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Immune response to foreign protein
In the context of COVID-19, why is it possible to inject someone else’s antibody protein into a person without fear of stimulating an immune response. Does this indicate that, somehow, antibody conformation is universal?
Or rather ...
The immune system must differentiate between cellular and fragmentary material? It will attack any cellular material it deems ‘non-self’. But if foreign non-cellular material enters the body, such as dust, pollen etcetera we are in the realm of an allergic response. The allergic response is not absolute: only certain materials will cause a reaction.
So perhaps foreign protein, such as donor plasma products, are treated as potential allergens which, happily, do not cause an immune response; unlike midge spittle?

Educating I find that you differentiate "between cellular and fragmentary material", this brings up "MHC". People differ in their allergic reactions as they differ in their MHC?  If  any sole protein, is "no cell", it might still be about the MHC, of the "host". Not commonly  known is that antibody producing B cells take up isolated antigen without prior presentation by APCs. B cells then present on their MHC2 to   T helper cells that need presentation by APC.  Thesis: people differ in reaction because they differ in their MHCs presenting allergenes to TH1, 2 and their B cell's MHC2.

Interesting: Likewise it might be asked if T cell receptors are interchangeable between individuals - as antibody is another word for the B cell receptor turned loose from the B cells membrane.  Any T cell receptor isolated from one individuum and injected as "foreign" protein should be tolerated - it might even be taken from the horses' mouth as Behrings magic bullets were.

The complexity of the immune response requires foreign proteins to be bound first by presenting cells which happen to be like macrophages - cells that are like garbage disposals. Why some proteins are simply gobbled up and yet others are preserved and presented to the resident T cell helper population is related to the size and sequence of the protein. In other cases, even small molecules (allergens) can bind to native normal proteins and make them look abnormal.
The use of immunoglobulin (semi purified blood) was used in treating certain diseases in the past. These sera were usually developed from animals purposely infected with the disease. Though these proteins also elicited their own immune response (side effects) the kinetics of that event was days to weeks whereas the binding of the immunoglobulin to its target(the virus protein) is a first order event occurring in minutes. Clearance of that antibody antigen complex over hours to days Avoids the catastrophic exponential growth of the virus by keeping the numbers low. Eventually tho side effects WILL happen if you keep giving the serum

Activation of the immune response relies on the detection of structure features of the foreign molecule that marks it as distinct from host cells. In the case of immunoglobulin injection between a human donor and a human recipient, these immunoglobulins are naturally produced antibodies that the body makes to help you fight infections and to serve other functions for the immune system. Therefore, they do not have the structural features that can be recognized and mark them as “foreign molecules” by the immune system.
However, IVIG can cause some adverse effects such as headache, chills, etc. You can find more details in this paper.
Resources

Chaplin D. D. (2010). Overview of the immune response. The Journal of allergy and clinical immunology, 125(2 Suppl 2), S3–S23. https://doi.org/10.1016/j.jaci.2009.12.980
https://www.rheumaderm-society.org/ivig/
Guo Y, Tian X, Wang X, Xiao Z. Adverse Effects of Immunoglobulin Therapy. Front Immunol. 2018;9:1299. Published 2018 Jun 8. doi:10.3389/fimmu.2018.01299


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What allows diverse ecology to thrive despite forces reducing species diversity?
Ecology and business are a useful model for understanding one another. One species fills a niche until it is outcompeted by another just as one business fills a niche until it is outcompeted by another. Businesses adopt successful strategies and traits from others, roughly akin to horizontal gene transfer, and fail should they become no longer able to compete.
The breakdown of this duality reveals interesting questions about differences between the two where one would expect similarities. One big example of this, and the topic of this question, concerns the trend of de-diversification in business. Over time, competitive industries tend toward a decrease in number of companies (species) filling a niche, with major shocks (like COVID-19) tending to cause smaller businesses to go extinct, and the strengthening of bigger players. Once a powerful oligopoly is established, it is almost impossible to overturn.
Yet in Earth's history, there have been countless major and minor extinction events, and countless highly successful species dominant in their niche that have been successfully displaced by smaller, newer competitors. Why is it that new competitors can compete with entrenched incumbents in biology, maintaining species diversity in biology where it fails in business?

You are incorrect about the business part of this, as there are numerous examples of near-monopoly businesses being displaced by new competitors.  For instance, the US "Big Three" automakers losing market dominance to foreign companies, on-line retailers taking market share away from malls, cell phones replacing land lines...  And have you tried to buy an incandescent light bulb lately?

There's a lot to unpack here. I'll try to leave an answer later. I'll share one initial observation: You seem to strongly emphasize the inmpact of competition or competative exclusion, perhaps because it's so ingrained in the philosophy of capitalism. But there are a number of factors that go into determining diversity in an ecosystem besides just competition. Related keywords: Niche partitioning, cross-feeding, mutualism, community succession, niche construction, intermediate disturbance hypothesis.

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

I agree with jamesqf. It is not at all clear to me that ecology and business show any fundamental differences based on the information that you've presented, which is only a series of assertions. If jamesqf's counterfactuals are insufficient to convince you, it would be helpful to understand why not. If you have such information, it would be helpful to share it or link to it if you want a meaningful answer to the question.

source: Stack Exchange

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

sort: votes


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Humans best at long distance running: purely physiological or is it a function also of ability to pace?
I have read that although certainly other land animals are much faster over short distances, a human can run down any other animal over time, so that if a human is hunting like a gazelle, etc. eventually the human will catch up. I am wondering if this is purely a physical thing or if humans, knowing how to pace themselves, avoid exhaustion while the gazelle just runs as fast as it can and then collapses -- is it possibly because humans are smarter that they are better long-distance runners? (Now, some birds are able to fly for thousands of miles and I guess also in water we can't compete.)
EDIT: I understand that humans have some physical attributes that contribute to their long-distance abilities but is the ability to understand pacing also part of it?

there are studies of human biology which will list all the different physiology and ability-to-pace-iology (that's morphology?) specializations that make humans run long distances. I donno if you researched this at all, cos previous research is already good reading when you find it.

i will change question, because i have seen nothing about the mental aspects.

Humans are efficient runners, but just as a reference, I think there are some interesting answers here that call into question whether humans are really the best at long distance running. https://skeptics.stackexchange.com/questions/6114/can-trained-humans-run-faster-than-all-other-animals-on-a-marathon-distance

While humans are certainly in the upper ranks, they are not the absolute best.  Sled dogs almost certainly take first place, at least in decently cool weather.  Horses are a bit better (as measured by endurance races over the same course, e.g Tevis Cup vs Western States 100), but it's close enough that some humans are better than some horses. But the real factor here is something you haven't mentioned: intention.  AFAIK humans are the only mammals (migrating birds are something else entirely) that deliberately set out to run long distances.

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


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How is Open Reading Frame (ORF) chosen?
I understand that AUG is the "start codon", and, because of this, most proteins begin with methionine as their first amino acid.
However, this ORF problem on Rosalind.info states that "AUGCUGAC... can be translated as ...AUGCUG..., ...UGCUGA..., and ...GCUGAC".  That is, something (the Ribosome?  The GTP cap mentioned here? Something else?) must cause the translation to be shifted by one or two nucleotides in the sequence.
My first question is :  What mechanism(s) cause(s) this shift in translation to another Open Reading Frame (ORF)?
Specifically, I want to know how the start codon, AUG, can have one ("A") or two ("AU") of its bases ignored in the Ribosome during translation.
My second question is : How often does this happen?  That is, what is the percentage of (known) proteins that start with methionine vs. the percentage that start with something else due to this "ignoring" of the bases of the start codon?
I am interested in the answers for both prokaryotes and eukaryotes.

This is standard material you will find in any modern textbook of biochemistry or molecular biology. Aspects of it have also been discussed here, but I advise you to start with NCBI Bookshelf — a textbook generally provides a better explained and illustrated account of an elementary topic. Here are links in Berg et al. to accounts of prokaryotic and eukaryotic initiation of translation.

I now suspect that you are being mislead by the use of the word "can". In problems of this type "can be translated" refers to the pure informatics conceptual possibility, without any reference to biological reality, except, in this case, that of the genetic code. It is a question of considering the six possible reading frames of any stretch of DNA, and deciding which have the theoretical potential to encode a protein — see my answer to this question. The biology depends on transcription as well as the translation mechanism referenced above.

David the part that confuses me is how the start codon, AUG, can have one or two of its bases ignored (skipped over).  I would expect "AUG" to always get translated.  I don't understand how the "A" or "AU" can be skipped, as the start codon has a specific function in the Ribosome.

@GregThatcher I do not understand what you mean by "A or AU can be skipped". 1) Do you mean at translation initiation? E.g which start codon to choose if "AUGAUG"? 2) Or do you ask what happens when the ribosome encounters a "AUG" in a different frame, e.g. "TAU"G? I feel like Joshua Morris great answer below should answer the second option.

@dtrades, from the Rosalind.info problem statement above, "AUGCUGAC... can be translated as ...AUGCUG..., ...UGCUGA..., and ...GCUGAC".  The first sequence shows "AUG", the second sequence truncates the "A", the third sequence truncates the "AU".

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

It’s the hypothetical “can” applied to the interpretation of a fragment of information written without spaces between each word (codon). Roman inscriptions in Latin are like this, as are the German equivalents of English noun phrases. As an example, suppose such a Roman inscription in English rather than Latin, in which the fragment you have found reads ...MASHIT... You do not know without determining where the sentence begins whether it is referring to a popular recording by a former US President, a call to vandalism,  or maternal faeces. The ribosome decides by the mechanisms I referenced.

@GregThatcher I hope I now understand your confusion. DNA is long. X = "AUGCUGAC" will always have other sequences around it. If there is another 'AUG' before the X sequence it can be read as either "'...'AUG'CUG'...,...'UGC'UGA'... or  ...'GCU'GAC'" depending on the reading frame as explained in Joshua's answer. IF translation initiation happens at the 'AUG' of the X, there is only one possibility: AUG, nothing will be truncated.

I understand now, thanks @dtadres.  It sounds like the Rosalind.info question was written in a confusing way.  They probably shouldn't have used a sample sequence starting with "AUG", when they meant that that particular "AUG" occurred after another start ("AUG") codon.

Question's link  "this ORF problem on Rosalind.info" doesn't seem to be valid? It seem last comment by Greg Tatcher answers the question. Probably it's in the "can", indeed. I bet It's about the theorem that there are 3 and only 3 possibilities to frame, nothing more implied.

Tl Dr: In the rosalind example they are showing the 3 reading frames that stem from the definition of a reading frame(non-overlapping triplets), not an example of open reading frames. Open reading frames are non-overlapping triplets between a start codon and a stop codon.
Its important to step back and understand what is meant by reading frame first.  It has been determined experimentally that translation occurs in non-overlapping triplets.  That is to say that if the ribosome starts reading at position n it will translate n, n+1, and n+2 into an amino acid, then it will start at the next non-overlapping position which is n+3.  For example, in the sequence: ABCABCABCABC if you start at A it will read ABC ABC ABC.... But if you start at B you will have an equally valid reading frame by the definition of a non-overlapping triplet and it will read BCA BCA BCA.  If you start at C it will read CAB CAB CAB.  What would happen if I start at the next A? ABC ABC ABC... See how you are back in the first reading frame?  No matter how long a given sequence it will only have 3 reading frames.
Why does that matter if they all start at an AUG?  You don't know which AUG translation starts at.  Not all AUGs are actually used as the first codon in translation, in fact, most are either internal to a translated protein or not translated at all.  An open reading frame is any sequence starting from an AUG to a stop codon.  An open reading frame can be within another open reading frame. E.g: AUGCTAUGGCGAUGUUAGAUGA. All of the valid open reading frames are:
    AUGCTAUGGCGAUGUUAGAUGACUAACUAA

    AUG CTA UGG CGA UGU UAG
         AUG GCG AUG GUU AGA UGA
               AUG UUA GAU GAC UAA
                      AUG ACU AAC UAA

What do you mean by "triplet pair"? It is a term that I have  never encountered and does not come up in a Google search (except in its chemical meaning) even with DNA appended to the search term. It seems to me that it is incorrect.

Not sure why i put that.  Edited.

A shifting of the reading frame downstream of a given point can occur with either an insertion or a deletion of a nucleotide.  I encourage you to pick a point after aug in my hypothetical sequence and add one nucleotide (A U G C) and see what happens when you group them into codons, then add one more and then another after that.  A change in the reading frame can cause the ribosome to encounter a very early stop codon and produce a non-functional protein. A great early experiment by (Brenner et. all, 1961) carried out this experiment inducing point mutations in viruses.

http://www.ehu.eus/biomoleculas/proteinas/pdf_doc/genetic_code.pdf

Basically one insertion/deletion shifts the reading frame and at some point downstream of that a stop codon occurs far too early.  An additional insertion/deletion (++ or --) it shifts reading frame to the third one and remains disabled.  If you add one more (+++ or ---) the reading frame is back to the original one and functionality reemerges.


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ID request - larvae on potato plants
Several of these were on my potato plants in Washington state, USA. This one about 7mm in length, some were a bit larger. They were moving in an inchworm-like fashion, but only by touch - I don't think they have eyes.

This specimen was photographed after placing in isopropyl alcohol, which changed the color (it was almost white while alive) and the shape somewhat.

This larvae doesn't seem to match the common pests of potatoes. It is possible this larvae has been infected by a fungi and so is distorted in shape and colour.

@SergiiDymchenko — In the future please [edit] your post rather than putting important information into comments. Not everyone will read comments and they are also ephemeral, so they should only be used to discuss how to improve a post. Thanks!

One notorious pest of potato plants are cutworms. Unfortunately due to the the discoloration of the species I am not able to identify for sure which species of cutworm it is.
Cutworms attack a wide host of plants (more info here). According to that same website, the main ways to avoid the damage these larvae can cause are to:

Remove all plant residue from soil after harvest or at least two weeks before planting...

... plastic or foil collars fitted around plant stems to cover the bottom 3 inches above the soil line and extending a couple of inches into the soil can prevent larvae severing plants; hand-pick larvae after dark; spread diatomaceous earth around the base of the plants (this creates a sharp barrier that will cut the insects if they try and crawl over it); apply appropriate insecticides to infested areas of garden or field if not growing organically

These larvae come from a large variety of insects so don't associate them too quickly with one insect or another (many websites associate them with moths but that is not always necessarily accurate).
Here's a source that elaborates a bit more on how to treat them plus another source for how to use pesticides in a garden safely (if no other option is convenient).


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Can the shoulder bones grow after the growth plates have fused?
Body builders have broad shoulders. If one start lifting weights after one's growth plates have fused, can one still increase the width of one's shoulders? If yes, does that mean shoulder bones can grown longer?
Which bones, (if any) can grow longer after growth plates have fused without causing an abnormal condition like acromegaly?

That is mostly muscle, not bone. Regardless of how much bone can or can't grow, muscle can hypertrophy more.

Why do you think exercise would cause bones to grow?

Regardless of growth plates, exercise does not cause bones to get longer or wider than they would have without exercise.
Each bone is like a sponge, it grows to a predetermined size as regulated by your DNA. Exercise makes the bone more dense and stronger. The more you exercise, the more stress your bones are under.  The bones respond by getting denser and stronger.

Like most organs/tissues, skeletal bone is constantly remodeling. Bone remodeling is a lifelong process where mature bone is removed (a process called resorption) and new bone is formed (called ossification). Cells called osteoclasts are responsible for the breakdown (resorption) while cells called osteoblasts handle new bone ossification. When we are young, we make new bone faster than we remove old bone and we increase our bone mass. Through our 20s this starts to shift, and we begin to lose bone mass faster than it is created. Source


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What is the difference between floral primordia and floral buds?
As we know an axillary bud differentiates to form a floral bud, but what is a floral primodium?

Welcome to Biology.SE! I made some changes in your wording — please [edit] if you think that I've changed your meaning. Please note that we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Finally, please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

A primordium (plural: primordia) is the first recognizable manifestation of a biological structure. In the case of a flower this will be a small meristematic bump typically at the periphery of a shoot apical meristem.
In contrast, a flower bud is generally used to describe the entire structure including the meristem and any associated structures (such as bracts) that can develop into a flower. This structure often goes through a period of dormancy.
Another way of saying this is that, in the context of a flower, a primordium is a group of meristematic cells that has not yet formed any lateral structures, while a bud contains a meristem and its associated lateral structures. Note however, that I believe I've seen bud used as a synonym for primodium in some cases.
Another difference is that primordia are (usually) microscopic structures, while buds are (usually) macroscopic (visible to the unaided eye) structures.


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identification request - tiny flies invasion
Since they are tiny, this is the best photo I can do:

We are in Berlin, Germany. It has become very hot outside and the flies have invaded us for the last couple days.
The insect is about 1mm long, 0.2mm wide, they are absolutely tiny. They fly but seems to like camping on the ceiling.
The have come in massive numbers, probably over a thousand, but they're so small we barely see them. They don't seem to be interested by our food, nor water, etc but rather just stay in cool and darker areas.
Since we have a newborn, I don't want to use insecticide to get rid of them, so I'm trying to figure out what they are and then.. what to do next :) Right now I am welcoming spiders!

Probably some Thrips species (aptly named "Gewittertierchen" in German). At worst, they are a nuisance.


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identification request - medium size fly invasion
I have two invasions going on!
the one here: identification request - tiny flies invasion
and this one:

We are in Berlin, Germany. This fly is 2.5mm long vs 1mm wide, and seems to like the dark and colder area of the apartment. They arrived at the same time as the tiny ones in the other link, but they don't look similar, so I don't think this is the adult form of the other kind but maybe I'm wrong.
They came with the heat, looking for shelter.

Without a clear view of the wing venation any answer would be sheer speculation; if the critters are still around and you can get a photo showing all the wing venation clearly (all we can see for certain at present are the ends of two of the longitudinal -- as opposed to cross -- veins) adding such would help immensely.

@ArthurJFrost, we're currently in another country; but when we're back I will check if they are still around


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Why Vibrio Cholera produce its toxins?
I was wondering, why V. Cholera synthesize toxins which induce in humans diarrhea? I know that diarrhea is protective mechanism for humans, to get rid of bacteria. But why V. Cholera just stop producing it? What is its function in bacteria? In which bacterial metabolism it is involved?

Which of these questions do you most want to see answered? One of the questions you ask is very interesting to me, but I would not be interested in answering them all. Can you narrow this down to one (maybe two) question(s)? Thanks.

What is its function in bacteria?

Then may I  suggest you edit your question to basically just that? Because that is a very interesting question. Also, it would help if you included any research you've done to answer the question. Thanks! :)


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Relationship between blood pressure time series and ventricular dynamics of the heart
The answer to this question is probably very straightforward, but I have actually had some difficulty finding an explicit answer online.
To what extent does the oscillatory pattern of arterial blood pressure (over small increments in time) mirror the oscillatory pattern of heart beat. For simplicity, imagine my heart beat signal is a binary signal where 0 means blood is not being ejected and 1 means blood is being ejected into circulation.
Said differently, if I detect a transient (where the interval of time is less than one second) increase in arterial pressure (e.g. a local peak), can I always accurately map that event to the "causal" contraction of the ventricles during blood ejection?
Similarly, can I use an arterial blood pressure time series to accurately recreate the binary signal of the heart beat? (Though, perhaps there will be a slight time shift due to the propagation speed of a pressure wave).
To provide another silly example: if my arterial pressure time series has 60 peaks (and corresponding "separating troughs"), can I confidently assert that the heart beat 60 times?

What happens when you take a pulse?

@BryanKrause ehhh. I was hoping for a legitimate paper. Taking a radial pulse is likely a grandfathered in practice that predates technology from the past 50+ years...I'm reluctant to claim something as canonical in the absence of quantitative evidence. I did not know if there was some paper that simultaneously measured time series of a ventricular valves open/close states and an arbitrary artery's vessel pressure. Certainly the radial pulse can be used as a proxy for heart beat (that's why it's a grandfathered in practice) but can it capture ectopic heart beats that eject very little blood?

Be careful not to ask an "XY" question. If you want to ask about ectopic heart beats then ask about that rather than the vague question you wrote here.


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Is Brain Eye connections reversed in all animals or just Humans?
I know that Brain Eye connections are reversed in Humans,

Left Hemisphere controls the Right eye/Right side of the body
Right Hemisphere Controls the Left eye/Left side of the body

Is it true in other animals like Birds,Cephalopods and other creatures?
Are the optic nerves physically connected in reverse or is it internally mapped ?

The premise with which this question starts is incorrect. It is not true that the left cerebral hemisphere exclusively 'controls' the right eye, or the other way round, in humans. (See https://www.kenhub.com/en/library/anatomy/the-visual-pathway for details.)

The statement is correct. A hemisphere does control the contra-lateral side of the body exclusively (e.g. hands, legs...), with very few exceptions including the eyes where a hemisphere controls both eyes equally (Hering's law of equal innervation) but for eye movements in the contra-lateral side exclusively. Your reference is about visual inputs, which is a completely different story.

That's not completely true. In mammals, including humans, the left of an image projects to the right of each of your retinae (this is due to the eye working like a camera obscura), and conversely for the right of an image. So you have 2 eyes, each eye receives mostly identical information but one is on the left and one is on the right of your body. You must somehow recombine this information together in the visual cortex. The way this is done is through the optic chiasma, where roughly half the nerves from the nasal parts (the half closer to the center of your body) of each retina cross. Then connect to a relay called Lateral Geniculate Nucleus and then connect to the brain. Below you can see a drawing from Ramón y Cajal, who first proposed this theory, depicting the process.

As you can see the points on each retina that receive information from the same parts of the visual field (here represented by the arrow) project to identical locations in the brain. So there is not a complete decussation (anatomical name for a crossing of nerves) like for muscles, but only a partial decussation of about half in humans.
Although y Cajal was the first to explain exactly why it makes sense to have partial decussation, this phenomenon had been known for a very long time. In facts Newton (hardly an anatomist) discusses that phenomenon in his Optiks and suggested that it might be related to the amount of overlap between the 2 eyes. So the more overlap, the higher the amount of partial decussation. This rule, later called Newton-Muller-Gudden law by Walls, seems to be approximately correct for mammals. However, as noted by Walls, there is no evidence of partial decussation in vertebrates other than mammals. Meaning that the decussation is complete (like muscles). In his Optiks Newton concludes that (I'm paraphrasing) if his theory is right then animals with no binocular overlap should have no decussation, which if he is well-informed is true for chameleons. His theory was indeed right but he was misinformed, chameleons have complete decussation.
Finally non-vertebrates do not have "contra-lateral" brains. They do not have this strange property of having each hemisphere mostly connected to the opposite side of their body. Therefore they have no decussation at all.
So in short: vertebrates-mammals = partial decussation ; vertebrates-non-mammals = total decussation ; non-vertebrates = no decussation.
Although dated, Walls book remain the most complete reference discussing decussation:
Walls, G. L. (1944). The vertebrate eye and its adaptive radiation.

According to Wikipedia, the nerves cross in all the vertebrates:
In vertebrates with a large overlap of the visual fields of the two eyes, i.e., most mammals and birds, but also amphibians, reptilians such as chameleons, the two optic nerves merge in the optic chiasm. Part of the nerve fibres do not cross the midline, but continue towards the optic tract of the same side. The purpose is so that the part of the visual field that is covered by both eyes is joined so that the processing of binocular depth perception by Stereopsis is enabled.
https://en.wikipedia.org/wiki/Optic_chiasm


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Quantification of various amino acids from bacteria?
I would like to characterise how much of various (uncommon) cytosolic amino acids  are produced in bacteria, and was wondering if there are good suggestions of how to go about doing this. I know that chromatography is a good end-point analysis once I have isolated a fraction of what I suspect contains the amino acids; however, I am unsure about the smartest way to do the 'rough' initial purification prior to chromatography.
I know that you in general lyse the cells, pellet cell debris and then start some form of purification. I have also heard of certain resins that can bind natural products (e.g. Diaion® HP20, synthetic adsorbent resin) had thus aid the first purification step of the amino acids. Do people have experience with this? Are there also good solvents for separation of amino acids from lysate, that could be used in the first step (phase separation)? Does someone have any experiences with this? Any alternative suggestions would be appreciated.

Please clarify what you are trying to characterize. 1) You seem to be using amino acid and "natural product" as if they were synonymous, but amino acids are only one type of metabolite that you could call a "natural product". IMO "natural product" isn't a helpful categorization since it could refer to anything made by an organism — do you have a more specific definition? ——— 2) Do you have a defined list of what you want to characterize or are you interested in "fishing" for all molecules that fit certain criteria?

Yes, amino acids of various kinds (common and non common). I thought this would be specific enough? Amino acids is a type of molecule with the amine and carboxylate group on each end, and various side chain (depending of which amino acid it is). Overall they are very small molecules (under 300 g/mol).

I edited your post to something I find clearer — please [edit] if you feel that I've changed the essence of your question. Is there some reason you picked Diaion HP20? I had a quick look at the Sigma page for that resin and its description doesn't sound promising to me ...

Diaion HP20 is simply the only one I have head of, and the reasons I was asking what people think about it (or perhaps have head of something better?). Thanks for the edit - this is much better!

It sounds like you'll need to do a protein hydrolysis reaction to seperate the cellular proteins into individual amino acids. This book chapter compares different methods and their various pros and cons (https://link.springer.com/protocol/10.1385/1-59259-342-9:111). If you don't have institutional access, just find a paper that does a similar analysis to the one you want, and reference the methods. Just make sure they did a decent job of validating it before you used it. Published method does not always equal valid method.

A good approach could be to use GC-MS to identify cytosolic metabolites. When focussing on cytosolic amino acids, it might be useful to precipitate the proteins in a purification step and continue with the soluble fraction. Subsequently, a derivatization is done. The mass spectrometry helps to better identify the amino acids. This article by Phelippe et al. can give a good start.

Thanks, this was exactly the type of literature I was looking for! I filtered the lysate solution and I am now attempting a freeze-dry, to then resuspend it in some type of solvent that proteins dont like (might be a good way to completely remove them) - before e.g. GC-MS. I will have a look at the paper!


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Phytomass and photosynthesis
I have been introduced to the term "phytomass" and I was wondering if phytomass can be both photosynthetic and non-photosynthetic?

"Biomass is defined as live material, necromass as dead, attached material.
Biomass + necromass form the "standing crop" or phytomass." (from https://link.springer.com/chapter/10.1007%2F978-3-642-68786-0_22)

But even if we were only talking about biomass, there is only a loose correlation between that and photosynthetic activity -  think about single-celled algae, where 'every' cell is photosynthesizing, versus trees, where most cells are non-photosynthesizing, and there may even be times where none are (in trees that loose their foliage in winter).

Oh I see. Is true though that phytomass has both photosynthesising and non-photosynthesising components (with the majority being non-photosynthesising)?

That depends on what those 'components' are - if you are counting cells, the answer is a clear yes, if you are counting organisms the answer would be no, and if talk about mass, i don't know.  - 'Phytomass' and 'biomass' are both in need of a qualification if you are going to use those terms - 'biomass' might also be the sum of all living organisms, and is also sometimes used for some types of harvest (plant matter for instance), where the 'bio' only refers to the formerly living state of the matter...

.. also note that in my answer - citation the phytomass only comprises 'attached' dead material, whereas sometimes it can also comprise all dead former plant material.


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What's the difference between the terms "muscle" and "muscle organ"?
Foundational Model of Anatomy distinguishes between Muscle organ and Muscle. What's the difference between the two?

Your links do not work. If there is relevant info at either link, please quote it as necessary in your post. Also, please clarify what you are referring to regarding "Foundational Model of Anatomy". If this is a book, please include a more complete citation (i.e., include authors, year, edition, publisher). Thanks

The word "muscle" is applied to both the organ and to the tissue.

There are 3 types of muscle tissue: skeletal, smooth, and cardiac.

Below is a decent quote from SEER explaining this (my emphasis added):

A whole skeletal muscle is considered an organ of the muscular system. Each organ or muscle consists of skeletal muscle tissue, connective tissue, nerve tissue, and blood or vascular tissue

If the word "muscle" is used on its own (i.e., without specifying "muscle tissue" or "skeletal muscle"), it is typically referring to the whole skeletal muscle organ.

Examples: chest muscles (pectoralis muscles), thigh muscles (quadriceps and hamstrings), etc.

Note: the word "bone" is used in a very similar manner.

"Bone" can refer to the entire organ (e.g., femur) or to one of the two recognized bone tissue types (compact bone and spongy bone).

In the context you state, seemingly nothing. "Muscle" is listed as a homonym of "Muscle organ". So it seems, for the sake of the website you like to, there is no difference (unless they are using homonym differently).


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Can anyone identify this spider for me, please?
I live in Northern Indiana and I’ve seen 3 of these spiders in my house before, all different ones. When I first saw it, it scared me since it’s a pretty big spider in my opinion from what I usually have seen around here. This spider was bigger than a quarter all together. I know it’s not the best picture, but this is it on the wall a while ago. Also was a very fast spider so I couldn’t capture it too well. Are they harmless? I woke up with a bite today and then I remembered this!

The spider on your ceiling looks like a sac spider, more a Cheiracanthiid (like a yellow sac spider) than a clubionid (a leafcurling sac spider).
But the colour contrast of the dark red thorax to yellow abdomen suggests it may be broad-faced sac spider, which a is actually classified closer to a wolf spider than to the above two sac spiders. It is considered non-aggressive and non-harmful to humans.
It is hard to tell from the photo whether the cephalothorax is actually red or just dark. So you are probably the best judge from here.
Compare what you saw to:

trachelas tranquillus (broad-faced sac spiders) https://bugguide.net/node/view/26291/bgimage?from=72
cheiracanthium (yellow sac spider) https://bugguide.net/node/view/3383/bgimage?from=0

I would second Trachelas tranquillus.  Nice flat face and two-toned body (dark reddish front and whitish back).  These are commonly found in houses during the fall (when they come in to overwinter) and the spring (when they re-emerge with the return of warmer weather).  They can bite, but rarely do so without extreme provocation.  Not significantly venomous to humans.

I'm also from Northern Indiana. There's only two spider species in the area that are venomous: the Brown Recluse and the Black Widow. It's hard to tell from the picture, but I'm fairly certain that its not a Recluse, and it's definitely not a Black Widow. My best guess would be a Barn Tunnel Weaver.
For future reference: https://spiderid.com/locations/united-states/indiana/ has a list species, with pictures.
https://www.in.gov/dnr/entomolo/4542.htm for more info on Brown Recluses and Black Widows.

Hi, I'm a moderator here, but really terrible at identifying species besides ones I grow in my garden or those I catch fishing in local lakes. It seems you've provided some good resources, but we like answers here to be self-sufficient since links can break. Can you expand your answer to discuss particular features that led you to a specific ID?

the link provided has a "barn funnel weaver" but no "barn tunnel weaver". The spider in question does not resemble a funnel weaver. It looks like a sac spider. The link is also a very incomplete collection of spiders in Indiana. The link given also does contain trachelas tranquillus (albeit the picture on that site appears to be a very gravid one) but I believe that is what we are looking at here.


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How does the DNA cross through bacterial cell wall during electroporation?
There exists a lot of literature on electroporation of Gram-positive and negative bacteria. Most of it gives an explanation that electroporation works by creating transient pores in cell membranes of bacteria for the DNA to pass through.
Both types of bacteria have a cell wall as well (differing in thickness). How does the DNA pass through the cell wall that it encounters on the way?

The bacterial cell wall is quite porous, and is not considered a permeability barrier for most small molecules. It mainly functions as structural support and to resist turgor pressures.
The average pore size of relaxed peptidoglycans were measured to have a radius in a range of about 2.0 to 2.5 nm, regardless of thickness (i.e. Gram + and Gram - bacteria have similar pore sizes), but when stretched under turgor pressures, peptiglycan is permeable to globular proteins of 50 kDa or more, while hyperosmitic shock of bacterial cells can trigger the release of proteins up to 100 kDa in size (Vollmer et al., 2008). That equates to ~6.5 to 8.5 nm in diameter by one method of estimation.
A single strand of DNA double helix is around 2 nm in diameter, so it stands to reason that even a circularized plasmid could potentially pass through pores just a little more than 4 nm wide.
Reference:
Vollmer, W., Blanot, D., & De Pedro, M. A. (2008). Peptidoglycan structure and architecture. FEMS microbiology reviews, 32(2), 149-167.

Good answer (+1) and you've done a nice job of providing a relevant supporting reference. However, in the future please include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. I've formatted your reference in way that minimizes changes to your answer, but this is another good example of how to format references.


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How does a sheep's fleece impact its tolerance for high temperatures?
I am interested in whether a sheep endures more stress when its environment is hot if it has a full fleece or if it is recently shorn.  Put another way, at the extremes, is a sheep more likely to die due to high temperatures if it has its fleece or if it does not?  If the answer depends on breed, what are the biological differences that cause one breed to interact with this element of its environment than others?
I am interested in temperatures around 90°F but if the answer differs at some temperature commonly experienced somewhere on Earth, that would be interesting to know as well.
I am interested in modest relative humidity values, in the 40%-60% range, but again if the answer differs outside of that range it would be interesting to know about.
I considered asking this question on a physics stack exchange (where a sheep might be modeled as, say, a radiator with or without insulation) but I'm particularly interested in the answer for real, actual sheep - biological processes and all - and not just a spherical sheep of radius r.

Wool serves as a good insulator, meaning it doesn't allow warmth to escape the wearer easily allowing the wearer to remain warm. Furthermore, wool helps maintain a dry environment by absorbing moisture from the air (and sweat) which can also keep you cool during summer.
Here's a link that talks more about this for both wool wearers and sheep: https://shepherdsdream.com/blog/wonders-of-wool/how-wool-keeps-us-cool/

Thanks.  Wicking seems like a really good point.  I had the impression that sheep don't sweat but https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1365279/pdf/jphysiol01094-0027.pdf apparently contradicts this notion.

Yeah, there are only a handful of mammals that have some form of perspiration.


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What is this creepy little thing that I found sticking on my bathroom wall?

I found this creepy looking thing hanging on my bathroom wall. This is actually the 2nd time I have seen it. The first one I saw looked kind of dried up already stuck in between the walls. But this looks fresh and new. It's scary and gives me goosebumps just looking at it. Can somebody pls help

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — photos must be uploaded; 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) an estimate of the size of the organism; and 4) the species-identification tag. I fixed 1 & 4 already, but please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

This is the pupal stage of a lepidopteran (i.e. a butterfly/moth). The pupa is encased in the brown silken cocoon in the centre of the 'net'. The 'net' itself is built from the setae (hairs) of the caterpillar, which it sheds prior to cocoon formation.
Here's some photos of similar formations:

http://www.richard-seaman.com/Insects/Vietnam/Highlights/index.html#Chrysalis
https://www.nhm.ac.uk/wpy/gallery/2019-the-hairnet-cocoon?tags=ed.current
https://besgroup.org/2015/11/05/a-parasitic-fly-emerged-from-the-cocoon-of-a-footman-moth/


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What is a "fairy smile"?
From Hrdy and Burkart (2020):

At birth, both chimpanzee and human newborns seek out eyes, are capable of mutual gazing, and caught just right, may imitate someone else’s outstretched tongue or other facial expressions. Both species exhibit reflexive ‘fairy smiles’, soon to be replaced by more open-eyed ‘social smiles’ in response to someone else.

Welcome to Biology.SE! Nothing relevant comes up with a Google Scholar search, so this may be an idiosyncratic expression. I suggest you contact the authors ...

From Sarah Hrdy (email):

A “fairy smile” is a reflexive smile that spontaneously and briefly flickers  across the face of a newborn baby.  Some years ago, Tetsoro Matsuzawa discovered that these occur even before birth, en utero in chimpanzees! (Long story, but Tetsoro was using laser probe with a camera on a highly habituated pregnant chimpanzee female, accustomed to working with him to learn this). So of course do humans en utero.  After birth, one may see a reflexive “smile” flicker across the face of a baby even while sleeping —no outside stimulus or engagement with another person needed, tho may occur in response to a sound. "Fairy smiles" are different from “social smiles” that emerge later, and occur in response to someone else speaking to or smiling at them, etc.

I grew up in the southern part of the U.S. and people around me used the term,  but now that you ask, am curious to know where this term to describe “reflexive, non-social smiles” in newborn babies comes from.


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Which is the most extreme thermophilic bacteria known?
Extreme thermophilic bacteria thrive at any temperature above 40/50°C. Thermotoga Maritima seems to be the bacteria that can survive at the highest temperature up to 90°C (reference 1, table 2). I wonder if there is a more exhaustive list of extreme thermophilic bacteria and if there is a known bacteria that can survive at higher temperatures than Thermotoga Maritima.
References:
Ref.1 Front. Microbiol., 05 November 2015 | https://doi.org/10.3389/fmicb.2015.01209
Extremely thermophilic microorganisms as metabolic engineering platforms for production of fuels and industrial chemicals

There is also the bacterium Aquifex pyrophilus which is reported to grow  up to 95°C. I don’t know if this is the most extreme temperature reported for bacteria.

Geogemma barossii, initially designated Strain 121, can survive and reproduce at 121°C, with an optimal growth temperature of 103°C. It's not a bacterium though, but a member of the Archaea domain.

Here is a link to an online lesson covering thermophilic and hyperthermophilic bacterial and archaea. https://courses.lumenlearning.com/boundless-microbiology/chapter/thermophiles/

Methanopyrus kandleri strain 116, another archaeon, is reported to grow up to 122°C with an optimum growth temperature of 105°C. In the paper they also explain that it is difficult to compare this species with others from different studies due to the dependence of growth temperatures on culture conditions.

Is this the same as what grows at Yellowstone's geysers? Because they say "The water can be as hot as 204 degrees and the steam can exceed 300 degrees." That's on the Fahrenheit scale. Converting to Celsius, it's 95.5 and 148.9. https://whyy.org/segments/the-biodiversity-of-heat-loving-bacteria-in-yellowstone-rivals-a-rainforest/


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Interpretation of Pangenome: high number of accessory genes
I performed a pangenomic analysis on a collection of 52 strains belonging to the same genus (some 5-6 different species). All the strains were isolated from the same environment: interior compartment of surface-sterilized plant root.
Now, the results of my analysis (I used the R package FindMyFriends) indicated a total of 32911 gene groups divided as follow:

581 core (present in 95% or more of the genomes)
6116 shell (present in 15 to 95% of the genomes)
26214 cloud (present in up to 15% of the genomes)

This results are quite unexpected. Even though it is typical that most gene groups get labeled as cloud or accessory, it surprises me that the percentage is so high! Especially given the common origin of those strains.
Other software I tried (Roary, BPGA, microPAN) gave similar or more extreme results, so I can exclude a technical error.
Therefore, if anyone has some experience with pangenomic data, some input on how to interpret this data would be greatly appreciated.

Don't know this area, but have you considered the possible presence of other organisms' DNA from contamination or the presence of eukaryotic (e.g. fungal) or prokaryotic cells inside the root tissue sample?

Welcome to Biology.SE! I did an [edit] that I think improves the readability of your question (e.g.s: your use of "begets" didn't make sense to me, and "worst" means most negative, which feels ... unnecessarily subjective) . Feel free to make more changes if you feel I've altered your meaning.  ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

@Rob, I'm unfamiliar with BGPA and microPAN, but I've used Roary and PanPhlAn. Some questions so that I can better understand your system: What is the average size (+deviation) of these 52 genomes?  Are these draft or finished genomes?  If draft genomes, how fragmented are they (how many scaffolds, on average)?

@mgkrebbs I would exclude that as the process of binning during the assembly should have taken care of that

@Dirigible The average size is 5.7 MB with SD of 1.2. I did not process them myself, but they are drafts, with an average of 76 scaffolds. However one of the genomes is almost double in size compared to the others and I believe I should probably discard it.


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Would tattoos be considered a phenotype?
I'm trying to understand how broad the definition of "phenotype" is. If someone gets a tattoo, would that tattoo be considered part of their phenotype?

The fact that the two posted answers disagree is maybe a good argument to say that the answer is not obvious and the post does not "lack research". I am upvoting.

Hereditary biology doesn't often extend to human artwork, so it's a moot point. Tattoos fall into the realms of social sciences / human sciences and they are not very useful for measuring genetics, which is what genotype and phenotype are aimed for.

Tattoos are not considered part of genetics, a scientific measure of genetic heredity, and no established science paper would quantify tattoos as an indicator of biological phenotype. Tattoos are anthropology, artwork, they would only be referenced as phenotype in a joke paper.

Broadly speaking it most likely is. The exact meaning of phenotype has changed quite a lot over the years. There isn't a clear distinction between what should or should not be included in the definition, and reasonable people can disagree on sound arguments.
Phenotypes were defined by Johanssen in 1911. His definition was "All “types” of organisms, distinguishable by direct inspection or only by finer methods of measuring or description, may be characterized as “phenotypes.”". So in his definition a phenotype is a class of individuals that share a common observable property. Take Mendel's experiment: short and long peas are 2 phenotypes. From heredity we can infer multiple genotypes. An identical phenotype (tall) can result from 2 different genotypes (tall-tall, or short-tall). That is why the distinction is important, because truly understanding genetics will require not only to understand the genetic makeup of individuals (we have more or less solved that), but more importantly how the genes are expressed into a phenotype. Keep in mind all of this was speculated long before we actually found out what genes were. Ironically, Johannsen thought it was an idle pursuit: "The question of chromosomes as the presumed “bearers of hereditary qualities” seems to be an idle one. I am not able to see any reason for localizing “the factors of heredity” (i.e., the genotypical constitution) in the nuclei.".
At the time, genes were really thought to produce strict discrete categories of individuals that were slightly smoothed out through random individual variations. Over time it became obvious that Mendelian traits were more the exception than the rule and that trying to classify individuals in discrete categories was not really helpful. So over time phenotype became to used for traits instead of individual. That's the way I hear people use it today at least (i.e. we would call "being tall" a phenotype of peas, and not "all peas that are tall").
So the modern definition of a phenotype is the observable characteristics of an organism, anatomical, physiological or behavioral. The first 2 points are easily accepted and uncontroversial. But there is debate about what exactly should be included in "behavior". I'm going to ignore behavior for now.
An important point, and I think this is where there is disagreement between Remi.b and me, is that a phenotype must have a genetics basis. I realize this is not explicitly mentioned in any definition, but that is very much the way people mean it. And if not, the definition is totally meaningless. Take the example of a monkey missing a finger congenitally. This is a phenotype, it is due to its genes. If the monkey is missing a finger due to a fight, this is not a phenotype because genes have nothing to do with it (again, ignoring behavior for now).
So, in my opinion, what would not be a phenotype is something that you could conclusively prove to have no genetics basis whatsoever. That's an extremely (impossible) hard case to make. But in retrospect I was perhaps to quick to include behavior in the definition, and this is due to my own biases as a behavioral neuroscientist.
I think this is the narrow definition of phenotype and I don't think anyone would disagree up to that point. You might notice that there has been no mention of evolution so far. It is because genetics and evolution have been developed independently, and even though everybody was quite aware they must be 2 sides of the same coin evolution is not directly relevant to the genotype/phenotype distinction.
This is when the definition of phenotype started to be extended beyond purely physical traits (people included behavior in phenotype but they mostly meant things like gait that require a behaving animal to measure, but it is not behavioral in the broad sense). I see 2 reasons for that change, and R Dawkins was largely involved in popularizing these ideas. First as genetics and evolution started to be integrated together, it became obvious that genes must be selected through evolution, and that phenotype must reflect something related to fitness. W. D. Hamilton did important work on the topic and his ideas were popularized in the "The Selfish Gene" from Dawkins. The second idea is the ethological "revolution" from Tinbergen and Lorenz. Until then animals were seen as automatons (following Descartes) that behave the way they do because of simple conditioning. Ethologists showed that complicated behaviors such as courtship or altruism are instinctive, and therefore must have a genetic basis (Hamilton also worked on altruism a lot). A new generation of scientists pushed things even further with people like E. O. Wilson who studied the social life of insects, J. M. Smith who showed that individually detrimental behaviors can be optimal at the scale of a population etc.
At this point it became clear that the definition of a phenotype was too narrow, because behaviors are (at least partly) related to genes and therefore must have been shaped by evolution. This is the idea put forward by Dawkins in his second book "The extended Phenotype" where he explicitly makes the case that the definition of phenotype should be enlarged to include behaviors such as courtship, nest-making and the like (Dawkins was a student of Tinbergen so it's not entirely surprising he is biased to like animal behavior). Although these 2 books became very popular and widely read in the general public, they were actually meant mostly for biologists. Note that the extension of the definition of phenotypes shifts the focus from pure genetics to evolutionary theory as the rational for extending phenotypes is that more stuff than pure physiology contribute to fitness. That's not entirely relevant to the genotype/phenotype distinction but there is a great interview of Smith by Dawkins where he discusses a lot the history of genetics, evolutionary theory, and the socio-political debates behind it (link below).
So today some behaviors are widely, and I think uncontroversially, thought to have a genetic basis and therefore should be considered a phenotype. This is the second part of the disagreement between Remi.b and me (which derives from the first). If phenotypes must have a genetic basis, then how do you know that a behavior has a genetic basis or not? The gold standard is to show heritability of the trait in a twin-study. If the trait co-occur more in identical twins than fraternal twins, and/or in identical twins raised separately than expected from chance, then you know with confidence that this trait is partly genetically determined. Most famously, for example, this is known to be true for sexual orientation. So I am not saying that a phenotype can only be inherited. Obviously a random mutation is a phenotype but has not been inherited. But to show that a behavior is genetically determined I don't know how you can do that without showing heritability (but I'm not a geneticist so maybe there are other ways). Siddhartha Mukherjee's The Gene is a very good summary of the state of the art in that area.
So where does that leave us concerning phenotypes and tattoos? Well if you agree that behaviors should be considered phenotypes, such as courtship, nest-making in birds, aggressive displays in monkeys... Then I see no reason not to include tattoos in it. Any criterion you apply to "animals" should apply equally to humans. Some birds decorate their nests with flowers as part of courtship. The question left is whether it has a genetics basis or not, and I think you are very likely to find that getting tattooed would co-occur more than expected from chance in twins. Of course the tattoo is not genetically determined. It's probably something like open-mindedness, but a tattoo is observable and open-mindedness is not. This definition of phenotypes means that you can more or less already include quite a lot of things in it. So I can see why someone would disagree with extending the definition of phenotype beyond pure physiology. But clearly phenotypes must be linked to genetics otherwise the definition is purely meaningless.
Johannsen W. The Genotype Conception of Heredity. The American Naturalist 1911;45:129-159.
Dawkins, R. (2016). The selfish gene. Oxford university press.
Dawkins, R. (1982). The extended phenotype (Vol. 8). Oxford: Oxford University Press.
Tinbergen, N. (1951). The study of instinct.
Lorenz, K. (2013). The foundations of ethology. Springer Science & Business Media.
Smith, J. M. (1982). Evolution and the Theory of Games. Cambridge university press.
Wilson, E. O. (2000). Sociobiology: The new synthesis. Harvard University Press.
Siddharta, M. (2016). The gene: An intimate history. Scribner, New York, 9-9.
https://www.youtube.com/watch?v=0b0Nm_L3TKg&list=PLVV0r6CmEsFzJSvAc4MBuUP_GrjO1lLHp

I developed my answer quite a lot, but I'm still making the exact same point, just more clearly. I also included a short history of the notion of phenotype to explain why the meaning has changed and why it's still unclear what should or should not be included in it.

Standard definition of "phenotype"
The term phenotype is generally not clearly defined. Most often, textbooks will define a phenotype as any anatomical, morphological, physiological or behavioural observable characteristic of an individual. This definition is somewhat vague as it is unclear how far reaching the impact of the behaviour can be. To my knowledge, the only clear definition of a phenotype is its broadest definition as popularized in the book The Extended Phenotype.
The Extended Phenotype definition
In its broad definition, a phenotype is any manifestation in the world of the presence of a given genotype. I am unsure of the detailed presentation of this definition in the book but here is briefly my extended definition.
With the "extended definition", an individual phenotype is not limited to its body. Consider a bird nest as an example. In the "standard definition" only the bird building the nest has a phenotype, the nest itself in not part of that phenotype. With the "extended definition", the nest itself is part of the phenotype of the bird who built it.
With the "extended definition", an individual phenotype is not limited to its temporal existence. An individual can have much consequence to the world after its death. For example, the stoic philosophy of Marc-Aurel Caesar that has affected many people's life after his death is still part of Marc-Aurel Caesar's phenotype.
In short, imagine a world with and without an organism. The difference between these two worlds is the phenotype of that organism. Given the fantastic complexity and connectivity among events in the world, a lot of the world's properties can then be considered part of an individual phenotype.
Which definition is correct
Well, a definition is never correct or wrong. It is just a definition. But let's talk about clarity, uses and fit to theoretical models for both definitions.
Clarity
It is somewhat unclear what consequences of the genotype in the world are still included in the "standard definition" of phenotype. As such the "standard definition" is somewhat unclear.
Uses
For the vast majority of purpose authors use the term phenotype to refer to specific characteristics and therefore, the detailed definition does not matter.
Fitness of theoretical models
In theoretical work, the extended definition is the only definition that fully satisfy our models of ecology and evolution.
Phenotype and heritability
In a comment under the original post @Dirigible's said

No. Phenotypes are qualitative and quantitative characteristics that
arise from the interaction of an organism's genetics (genotype) and
the environment. There are no genetic determinants for tattoos. This
question lacks background research and I'm suggesting that it be
closed.

There might be confusion with the concepts of inheritance and of heritability here. Heritability of a given quantitative phenotype is the fraction of variance of this phenotype in the population that is explained by genetic variance (see this post for more info). If a phenotype (that has some non-zero variance) has no underlying genetic variance, then this phenotype is not heritable. But it still remain a phenotype.
By saying There are no genetic determinants for tattoos as a way to justify the No starting the comment, the comment sounds like (whether or not it was the poster's meaning) a phenotype is a phenotype only if it is heritable. I would strongly disagree with this claim.
More straight forward, @baca in his/her answer said
What would not be a phenotype is something that you could conclusively prove to have no genetics basis whatsoever.

Again, I disagree with this claim.
On top of that, I would argue that tattoos are very likely genetically determined. There are probably genetic determinants for liking tattoo. Probably for liking art in general. There are probably genetic determinants to joining gangs (such as loci affecting aggressiveness for example) that sometimes use tattoos as symbols of membership. There are skin conditions that prevent people from getting tattooed and some of these conditions are likely to be heritable.

A phenotype must have a genetic basis. That's the whole point. Otherwise it's just a normal, random, characteristic. To prove a genetic basis it must be heritable. Period. That's not up to discussion, it's the very definition of phenotypes, that were studied by Mendel without even knowing about evolution or genetics.

@baca I think you are confusing the concept of "heritability" and the slightly undefined concept of "genetic basis" or "inheritence". Something can be "inherited" without being "heritable" (at least by the commonly used quantitative genetics definition of "heritable"). You might want to have a look at this post (already linked in my answer). Also, some phenotypic variants may be caused by environmental factors (e.g. getting bitten by a predator).

If a phenotype has to be heritable then infection can’t produce a phenotype.  Neither could stress. In the literature we normally call the behavioral responses to such things phenotypes.

Absolutely, a phenotype may not be expressed, it also depends on the environment, we agree on that point. But it's still inherited. Otherwise, please, could either of you tell me what is not a phenotype? An infection can reveal an underlying genetics predisposition (like smoking inducing lung cancer), but without that genetic predisposition, which is heritable, then it's just what it is: an infection.

I've made some mostly minor grammatical changes that I hope improve readability. ——— Comments: 1) Your answer seems to end abruptly mid-sentence — did something get cut off? 2) Can you provide references for "In theoretical work, the extended definition is the only definition that fully satisfy our models of ecology and evolution." 3) No one else posting here has used "heritable" or "heritability", so I think that part of your answer may not be relevant ...

I might have been a bit too quick to accept this answer, since there seems to be some debate about its validity, so I've unaccepted it for now. Depending on the results of the discussion and such, I will accept it again later.


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Time scale for cAMP-dependent pathway cascades
What is the time scale for cAMP-dependent pathway cascades that start at the level of ligand binding to a G-protein receptor and finish at the level of gene transcription regulation?
For example, when corticotropin releasing hormone binds to CRH receptor 1, a cAMP-dependent pathway cascade is initiated, which ultimately leads to an upregulation in the transcription of proopiomelanocortin (POMC) mRNA.
I recognize that this is a very broad question, that is likely highly case dependent (i.e. different from receptor-ligand pair to receptor-ligand pair). Nonetheless, are we looking at several hundred milliseconds? Several seconds? Several minutes?
In the case of CRH, how quickly does CRH-CRH receptor 1 binding lead to the upregulated transcription of POMC mRNA?
If there are any good sources to read about this, I would greatly appreciate it!


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What is the energy required for storing and performing computations in synthetic computational biological cells?
I want to know the energy costs of various computations performed through synthetic biological circuits in terms of ATP. I am primarily interested in storing of bits, addition, and multiplication operation.
Though I am able to get various papers on half-adders and logarithmic analog addition, I find there is a lack of precise energy costs in these papers. Especially I am not able to find the energy cost of multiplication in any of the papers, though I believe that multiplication can be done by adding two logarithmic terms, but is this the only way available?
There is one paper that answers some of my queries: Analog synthetic biology by R. Sarpeshkar.
Here the author gives at least an idea about the number of ATP required for doing additions for a certain biological environment for both digital and analog scenarios and also mentions some facts about how increasing the precision of bits lead to increase in protein copy number.
But I need more such papers that deal with multiplication, storing of bits in cells and their energy requirements in terms of ATP.
Note that I am merely interested in having some literature that deals with computation and its energy cost, as most of the literature that I encountered doesn’t mention how much energy in ATP is consumed in performing certain computation in a given biological environment.

Biochemical systems use ATP to perform chemical reactions or other energy-requiring processes. Addition and multiplication are abstract mathematical concepts that can be mimicked in computers by specific circuitry. If you wish to do likewise in biology (synthetic or otherwise) you need to set up some system that can perform some chemical transformations. The energy cost of such transformations will depend on their specific physical nature. It is therefore nonsensical to ask in abstract the energy cost of this. You will have to get to grips with the biochemistry of specific systems. Good luck.

The reason you aren't finding this information in the literature is that this metric doesn't match the way that most genetic circuits work.
You appear to be thinking about operations in genetic circuits as being like instructions on an electronic processor. In that world, an instruction starts, executes, and stops, and you can measure the amount of energy consumed between the start and the stop.
Most genetic circuits, however, are more like wiring up electronic circuits like NOT and NOR gates. The computation is thus not discrete but continuous in time. One can certainly still consider the operating burden of each device on the cell, but (1) the load is strongly dependent on the particular state of the device (e.g., high output vs. low output), and (2) ATP availability is typically not the limiting factor.
Thus, your question is simply not one that most practitioners would find meaningful to answer. Even in the Sarpeshkar paper that you cite, by the time he gets to discussing actual experimental results, the numbers are expressed in terms of fluorescent protein concentration rather than ATP.
If you want to understand the burden of genetic circuits on cells, a much more relevant starting point is the recent paper "The Effect of Loads in Molecular Communications" from McBride, Shah and Del Vecchio

This addresses, rather than answers, the question; but is, I think, preferable to continuing to discuss the problem in comments.
As I understand it, the question deals with the use of genetic circuitry in synthetic biology to perform mathematical calculations in an analogous way to that done in computer systems. By genetic circuitry is meant the induction and feed-back regulation of transcription of certain engineered genes in the DNA of living (presumably bacterial) cells by protein molecules (together perhaps with small-molecule inducers). Such systems are modelled on natural bacterial operons.
While some of the users of this site may be familiar with synthetic biology of this type to produce bacteria with practical applications based on sensing environmental molecules, I imagine that very few will be familiar with their abstract use for mathematical operations. Certainly, although I subscribe to Nature, I had missed the 2013 article on this topic by Daniel et al. (Nature 497, 619–624), which it would take me some effort to master. Therefore the poster should not be surprised if his question has few takers.
Those who are interested or involved in synthetic biology are unlikely to have been concerned with the energetics of these circuits. Certainly RNA transcription involves the hydrolysis of phosphodiester bonds of nucleoside triphosphates, but one takes this as read, and assumes the bacterium will be in an environment where energy sources are available for growth.
Out of interest I glanced at the introduction to another paper involving Sarpeshkar — Philosophical Transaction of The Royal Society A (2014) 372 1–22 — and read the following:

Every living cell within us is a hybrid analog–digital supercomputer that implements highly computationally intensive nonlinear, stochastic, differential equations with 30000 gene–protein state variables that interact via complex feedback loops. The average 10μm human cell performs these amazing computations with 0.34 nm self-aligned nanoscale DNA–protein devices, with 20 kT per molecular operation (1 ATP molecule hydrolysed), approximately 0.8 pW of power consumption (10 M ATP s−1) and with noisy, unreliable devices that collectively interact to perform reliable hybrid analog–digital computation.

So it would appear that Sarpeshkar or others are citing the energy used per molecular operation taken apparently as 1 ATP equivalent needed for each NTP addition. (This seems to me incorrect, as the cleavage of NTP to NMP + PPi means 2 phosphodiester bond equivalents of energy are used.)
As far as I can see — and I may well be wrong — the answer to the poster’s question would seem to lie in learning how many molecular operations are involved in performing the particular mathematical operations in the systems described in these papers. I suggest he has more chance of discovering that by reading the papers and calculating how much RNA is synthesized in each operation — or even contacting their authors — than by asking on a general biology forum, like this.


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Help Finding Specific BlaZ Gene Type Sequences on Genbank
I am doing an undergraduate research project that involves blaZ gene typing for different strain types of Staphylococcus aureus bacteria; for reference, here are some of papers on this topic that explore resistance abilities of the blaZ gene and four different beta-lactamases that can be produced:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3421557/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC188454/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC106017/
Right now, I need to be able to align blaZ gene sequences in plasmids (or chromosomal regions, when looking at type B blaZ genes) of different S. aureus strains to the four blaZ gene type (A, B, C, and D) reference strains as mentioned in the first paper. The first paper provides the following strains as "reference strains": type A, PC1; type B, 22260; type C, RN98; and type D, FAR19. However, I can only find the nucleotide sequence for PC1 and the partial sequence for 22260 on Genbank; when I search for RN98 or FAR19, no relevant results come up. Even though these gene type sequences should only be distinguishable by several SNPs, it's important that I have references for all four for the most accurate strain typing.
In the last paper, I noticed they provide some of the differences between all four blaZ gene type nucleotide sequences, but not in a "from start to finish" order (i.e. the numbering above the nucleotides is not sequential and the sequence comparison length overall is less than 846, which is the length of the PC1 coding regions). Please advise, as after countless searches on Genbank I still do not have the specific sequencing information I need for each blaZ type.

The sequences from that first paper probably weren't submitted to any database. If you want those specific sequences, you could try contacting the corresponding author.

You might have already tried this, but how about doing a BLAST search using one of the sequences you do have, and perhaps limiting the organism to Staph a.
More info:
The below article did a similar comparison and mentions types RN9 and FAR10, perhaps these are related (or  misspelled originally)  See below.
"Real-Time PCR Assay for Detection of blaZ Genes in Staphylococcus aureus Clinical Isolates" at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993521/
mentions:
"type A, PC1(pI254) and NCTC 9789; type B, 22260 and ST79/741; type C, 3804(pII3804), RN9(pII147), and V137; and type D, FAR10"
In any case I highly recommend going to your original article of interest, and use the "cited by" function to find more recent papers.

Thank you! I tried this and a list of S. aureus strains with significant alignments were produced. Unfortunately none of them contained the reference sequence strain types as mentioned in the paper, i.e. RN98 or FAR19, but another paper I found gave some information on the types of differences (and number of differences) between amino acid sequences in each one, so I might be able to look into that as well for deducing sequence differences.


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Is osmosis diffusion of water?
My textbook says this:

Osmosis is the diffusion of water.

Wikipedia says this:

The diffusion model of osmosis is rendered untenable by the fact that osmosis can drive water across a membrane toward a higher concentration of water.

It's my understanding that diffusion is passive transport, and it moves material from a highly concentrated area of that material to an area where it is in lower concentration. By this definition, it looks like Wikipedia is correct. But if for example, a cell is put in saltwater, water from within the cell would go out. Is this diffusion now? Which definition is correct?
I would just go with the Wikipedia definition because it actively describes its own definition as a refinement of the textbook definition, but the paragraph above in the article is a bit confusing to me.

Have you tried reading the sources at the end of the article?

This question is off-topic for Biology. It seems like you understand the process of osmosis, and are just curious if it's also a kind of diffusion. The answer to your question is either going to be based in physics or in the semantics of various definitions.

you will likely have better luck in the chemistry stack as this is only tangentially connected to biology.

Yes, In most cases, osmosis is the diffusion of water. To my understanding, what I think Wikipedia is trying to do is to assert the fact that osmosis is also be the movement of water from a region of lower water potential to a region of higher water potential. These kinds of contradictions, as much as scientists try to avoid them, still come to play because science is very complicated. Just when we start accepting a theory, it gets discarded by another theory.

Welcome to Biology.SE! First, while this looks like it might be a good answer it is to a question that is off-topic for this site (because it isn't primarily a biology question) and it is better to leave such questions unanswered. Second, for future posts please note that answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

Osmosis is about solutions (solvent + solute).
Osmosis is a movement of the solvent through certain types of membranes. These membranes let the solvent move across them, but not the solute. The process tends to balance the solute concentration on both sides of the membranes.
If we say that the solvent is water and the solute is salt (NaCl). Water will move from the side of the membrane where the salt concentration is low toward the side where the salt concentration is high. At the end of the process both concentrations will be equal.
In biology it is a very important process at a cellular level (cell membranes are semi-permeable membranes) but also plays a key role in food digestion or kidney reabsorption, for instance. Cells (bacteria) that are put in solutions with high concentration of salt die of loosing the water they contain.

First, while this looks like it might be a good answer it is to a question that is off-topic for this site (because it isn't primarily a biology question) and it is better to leave such questions unanswered. Second, for future posts please note that answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Why is there a distinction between an *allergic* and an *immune* response?
Our immune system has evolved to protect us against potentially dangerous non-self particles. I have difficulty in understanding why there is a distinction called an allergic response: what’s wrong with using the term immune response full stop? Surely a person’s immune system should react to a particle of grass pollen in EXACTLY the same way as it does to a non-self protein expressed on cells of some transfused blood. The mystery that I absolutely don’t understand is why our body can then differentiate the scale of the response.

Doesn't an allergic response involve completely different mechanisms from immune responses?  Certainly at a high level we see much different effects, e.g. allergies involve histamines so we treat them with anti-histamines, while immune responses involve fevers & white blood cell production.

Have you found a satisfying response? I am curious of how difficult it is to find information on this, and this being the only question our of 2 in stack overflow asking this

The trouble is, you can't live without being exposed to all sorts of non-self particles. Some of those particles signal an actual threat to your health (proteins associated with a disease causing virus), some are nearly harmless (bee stings), some are completely harmless (grass pollen or cat dander), and some are potentially valuable as part of a food substance (seafood or peanuts). Ideally you'd like your immune system to respond to the harmful ones, and ignore the harmless or useful ones. An allergy is defined as an unneccesary immune response to a harmless (or nearly harmless) substance.
You do want your immune system to deactivate venom from a bee sting, but you don't want it to react so strongly that as a side effect your throat swells up and you can't breathe. Most people breath in grass pollen every day of their live with no ill effects, so those folks who have an allergy to grass pollen are being made miserable by their immune system to no good purpose.
Ideally the immune system mounts a full response only when the presence of particular non-self particles is associated with other signals indicating that something "bad" is happening which merits an immune response. However, the process by which the immune system is regulated is incredibly complex, involving feedback loops from hundreds of different chemical pathways and dozens of different cell types. The process is imperfect. Sometimes it goes wrong, and the immune system mounts an aggressive response to a harmless foreign substance or even worse part of your own body.

Thanks, Charles. That’s an interesting point you make that our immune system can somehow associate a non-self particle with any damage it causes (prior to any immune system mediated damage).

"An allergy is defined as an unneccesary immune response to a harmless (or nearly harmless) substance.". The problem here is that the immune response also seems to be different in the case of exposure to an allergen and a pathogen, which as OP points out, implies the body is "aware" one is harmful and the other is not..

Allergy is an exacerbated inflammatory reaction of the immune system in reaction to small quantities of foreign inert substances called allergens. It is a clinical condition characterized by its symptoms: redness of the eyes, ocular and nasal discharge, itching, eczema, asthma, headache, digestive disorders and swelling.
The most critical clinical manifestation is the anaphylactic shock that may lead to death.
The immune reaction is triggered by pathogens (viruses, bacteria, parasites) that have the ability to replicate within the body.
Both the allergy and the normal immune reaction share the same principle: a primary immune response where the immune system learn about the antigen/allergen, and a secondary immune response where it can unleash its full potential (too much in the case of allergy).


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What "algorithm" are carnivorous larvae using when foraging?
What algorithms are carnivorous larvae (lady bugs like Adalia bipunctata, Coccinella septempunctata, common green lacewing (Chrysoperla carnea) or hoverfly (Syrphus)) using as they are foraging for aphids?
Is it just random walk or something more efficient?

I'm going to assume that when you say algorithms, you mean the forms of innate behavior an organism may have relating to their senses (e.g. when sunlight is detected by a worm through the photoreceptors in their skin, it will move towards the opposite direction of the source of light to stay in their preferred environment).
These mentioned species of insects are very different taxonomically, but their number of sensory organs are for most part similar including during larval stages.
Examples of innate behavioural responses seen in invertebrates include taxis and kinesis.
Taxis is a change in movement in response to an environmental stimulus – either towards (positive) or away (negative)
Kinesis is a change in the rate of activity in response to an environmental stimulus
So, when talking about rough algorithms, when a larva detects a particular stimulus (e.g. chemicals of prey via chemoreceptors),  The organism will either have a 1 or a -1 value for Taxis response (e.g. it runs towards or away from the prey), and a rate of activity relative to taxis which represents kinesis (e.g. it gradually moves faster towards the prey as the chemical stimulus becomes stronger (meters per hour for example).
So, you could say that the theoretical formula/algorithm for hunting prey relating to the chemoreceptors as an example would be:
Taxis ('1' or '-1' to symbolize moving towards or away from a prey) multiplied by the number of 'prey' chemicals received by the chemoreceptors equaling the strength of the larva's response which could be (as an example) translated to the velocity of larva
Of course all the other senses such as photoreceptors and the chordotonal organ (vibration sensor) must be considered and I couldn't find any actual algorithm for how these species hunt. This is just a way to percieve how insects both in and past their larval stages respond to stimuli through their innate behaviour.

By "Algorithm" I mean: Suppose you want to implement an algorithm on a computer that indistinguishably mimics the animal's behaviour provided they get the same input information, i.e. no mathematical / statistical analysis (or other mathematical approaches for that matter) is able to distinguish the outputs of either algorithm. Given such a setting, what algorithm will the programmer get? Just random walk with specific average path length (which may depend on the habitus of the plant being foraged on) or something more or less efficient, and what algorithm is it specifically?

Are you saying that it's not known what algorithm(s) -- with "algorithm" according to your definition or my definition from my other comment at your disposal) -- these animals are "using"? Is it a (current) research topic?

Unfortunately I am not experienced enough to know whether there is an algorithm that can "indistinguishably mimic an animal's behaviour provided they get the same input information" Animals in general have so many senses and chemical reactions that determine what they next action will be. As far as I know, perfectly simulating most if not all organisms is currently not an achieved goal as of yet.
If it's any help... larvae usually wonder randomly at a more or less steady pace until they sense the chemical signature of a prey/food.


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Regarding the role of enzymes
Textbooks commonly state that the role of enzymes is to speed up a chemical rxn by lowering its activation energy.
However, I'm unsure what enzymes like helicase, DNA/RNA polymerase, and restriction enzymes have to do with lowering the activation energy. Isn't helicase's primary role, for instance, to unwind double-stranded DNA?

What is the problem with the enzymes you mention? They all catalyse chemical reactions which have activation energies. Those for polymerases should be self-evident. If you are unaware of the reaction catalysed by helicases, consult the relevant Wikipedia page, for example.

All reactions require an amount of energy to proceed called the activation energy. Enzymes lower that activation energy through various means. An example here is the unwinding of the double-stranded DNA requires breaking hydrogen bonds. Energy needs to be supplied for the reaction to proceed. The rate of the reaction can be  described by Arrhenius' equation

You can increase the rate of the reaction, or decreasing the activation energy. Enzymes are required to do that at physiological temperatures by lowering the activation energy, because increasing the temperature is usually not an option.
The enzymes you mentioned are no different.

Helicase also hydrolyzes ATP.

Your answer seems to me misleading. Whether a chemical reaction requires energy or releases it is irrelevant to the requirement for an enzyme. Both types of reaction have an activation energy barrier to overcome. What is pertinent is that it is a chemical reaction which helicase catalyses — as has been mentioned, one involving the hydrolysis of ATP.

Yes, an amount of energy is needed to overcome the activation barrier. Mentioning that helicase requiring ATP doesn't contribute anything to the answer.

Since some might not consider the breaking of hydrogen bonds in DNA to be a chemical reaction, it might not then be immediately obvious why helicase is considered an enzyme without accounting for its hydrolytic activity.

@canadianer — Strictly speaking I gather that it is a process in which chemical energy is converted into mechanical energy like other molecular motors. I’m not an expert on such, but it would seem to me that whatever the molecular details of this conversion, there must be an energy barrier for an enzyme to be required. However, if we throw out the nonsense about polymerases from the question, it may be worth considering helicases alone and in detail. As I have already said, I think this answer is bad as it suggests that an enzyme is needed because the process has a positive delta G.


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Are there any DNA viruses with junk DNA in them?
I know mimiviruses and pandoraviruses have orphan DNA - DNA that is not found in other species - but this is DNA that codes for proteins. I am not able to find out if they contain junk DNA. By junk I mean DNA that does not have ANY function at all. Sort of like the junk DNA in the human genome put there by retroviruses, DNA that just sits there, doing nothing, just going along for the ride.

The terms junk DNA and non-coding DNA mean very different things. Non-coding DNA would include the part of a promoter that binds RNA polymerase but is not transcribed and other similar and regulatory regions that bind proteins (and also strictly speaking the parts of a gene that encode the untranslated regions of a mRNA transcript). Junk DNA can be taken to mean functionless DNA, although that begs the question whether it is DNA that has a function that has not been elucidated. Could you please clarify what you mean and amend your title accordingly.

To help get an answer to the "junk" part of your question, you might be interested in a similar question I asked about parasitic code in viruses: https://biology.stackexchange.com/questions/92829/do-any-known-viruses-contain-junk-or-parasitic-genomic-information

I should have been clearer. By junk DNA I mean functionless DNA that is known to do nothing. Not promoter regions or regulatory sequences. On a related note, are there retroviruses that infect other virues - that insert their own code in the code of a bigger virus? If so, can some of this code get deactivated or mutated over time to become functionless?

Best not to use the word code for genomic DNA. First because of the confusion with the genetic code, which is a cypher; second because you’re interested in non-coding DNA. How can you envisage a virus infecting a virus? Think about the nature of viruses. And if you include transposons as junk DNA you are stretching things as they encode the ability to transpose themselves.

Viruses typically don't have junk DNA-so to speak because of their tiny size. When the particles (of virus) are so small, there really isn't any space for "junk" or extra DNA.
That being said, while viral DNA replication, there may be some errors that may make the virus DNA unable to code for proteins or "junk". While this is an interesting proposition, the mutations that occur in almost cases do not make non functional proteins but mutated proteins which make the viruses more virulent (more true in case of RNA viruses...which mutate a lot faster).
Regarding virus infecting virus, putting its own code it "kind of happens" but not as you would expect. I am listing 2 such examples here-

There are some viruses called satellite viruses and viroids which depend on "donor" larger viruses for some of the proteins they need for replication. This means a satellite virus can survive in a host only if the donor virus is present.

In animals like pigs, when different strains of Influenza virus infect together, while virus assembly genetic material (RNA) of one strain can enter into the other....creating completely novel strain.

Hope that answers your question. Please feel free to ask for clarification. Thank you and have a nice day.


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Is evolution the reason why water is colourless for our eyes?
Liquid water is transparent to most of the visible spectra, whereas it absorbs infrared.
Similarly, the air is almost transparent to the visible spectra too.
Could these be the reasons why our eyes evolved to "see" the visible spectra, and not IR or UV?
(Also, are there other animal species for whom water is not colourless?)

Human eyes are too big to see UV. Animals that can see UV have eyes of a few millimeters. Frogs and snakes are vertebrates that can see IR using an enzyme related to vitamine A, althouth mammals mostly just see color. Sea mammals only see green. The most recent photoreceptor change in primates is the acquisition of red photoreceptors to see fruit in trees, so we can't say that changes in vision have co-incided with their investment in marine and riverine environments.


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Is there an antidote for caffeine, e.g. as a supplicant for caffeine-intolerant persons?
First, let me state I'm not talking about a medical emergency. No one is in a serious condition.
My girlfriend is, we think, caffeine-intolerant. She loves the smell of coffee and the habit of coffee drinking, so naturally she risks drinking caffeinated beverages every now and then, even knowing she'll suffer. She experiences the regular effects of coffee, but they are uncomfortably strong and last much more time than usual. We've read that it's because her body metabolizes caffeine slowly, likely due to a gene mutation. We think it's not caffeine allergy.
We were wondering if there's kind of an antidote, a molecule which metabolizes or deactivates caffeine specifically. Then one example use could be

drink regular coffee;
wait some time (e.g. half an hour);
take a pill to take care of the excess caffeine in your bloodstream.

We're asking mostly out of curiosity - she's not that addicted to coffee as to actually take pills just to be able to drink it. The real (bio-chemical) question is - can an antidote, which targets a this very specific molecule, be actually manufactured? Or is it that it's not researched purely because of market size reasons?

Why not just drink de-caffinated coffee?

@CharlesE.Grant, she still gets some of the symptoms if she drinks decaf e.g. three days in a row. We think the prolonged exposure to even relatively small amounts of caffeine is what's bugging her.

Is it that it's not researched? Probably this. I've looked through literature and there seem not to be any references to any things studied which may sequester or adsorb caffeine, save for activated charcoal. People with hypersensitivity to caffeine usually have a gene variant which is involved in metabolizing caffeine in the liver. Aside from a hypothetical gene therapy, the best course of action would be to avoid it, especially if she is not in any way addicted. Can an antidote be manufactured? Yes, it is almost certainly possible, though I don't think it'd be profitable nor advisable.