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When is Semelparous reproduction most likely to be favoured?
Under which of the following conditions is Semelparous reproduction (where organisms produces all its offspring in a single reproductive event) is most likely to be favoured? (A) Adult survival rate is low. (B) Adult survival rate is high. (C) Breeding is perennial. (D) Breeding is seasonal.
Adult survival rate being low makes the most sense since only would an organism want to reproduce as soon as it could and also all at once. At the same time, seasonal breeding also doesn't seem far off meaning an organism would only produce all its offspring in one particularly favourable season a d in it, it produces all of it.
This is from an entrance test for a research institute. I am confused between A and D. Reading about Semelparous reproduction didn't help. Please help me solve this one.

Please do not post text as images. It discriminates against blind and partially sighted people who use screen readers. And if you post this sort of homework question we require more evidence of effort than "reading about Semelparous reproduction didn't help". What did you read? Why didn't it help?

I feel like you're just out to hound me, David. You have been nothing short of uninviting until now. You told me about the images in my other question and I then wrote the question in the details. You could've just said remove the images as well. About the question, I did say that I was confused between A and D, both of which are almost correct and should tell you that I at least know what I'm talking about and am not just here to get the answer. In any case, I have complied to both your complaints.

I know you're just following the rules and that my opinion doesn't matter to you but if you could just be a bit nicer with the tone, it would be more fun. If you see the comments on the first answer you'll even see that I discussed the answer with JayCkat who further cleared it up for me.

I commented on this question unaware that the other question I had commented on was also from you. (Easy not to notice on the phone.) Otherwise I would have probably held off. It's not you I have it in for, it's MCQs in general. They are allowed here with certain provisos, but I feel that these must be strictly adhered to, as they are really not  biological questions of general interest.

Duly noted. I disagree about MCQs though. I think well-formed MCQs are very good fuel for discussion and for checking concepts of school students/undergrads.

All its offspring in a single reproduction event.
All and single are the key words here. Ie this organism produces all its offspring that it will ever have in one event.
When breeding is seasonal- however this does not exclude organisms that can produce several batches of offspring over several seasons. Animals like deer and bears. They reproduce seasonally but are able to live several seasons and thus are able to produce several batches of offspring.
For an organism that only reproduces once, the important factor is survival of the adult animal. If the adult animal does not live long (due to predators, climate), you could expect the animal to reproduce only once and die.

This was my thinking as well. But don't you think the predation pressure could be present on the younger forms as well, and not only adults? That adds a bit a of a twist. Although, for all intents and purposes, A seems to be the most appropriate answer. Thanks.

Not really. Offspring are cheap. If there isn't so much pressure on adult form, the adults can continue to produce offspring.


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What is the meaning of "Rb is in the active state"?
I am reading about cyclins, cdks and Rb (Retinoblastoma) and some of the terminology is not clear to me.
I understand that when CDK phosphorylates Rb, it disconnects from E2F, and E2F can act as a transcription factor. My question is about the terminology.
My questions are:

When people say "Rb is active", do they mean "active = phosphorylated state" (where E2F is free from Rb) or do they mean "active = not phosphorylated state"?

Does "active cyclin" means cyclin is going to join CDK and cell cycle proceeds? or is "active cyclin = cyclin is not activating CDK and cell cycle paused"?

Active CDK means CDK is activated by cyclin and cell cycle can proceed?

In general, Maybe one can say that binding (Rb with E2F or Cyclin with CKD) means activation and disconnecting means inactivation?

Thanks!

(Image source: Kolch, Walter, et al. "The role of Raf kinases in malignant transformation." Expert reviews in molecular medicine 4.8 (2002): 1-18.)

The terminology of "Rb is active/inactive" refers to the activity of inhibiting E2F.
So active Rb inhibits E2F, while inactive Rb doesn't inhibit E2F.
With regard to Rb and phosphorylation - the story seems to be more complex ([1] describes Rb as an enigma).
According to [2] (this quote is from the summary of the paper by eLife):

Narasimha, Kaulich, Shapiro et al. now present biochemical analyses of
  Rb proteins that show— completely unexpectedly—that the cyclin D
  complex adds just one phosphate group to Rb during the G1 phase,
  although this group can be added to one of fourteen different sites.
  The resulting 'mono-phosphorylated' Rb varieties can each sequester
  different transcription factors and stop them working.At the
  restriction point, many more phosphate groups are then rapidly added,
  and the Rb protein is inactivated by a different cyclin. This
  cyclin—called Cyclin E—then drives cells into the next phase of the
  cell cycle. Establishing how cyclin E is activated is a priority for
  future research.

+ 3. Wikipedia's Cyclin-dependent kinase (CDK) page says:

By definition, a CDK binds a regulatory protein called a cyclin. Without cyclin, CDK has little kinase activity; only the cyclin-CDK complex is an active kinase.

Wikipedia's Protein kinase page says:

A protein kinase is a kinase enzyme that modifies other molecules, mostly proteins, by chemically adding phosphate groups to them (phosphorylation).

And here is a nice visual explanation from Life: The Science of Biology (10th edition):

So both "active CDK" and "active cyclin-CDK complex" (and according to the other answer, also "active cyclin") refer to the case in which a cyclin is bound to a CDK to form a cyclin-CDK complex, such that the CDK might phosphorylate some substrate.
(I didn't mention the cell cycle here on purpose, as I am not an expert, and so I am wary of claiming that an active CDK always pushes the cell cycle forward. If I understand correctly, we still don't know exactly how each cyclin-CDK complex affects the cell cycle.)

As for your last question:

In general, Maybe one can say that binding (Rb with E2F or Cyclin with
  CKD) means activation and disconnecting means inactivation?

As mentioned above, you could say that about a cyclin and its CDK.
Unfortunately, you can't say that in general. E2F here is a counter example (it is inhibited when Rb binds to it and activated when Rb disconnects from it).
However, you could say that in general, when something binds to a protein, the protein might change its shape, which might lead to activating or inhibiting some function.

[1] Dyson, Nicholas J. "RB1: a prototype tumor suppressor and an enigma." Genes & development 30.13 (2016): 1492-1502.
[2] Narasimha, Anil M., et al. "Cyclin D activates the Rb tumor suppressor by mono-phosphorylation." Elife 3 (2014): e02872.

Rb: The underphosphorylated, active form of RB1 interacts with E2F1
  and represses its transcription activity, leading to cell cycle
  arrest. (UniProt: P06400)
Cyclin-D: Regulatory component of the cyclin D1-CDK4 (DC) complex that
  phosphorylates and inhibits members of the retinoblastoma (RB) protein family including RB1 and regulates the cell-cycle during G1/S
  transition. (UniProt: P24385)

Active cyclin-D (i.e., cyclin-D in complex with CDK4) phosporylates (i.e., inactivates) Rb.

This answer makes complete sense to me and probably most folks who answer questions here, but given OP's confusion it might be helpful to explain a bit further and state very explicitly what's going on.

source: Stack Exchange

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

sort: votes


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Land Shrimp Sighting (Western Europe): What is it?
This approx. 6cm long insect was moving rapidly across the asphalt in a wavy/jumpy motion. It makes me think of a shrimp. It has a kind of widened head like a hammerhead shark.
I got two shots with my smartphone camera. Not the best quality.
What is it?

Position: Western Europe
Season: Start of Summer (June 20)
Time of day: Mid-morning
Location: Next to a largish marsh area currently kept as mini natural reserve in the middle of agricultural fields after large-area
school buildings got dropped on the landscape. Sadly this area is
likely to be marred by additional construction soon, the money is
just too good and attracts sharks and brown envelopes.

The size (~2 inches), broad "quadrate" head, and long posterior abdomen leads me to believe this is a relatively large larva of a Predaceous Diving Beetle (family Dytiscidae).

The larvae are sometimes called "water tigers" due to their large mandibles and voracity as aquatic predators.

One possible example:

 Dytiscus marginalis; Sources: Left: Wikipedia, right: Wikimedia
From Wikipedia:

When still in larval form, the beetles vary in size from about 1 to 5 cm (0.5 to 2.0 in). The larval bodies are shaped like crescents, with the tail long and covered with thin hairs. Six legs protrude from along the thorax, which also sports the same thin hairs. The head is flat and square, with a pair of long, large pincers.

The larvae of these insects are found across the globe in most surface waters (lentic and lotic), and they are known to leave the water to dig a suitable terrestrial site in the mud to pupate (Miller & Bergsten, 2016) -- this is likely why you saw this fairly large individual on land near your marsh.
Distinguishing species:
Your image does not provide enough detail to convincingly distinguish to species. I will provide some general details below, but I'll also mention that many species are only differentiated by internal or microscopic differences (e.g., male genitalia; Miller & Bergsten, 2016), and that even more macroscopic differentiating details tend to be on the ventral side of the insect (which is not visible in your image).

I couldn't find any accessible keys for the larvae of European or even more broadly Palearctic species.

Larval keys do exist, though just for other regions of the world (e.g., Michat et al 2008 for Argentina and Watts 2002 for Australia) or for only narrow taxa (e.g., Fery 2003 or Holmgren et al 2016).

Pederzani (1995) provides a global key for adults.

Miller and Bergsten (2016) supposedly provide a fairly stellar global-focused key to genera, but I could not find access to it online.

Some characteristics of note:

Larval characteristics of the family (from WV DEP): two claws on each leg; legs 5-segmented; abdomen usually terminates in a pair of urogomphi

Differentiating characteristics between common genera Dytiscus and Cybister available on bugguide.net

You can find some similar looking species here, and -- although from USA -- this Dytiscus species shares similar dorsal paired/longitudinal striping, number of body segments, and similar caudal anatomy.
Certainly, the similar-sized (up to 60mm), double-striped, European species, Dytiscus marginalis (the Great Diving Beetle), that I show above could very well be your species.

Citations:
 Fery, H., 2003. Dytiscidae: V. Taxonomic and distributional notes on Hygrotus Stephens, with emphasis on the Chinese fauna and a key to the Palearctic species (Coleoptera). Water beetles of China, 3, pp.133-193.
 Holmgren, S., Angus, R., Jia, F., Chen, Z.N. and Bergsten, J., 2016. Resolving the taxonomic conundrum in Graphoderus of the east Palearctic with a key to all species (Coleoptera, Dytiscidae). ZooKeys, (574), p.113.
Michat, M.C., Archangelsky, M. and Bachmann, A.O., 2008. Generic keys for the identification of larval Dytiscidae from Argentina (Coleoptera: Adephaga). Revista de la Sociedad Entomológica Argentina, 67(3-4), pp.17-36.
Miller, K.B. and Bergsten, J., 2016. Diving beetles of the world: Systematics and biology of the Dytiscidae. JHU Press.
Pederzani, F. 1995. Keys to the identification of the genera and subgenera of adult Dytiscidae (sensu lato) of the world (Coleoptera Dytiscidae). Atti della Accademia Roveretana degli Agiati, Serie 7 B, 4: 5-83.
Watts, C.H.S., 2002. Checklists & Guides to the Identification, to Genus, of Adult & Larval Australian Water Beetles of the Families Dytiscidae. Noteridae, Hygrobiidae, Haliplidae, Gyrinidae, Hydraenidae and the SuperfamilyHydrophiloidea (Insecta: Coleoptera)., Cooperative Research Centre for Freshwater Ecology, Identification and Ecology Guide, 43.

This is my 200th (gold badge) [tag:species-identification] post :). NEAT!

Congrats!!! Well done and well earned. :)

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Why is the relative expression in qPCR so low?
When analyzing different mutations through qPCR I found the $2^{-\Delta\Delta ct}$ value for each mutation. All the mutation have similar values compared to the wild type gene, however one of the mutation has an extremely $2^{-\Delta\Delta ct}$ value. Having $1$ for the wilde type, and an average of $0.9$ for some mutant genes, the exceptional case has a $0.05$ value.
I think one could argue that this mutation deletes a sequence from the wild type gene, but I believe other things can be suggested from this.

It may be a particular mutation that affects expression altogether. Through qPCR you're able to tell the relative difference in mRNA levels of a particular gene between, say, a WT and a mutant. It may be that this particular mutation damages some regulatory sequence within the body of a gene (e.g. a downstream promoter element) or some regulatory sequence upstream. To me, this suggests that you're dealing with such a case here. Anyways, you'd need more data to tell for sure. You should have the mutation mapped, if you haven't already and check if the primers you used were  okay. This mutation clearly hampers expression, as long as everything was okay with the procedure.


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What promoter is required for expression of a human protein Y in bacteria?
This is the actual question. It's from an entrance test for a research institute:
A scientist wants to express human protein Y in bacteria. For effective expression of this protein he should use
(A) promoter of human gene Y. (I think this is the correct one)
(B) promoter of bacterial gene.
(C) operator of any human gene.
(D) operator of any bacterial gene.
I think my answer is right although I am not sure if my thinking is entirely correct.

Homework questions are not allowed unless you show your attempt at an answer, so please share your thinking.

I am pretty sure there is no way to convince you but this is not a homework question. It's from an entrance test for a research institute in my country.

I believe you, though some level of effort is expected for all questions. Here's a leading question: why would bacterial transcription factors recognize a human promoter?

My guess is that they probably wouldn't? Instead the prokaryotic RNA polymerase is more likely to recognise a bacterial promoter. But I don't know if a bacterial promoter could work with a human gene, hence the confusion.

Yes, that's correct. The promoter essentially directs RNA polymerase to start transcription at a specific point, but transcription initiation isn't generally concerned with what comes after the transcription start site. Bacterial promoters (and viral promoters, which have coevolved to be recognized by bacterial transcription factors) are used frequently for heterologous protein expression.

That clears it up. Since prokaryotic RNA polymerase doesn't recognise an eukaryotic promoter AND promoters aren't concerned with what comes after the transcription start site, a prokaryotic promoter should be employed for the expression of a human protein in bacteria. Answer should be B. Thank you for helping me arrive at the answer. Although I didn't know about heterologous protein expression, I could answer (after some prompting by you of course) it by using the knowledge of prokaryotic and eukaryotic RNA polymerase.

I am sorry. I was not aware of that. I will correct it right away.

I'm afraid that "My query has been solved… details in the comments" just will not do. This is not how SE works. The poster is allowed to accept an answer, but the votes of the list indicate general opinion on the answer. If there is no answer the question has not been answered. Either withdraw your question or arrange with @canadianer for an answer to be posted. Please.

I have removed that last line.I hope there are no further transgressions on my part.

Canadianer has very deftly enabled me to arrive at the answer with knowledge I already had. I attempt to explain the same here.
We know that eukaryotes and prokaryotes have different RNA polymerase (enzyme responsible for transcription) enzymes. Eukaryotes have three different RNA polymerase, each responsible for synthesis of the three different types of RNAs. RNA Polymerase II is responsible for mRNA synthesis in eukaryotes. It recognises the eukaryotic (or say, human) promoter present in an eukaryotic cell. On the other hand, in prokaryotes, there's only one RNA polymerase responsible for synthesis of all the types of RNA.
Coming to the question, using a human promoter is probably logical since it would be ideal for initiation of transcription of the said human gene Y. But this is not true because a promoter is only responsible for recognition by RNA polymerase and allowing it to move further and transcribe the DNA sequence i.e. it doesn't matter what comes after a promoter. Also, prokaryotic RNA polymerase is unlikely to recognise the sequence of a human promoter. It is much more likely to recognise a bacterial promoter. Since a promoter's function is limited to allow recognition, it doesn't matter that it's a bacterial promoter as long as it can be recognised.
The two options about operators weren't a confusion for me since I already know that they don't have much to do with expression of gene as much as regulating it. Besides, any operator used would also require a promoter in any case, since that is how transcription is initiated.
Thus, the scientist should use a bacterial promoter.

You're welcome. Credit goes to you.


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Which components grow in size but not in number and which grow in number but not in size?
During growth of an individual animal some components of the body grow in size but not in number (type 1) while some others increase in number but not in size (type 2). Which of the following is correct?
(A) type 1: bones and muscle cells; type 2: hair follicles, red blood cells and epithelial cells.
(B) type 1: bones and red blood cells; type 2: hair follicles, muscle cells and epithelial cells.
(C) type 1: hair follicles and muscle cells; type 2: bones, red blood cells and epithelial cells.
(D) type 1: epithelial cells and bones; type 2: hair follicles, red blood cells and muscle cells.
I know muscle cells only grow in size. I am unsure about hair follicles, which is why I am confused between options A and C. I am also confused about bone growth. Does it ever increase in number? It would be nice if someone could clear that up.

Welcome to Biology.SE! Did you ever see giant hair follicles in adults? :)

I'll admit I didn't think of it that way. So do they increase in number then? And what about bones?

Well, either they grow in number, or, if they stay the same size, they become less and less dense when we grow up. Which option do you think is the correct one? Also, have a look at this page. Can you tell something about bone cell growth?

(It's not that I don't want to give you the correct answer straight away; it's just, you know: "Give a man a fish, and you feed him for a day. Teach a man to fish, and you feed him for a lifetime.")

Clearly they become less and less dense, duh. Also a new bone would require more osteoblasts and since they don't divide, bones don't grow in number? I like that you want to me to learn to think for myself but you pretty much gave away the answers. :D So bones, muscle cells and hair follicles don't grow in number? None of the options are correct in that case.

No, come on, if they become less dense we would have the same number of hair as babies and as 2 metres tall individuals, and it seems unlikely to me that a basketball player and a newborn baby have the same number of hair, isn't it?

This means that the number of hairs you had on your head when you were born and now is the same. I don't think so, right?

You're right. I got confused. I'm not thinking straight. They grow in number. I think that solved my question. Answer should be A. Thank you for being so patient. You're a good teacher. :)

You're welcome, Fenil. Remember: common sense before biology ;)

I posted an answer summarizing the process we underwent to get a solution, so that you can upvote and accept it and the question can be regarded as solved :D

I am not sure if I can upvote. The +1 seems to go away after a bit. I think it's because I don't have enough reputation. This feels like a dystopia movie. Not complaining, though.

Strange, according to this you should be able to upvote answers on your own questions... Well, surely you have the privilege of accepting the answer by marking the tick sign at the left of the answer. :)

Done. BTW, is there any chance I can talk to you properly somewhere? I don't have anything in particular to ask. I would just like to get to know you a bit, since I plan to pursue to biology in college as well and probably head into research.

Sure! We can talk in chat here. You still don't have enough reputation to talk there; I'll proceed and up vote two of your question so that you gain it.

We navigated through this question with Fenil in comments, I'll resume the answer here:
Osteocytes
We know from this page that "osteocytes have an average half life of 25 years, they do not divide" and that "when osteoblasts become trapped in the matrix that they secrete, they become osteocytes. Osteocytes are networked to each other via long cytoplasmic extensions that occupy tiny canals called canaliculi".
We can thus conclude that bone cells don't grow in numbers, but in size by their cytoplasmic extensions.
Hair follicles
Well, we draw the conclusion that hair follicles grow in number and not in size based on the following common sense observations:

We don't get to see tiny hair follicles in babies and giant ones in adults;
If they don't grow in size, either they grow in number or they become less and less dense as the skin surface grows with age. If the latter, we should see the same hair number in babies and in adults, whichever their height is, and this is obviously not the case.

So, they grow in number.
The answer is $A$.


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Is there a name for the behavioral phenomena of when animals like ants sacrifice themselves?
Title says everything about the first question.
The second question is: does the special case when ants apparently explode, https://www.washingtonpost.com/news/morning-mix/wp/2018/04/20/meet-the-exploding-ant-which-sacrifices-itself-for-its-colony/?noredirect=on&utm_term=.b56b0100a88b have its own name or does it fall under the same previous term?

The term you're looking for is altruism. According to Wikipedia, altruistic behaviour "allows an individual to increase the success of its genes by helping relatives that share those genes." Someone correct me if I am wrong but this means that this behaviour evolved by natural selection because it ensures the survival of a species in most cases. The link about exploding ants is probably a nifty example of altruism.


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How are ants able to dig with such pointy limbs?
Digging is usually efficient with somewhat broader structures shovels, no one tries to shovel with an ice-pick. Given that ants have very pointy mandibles and thin wispy legs, how are they able to dig anything? Is it  honestly solely by the means that the granules of soil are somehow coincidentally always the right size to fit in their mandibles?

Wow nothing after all this time, I didn't think this would be that hard of a question.

"pointy" is relative term. Try to shovel pieces that are 1m/3ft wide using garden shovel. You look at ant with your eyes, not ant's

It is a relative term, but that doesn't magically make it any less true. Obviously we are talking pointy relative to a human scale, often able to pierce human skin at terrestrial pressures. If we need additional information about the detail of their body at a finer level of observation, that is still relevant information towards answering the question.

what have you done to asnwer this quesiton?

I did research on people who raised ant farms. I was lucky enough to find a video that showed a close up of ants digging in a glass vial and it showed that they were moving artificial granules. However, this is not the same as their natural environment, so I don't actually know of the granules are realistic or if the ants instinctually adapted to the artificial granules. There's plenty of random sites giving vague entries about what ants use digging for, but there is little on the actual mechanics of how they are able to dig in regular dirt in the first place.

Wow, STILL no answer, maybe a research paper can be written about this since the answer is so pervasive. I've had that happen before, I did research on the mechanisms of ants ability to stick and discovered that their saliva contributed to it over smooth surfaces.


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What's the name for this kind of pointy/raised texture in animals?
I was in a store and I saw a jackfruit, seen here https://livenaturallymagazine.com/all-about-jackfruit/ with this sort of...scaly yet round and also pointy texture.
Then, I could have sworn I saw some kind of texture like this on animals, so I tracked down a couple images, like the back of a bearded dragon https://shannonwild.photoshelter.com/image/I0000Wf4WI2Vn.V0 and the pads of an owl
https://i.pinimg.com/originals/a1/94/07/a19407eff53e0fd06c48144c4541e3d8.jpg
What is the name for this semi-spiky texture, and what is the practical use of its topology?

I don't really know, however I have my suspicions. My initial guess would be the following. For the bearded dragon, I'm guessing it aids in defense. Small spikes protect against attackers. For the owl's feet, I would guess that its utility is completely different: friction. Friction helps holding on to the environment.


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Identifying flying insect from southern Poland / Upper Silesia area
Yesterday evening, I spotted this quite huge insect at my home in southern Poland (the exact location of the place). Unfortunately, I have only a very low quality pictures available at the moment:

Some details:

found in southern Poland / eastern Europe,
about 3 cm long,
quite fat (if I may say so),
seems to have 4 pairs / 8 legs in total,
airborne / able to fly (though quite slowly).

The quite huge (as per typical insect in Poland) size of this species was kind of surprise for me, but its behavior was even more surprising to me:

As pictured, it was able / willing to rest (copulate?) one on another even in groups of three (I failed to picture this), remaining still / not moving at all even for as long as half of hour.
After such resting / copulation ended or was interrupted the species on top was thrown off, falling down to the windowsill beneath.
It was then lying there up-side-down on its back, again remaining still and not moving at all even for 10-15 minutes.
Then it was kind of waking up from some kind of stasis, turning over walking a little bit around the windowsill.
Then it was flying up, flying around a little bit.
Finally, it was trying to rest / copulate with the species still on my window's mosquito net (or with the couple being there).

And then, the whole cycle was repeating until (late evening) only one species remained on mosquito net, which was also gone late in the night (not found the following morning).

Did they make any sounds while flying?

I believe, not.

Found it, with a lot of help from my local neighbors. It is Melolontha melolontha or cockchafer.

From English Wikipedia:

The cockchafer, colloquially called May bug or doodlebug is a European beetle of the genus Melolontha, in the family Scarabaeidae.
Once abundant throughout Europe and a major pest in the periodical years of "mass flight", it had been nearly eradicated in the middle of the 20th century through extensive use of pesticides and has even been locally exterminated in many regions. However, since an increase in regulation of pest control beginning in the 1980s, its numbers have started to grow again.

Here, where I spotted this insect (Upper Silesia) it is called in local language (in Silesian language) "julik", which is quite correct, since they seems to appear in July.
However, as per above cited part and as per Polish counterpart to above cited article, officially this insect is called after May, either "May bug" (English) or "Chrabąszcz majowy" (Polish). Most likely because adult forms of this species appears mature by the end of April and through May.


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Can men also become only bald on their legs?
Often hair loss that primarily affects the top and front of the scalp will happen to men (and female) during aging. Male pattern hair loss is believed to be due to a combination of genetics and the male hormone dihydrotestosterone.
Men with androgenic alopecia typically have higher 5-alpha-reductase, lower total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT.
The question is whether this kind of balding is only present in the hair of the scalp or can this proces also happen on the legs (or other parts of the body)?

Hair loss is known as alopecia, and is often associated with hair loss on the head. This type of hair loss is most noticeable, but hair loss can occur in nearly any part of the body, including the legs (source: Healthline). As an anecdote - my father in law (65+) has lost all his hair on his legs. This hair loss is referred to as anterolateral leg alopecia
About 35 percent of older men have this condition. The exact causes of anterolateral leg alopecia are unknown, but there may be a genetic component.
Age related hair loss in men is referred to as male pattern baldness, or androgenic alopecia. This type is related to hormones and certain genes.

For those who are interested, here is the current best genomic predictor of male-pattern baldness. Currently, about 15-20% of the variance in liability can be predicted directly from DNA (will increase when better data comes).


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Is it Theoretically Possible to Create a Male clone from the donor Cell of a Female?
I understand that Dolly the Sheep was created without the presence of a sperm cell. Instead, nucleus DNA from somatic cells of adult sheep were used. Since Dolly was female, i am assuming that the nucleus DNA used came from a female sheep. So, i want to know if the sex of the resulting clone is determined by the sex of the donor animal. Also, in light of the science behind sex determination in clones, would it be theoretically possible to create a male clone where a single woman contributes both the egg and somatic cells used in the cloning process?

AFAIK, mammals use sex chromosomes to determine male vs female, with males carrying a copy of the Y chromosome. It is possible to have a male with 1 Y and 2 chromosomes. So, i would guess that if you took a female embryo and microinjected a Y chromosome into the embryo at the single-cell stage, it MIGHT develop into a male.

is there any research that has been done on this topic?

I guess not specifically on creating male clones from females, but there have been IVF embyros created using 3 "parents", where one person provided healthy mitochondria to replace the mother's faulty mitochondria.

Maybe some of you could see this and I don't have to ask the question (something stressful to do in StackExchange): would it be possible to clone a female mammal from a male one, the female having two copies of the X chromossome from its male donor? If so, barring mutations, wouldn't the offspring of these be, "in a sense", like "clones" of their parents? I wonder what would happen if this pattern of mating would continue through generations. Assuming an eugenic mammal was the original male donor, I think this could help discover any "bugs" in the eugenics process by exacerbating them?

So, i want to know if the sex of the resulting clone is determined by
  the sex of the donor animal.

Generally yes for mammals and birds. In animals where the sex is determined by sex chromosomes, the sex of the clone will be dependent by the sex of the donor.
In animals (ie turtles and crocodiles) where the sex is determined by external factors (ie temperature), then the sex of clones will not be dependent on its donor.

would it be theoretically possible to create a male clone where a
  single woman contributes both the egg and somatic cells used in the
  cloning process?

Short answer is No.
Sex in mammals and thus humans is dependent on presence or absence of the Y chromosome. If the Y Chromosome is present, the mammal is male. If absent the mammal is female.  So a woman does not have the Y chromosome. Hence it is not possible to create a male from her genetic material.
Longer answer... anything is possible. A woman does not have a Y chromosome, so if you added a Y chromosome to one of her ES cells and then used those cells to form the inner cell mass of a blastocyst, then yes you can get a male.


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Why aren't "Water Giraffes" a thing?
If we assume that the Brachiosaurus and the modern Giraffe with their long necks both came to be by the need to reach higher-situated vegetable nutrition (which is a somewhat controversial assumption to make, I understand Evolution of long necks in giraffes), what biological reason is there we don't see any kind of modern day equivalent to the Elasmosauri?
Put differently, what environmental factor promoted the evolution of water reptiles with extremely long necks that ceased to exist in a post-cretaceous world? What benefits did Elasmosauri have that later water creatures would not?
Assuming that evolution is shaped by environmental factors, of course.
(And assuming the "water giraffes" weren't simply called "hydras" and extirpated by the ancient greeks. :P )

I think you already visited this Wiki page, but just in case you didn't I'll post it here: Neck movement in Elasmosaurus.

Do we not? https://en.wikipedia.org/wiki/Heron https://en.wikipedia.org/wiki/Hydrophiinae

Are there any existing environments where such long necks would be advantageous, and which are large enough to support a population of Elasmosaurus-sized creatures?  Such necks are certainly common in aquatic birds: not just herons, but geese, swans, cranes, flamingos...

Is your question simply: Given that elasmosaurs went extinct, why did an analogue of elasmosaurs not evolve after the Cretaceous?

@kmm rather late answer to your comment, but yes, that's the question.


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Why are there not two trees of life?
Life on earth started an estimated 3.8 billion years ago, very soon (in geological time) after the earth’s surface cooled to become solid and the first oceans formed. Nowadays, we believe that all living things can trace their ancestors back through a multi-branched tree of life, to this first living thing.
How do we square this rapid appearance of life, with the fact that it only seems to have developed once? In other words, we didn’t have life starting up in 10 different places on earth, giving rise to 10 different trees of life, why did we see only one?
In a variation on Richard Dawkins’ Selfish Gene, is it possible to think about a Selfish Tree?
Once the first tree of life arrived, it set about changing the atmosphere and environment generally, multiplying the number and range of species to fill every available niche (eg cold, hot, land, river, ocean, acid, alkali, large, small) in order to leave no space or circumstance for a second tree of life to spring into being.

@David - Maybe it's a pun? I think it's a pretty good pun. Trees do change the atmosphere without the assistance of anthropormophic nonsense...

Have you found a convincing argument in these two and a half years ?

The emergence of life out of matter is a very rare event.
The chance of having such event occurring more than once in a small time-frame is very little.
If the time-frame is large enough, then "New Life" could emerge again. However, in that case, the new emerging living organisms would be extremely disadvantaged by the presence of the "Old Life", already evolved to efficiently compete for energy sources etc.
Any new, barely functional, primordial life form cannot outperform the already existing ones, thus it would undergo extinction pretty soon. And that is why we ended up with a single tree of life on this planet.
Some links for further reading:
http://www.science20.com/stars_planets_life/calculating_odds_life_could_begin_chance
http://www.science20.com/news_releases/the_mathematical_probability_of_life_on_other_earth_like_planets
https://www.sciencedaily.com/releases/2018/01/180108090109.htm
https://www.scientificamerican.com/article/universal-common-ancestor/
https://www.nature.com/articles/nature09014
https://link.springer.com/article/10.1007%2Fs00239-010-9407-2
https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793%2896%2900631-X
https://www.sciencedirect.com/science/article/pii/S0022519318300419?via%3Dihub

"Any new, barely functional, primordial life form can not outperform the already existing ones, thus it would undergo extinction pretty soon. And that is why we ended up with a single tree of life on this planet." - I don't see how this is "by chance."

"The chance of having such an event occurring more than once in a small timeframe is very little." So, having two trees of life is unlikely, not impossible. Thus, it's still a matter of chances.

By that definition, just about everything and anything is by chance. I think your answer would be better if you left out the first line, and moved your last paragraph up top.

Mmm... Agree  I'll change my answer

Do you have a reference that clearly state the life originated only once? It actually feels more likely to me that there has been a number of abiogenesis events with creation of life-life creatures (but really at this level we come to the difficulties of defining what is 'life') but only one lineage made it over more than a few years and quite convincingly, one one lineage made it to today.

@Remi.b I didn't read that claim in this answer anywhere. I think it could be added that there could have been, and likely were, many events that you could consider as building toward some emergence of life, but once something fairly organized took hold it would have had too much advantage to be supplanted.

@BryanKrause The answer starts with The emergence of life out of matter is a very rare event which I took as suggestive that it is sufficiently rare that it only happened once but I agree that I might be doing a little bit of a stretch here.

@Remi.b I am looking for proper references to add. In general, I agree with you. It is a speculative answer since we don't have the evidence of any life-form differnet from the one we know. To my understanding, if the emergence of life would have been "commonly spread" then we should have evidence of it. Of course a "life-form" can exist for a shost time and then go extinct without leaving traces. But then again, that means that the emergence of a "strong enough form of life" is rare, and the most probable scenario is to have only one form of it taking over at the beginning.

I only read one of your links (the Nature article.) It doesn't support your answer the way you think it might.

@anongoodnurse It's just to start thinking about it. The basic idea is: taken separately, each event, like the emergence of a single chemical network, it's fairly common. If you mix "some random ingredients" you will get some reaction. If you apply selective pressure and reproduction, you will get improvements in the reaction rate. However, the chain of event that needs to happen to get a protocell is really long. The probability of each step, summed up, makes the emergence of life a pretty rare event.

Yes, I would agree that the emergence of complex life is a rare event, but I would disagree about simple life forms. If conditions were perfect for it to happen once, why not a hundred times? A thousand times? A million times?

This also explains why, experimentally, we can produce DNA/RNA peptides and membranes starting from simple chemical compounds quite easily, but we cant easily reach a higher level of complexity. To mix all together and get a protocell out of it is orders of magnitude more difficult. Indeed we are not yet able to produce a living protocell out of matter.

@anongoodnurse Indeed it could have happened. But then why don't we see the discendants of those hundreads of thousands emerged life forms? Probably they never kick off. As far I can tell, only one form of life managed to make it. A DNA/RNA-based protocell. Al the rest that was in the primordial pound, didn't make it, so ultimately, I do not consider it life. Of course it is matter of definition. If you consider some chemical system able to reproduce for a week and then disappear life, then I accept your point of view. But I consider such cases "failed starts" instead.

@alec_djinn "...I do not consider it life." Nonsense. I'm not talking about amino acid soup. I'm talking about life. Life is life, and the definition changes with new discoveries.

...all living things can trace their ancestors back through a multi-branched tree of life, to this first living thing.

I don't know exactly how anyone can claim that life arose on this planet only once. For all I (maybe 'we') know, it may have arisen a number of times, but only the most well-suited survived/adapted on this planet in its then-conditions long enough to begin a record of the type we now call the 'tree' of life (complex/eukaryotic organisms). You can't 'know' what you don't know. You can theorize, but you can't know.
Scientists make new discoveries all the time. There was a time (lasting millennia) when men of science* believed that life (in the form of a mud fish, for example) came from non-living matter (a mud puddle, in this case.) When that idea became laughable, the microscope was invented, and people still believed that microscopic life (bacteria, for example) arose from the proper conditions (a hay infusion, in this case.) It wasn't until Pasteur climbed the Alps with his experiment that spontaneous generation was finally put to rest.
At one point, we thought Homo sapiens were the only humans. We didn't know bacteria could live in the stomach, or in a lake full of arsenic.
How do we know what to look for when we talk of "life" if it's not life as we know it? We need to keep studying, keep thinking, keep our minds open about 'life' to find out more about it, like how many times it is likely to have arisen.
*I'd like to think that women of science knew better but were simply ignored.

I'm sorry, I think I don't get your point. Are you proposing that living forms of a second tree of life may still live on earth without us knowing?

I wouldn't say trees. Tiny shrubs or smaller, though, yes, past and present. Do you find that difficult to fathom?

I think you may need to state it more clearly, then :) also, see my comment on Samid's answer for my objections to this (albeit fascinating) hypothesis.

I don't really see the point. Sure, what you're saying is true in general about science: there is always more to discover, and there is room to be wrong about previous theories that were thought to explain certain phenomena. However, this is true in general and not specifically related to this question. The original question could simply then be rephrased as 'Why is there only evidence for a single tree of life?' This answer doesn't really address that. Also, the quip about gender is honestly totally out of place and should just be removed.

There's a serious answer here: the first paragraph (I'd ignore the rest).  We have no evidence of any history life on this planet before colonial or multicellular organisms formed clumps large enough to fossilize (and even then the evidence is unclear and debatable).  There could have been several microscopic replicating (living) systems that formed before the one we see today formed.  If they existed, they apparently died out, unsurprisingly without leaving macroscopic evidence of their existence visible today.

@Eff You are entitled to your opinion, as am I. Write an answer if you don't like mine. Crick is brilliant, Watson is an idiot, and Rosalind Franklin was dismissed. As to my answer's relevance to the question, again, write your own answer. I believe mine answers the question, and I'm not alone in science to believe what I do.

"There was a time (lasting millennia) when men of science believed that life  came from non-living matter."  I'd argue that the current prevailing opinion still looks for that mud puddle that life came from.  We've just pushed that mud puddle back roughly 4 billion years, and we call it an ocean now.  How far we have come from those barbaric days =)

Molecular phylogenetics, among other lines of evidence, strongly suggests that all extant life shares a universal common ancestor. However, this analysis is confounded by horizontal gene transfer. The following hypothetical figure, for example, explains how genetic phylogeny (right side of the image, this is what we are able to observe) may not represent true evolutionary relationships (left side of the image, this is what we are trying to infer) in the presence of horizontal gene transfer (represented by an arrow):
Martins L de O, Posada D. 2013. Proving universal common ancestry with similar sequences. Trends Evol Biol 4(1):e5.

While this problem can potentially be overcome by considering many genes, this becomes more difficult the further back in time you go, and impossible if you consider primitive life (such as an RNA world), about which we know very little. Assuming multiple origins of life, horizontal transfer of heritable information soon after their generation could be possible, as well as undetectable today. This creates a rather tangled tree, as visualized below:
Smets BF, Barkay T. 2005. Horizontal gene transfer: perspectives at a crossroads of scientific disciplines. Nat Rev Microbiol 3(9):675-678.

It is also possible that life originated multiple times on Earth, but only one "tree" survived to the present. In this scenario, there are multiple trees of life with many extinct and only one extant.
To sum up, the answer to your question is not known.

Definitely this. I'd expect that at the beginning of life informaron exchange was very permissive and fluid, with a lot of environmental DNA caught up by the protocells.

@LinuxBlanket That’s my intuition as well, but it seems unknowable.

What we know is that there's a single (more or less) genetic code, so even in the case of multiple origin of life, one code has dominated the "life scene". Do you know something about the evolution of tRNA?

@LinuxBlanket Yes, something, but certainly less than I should. Why?

It is entirely possible it did arise multiple times and we are the results, one of the nicer aspects of nucleotides is they can combine, it is possible different independently derived gene lines combined in the early stages. In our best guesses about what the most primitive forms of life would be like it is fairly easy to combine them. We simply don't know enough about exactly how the earliest life was structures to say with any certainty one way or the other. it could even be yes and no with life that was not compatible with this cooperation being driven to extinction by the cooperating ones. But as others have pointed out the window for this to occur is small, once the first form of life evolved the ability to breakdown larger molecules for raw material newly evolved life would be doomed, as would earlier ancestors of this "predatory" line. Life would literally clean up the traces of its early origins.

What is "life?"
It turns out to be a surprisingly tricky question.  Even descriptive lists like the one on Wikipedia  fall just a hair short of actually being a definition.  Through the years life has been famously easy to intuit and understand, and famously hard to analyze and pin down.  Whole branches of philosophy deal with that question.
This creates an uncomfortable challenge in answering questions like this one.  It's possible to define "life" in such a way that, if we were to look into the past with a magical crystal ball, we might find existed "outside of our tree."  I might then say "no, that's not how I define life," and pick some minor detail which exists in our tree but not in this "second tree" and add that to my definition.  Because there's one one overarching agreed upon definition with clear crisp edges, there wont be one clear agreement.
What we can say about the past is that the observed facts regarding the origin of life are consistent with the theory that life sprang up once, and only once.  That is intentionally shy of the wording you used.  I, personally, have problems with science using phrases which overstep the bounds of what it can actually prove, so I prefer to use more restrictive phrasings when the going gets tough.  For 99.9% of the time, "life originated once" is a sufficiently clear phrasing.  For the 0.1%, like this question, it's nice to rely on more precise wording. (and I'm open to any suggestions on more precise wordings in the comments)
I will note that we do find things that occurred more than once in the evolutionary tree.  It is currently believed that wings and flight evolved four separate times: insects, birds, bats, and pterosaurs.  To use the more precise phrasing, the observations in the fossil and genetic records are consistent with the hypothesis that they evolved four times, and rather contradictory with the hypothesis that they evolved just once.
That's not to say that's direct evidence in relation to your question, but I think it does point out the fact that scientists do indeed look for something happening more than once.  It would be an interesting result for them.  To date, nobody has been able to make a solid argument to show that life did indeed evolve twice.  Thus, a "second tree of life" gets relegated to the same dusty corner as Russel's Teapot.

If we look for life based solely on characteristics we've observed from the tree of life, then we will only find life forms connected to that tree. What I mean is, our current understanding of life revolves around cell theory, therefore whenever scientists go out to look for new life, they look for characteristics related to the cell.
May be another life form or tree exists that isn't derived from the cell. Food for thought.

But I think we can agree that the tree of known life, let's call it like that, has wildly outperformed the second one, at least in term of "visible" organisms in most terrestrial and aquatic niches. Also, features of life (birth, death and reproduction) aren't that subtle, I think we would be able to spot them if we came across them. What do you think?

@Samid "solely on characteristics, we've observed from the tree of life" what do you mean with this? We started distinguishing life from matter way before any tree-of-life concept was defined. Only when we started digging into the cellular and molecular biology of the various organisms on this planet we recognized their common origin. If we would have found organisms working with different chemistry, far from DNA and proteins, then we would have adjusted the tree-of-life accordingly. But up to now, all the living creatures we have examined have shown strong similarity at many different levels.


text:
What is meant by "a codon codes for an amino acid"?
What is meant by "a codon codes for an amino acid"? Does it mean in order to build that amino acid you must combine those three nucleotides?
Does it mean anything more than provides the instructions for manufacturing that amino acid.

It does not means "provides instructions for manufacturing an amino acid".  How could three little letters encode so much?
A codon is a three nucleotide sequence that matches the anti-codon of a t-RNA molecule capable of carrying one kind of amino acid.  The GGG codon, for instance, binds the t-RNA that binds to glyceine.  So the codon GGG in an mRNA ends up amounting to "put a glyceine here in the amino acid chain"

I'm not sure this kind of question should be answered. I know it's easy to toss off a quick answer to help the OP, but should this not be closed instead of posting an answer? Maybe a comment if you want to help? I would liken it to asking for a dictionary definition on EL&U... OT due to lack of research.


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Does recombination slow mutation accumulation in sexual populations? Is there any evidence?
Mullers Ratchet is the process by which asexual organisms would accumulate mutations without bound. It is claimed that sexual organisms would slow this mutation accumulation through recombination. Is there any evidence that recombination achieves this? Preferably experimental evidence.

It's a good question and one without a wholly satisfactory answer.  Here's a nice review from 2012 outlining the theoretical questions regarding Mueller's ratchet and recombination.
There also is "unequivocal evidence that deleterious mutations accumulate in low recombining regions of the genome, due to the reduced efficacy of purifying selection. " So if you accept this correlation between recombination and removal of deleterious mutations, then studies such as these are compelling evidence of what's happening in real populations .
One other thing to keep in mind that in terms of experimental evidence, it is non-trivial to translate theoretical measures of fitness (e.g. "selection coefficients") to something that we can directly measure in real populations.  So even determining if there is an increase/decrease in deleterious alleles is going to dependent on having useful data in the first place. The assignment of "true" measures of selection on individual genotypes is the mainstay of experimental evolution (nice review here) and is very labor intensive. Moreover, the vast majority of this work has been carried out in bacteria (due to their short generation times) so effects of recombination are not addressed. Nevertheless there are some cool comparative studies in yeast showing how recombination can make selection more efficient.

There have been a ton of mathematical arguments and computer simulations demonstrating Muller's Ratchet and its relationship to asexual reproduction. However, as far as I know, the experimental evidence is still hotly debated. The debate generally revolves around whether a given biological system fulfills the conditions necessary for the ratchet to operate. Here are a couple of relevant papers:
Quantifying the genomic decay paradox due to Muller's ratchet in human mitochondrial DNA.
Asexual Amoebae Escape Muller's Ratchet through Polyploidy

Mutations that are positively selected reduce the ratchet effect in large asexual populations. They spread, eliminating everything else, and so other mutations only matter if they happen in descendants of those mutations. It's as if the average population size is smaller.
Unfavorable mutations can hitch-hike with the selected ones, but only if they are unimportant enough that the combination is still selected.
Sexual reproduction reduces the ratchet effect to single linkage groups. But it allows things like meiotic drive. Mutations that result in the mutant version distributed to more than half the offspring can still be selected even if they reduce survival of the offspring later. And that happens a lot faster than the ratchet.
Experimental evidence -- that's hard. Maybe you could grow haploid yeast that don't do sex over a long period in a particular environment and measure changes in fitness in that environment. (The obvious way to measure changes in fitness is to grow them mixed with the wild-type and see how long it takes one to outcompete the other.)
Grow other yeast that do some recombination in the same environment and see whether they evolve faster. (Again, grow them together and see which one consistently wins.)
Some yeast that look reliably asexual have rare events that turn on sexuality. For example if they are all the same mating type, they can rarely have something that turns an individual into the other mating type. If your asexual populations have that happen while the experiment is running it contaminates your results. So be careful about that.
It looks like a whole lot of work. If the sexual form usually evolves faster then you have done a whole lot of work to show what almost everybody already believed.


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Melatonin production, sleep, and "cyan light"; how might this finding be possible?
The BBC News article Cyan colour hidden ingredient in sleep describes research that suggests melatonin levels as measured in saliva could be affected by the presence or absence of cyan color in a displayed screen, even when the color balance was adjusted so that the difference was not visibly perceptible.

The colour cyan - between green and blue - is a hidden factor in encouraging or preventing sleep, according to biologists.
University of Manchester researchers say higher levels of cyan keep people awake, while reducing cyan is associated with helping sleep.
The impact was felt even if colour changes were not visible to the eye. (emphasis added)
The researchers want to produce devices for computer screens and phones that could increase or decrease cyan levels.

Is cyan going to keep you awake?

I am guessing that this even possible because color perception comes through the sensitivity of three (or four?) color channels and so two different spectra can appear to be the same color. An example might be that a green wavelength might appear to be the same color as the mixture of a blue and a yellow wavelength if properly adjusted.
But if the two stimuli are adjusted to have the same or similar mix of signals in the individual's color receptors, how might the melatonin production still be affected?
edit: According to Wikipedia, monochromatic light would have a wavelength in the range of 490 to 520 nm, and if you wanted to create a visual impression of cyan, you'd use a mixture of Green and Blue channels:
Wavelength    490–520 nm
Hex triplet   #00FFFF
sRGBB         (r, g, b)   (0, 255, 255)

Melatonin production is in response to photoreceptors in the eye, in part, the same photoreceptors in rods and cones that process and transmit information about the wavelength of light (eventually) to the visual cortex for vision. However, @uhoh was right to wonder whether there might be a separate receptor input for melatonin production.
There is an additional opsin (photosensitive protein), found in the ganglion cells rather than the rods and cones, that is sufficient for responding to light and causing the production of melatonin by the pineal gland (mediated by the suprachiasmatic nucleus of the hypothalamus). Processing of light signals by the circadian system is quite separate from processing by the visual system. This is discussed briefly in Chapter 47 of Kandel's Principles of Neural Science, but you can read more about it in this review.
The pathways involved in receiving and processing light as an input to the circadian system were discovered relatively recently. Consider that the optic tract was discovered in the 3rd or 4th century BC, and the retinohypothalamictract was discovered in 1971.

Thanks! As in everything else in biology, the closer one looks, the more complicated (or at least complex) it turns out to be.

I am guessing that this even possible because color perception comes through the sensitivity of three (or four?) color channels and so two different spectra can appear to be the same color.

While this can happen, this is probably not what the article is referring to.

But if the two stimuli are adjusted to have the same or similar mix of signals in the individual's color receptors, how might the melatonin production still be affected?

I would guess that the caveat here is "visible to the naked eye" -- that is, the viewers didn't consciously perceive the cyan color. That doesn't mean that your eye didn't transmit its presence, as vision is the most "processed" sense we have. The screen you're reading this on is made up of RGB pixels on a scale small enough that your brain blends them together to construct an image made of the average color of the pixels.
It's very possible that there could be some cyan colors mixed in right now, but not in high enough concentrations for your brain to average them out into something you consciously "see".
For the experiment it's probably something similar: The cyan was there and picked up by the eyes, but the post-eye processing performed by the brain filtered it out from conscious view. That, however, doesn't mean it can't impact other portions of the brain. You still perceived it, it might still have an effect elsewhere, but your brain just isn't presenting it to you as "important" information.

I'm wondering if the receptors that lead to this response are completely separate from those used for vision. That might be a good avenue to explore.

@uhoh that's an excellent thing to wonder. Good instincts!


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If I expose a bowl of curd to sunlight,then will the bacteria undergo mutation?
Since bacteria undergo mutation while exposed to the sunlight, if a bowl of curd is exposed to sunlight, will the bacteria undergo mutation?

Mutations happen all the time. It does not take sunlight for mutations to happen, whether in bacteria or in eukaryotes. It mainly just take DNA replication for mutations to happen.

Spontaneous mutations occur in all cells (more frequently in bacterial cells) whenever DNA replicates.
No matter the location of the curd, bacterias from that enviroment will have muattions because they replicate.
 UV rays from the sunlight will also cause some mutations and extensive DNA damage in some bacterias that will eventually die, while others will get mutations that aren't as harmful for the cell.
Human cells, compared to bacterias have proof-reading and safety-check mechanisms that prevent mutated cells (UV damage, normal replication, viruses, etc) from spreading around-cancer.


text:
Sound volume drop when falling asleep in an airplane
Note: This question has nothing to do with pressure change.
When I'm flying in an aircraft at cruising altitude, the monotonous sound often lulls me to sleep. I've noticed that just as I am on the verge of drifting off, the perceived sound volume drops significantly. I then notice what is going on and the thought awakens me a bit and the volume snaps back to normal. I verified that the actual noise in the airplane stays constant while this happens.
I always try to hold on to the state where the sound is quieter, but it is very difficult to do while at least a bit conscious. That's why I suspect that it could be part of the process human brain goes through normally when falling asleep. Perhaps it happens every time, but I do not notice because I only ever sleep in such a noisy environment when flying.
I asked a bunch of friends and some of them experience the same phenomenon. I was unable to find any relevant scientific literature mentioning it, though.
What causes this fascinating phenomenon? Does it have a name? Has it been studied?

Cruising planes do throttle down sometimes which does decrease the sound level. Is it possible that the causality is reversed? That is, you are trying to sleep and are finally able to drift off when the noise level decreases.

@CharlesE.Grant I have ruled that out. The actual volume stays constant the whole time. The people sitting next to me never perceived any change. If the plane's engines were throttling up and down like that, it would be called surging and the plane would be in big trouble. I am absolutely certain that this is something that happens to me, not the airplane.

Have experienced this myself.  It is as if the part of the brain responsible for sensing or initially processing the sound falls asleep a bit faster than other parts involved in monitoring that sound consciously.  Sound fades out then suddenly slams back to full volume along with full awakeness.

Is it possible that you are equalizing the  pressure in your ear canal unknowingly when the perceived volume changes? The pressure differential between the external and middle ear is an important factor in hearing ability (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985947/) , so that might be related.

@ASimonis Not unless drifting in and out of consciousness changes the pressure somehow, which I doubt. Moreover, this is happening during the most boring parts of the flight at cruising altitude when the pressure is unchanging and I'm already accustomed to it. It also felt distinctly... software-caused.


text:
Protein - one polypeptide molecule or a collection of molecules?
I'm struggling a bit in Bio 111 with confusing terminology between the terms "chain" and "molecule". I understand the primary structure of a protein is a chain of amino acids connected by peptide (covalent) bonds - easily a molecule. And the secondary helix structure could be a single molecule/polypeptide chain. Up to this point, chain = molecule. But a beta-pleated secondary structure would have to be two or more chains (molecules) connected by hydrogen bonds. No? Or is a beta-pleated sheet considered one molecule? One chain?

beta pleats can still be a single chain and molecule, don't forget proteins fold which ba bring distant portion of the ame chain together.

Thanks John. But I think beta-pleated sheets must, by definition, be multiple molecules if you accept that a molecule is defined as consisting of only covalent bonds. I think I finally pieced the different terms together and cam up with definitions that work. I sure would like confirmation from anyone more knowledgable.

I think you are confused about what a beta-pleated sheet is, the secondary structure of a pleated sheet can and usually is made from a single amino acid chain. https://d1yboe6750e2cu.cloudfront.net/i/876db44ecaf5510a0c2438178140fcee11f39634

Chain yes. But a beta-pleated sheet has polypeptide chains connected "head" (carboxyl) to tail in alternating directions according to the definition of Secondary Structure in my textbook. That being the case, the head-to-tail binding can only be hydrogen bonding - much like the pairs of strands (molecules) of DNA in a helix.  And if molecules only contain covalent or ionic bonds, then the beta-pleated sheet may be one chain but it is multiple molecules.

no look at the image I linked it is a single chain, covalent bonds all the way through, that folds back on itself forming additional hydrogen bonds. DNA is the wrong analogy RNA which can fold back on itself and link is a better comparison. Here is another even better illustration. https://upload.wikimedia.org/wikipedia/commons/thumb/1/10/Alpha_beta_structure_%281%29.png/270px-Alpha_beta_structure_%281%29.png

Thank you for staying with me on this one, John. The link you provided was of a very small picture and I was unable to make out the detail. So I searched wikipedia and came up with this: https://en.wikipedia.org/wiki/File:1gwe_antipar_betaSheet_both.png
It shows that the tails and heads of the amino acid molecules are attached to each other by hydrogen bonds.

Let us continue this discussion in chat.

This sort of question is easily answered by consulting and carefully reading an introductory biochemistry text, like this section of Berg et al. on line. However, as the diagrams of β-sheets can be confusing, I will summarize.

The amino acids linked by covalent peptide bonds produce a protein molecule in the form of a single polypeptide chain.
This polypeptide chain folds into a specific shape in three-dimensional space, its conformation being maintained by weak non-covalent interactions — ionic bonds, hydrogen bonds and Van der Walls interactions. (Often referred to as protein tertiary structure.) Proteins that have a roughly spheroidal shape (rather than being long and extended) are referred to as globular proteins.
Often the three-dimensional structure has large regular components (often referred to as secondary structure) because of the potential for repeated hydrogen bonding between the CO and NH of the repeating peptide bonds.

Molecular diagrams to illustrate the type of secondary structure known as the β-sheet generally show just a section of the polypeptide chain for clarity, as in the left-hand illustration from Berg et al., below:

This may give the impression that two separate chains are involved†, but cartoon representations such as the one on the right (also from the same section of Berg et al.) show that for globular proteins this is not so.
In the diagram the flat blue arrows represent β-strands that are hydrogen-bonded to one another to form a twisted barrel-shaped β-sheet. The yellow ‘rope’ between the arrows represents the continuation of the chain in the non-sheet areas of the structure.
So the possibility for confusion arises primarily from the difficulty of showing the detailed pattern of hydrogen bonding in the whole of a large protein. (Although it may also arise from the fact that it is easiest to illustrate β-sheets using the diagrams of silk fibroin — historically the first to be described — in which the sheets are very regular and flat. To an extent this is misleading as the right-hand side of my diagram indicates.)
†Footnote
Fibrous proteins, such as silk, exist in which β-sheets are formed between many different chains. The identification of the individual chains can be made unequivocally, e.g. on the basis of the gene sequence, and it is clear that the higher-order structure is composed of many individual molecules. In smaller higher-order structures, e.g. tetramers of globular proteins held together by weak non-covalent interactions, the semantic question of whether a molecule can be made up of several individual chains arises. In my opinion, this question is best ignored, unless one is studying the biophysical chemistry of proteins.

Well David, as it happens, my question is a result of taking Bio 111 in college right now. Our Pearson textbook doesn't show the ends of the polypeptide chains in the illustration of secondary structures. The illustration on the left in your answer would have provided great insight but doesn't explain the fact that proteins are called "molecules" in other parts of the text. The consensus I'm receiving is that there is no clear consensus on the definition of "molecule" with respect to bonding. Everyone does agree that hydrogen bonds between water molecules do not make all of them one molecule.

My answer assumed that you were taking an introductory course which included something about proteins, and this was likely to be dealing predominantly with globular proteins. If there is any aspect of it that is unclear or which you dispute, please tell me. As regards the meaning of the word molecule in relation to proteins in general, this is another question and concerns mainly higher order structures. If this really interests you, please ask it as a separate question. However, of one thing there is no doubt: the polypeptide chain translated from a mRNA encoded by a gene, is a molecule.

@Byron1948 your question is a natural one for someone approaching protein structure after some chemistry. Has David answered your question? Do you see that the atoms in the $\beta$-pleated sheet are in fact all connected by covalent bonds (in addition to hydrogen bonds); that the molecule is just long and flexible enough that more than one type of interaction can be involved?

Thanks Dan. No, I don't think I have a clear answer yet. The illustration on the left of David's first comment show hydrogen bonds a the ends of the polypeptide chains (the dotted lines). I'm looking for a definition of molecule in terms of bonding. If the definition is "multiple atoms bonded together", then fine. Technically all water in a drop is one molecule due to hydrogen bonds. But this doesn't sound like a reasonable definition to me. What am I missing?

@Byron1948 — Your question related to text book diagrams of beta-sheets of proteins, leading to the statement: "But a beta-pleated secondary structure would have to be two or more chains (molecules) connected by hydrogen bonds. No?" My answer was "No" — the diagram (unless it stated it was silk fibroin) represented hydrogen bonds between parts of a single polypeptide chain (and not at the ends, as you state). If you want to discuss the meaning of the term "molecule" start with Chemistry SE. Ask separately about protein molecules here when you are more familiar with different proteins.

So, dotted lines aren't hydrogen bonds then. Guess I was misinformed.

@Byron1948 — A Polypeptide chain has two ends (also referred to as termini): an amino end (with a NH3+) and a carboxyl end (with a COO–). Neither of these is portrayed in the left side of the diagram (all COs and NHs) and, indeed they are never parts of beta-sheets as they are chemically different and not part of peptide bonds. Nor, in globular proteins are they generally even near beta-sheets, as the right hand part of the diagram illustrates. And btw., although I am sure it was not intentional, the phrasing of your comment is close to violating the list's "be nice" ethos.

Thank you for the clarification. I have, as you suggested, turned to the Oxford Chemical Dictionary in order to better understand precise definitions of these terms. And, although some answers come across as pedantic and condescending, I have no intention of violating the "be nice" ethos. Most of the time I find StackExchange to be a very helpful resource.

This may be of additional help, as I used to struggle with the difference between a peptide and a protein too.
A peptide is a single, short chain of amino acids (approx. <50 amino acid length). It's a single molecule.
A protein may or may not be a single chain of amino acids. It may or may not be a single molecule, it could be several molecules adhering to each other.
Hemoglobin is a protein. It's constituents, alpha- and beta-globin, are peptides. It's correct to refer to each of them as proteins, too. Alpha-globin is definitely a protein. What you would never say, however, is that "the hemoglobin protein is composed of four proteins", two alpha-globin and two beta-globin proteins, even though it is most certainly technically correct.
If you want to be extremely pedantic, hemoglobin is a single (metallo)protein composed of four peptide molecules, which behaves as a single unit, hence why it can be colloquially but not strictly referred to as a molecule.

This is not completely right. A peptide is seen as a short chain of amino acids linked together. More complex proteins are referred to as polypeptides. Today, proteins are seen as the functional unit built from polypeptides or peptides - sometimes more than one. But a protein can also consist of a single polypeptide. What matters here is the 3D-structure.

I don't understand how this disagrees with what I wrote. It's exactly re-written. Polypeptides are multiple peptides, hence 'poly'. Proteins are either peptides or polypeptides. Peptides are arbitrarily "short" single chains. Which part is not right?

Peptides are explicitly short - not only a single chain.

I've updated my answer. 20 years ago I was taught (and older generation scientists) say that a peptide is <100 AAs long. Wikipedia states <50. I guess it's arbitrary and fashion-sensitive, but we can agree it's a "short" chain.


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Are there any proven ways to increase the rate of bone remodeling in humans?
I'm not asking for anything specific -- just wondering if there's any data, studies, or etc. that show a possibility in increased bone resorption and turnover (bone remodeling/Wolff's Law) from certain procedures (whether it be diet, supplementation, drugs, surgery/experimentation, exercise/habits, etc.)
For example, comparisons between studies of people that show bone remodeling faster under different circumstances that can prove a specific method one can use to apply
By "increase" I mean anything that allows the human skeleton to be replaced faster some way

How can I clarify to make it sound as if I'm not asking for something specific then?

There, I clarified -- check the new title.

The main factors affecting bone remodelling are the person's age, and the load applied on the bone. It is known that in relation to fracture healing, younger children remodel much faster and more effectively. This allows surgeons to accept very displaced fractures in young children without having to restore original anatomy as remodelling will take care of that naturally. Here is an example:
http://www.brokenarmanswers.com/arm-still-crooked-cast-comes-off/arm-fracture-remodeling-children/
The reason is that bone absorbs in areas under less loading, and forms along load lines. The shape of bones therefore follows the shape and alignment of surrounding muscles, which apply some form of load even at rest due to muscle tone. The process of bone absorption and formation is much more efficient and faster in younger people and becomes slower with age. This also explains why bones become osteoporotic in people who can't weight-bear for a lengthy period of time, or in astronauts who spend long periods in zero gravity.
A well known method to accelerate fracture healing is to load the fracture as early as possible. This is the main principle of the dynamic compression plates where the holes of the plate are designed as oval rather than circular, so that when an off-centred screw is tightened, it pulls the plate in a direction that results in compressing the fracture to promote bone healing. Here is an illustration to demonstrate this technique:
https://www2.med.wayne.edu/diagRadiology/RSNA2003/Compression_Plates_Overview.htm


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Is each blade of grass an individual plant or not?
Sometimes when I do gardening, I notice multiple blades of grass appear fused together at the root, yet still appear to be segmented. When I look at images, I get some that suggest each blade is an individual plant like this one, and I find ones that suggest they're fused together like this other one, and I wouldn't know if they're actually fused or if they just have a tendency to have seeds or roots distributed in a clumped manner as some survival strategy.
Should it be assumed that each individual blade of grass is a separate plant, or otherwise how many blades are part of the same plant?

Each blade of grass is part of the grass plant and may have multiple blades.  Clumping grasses, when mature, can spread producing multiple shoots with additional blades.  The number of blades would depend on the type of grass and individual seed, but the clumping grasses tend to produce 10-16 leaves/blades.

Source: Poaceae - Wikepedia

They are clones, technically a single plant, even if disconnected at some point. Usually they are connected through the root system, through a rhizome which will produce additional shoots that go up vertically above the ground. Once a decent root system has developed, new offshoots (of the same plant) will continue to grow vertically, even if separated from one another.
This is a bamboo grass,

In a bamboo forest (or any patch of grass), it is possible that entire groups of trees are actually just one plant.


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Why didn't people taking up the Ice Bucket Challenge die?
I recently came across Vagal Inhibition. That article says,

(5) Sudden immersion of body in cold water.

can cause vagal inhibition and ultimately death.
Recalling the Ice Bucket Challenge. Going by what the above article says, shouldn't many of the participants have had a vagal inhibition ?

For one thing the ice bucket challenge is not immersion, you also might want to look at the mammalian dive reflex.

Theoretically, any treatment can cause death. Drinking water can be lethal and oxygen is highly toxic and a strong oxidizer.
To quantify toxicity we usually use Median Lethal Dose (LD50) metric. That is a dose at which half (50%) of test group is going to die.
To answer "Why didn't people taking up the Ice Bucket Challenge die?":
Dose that people used was not high enough to cause any significant increase in mortality. Maybe some people did die, but it was just masked by other news (to some degree)


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What is the etymology of "moura" in Mourasuchus?
Mourasuchus is a unique species of prehistoric crocodile so far discovered. It is a filter-feeder and has shared its habitat with Gryposuchus and the more fearsome Purussaurus in the Miocene Era --  reptilian counterpart of the Whale shark and Basking shark.

The original description of the species was given in 1964 by Llewellyn Ivor Price in:

Price, L. I. (1964). "Sôbre o crânio de um grande crocodilídeo extinto do alto Rio Juruá, Estado do Acre". An. Acad. Brasileira Ciên. 36 (1): 59–66.

As such, it seems plausible that the name means 'crocodile of Moura', Moura referring to Rio do Moura, a river in the Brazilian state of Acre where the animal's fossils were discovered.

Fossil crocodilians from Colombia and the Cenozoic history of the Crocodilia in South America (Langston, 1965) has the original description of Mourasuchus, so that would be the definitive source and contain the etymology. Unfortunately, copies of that book appear to be rare and the text not available online.
But guessing that "moura" is Latin or greek in origin leads to a promising result. Moura is the feminine of mourus, which comes from the ancient Greek for "black," "dark," or "obscure."


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Does contracting Rubella give one some kind of immunity to Measles and vice versa?
Both these diseases- Measles and Rubella, have very similar symptoms, have similar complications and are often confused for one another. And both the diseases have a common MMR vaccine. So, are the culprit viruses also related, so that contracting one can give one at least partial immunity to the other as well?
The similarity in symptoms is striking. Both the diseases may start with cold and fever. Both give one rashes, that start from face, and spread to rest of the body. Both have similar complications associated with them like brain infection. In the end, both can cause miscarriage, preterm birth, or stillbirth, as well as a variety of birth defects in pregnant women.
I know from this source that lab tests exist which can tell whether a person has immunity to one of the MMR diseases (Measles, mumps and rubella) and not the other, implying that there is a possibility of immunity to one and not the other. But since the vaccines like MMR only ensure immunity for 99% people who get the shot, my question is- does there exist partial immunity (in some people and not others, or in less severe attack and not otherwise) to Rubella if one has contracted Measles before and vice versa?

Short answer: No, there is no cross immunity between these two diseases. Having the same symptoms doesn't mean that diseases are related.
Both have in common that they are caused by viruses, but similarities end here. Rubella is caused by the rubella virus, which is the only member of the genus Rubivirus and belongs to the family of Togaviridae and are encapsulated positive strand RNA viruses.
Measles on the other hand are caused by the measles virus, which belong to the genus Morbillivirus within the family Paramyxoviridae and are negative stranded enveloped RNA viruses.
Historically speaking, the measles vaccine was available first in 1963, with mumps following in 1967 and rubella in 1969. All three are attenuated live vaccines which have been combined into a single vaccine in 1971. The sequence of this developments also shows that there is no cross immunity. You wouldn't develop another vaccine, when the disease is already covered by another. Drug development is a very expensive business.


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How increased potassium intake increases sodium excretion?
"K+ antagonises the biological effects of Na+". I have been reading the same many times without any explanation. How actually (mechanism) K+ helps excretion of Na+?, their interactions? And eventually lowers blood pressure?

That's because cell membrane could have a protein, called Na/K pump who's able to regulate the level of Sodium/Calcium using the energy gained by the hydrolysis of a phosphate bond from ATP.


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Differences between Heracleum mantegazzianum and H. sphondylium
I have heard about the hazards associated with Giant Hogweed and the trouble is when trying to identify it, it is very similar by the looks to normal hogweed.
When fully grown, there is a big difference in height with Giant Hogweed (hence the name Giant Hogweed, but when it is small, how can you tell the difference?
Giant hogweed (Heracleum mantegazzianum)

Image from WikiMedia
Hogweed (Heracleum sphondylium)

Image from WikiMedia

Yes, the species can be identified by the shape of the leaves. The leaves of H. sphondylium are more or less flat (in one plane); the leaves of H. manteggazianum are more crisped and much more pointed.
Here are two pictures from the Dutch wikipedia (h. sphondylium last):


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Lizard Identification
What is this lizard?

Seen in Hollywood, Florida, on a golf course. It may have been an escaped pet and was approximately 17" long.


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How did genome replication first synchronise with cell division?
It is obvious that cell division in living organisms is now synchronised almost perfectly with DNA replication and, furthermore, the line of division has to intersect exactly the space between the two copies of all the DNA molecules in the cell.  I know that as otherwise, most cells would be either empty or have a lot of excess DNA strands, which would lead to an eventual termination of replication due to scarcity of resources and energy required to trigger it.
Some theories (https://www.ncbi.nlm.nih.gov/books/NBK26876/) suggest the first protocell might have formed by a liposome simply gobbling up a self-replicating molecule. However, how would the molecule then 'know':

when exactly it should replicate so that the replication coincides with the liposome diving and
where in the molecule it should be located at the time of division, so that its copy ends up in a different daughter cell to itself

?

I obviously don't know the answer as there isn't a proven hypothesis yet. It seems to me plausible that by chance alone (i.e. no molecular knowledge required), a small fraction of the early protocells ended up dividing with enough self-replicating material randomly spread among the two daughter cells for them to grow and repeat the duplication process until it became controlled and perfected giving those cells an evolutionary edge.

@cagliari2005 that would still be one division. In order for synchronisation to have developed, millions of synchronised replications must have taken place.

Agree, but if the number of protocells is sufficiently large at each duplication phases, then while the vast majority will fail at duplicating, the few that made it will slowly evolve to perfect the mechanism (i.e. think about a population of protocells rather than single individual cells). I also wouldn't be surprised if this mechanism didn't evolve linearly but rather made several evolutionary jumps. But again, this is mere speculations and while I found the question interesting, the answer is unfortunately bound to be speculative.

@cagliari2005 I am really not sure (in fact, pretty sure that the opposite is true) such a mechanism would have any evolutionary advantage over molecules outside of the cell, if only one in many could successfully reproduce. My own theory is that at first, many molecules were able sustain themselves in one protocell, which eventually ripped apart due to excessive tension exerted by the molecules. As it did, roughly half the molecules went into one daughter cell, and half went into the other. Then, as you say, perhaps a more efficient mechanism evolved in an evolutionary jump.

That is definitely a possible theory :)


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What animal does this skull belong to?
This skull was found in Greece, about 40 years ago, possibly in the island of Euboea (there is uncertainty about the area it was found).

The length from nose to the end of horns is 67 cm. The skull's length without the horns is 42 cm. Just for reference, the floor tiles in the pictures have a side of 33cm.
What could this animal be? It does not have to be native to Greece, even though a native animal would be more probable.
Update:
The size of the skull points to an animal larger than a goat. It looks more like an antelope, a gazelle, or even a deer.  Only deers are native to Greece, however the horns look nothing like deer.
I believe the horns are the key to unlock this mystery.

Lichtenstein hartebeest possibly a female looking how thin the horn base is

Its definitely a bovid, most likely an african antelope specifically a Hartebeest or Alcelaphus buselaphus . There are several sub-species but those horns are a dead giveaway. The the horn do vary a bit by sub-species. The Neumann's or Tora hartebeest might be your best bet but I can't be 100% sure. They are all popular hunting trophies since forever and are even kept in some european game reserves so it is not that hard to find there skulls in private hands. Search "hartebeest skull" and you'll find a million of them so you can try for a more exact match.

There is limited information using only the bones and horns. But I suspect that is a Kri-kri or Cretan goat based on the reported location and the features of the horns.
Greece is trying to standardize its goat pedigrees by further classifying them based on regional names and features. This could be more specifically a Skopelos goat but I doubt it based on the horns being so short. As you report the length of the horns to be 25cm that puts a lot of evidence as this being a  Cephalonia/Kefalonia/Kefallonia goat depending on how you want to spell it. These Cephalonia goats have an average horn length of 25cm.

Thank you for your answer (+1). My impression is that this animal is too large to be a goat. It looks more like an antelope or gazelle. Moreover, the horns do not match the ones I see in pictures of kri-kris or other types of greek goats.

Yeah they are quite thick


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Would butterflies prefer drinking blood over nectar?
Knowing that butterflies will drink carrion blood and nectar, I wonder if they would prefer one over the other? The blood has more nutrients like iron and copper that the nectar would not have. Or do they not need nutrients outside of what is found in nectar?

Well nectar contains a lot of sugars which provide a quick fix of energy. It is quite similar to humans in which our bodies much prefer the breakdown of sugars rather than protein or fat breakdown. Blood may provide important nutrients but it lacks a lot of the sugars that nectar has, like fructose, glucose, and sucrose.


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Are there disadvantages to using Rhizobium rhizogenes for genetic transformation?
Rhizobium rhizogenes causes hairy roots, which are transgentic. Are the transgentic roots able to eventually grow normal roots or will they always be hairy in the transgenic organism?

After integration and expression, in vitro or under natural
  conditions, the hairy root phenotype is observed, which typically
  includes overdevelopment of a root system that is not completely
  geotropic, and altered (wrinkled) leaf morphology, if leaves are
  present.  - Cardarelli M, Mariotti D, Pomponi M, Spanò L, Capone I,
  Costantino P. 1987. "Agrobacterium rhizogenes T-DNA genes capable of
  inducing hairy root phenotype". Molecular and General Genetics
  209(3):475-480.

Is this permanent or temporary?


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Why do most theories assume "only" sexual reproduction can cause genetic diversity?
The reason cited for sexual reproduction trumping over asexual reproduction broadly relies on the advantages of genetic diversity.
This completely overlooks the fact that a mutant which is able to reproduce asexually with some amount of genetic variation (editing, randomizing etc) would have more inclusive fitness?

Actually, the idea that sexual reproduction promotes genetic diversity is a more a  myth that a reality. If you actually look at papers the develop models of the evolution of sexual reproduction, they rather talk about the evolution of a modifier locus and the importance of recombination and linkage disequilibrium. In any case, "promoting genetic diversity" is not a reason for which sexual reproduction would evolve as it refers to a species wide statistics. Finally, seeing diversity as "beneficial to the species" is also a potential misunderstanding.

Your question is based upon the false belief of what models of the evolution of sexual reproduction tell. It is also based upon other misunderstandings explained above. For these reasons, I am voting to close.

I did not imply group selection. I was just stating that the books I have read (introductory) state that sexual reproduction survives mutant asexuals because of the advantages of genetic intermingling (e.g. the Red Queen hypothesis), this has the side effect of promoting genetic diversity.

Can you please clarify sexual reproduction survives mutant asexuals? Also, just after you say because of the advantages of genetic intermingling (e.g. the Red Queen hypothesis). I don't know what you mean by "genetic intermingling" but RQ hyp. refers to an evolutionary arms race and does not (directly at least)  "explain a fitness advantage".

This is a pretty big question so I'm going to focus on the core points.
It's not nearly so either-or, and really a range of two things: trait diversity and stability. Sheer diversity isn't sufficient to improve rate of adaptation. Stability in the sense that it's a good idea to hold on to successful traits.
In sexual reproduction, you have two sets (one set of traits from each parent) of proven survivable traits to draw from. Very roughly, it doubles the amount of positive feedback toward maximizing fitness for the environment the pair finds themselves in - of which pathogens are a major and quickly changing component.
In asexual reproduction, you have a single tested set of traits. Asexually reproducing organisms thus depend on things like horizontal gene transfer - proven traits from another organism. This has the effect of prolonging the amount of testing that takes place (one organism vs two), causing asexual organisms to be more adaptable to the circumstances they find themselves in compared to sexually reproducing organisms and vice versa.
Where I have written "proven" here, I am referring to the fact that the traits in question have survived in combination with the organism's other traits, as opposed to a totally new mutation that could have consequences before the organism has a chance to reproduce.
Related literature

Genetic variation in organisms with sexual and asexual reproduction
"With realistic environmental changes small alterations in any particular measurement or trait are usually sufficient to keep up with the changes, but fitness, since it depends on a large number of traits, will be selected with greater intensity, which may be enough to confer a distinct advantage on sexual reproduction." An advantage of sexual reproduction in a rapidly changing environment.
Bacterial adaptation to pathogens: What antimicrobial resistance has taught us about horizontal gene transfer.

Can you please backup your claims with a reference? I don't understand what you call 'trait' here. It sounds like you confound number of parents with number of traits. There are fair number of literature on the evolution of sexual reproduction but I have never seen anything sounding like your answer.

Is there any study on HGT being used particularly by asexually reproducing species? If this is an evolutionary winning card, I'd expect it to show a high prevalence for instance in rotifer Bdelloidea.

Yeah: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632278/


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Please help identify insect found indoor in Malaysia, south east Asia

Found this insect in my home. About half an inch long. Would appreciate it if any of you could help me identify it. Thanks.

that's a cricket

In the USA we call these insects crickets. Because they make a noise that sounds like the pronunciation of their name. This one looks like a male with two cerci.


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Identification of beetle: black with orange stripe and 2 orange dots
I found the following beetle in a wooded area in Essen, Belgium. Does anybody know what species it is? Thanks in advance.

Looks very much like Nicrophorus investigator https://www.pinterest.com/pin/815362707508687290/


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What is this hopping insect?
What species is this jumping insect?
Found in the United Kingdom in summer.
About 1 cm body length + 1 cm feelers.

The well-developed jumping legs indicate Orthoptera. The undeveloped wings show that it is an immature. The long antennae say Tettigoniidae. I don't know the species.

It looks to be a bush cricket of the Leptophyes genus.  Possibly Leptophyes punctatissima, also known as the speckled bush cricket - not sure if the one in your image is speckled or not.  It is endemic to Europe and can be found in the UK.

Photo source: Wikimedia commons - Leptophyes_punctatissima

Where should I find the speckes if there are any? Are they those orange spots on the back on your photo?

Oh, it's probably all these little dots on the body! I didn't notice them at first.