formula written correctly?" translated from Lithuanian to English. I would appreciate some guidance.

These are floral formulas, a way to succinctly describe how many petals/sepals/pistils/... the flower contains, and their relations (free, fused, ...). The wikipedia page describe the meaning of each symbol.
For example, for the first one :

Up arrow : symmetry along the vertical axis
K(6) : 6 sepals (K), which are joined (parenthesis)
C(2.3) : Two large petals, three smaller, joined. (not sure on the exact signification of 2.3)
A2 : Two stamen, not joined
[C(2.3) A2] : the petals and stamen are fused
G(2) : two fused carpels

Continuing with that example, it seems to me the first formula is not correct given the schematics below : there are 4 carpels. Though I'm no botanist.