text:
What do oxpeckers eat from thick-skinned hippopotamuses and rhinoceroses?
Noted for their thick skin are both rhinoceroses (1.5 to 5 cm) and hippopotamuses (6 cm).  They are further noted for their symbiotic relationship with bird called an oxpecker:

Both the English and scientific names arise from their habit of perching on large mammals (both wild and domesticated) such as cattle, zebras, impalas, hippopotamuses, or rhinoceroses, and giraffes, eating ticks, small insects, botfly larvae, and other parasites.
Oxpecker, Wikipedia

I feel like the thick skins of rhinoceroses and hippopotamuses would make them invulnerable to many parasites (such as those listed above), so I'm interested in finding out more specifically what oxpeckers eat from the skin of these two mammals.
Question: What do oxpeckers eat from thick-skinned hippopotamuses and rhinoceroses?
In the case of hippopotamuses, I feel like their semi-aquatic lifestyle would further impact many parasites.

I think you should (re)read that Wikipedia article — later on it says "They feed on ectoparasites, particularly ticks, as well as insects infesting wounds and the flesh and blood of some wounds as well. They are sometimes classified as parasites, because they open wounds on the animals' backs." There are also numerous references at the end of that article including at least one about rhinos ...

Thanks!  I admit it, I didn't read that part of the Wikipedia page prior to posting.  Although I'm still uncertain as to how oxpeckers use them as a source of ticks despite their thick skin, and, in the case of hippopotamuses, being submerged for large amounts of time.

That's the point — they appear to primarily use them as a source of blood. Think of them as little feathered vampires.

many is not the same as all


text:
Does the 'President' have 2 Billion Leaves?
The world's second-largest known tree, the President, in Sequoia National Park is 3200 years old and is said to have 2 billion leaves (Source: https://youtu.be/vNCH6uhB_Bs?t=59).
Is this correct? And how was this number arrived at?
In other words, how is such an insanely large number possible?

The US National Park Rangers count them. But that makes it a mathematical question, not a biological one, so it should be obvious that it is off topic here.

Strictly speaking, S. giganteum is a conifer so it has needles, not leaves. So count the individual needles on one twig (they're really small), multiply by the number of twigs per branch and the number of branches on the tree.

@David That number was obviously not 'counted'. It was arrived at by an estimate based on botanical facts.

@jamesqf Thank you! That explains the huge number which was my primary curiosity. Could you please add it as an answer so that I can accept it?

If you know the answer, why ask the question?

@David I want to know what botanical facts made that estimated number so huge.

Botanical facts? I imagined they extrapolated from the empirical observations of the numbers of leaves per branch and the number if branches per metre rise in the trunk, allowing for the pattern of sub-branching. But it is hardly a question of biological principle. As I have indicated, it may be answered by some general mathematical formula, if you plug in the constants. A good scientific exercise, but not a question likely to find interest or answer here, I would imagine.

@Ritesh Singh: Because it's not an answer, just my guess at how that number might have been arrived at.  I don't know how whoever did that video got their number...

@jamesqf It is closest to an answer. My main question was how is such an insanely large number possible.

@RiteshSingh, I upvoted your question. As a physicist that's a member of a lot of Stack exchanges, I wonder if you could help us by committing to the Materials Modeling proposal? We really need help, and would very much appreciate if you could commit!

@user1271772 Done sir/madam, Thank you! :)

@user1271772 Also recruited a few friends to commit to it :)

@RiteshSingh! Thank you so much !!!!!!

One way* to come up with an estimate of how many leaves - or needles, in the case of Sequoiadendron giganteum - is simply to count the number of leaves on a twig (or a number, to get a good average), then the number of twigs on a branch, and then count the branches on the tree, after which it's just multiplication.
Now one reason that the number seems so high is the way the needles grow.  Unlike for instance pines, which have long needles arranged in sparse clusters of 2, 3, or 5, or spruce & fir, which have medium needles arranged along the branches, the sequoia has lots of tiny needles arranged on twiglets.
Link with picture of sequoia needles: https://www.monumentaltrees.com/en/trees/giantsequoia/giantsequoia/
Picture of pine vs spruce & fir: https://www.finegardening.com/article/fir-vs-spruce-vs-pine-how-to-tell-them-apart
*But I don't know whether it's the way used to get the number in the link.

Thank you for the pics. This answer completely satisfies by curiosity! :)

source: Stack Exchange

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

sort: votes


text:
Is molecular oxygen (O₂) consumed in any process (in humans) other than acting as an electron acceptor for the ETC?
I know that molecular oxygen (O2) serves as the electron acceptor in Complex IV of the electron transport chain, which maintains the proton gradient that produces ATP for, as far as I know, every cell in the human body.
Is this the only reason we need molecular oxygen for life, or are there other vital functions (i.e. necessary for life) that molecular oxygen serves within the human body?
Edit
For clarification, there are probably well over a million oxygen-containing compounds, from water all the way up to the largest proteins, which perform repeatable roles in basically every system of the body. But in cases where oxygen is exhausted, specifically consumed requiring a continuous supply of new oxygen, what roles does oxygen serve with the exception of serving as electron acceptor in Complex IV of the electron transport chain?

Are you asking about molecular oxygen, rather than all the roles of oxygen containing compounds? I'm not sure why you're getting the downvotes, but maybe clarifying this will help you get a more favorable response ...

@tyersome The original intention was to capture purposes served that consume oxygen in a one-off process, rather than incorporating it into components that can be reused. The significance here is that the vast majority of the oxygen balance in the body will go into processes that consume oxygen, rather than incorporating it. Yes, oxygen-containing compounds will eventually degrade or be removed from the body and require replacement, but in studying oxygen balance, it is these consuming processes that hold the most sway, and I'd like to gain a better understanding of these processes.

So, would it be accurate to say that the question you want to ask is something like:
'Does molecular oxygen (O₂) have any roles other than as an electron acceptor for the ETC?'

@tyersome Not necessarily, because molecular oxygen can be transformed before it is consumed in a different form, so that would be just slightly too specific a phrasing

OK, but the question as written isn't specific enough since it would seem to include  roles of water (and almost every biomolecule since they mostly contain oxygen) — i.e. all of biology! ——— How about: 'Is molecular oxygen (O₂) consumed in any process other than by acting as an electron acceptor for the ETC?'

@tyersome Works for me! Feel free to make the edit so you get the credit

Molecular oxygen also has roles in antimicrobial defense1,2. Specifically macrophages use O2 to create cascades of reactive nitrogen intermediates (RNI) and reactive oxygen intermediates (ROI; aka ROS) — these compounds have antimicrobial effects.
The RNI cascade starts with nitric oxide (NO) and is catalyzed by a nitric oxide synthase, which converts arginine and O2 into citrulline and NO.
The ROI cascade starts with superoxide (O2•-) and is catalyzed by a NADPH oxidase, which transfers an electron from NADPH to O2 creating superoxide.
Figure 1 from2 gives an overview of these reactions:

Legend for figure 1:

ROI and RNI production in mammalian cells via phox and NOS: parallel but connecting paths. Nitroxyl anion (NO−), a one-electron reduction product of nitric oxide (•NO), is unlikely to arise from •NO under physiologic conditions, but is considered by some investigators to be a primary and more toxic product of NOS. Reaction of RNI with cysteine sulfhydryls can lead either to S-nitrosylation or to oxidation to the sulfenic acid, as well as to disulfide bond formation (not shown), all of which are potentially reversible. Peroxynitrite anion (OONO−) and peroxynitrous acid (OONOH) have distinct patterns of reactivity, but for simplicity, the text refers to both as peroxynitrite. OONOH spontaneously decomposes via species resembling the reactive radicals, hydroxyl (OH•) and/or nitrogen dioxide (•NO2). When L-arginine is limiting, NOS can produce superoxide (O2⨪) along with •NO, favoring the formation of peroxynitrite.

References:
1: Weiss, G., & Schaible, U. E. (2015). Macrophage defense mechanisms against intracellular bacteria. Immunological reviews, 264(1), 182-203.
2: Nathan, C., & Shiloh, M. U. (2000). Reactive oxygen and nitrogen intermediates in the relationship between mammalian hosts and microbial pathogens. Proceedings of the National Academy of Sciences, 97(16), 8841-8848.

This is very interesting. However the text under the figure makes the figure itself unreadable on my phone. Could you possibly separate the two?

@David — Gladly. Does this work better?

Yes. That’s fine. Thanks.

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


text:
Are hormones antigenic?
I have been asked whether hormones are antigenic.
I would have to think that the answer is no because they are used as various drugs such as FSH in infertility treatments without the need of immunosupressants.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, you would benefit from reading up about antigens.  ——— In general, 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). Thanks!

Where did your question come from? Are you sure you are quoting it correctly? Both testosterone and insulin are hormones, but they are very different in size, which influences their antigenicity. And my phrasing of the last sentence was deliberate, we don’t talk about molecules having antigens, but being antigens or having epitopes, and the question is generally whether they are recognized as foreign antigens by species other from those in which they originate. So you need to try to get the question clear, before you or anyone else can attempt to answer it.

Hormones have antigens.  Usually they are antigens our immune systems recognize as self.
Pretty much any big biological molecule will have antigens.  FSH is no exception.  The binding of FSH to anti-FSH antibodies (in a laboratory system) is one way to measure FSH levels in a human.
 Definition and Measurement of Follicle Stimulating Hormone

B. High-affinity binding assays
  1. Immunoassays. Immunoassays are widely used for clinical determination of FSH for diagnosis and in physiological studies
  because they are rapid, readily available, relatively cheap, and
  sensitive... Most commercially available assays are now based on
  sandwiches of monoclonal or monoclonal-polyclonal antibodies with a
  variety of detection modes and are generally more sensitive and
  precise than one-site assays. The latter assays are highly specific
  and may exclude some forms of the hormone of interest (e.g., Ref.
  176).

The antibodies used to measure FSH are from other species of mammals - usually mice but sometimes other animals. People (and other animals) normally do not form antibodies to molecules that have been present in their bodies since development.  The immune system is educated early on about what is self and so exempt from attack.  Mouse FSH is antigenically different enough from human FSH that mice can be induced to form antibodies against human FSH and then those mouse antibodies are used to make the lab test.   You can find out how those tests work with a little googling because they are for sale and their owners will brag about them.
It is possible to form antibodies against your own FSH or any other biomolecule in your body.  That is autoimmunity and usually that is not good.  The woman in the linked article was infertile because of antibodies against FSH.  Her FSH level was very high because her pituitary was cranking it out.  Her immune system bound it up as fast as it came out and so the FSH did not work.
Abnormally Elevated Follicle-Stimulating Hormone (FSH) Level in an Infertile Woman

We describe here a case of anti-FSH autoantibodies leading to
  persisting very high FSH serum levels in an infertile woman.

Bullet points

Any biological macromolecule has antigens.
The immune system may tolerate antigens it has been educated to recognize as self.
Sometimes the immune system becomes intolerant of an antigen it should recognize as self and attacks that antigen.  This is autoimmune disease.

As I mentioned in my comment on the question, we don't usually refer to molecules having antigens, but being antigens. We do refer to cells having antigens as they have macromolecules on their surfaces. You can easily check this by doing a Google search for "have antigens". It would be helpful to the poster and others to edit has question and your answer in this respect.

Antigenic sites are generally referred to as epitopes. They are not the same as antigens, which term is used to refer to the macromolecule with such site(s). Argue all you like, but scientific communication involves using, and introducing people to standard terminology that allows them to express ideas with precision in a way that is understandable to others. Not correcting novices for fear of offending them is selling them short


text:
Hollow stalks in celery
When cutting a section of a celery plant stalk it appeared hollow inside, i.e. the cortex was hollow and encircled by the cambium, the vascular bundles, some cortex and the epidermis layer, thus the structure appeared similar to the celery stem's one and to the one of many other vascular plants, but the cortex. I have struggled to find answers on this topic: the cortex has a pivotal structural role, since it becomes turgid and keeps the plant straight, not to mention its water storing properties. Then why would it be so thin in such an important part of the plant, (stalks develop into leaves)?

Can you post a picture of what you observed? ———
I've never seen a celery plant that had been allowed to develop branches, so I suspect you are talking about the petioles ("stalks") of the leaves. If so, it would be clearer if you edited your question to use the correct terminolgy ...

Celery is a wetland plant, and likes to have a constant supply of water. Other vegetables can "bounce back" after experiencing a short drought, but celery  usually has more difficulties. If the plant is young during reduced water, it typically will become dwarfed, and fail to grow to full size. If the plant is older, it will develop defects, and suffer long term damage such as what you have described.
Defects are also possible if the celery does not have sufficient micro nutrients, or if the weather is very warm during growth.
In short, this is caused by non-ideal growing conditions of the celery. The celery was stressed to a point where it sustained damage that it could not repair. Celery is one of the more difficult crops to grow because of how finicky it is to drought.
Sources:
-https://www.gardeningknowhow.com/edible/vegetables/celery/why-celery-is-hollow.htm
-https://harvesttotable.com/celery_growing_problems_troubl/
-Personal experience trying to grow celery

Welcome to Biology.SE! This sounds very reasonable, but your answer is much more likely to receive a favorable response if you [edit] it to include supporting references (primary literature is best, but a textbook or other authoritative source are acceptable). Without this your answer is indistinguishable from opinion and make it impossible for non-experts to verify your assertions. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


text:
What is the probability that a gamete will only contain father's chromosomes
As it is depicted in most textbooks, cross-over does not occur between the two "outer" sister chromatids. By independent assortment during Meiosis I, there is 1/2^23 chance that all father's chromosomes, with one pure father's chromatid, will end up in the same daughter cell. Does this mean that roughly one in eight million people does not have any genetic material from one of his grandparents or is there some more independent assortment during Meiosis II, which makes this outcome extremely unlikely? (more like 1/2^46)
More generally I would be interested in the probability that a gamete will contain more than 60% ,70%, 80% ... of only one of your parent's genes.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, it would be helpful if you could be clearer about what you are asking — for example, it seems that you sometimes use parent when you really mean grandparent. Thanks!

In organisms like humans it is VERY rare for sister chromatids not to undergo at least once crossover. You may want to look into the term obligate crossover. It's not entirely clear from your question, but your reference  to 'two "outer" sister chromatids" makes me wonder if you are confusing a convenience in drawing an illustration with a biological fact.

So if I understand it correctly, it is very unlikely that any of the four chromatids in the tetrad will remain unchanged after the crossover occurs, right?


text:
Are there any known microbes capable of living in almost pure carbon dioxide?
Some bioengineering is investigated in high carbon dioxide environments. Are there any microbes like bacteria or Archaea capable of living and multiplying in such environments?

It is not speculative to ask if a microbe can live in almost pure carbon dioxide.

@DavidJonsson Thank you for the edit, it improves the question immensely. In the previous form I would have certainly agreed with Willk.

Do you mean an atmosphere of co2/nitrogen like Earth had prior to the evolution of photosynthesis?  Presumably most of the bacteria from those days would be ok with a more or less pure co2 atmosphere, at least assuming they had access to water.

This is a much better question now! I think this could be even clearer if you made the 'Title' match the 'Body'. For example getting rid of the "almost pure" (which makes it sound like you're looking for something that can live on "dry ice" or in supercritical liquid CO₂) and being more specific — for example it seems like you might be interested in anoxic (oxygen free) environments ...

Also, are you only interested in organisms that are considered to be "extremophiles"? I found references to a non-extremophile that grows under Mars-like conditions ...

These aren't technically extremophiles, but one paper identified twenty species of bacteria that grow under a low pressure, mostly CO₂ atmosphere1.
One relatively well studied species is Serratia liquefaciens (a Proteobacterium) that has been shown to grow under

low temperature (0 °C), low pressure (0.7 kPa), and anoxic, CO2-dominated atmosphere-conditions intended to simulate the near-subsurface environment of Mars2.

References:
1: Schuerger, A. C., & Nicholson, W. L. (2016). Twenty species of hypobarophilic bacteria recovered from diverse soils exhibit growth under simulated martian conditions at 0.7 kPa. Astrobiology, 16(12), 964-976.
2: Fajardo-Cavazos, P., Morrison, M. D., Miller, K. M., Schuerger, A. C., & Nicholson, W. L. (2018). Transcriptomic responses of Serratia liquefaciens cells grown under simulated Martian conditions of low temperature, low pressure, and CO 2-enriched anoxic atmosphere. Scientific reports, 8(1), 1-10.

Capnophiles (from the Greek kapnós, meaning smoke) are organisms that thrive in the presence of high concentrations of CO2.  Some of these organisms have a metabolic requirement for CO2.
Many organisms present in the cow rumen are capnophiles by necessity, as CO2 is the major gas product of rumen fermentation (66% by molarity 1 ).  One such organism is Mannheimia succiniciproducens, which was shown to thrive in a pure CO2 atmosphere when compared to pure N2 and equimolar H2:CO2.

Under N2 atmosphere, cell growth and glucose consumption rates were much lower, suggesting that M. succiniciproducens, like other capnophilic bacteria, relies on a CO2-dependent metabolism. The glycolytic flux under CO2 was four times greater than that obtained under N2.
...
When H2 was present, cell growth rate and the glycolytic flux were lower. However, the relative succinic acid flux increased by 30% under CO2-H2, and the relative formation rates of ATP and NADH were higher in the presence of H2.

Many pathogens are capnophiles, including species of Campylobacter 2, Neisseria gonorrhoeae 3, and Haemophilus influenzae 4, though ideal culture conditions for these organisms call for CO2 concentrations around 5 - 10%.

References

Hong SH, Kim JS, Lee SY, In YH, Choi SS, Rih JK, Kim CH, Jeong H, Hur CG, Kim JJ. The genome sequence of the capnophilic rumen bacterium Mannheimia succiniciproducens. Nat Biotechnol. 2004 Oct;22(10):1275-81.
Dykes GA, Moorhead SM. Survival of Campylobacter jejuni on vacuum or carbon dioxide packaged primal beef cuts stored at −1.5 °C. Food Control. 2001 Dec;12(8):553-7.
Platt DJ. Carbon dioxide requirement of Neisseria gonorrhoeae growing on a solid medium. J Clin Microbiol. 1976 Aug;4(2):129-32.
Langereis JD, Zomer A, Stunnenberg HG, Burghout P, Hermans PW. Nontypeable Haemophilus influenzae carbonic anhydrase is important for environmental and intracellular survival. J Bacteriol. 2013 Jun;195(12):2737-46.


text:
Relationship between immunologic response to specific gluten epitopes and clinical antibody testing
Celiac disease is understood to be an immune response to certain proteins which occur in a group of cereals; most commonly they are glutens (wheat), secalins (rye) and hordeins (barley). A clinical test for celiac examines serum levels of two specific antibodies: Deamidated Gliadin peptide Ab IgG and Tissue Transglutaminase Ab IgA.
Is it possible to test positive for the above antibodies while being sensitive (raise an immune response) only to hordeins?
There are two components to this question:

Can a person be sensitive to hordeins while being unaffected by either wheat gluten or rye (secalins)?
Would the above test produce a positive result given only hordein-specific antibodies? In other words, is the test specific to wheat gluten antibodies or will antibodies to any gluten epitope produce a positive result?

The reason behind this question in a short case history:

Mature adult subject experienced mild/intermittent IBS symptoms, onset vaguely extending back several years. Diet notably included regular/daily consumption of wheat/rye products as well as intermittent (2-3/week) beer (barley).
Recent clinical screening for celiac (serum levels of Deamidated Gliadin peptide Ab IgG and Tissue Transglutaminase Ab IgA) performed to investigate cause of suspected osteoporosis; both antibody levels assessed as positive.
Symptoms apparently abated within about one week following an initial dietary change successfully removing only barley gluten (beer), while regular consumption of wheat/rye continued.

Observations suggest a specific response only to barley, and raises the question about specificity of the clinical antibody test.

You might find this answer to a related question to be of interest — it doesn't address celiac directly, but it does answer the first part of your question.

@tyersome it does help with general understanding. Still hoping for an on-point answer to reconcile some specific facts and observations.

I would recommend editing your question to focus on the IBS specific portions — since you already learned the answer to 1. and 2. I recommend rewriting your post to include that information and delete extraneous material. (The website keeps track of edits so you don't need to have an 'Edit' section.) This will show people that you have done your research and allow people to focus on what you still don't know, rather than getting distracted by questions for which you already know the answers. ——— Specifically, I would delete anything not relevant to understanding your final paragraph.

@tyersome Thanks for the suggestion; hope my latest edit does the job

You're welcome — this is much better! (+1) It's great that you've put in so much effort to improve your question. The only other suggestion I can make at this point is to include references for the background statements you make. In particular, references that describe the basis for the clinical tests might allow someone with the correct background to rapidly come up with an answer for you. This also provides a resource for other users and documents all the work you've put into your question! ——— I hope you get a good answer soon.

1) Can a person be sensitive to barley hordeins, while being unaffected by wheat gluten or rye secalins?
Possibly, but I haven't found a documented case.
According to What is gluten? (Journal of Gastroenterology and Hepatology, 2017):

A variety of sequences from α, γ, and ω gliadins, as well as from the
  glutenins, have been identified to activate coeliac disease. However,
  several hundred gluten peptides are predicted to be immunogenic and
  trigger the T-cell mediated response.6 The most immunodominant T-cell
  epitope is from α gliadin, although T-cell cross-reactivity against
  gluten-derived, secalin-derived, and hordein-derived peptides have
  been confirmed. Additionally, within each grain, there exists a
  distinct hierarchy of immunostimulatory gluten peptides.6 Of all the
  peptides known to stimulate the T-cell response in coeliac disease, a
  given patient may react to only a few.

However, according to Coeliac disease: immunogenicity studies of barley hordein and rye secalin‐derived peptides (International Journal of Experiemntal Pathology, 2016):

In conclusion, barley hordein and rye secalin appear to contain CD
  toxic epitopes that are found in wheat gluten, as demonstrated by the
  observed cross‐reactivity of CD‐derived gluten‐sensitive small
  intestinal T‐cell lines to wheat gliadin, barley hordein and rye
  secalin‐derived peptides.

2) Are the blood tests specific to wheat gluten antibodies?
I can't say for deamidated gliadin peptide Ab IgG test, but tissue transglutaminase antibodies IgA test (anti-tTG IgA) is not specific for wheat gluten; antibodies can be triggered by wheat gliadins, barley hordeins and rye secalins.
Gluten peptides (gliadins, hordeins, secalins) bind to tissue transglutaminase which deamidates them. Individuals with celiac disease have HLA DQ2/DQ8 dendritic cells, which present deamidated peptides to T cells, which stimulate B cells to produce antibodies against tissue transglutaminase:

In CD, deamidation of gluten by tissue transglutaminase (tTG) in the
  small-bowel lamina propria promotes presentation of gluten peptides
  (gliadin in wheat, secalin in rye and hordein in barley) by
  HLA-DQ2 or HLA-DQ8 dendritic cells to pathogenic local CD4+ T
  cells...The most widely used serological test is anti-tTG IgA
(Medscape)

3) Can barley affect the gut differently than wheat?
Possibly.
Nutrition and Celiac Disease (Nutrients, 2014):

There is very limited data looking at the effect of barley hordein or
  rye secalin on CD outcomes in the published literature (e.g.,
  [66,67]), but evidence exists that these prolamins induce effects
  different to wheat gluten, at least at an immunologic level.

4) Do positive DGP and TTG test confirm celiac disease?
The specificity of IgG deaminated gliadin peptide (DGP) is 98% and of IgA tissue transglutaminase (TTG) 95% (American Family Physician, 2014), so when both tests are positive, celiac disease is very likely. The final diagnosis is by histological examination of a tissue sample obtained by duodenal biopsy.
5) Is it possible that, in celiac disease, symptoms disappear after removing only beer, but not wheat and rye from the diet?
It could be possible to have celiac disease confirmed by blood tests without any symptoms despite consuming wheat, barley and rye. Beer could trigger symptoms by irritating the bowel, not by gluten, but by alcohol or other substances, like in people with irritable bowel syndrome (American Journal of Gastroenterology, 2013).

Thanks for the comprehensive answer. I was hoping for a more definitive answer, but this is very helpful and useful info.


text:
Are junk DNA's mb also counted when it is stated that human DNA contains 3mb?
The human DNA molecule (chromosome) is about 2 meters in length. See here. We have 46 of them so in total 92 meters (imagine we would place all our DNA in a row...)
In this article it is said that the Protopterus Aethiopicus (a.k.a The marbled lungfish) has the most base pairs (about 133mb vs about 3mb of the human genome) of all living beings (flora and fauna) residing in the DNA of its cells.
That's a huge difference! That's why I ask if junk mbs are accounted for too in the 3mb in human DNA.

Some notes and suggestions: 1) A diploid human genome is ~6.4 megabases in length — bases are not bits. 2) The relationship between DNA bases and genes is similar to that between letters and sentences — you will get a better response if your questions don't conflate these concepts. 3) Please don't refer to "junk DNA" — this is a misleading and inaccurate term. 4) You won't find a (reliable) source for your claim that human DNA contains the most "junk" because it isn't true! ——— I encourage you to make the time to understand the basics of genetics and molecular biology. ...

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. There are also online platforms called MOOCs that offer free (or very low cost) courses on a wide variety of subjects — two that 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.

@tyersome Information is measured in bits (or bytes). Not in bases. Well, you can assign one bit to one base, but basically this is the same. Do you have a source that my claim is not true? I referred to junk DNA as non-coding DNA. Just read! Thank you very much.

DNA is a molecule — the size you quoted is a length (in base pairs) not a measure of information content. The information content of a sequence that contains highly repetitive regions (like a human chromosome) is not equal to the sequences length and since DNA contains four bases it certainly is no way "basically the same"!

Well, anyway, this is not a question of what the unit of information is!

@tyersome Can you prove my claim wrong? After all, you say it's NOT true.

BTW: It is not called junk DNA, it is called non-coding DNA.

And? What do you want to tell me with this comment? Non-coding and junk is distinctively different. One doesn't code for proteins but contains a lot of regulatory (for example) information, the other one implies that it can be removed which it cannot. The term "junk" has no scientific basis.

That means the more non-coding DNA, the more complex the species. Or am I wrong here?

I have edit(ed?) the question. But before I submitted my question I was at risk to be blocked, so was to read!!!

In science it is generally expected that you do some research before making a claim, editorial articles are not research. there is a wonderful tool called google scholar that lets you search actual sources. https://scholar.google.com/

@john What can I do to improve my question? I've done it a zillion times now. Why can't I ask questions anymore? On which grounds has my privilege been taken away, though I think I know...

non-coding, information-rich, DNA

Since noncoding DNA contains many long repeating sequences repeated thousands or even millions of times, it is not necessarily information rich, and is often extremely low entropy.

Does human DNA contain that much (the most) non-coding parts?

No. The human genome is a midsized genome by eukaryotic standards, so it's not going to contain the most of almost anything because it isn't large enough. To put into context, the wheat genome has ~6 times as much noncoding DNA as the entire human genome. Then there is the lungfish, which could fit as many again copies of the wheat genome into it's noncoding DNA:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5718017/#Sec1title

Could it be that this huge amount is what makes us "free"? That thát's the reason why we differ from other species in an obvious way?

Our genomes are very average for eukaryotes, so not likely.

Has there any research been done to answer my claim?

Yes. The puzzling lack of correlation between genome size and organism complexity was an unsolved mystery in biology for about half a century. It was eventually resolved when high throughput sequencing combines with bioinformatics revealed that the actual information required to build an organism is very low compared to the typical size of a genome, and so factors other than information content drive genome size.
Also as an aside since I saw this in the comments: since a BP can have 4 values, it can store 2 (not 1) bits of information. Most BPs store less however because they are not random.

What about the length of human DNA? In comparison to other species?

Each base pair is 0.34 nm long. 3 billion * 0.34nm = 1 m per copy and you have two copies. You can do the math for other species.


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Is the biomass decreasing?
Is the overall biomass decreasing over time, and if yes, has that trend started within the last say $200$ years (about when industrialization started)?
EDIT. Let me add some of my own attempts to answer this question.
Reasons that the biomass might be decreasing. Humans have such a big impact on the environment that the current era is called the Anthropocene. Species are disappearing in masses. We put a lot of artificial chemical substances like pesticides and herbicides into the ground. All this makes it plausible that the overall biomass is decreasing. However...
Reasons that the biomass might be increasing. Humans are big animals, bigger than most species (and host to many bacteria). Their number has increased sharply in the last $200$ years. The $\text{CO}_2$ that humans output might lead to increased plant growth, and the higher temperatures might make macroscopic life possible in areas with little life.
Bottom line. It might be the case that animal biomass is increasing (due to human population growth), but the total biomass is decreasing because of the intense deforestation in the Amazon basin and other places.

What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Thanks for your hints - will do this!

@theforestecologist I chose to edit the answer, can you re-open it? Or is it preferable that I create a new thread?

Don't focus too much on land-based biomass. The impact of climate change and ocean acidification on plankton causes probably much larger changes of total biomass on earth than anything else.

I think you are looking for Net Ecosystem Production. Biodiversity seems positively related to NEP as e.g. concluded here. As we are causing the sixth mass extinction ceteris paribus the NEP should decline. Other factors that changed over the last centuries may increase NEP e.g. monocultural plantations can yield higher productivity in abundant resource environments.

Now as long as NEP is positive, I would expect the biomass defined as the mass of all living organisms to increase.


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Could Physarum polycephalum consume regular toenail fungus?
I just watched this video on physarum polycephalum, aka the "blob" and noticed how it consumes white fungus. Could it do the same maybe with human toenail fungus?

I am afraid your question is expressed in non-scientific terms, and requiring one to watch an external video to understand it, is not acceptable for this list. Your question is likely to be closed for lack of clarity unless you edit it so that it becomes comprehensible in itself. “Blob” indeed!

The site shows a related question that seems to be accepted : https://biology.stackexchange.com/questions/46192/what-is-this-white-stuff-inside-apples?rq=1 Your proposal sounds like a double standard :) I edited the question nevertheless.

— Unconvicted criminals do not create precedent for criminality. I know nothing about the question you refer to, and have no obligation to examine every question on this list. To accuse me of double-standards is absurd and offensive. Comments are to help people improve their questions, and I have done so in a manner that informs you of the “law”, not its transgressions. A more civil response would be to say thank you.

Thanks, of course :) The question was understandable though in layman terms, and that was the point. Science has to be inclusive and avoid scaring layman away.

Toenail fungus is deep inside the toenail.
Physarum would probably love to eat delicious toenail fungus if it could get at it.  But that fungus is down infiltrating the structure of the toenail itself, which is why topical treatments to the nail are (usually) ineffective at curing an infection with this fungus.
Toenails are durable and pretty impervious and the toenail fungus is safe down in there.  Physarum is a detrivore and I do not think has the enzymes necessary to penetrate the toenail and get to the fungus.  If it did I suspect it would be happy to eat toenail, fungus and all.  I would not want to have something like that on my toe.


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What is the difference between Molecular and Cellular tolerance?
Although I've read that there are three types of tolerance, molecular cellular and behavioural, I cannot seem to find any mechanism of cellular other than desensitization of receptors. If someone can clear it up, or inform me that cellular tolerance is not a thing, that would be much appreciated <3

Hi, and welcome to the site!  It would be best if you could include a bit of background research... what have you looked at already?  Please [edit] to clarify what research you have already done and what it is you are not understanding in your sources.  Thanks!

Personally, I find these distinctions a bit silly but I also understand they have some use.
People sometimes divide neuroscience into molecular, cellular, and systems levels of understanding. Molecular covers all the "one cell" phenomenon: expression of particular receptors or related proteins, for example. Cellular is one step above of molecular and considers the collection of all "molecular" entities and also considers a circuit level, recognizing that neurons exist among other neurons. Systems level neuroscience sometimes ignores these low-level interactions and sometimes embraces them, but overall is more connected to the behavior and state of the whole organism, approaching psychology.
The reason I think this separation is a bit silly is because, well, none of these levels of understanding are independent. That said, it's a good framework especially for novices to drive home that stuff happens at different levels of explanation. This is true for drug abuse as it is for many other concepts in neuroscience. It also lets someone that is writing a textbook focus on these different levels of explanation in sequence, in a way that is easier to process. A professional in the field is unlikely to draw the same boundaries, but they also have enough background to consolidate knowledge at all levels of interest.
I included a reference that makes the same distinctions I'm making here, but it's likely to be hard to find a canonical one. Different textbooks are going to draw different boundaries as they explain what we know in their own ways, and that's okay. I hope students recognize that A) There are different levels of explanation for neurobiological phenomenon, and B) These levels are interconnected. It's important to recognize that it's possible to study addiction at these different levels of abstraction; it shouldn't be important to draw boundaries between them, however.

Pietrzykowski, A. Z., & Treistman, S. N. (2008). The molecular basis of tolerance. Alcohol Research & Health, 31(4), 298.


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What are these near microscopic white bugs from my comb?
I saw a whole bunch of white bugs crawling on my comb in the medicine cabinet, they didn't photograph well but I did manage to get a bunch of them in mineral oil and eventually take some micrographs.
The good news is that a dermatologist says I'm not infested with anything and, after nuking the bathroom with poisons and cleaning products, they haven't come back.
Here's 3 different specimens at 40X and 100X.  The live ones seemed to be in the 0.2 to 0.8 millimeter range.
(Click for larger images)

What are these things?

excellent photos!  Thanks!

@JohnC (reacting to your comment below): your specimens do not appear to be the bird/rodent mites I'm familiar with. See Bug Identification: Tiny Bugs and Tiny white very hard cell bug! Please help to identify!. Your specimens seem morphologically different and smaller.

I agree with the answer given below that these are mites (8 legs helps to confirm this), but I'm not convinced that they're dust mites. I think you could also rule out Sarcoptes scabiei. Also doesn't look like any species of Cheyletiella I can find.

Do you have any pets or have you been around any animals lately? Do you have any animals living inside or outside the home? (even pests?). Do you have any bite marks or irritation? (if so, can you describe it?)

@theforestecologist, no animals inside home, no evidence of recent pests, no obvious bite marks, although itching has always been a thing with me.  I do work at an animal shelter, where are the animals have strong flea/mite/tick controls/medicines.

What country are you in? It seems USA "household" wood mites grow to about 0.5mm which is probably why could see them https://www.h2ouse.org/how-to-get-rid-of-wood-mites/

Those look like they could be dust mites and are certainly some sort of mite. Dust mites are found everywhere in homes and are around 0.2 mm in length.
Dust mites image by Gilles San Martin:

Dermatophagoide pteronyssinus (European house dust mite):

Dermatophagoides farinae (American house dust mite):

You can learn more about dust mites from the BBC and the US NIH.

The leg configuration does not match and most of my beasties are 2 to 3 times bigger than a dust mite. (Can you even see those with the naked eye?)

I've added a couple of images that appear to have been prepared more like to you did and which clarify that the leg positioning is very similar. Dust mites are visible (reported to be up to 0.3 mm) — if you are you sure yours reach 0.8 mm in size then they probably are a different species of mite.

I'm told elsewhere that my bugs are probably bird, or maybe rodent, mites.  I want to wait a couple days for more answers, then I'll accept one here.

Makes sense — there are also likely to be better sites for getting an answer than here. If you are in North America (USA or Canada) BugGuide seems like a good resource.


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What is this animal looking like an Axolotl?
My friend caught a strange looking animal and he's saying it is an axolotl. I keep telling him it's almost impossible, since they are almost extinct in their natural environment and he caught it in St-Larent River (Quebec, Canada)
Anyone have any idea what it is ?

Based on the size and location that appears to be a Common mudpuppy (Necturus maculosus). (Photo © Brian Gratwicke — CC BY)
The four toes visible on the front foot are also consistent with this identification.
This species is found throughout eastern North America and you can learn more about them from the Canadian herpetological society and iNaturalist.

@SamuelFyckes Note that just like the axolotl, it doesn't metamorphose to the adult stage - that's what makes them "strange looking" and similar. They're both salamanders that never "grow up".

I was thinking hellbender but I guess those don't live in Canada.

@prefectionist I'm definitely not an expert on amphibians, but a quick search suggests that the four-toed salamander is: 1) primarily terrestrial rather than aquatic, 2) much too small, and 3) looks nothing like the original photo. ———  If you have a better answer please post it — we need answers from experts, but that expertise must be demonstrated not just claimed.

Judging from the small limbs and overall size, it appears to be a large aquatic salamander, similar to Necturus maculosus, the mudpuppy. These have a pretty cosmopolitan distribution in North America, including into southern Canada. I can't tell from the photo if it has external gills.


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Can the word "Strain" be used to describe plants or is it used only for microorganisms?
I am trying to determine if I can use the word strain correctly as it is presented in the dictionary as "a variety of plant occurring naturally or developed by breeding" or should strain be used only to refer to subtypes of microorganisms such as a virus or bacteria. More specifically, would I be correct if using "strain" to refer to naturally occurring variety in plants?

I don't know whether it's "correct" or not - who's the judge of correctness here? - but it is commonly used to describe varieties of garden plants in catalogs & gardening books.

Yes, you would be correct in referring to a strain of a cannabis plant.
I have seen the term mostly applied to plants and microorganisms but it can also be used to describe genetically identical animals in experimental studies. Check out the Wikipedia article for strain and some of the sources in it where the term is used:

A strain is a low-level taxonomic rank used at the intraspecific level
  (within a species). Strains are often seen as inherently artificial
  concepts, characterized by a specific intent for genetic isolation.1
  This is most easily observed in microbiology where strains are derived
  from a single cell colony and are typically quarantined by the
  physical constraints of a Petri dish. Strains are also commonly
  referred to within virology, botany, and with rodents used in
  experimental studies.

More specifically, see this article about cannabis where the term 'strain' is used consistently:
https://www.biorxiv.org/content/10.1101/592725v1.full

I should mention the source of this question is a debate in the cannabis farmer community as to whether or not "strain" can be used to refer to naturally occurring variety in plants, so using a cannabis article for my purpose is too meta.

Your question is asking directly whether 'strain' is a term applied to plants. It is :) The idea is that the word 'strain' describes genetically similar organisms, regardless of whether they occur naturally or in a lab (also naturally after all).

@Hasselhoff It seems like you've run into an XY problem. In the future, it's much better to ask about your actual problem. In this case, your question could have been about whether "strain" can be used to refer to naturally occurring variety in plants - that isn't what you asked originally.

Fair enough.  Will edit the question.  pawelek zzz comment to JohnHadish's answer sbelow is also very helpful.  I would upvote and accept that comment as an answer if I could.

The word "strain" is colloquially used to describe cannabis, but is usually not used to describe other plants. The following are common terms for differentiating plant sub-species groups which are used by horticulturists, gardeners, evolutionary scientists and farmers.
"Breeding stock" is a breeding term used to identify genetic stocks in a breeding program. Breeding stock names are typically not ones that someone outside the breeding program would be able to identify, as they are used primarily for tracking hundreds to thousands of plants. Think of these as barcodes used to keep track of plants. Examples would be names like "WA38" and "WW_2019_7"
"Cultivar" is used to describe plants that have been released from a breeding program to the used in agriculture. These are typically hybrid plants, or plants with an interesting trait that the breeder selected for.
"Variety" is a tricky term. It is  used to describe breeding material once it is released to farmers in the case of most grain crops, and some major horticulture crops, but is also used to describe naturally occurring sub-species populations of plants (see below). In the case of grain, not all breeding material become varieties. To be released as a variety, the breeding stock must exhibit a trait that is desirable and unique from other already released varieties (i.e. different flavor, resistance to disease, drought tolerance, etc.).
A good example of varieties at the store would be apples. There are many varieties (Cosmic Crisp, Honey Crisp, Gala, Granny Smith, etc.) but they all still belong to the same species.
"Sub-population" is typically used to describe plant sub-species in the wild. This is a term that you may see in plant evolution papers. If a population of a species of plants becomes separated for a long enough time (we are talking evolutionary time here, i.e. 10's of thousands to millions of years) they may begin to develop novel characteristics. For example, the "Rocky mountain white fur" and the "California white fur" are the same species (meaning they can mate and have viable offspring), but they have traits unique to them. These are also often referred to as varieties.
The above descriptions, while useful, are often imprecise. All describe variation within a species, but the threshold for these designation is often based on easily observable phenotypic traits (i.e. flower color, height, leaf shape, flavor) rather than actually genetic evidence. It also does not help that these words are often interchanged (sub-populations are often referred to as varieties, varieties is sometimes interchanged with cultivar). This makes these terms tricky, and you must know the context they are presented in.
For your use, you can use "strain" and people will know what you are talking about.
For other plants you might find in a garden, you can usually refer to them as "cultivar" or "variety" and people will still know what you are talking about.
These terms have developed colloquial meanings as our understanding of plants and genetics has progressed. They are imprecise by their very nature, as they are attempting to describe differences in species at the sub-species level, and are arguably only describing variation that is interesting to humans. These terms are most useful within the context of a specific discipline, where their meaning is usually more constrained.
Sources:
http://kansasfarmfoodconnection.org/blog/2017/11/29/what-are-the-different-types-of-wheat
https://hortnews.extension.iastate.edu/2008/2-6/CultivarOrVariety.html
https://extension.unl.edu/statewide/buffalo/Yard/Cultivar%20vs%20Variety%2001-30-2016.pdf
Conifers of the Pacific Slope by Michael Edward Kauffmann

The word strain has been widely used in scientific publications to refer to identically genetic varieties of a specific plant species and is not restricted to cannabis. See this and this publications from late 90s related to Arabidopsis, common model organism for plants. And if you check in biorxiv for recent publications in Plant Biology you will see that it is still actively used (for many plant species, not only for Cannabis).

I usually have seen Arabidopsis referred to "accessions"/"ecotype" (for example, Col-0) and "lines" (for specific T-DNA insertions, or point mutations). This is the nomenclature that the salk institute uses: http://signal.salk.edu/tdna_FAQs.html
I was not aware that some people use the word strain, that is interesting.


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Why is the body not able to "detect" imbalances and defects on its own?
We all know, our body is able to roughly localize pain sources or react to imbalances or defects:

the stomach hurts because we may have eaten something spoiled,
muscles hurts after exercising too much,
we feel dizzy after we drank too much alcohol, and so on.

However, the body is not able to "detect" most of the  imbalances and their causes on its own. We certainly do not know why exactly we feel in a certain way, or which current issue is causing pain. We can't "listen" to our body to find out why we feel uncomfortable.
Let me give you some examples:

Our hand hurts because of the carpal tunnel syndrome, but we only receive the information that our hand hurts.
We feel tired, dizzy and suffer from headaches because of a vitamin D deficiency, but we only feel tired and dizzy instead of knowing that we are missing on the vitamin.
Our body reacts to a virus like influenza with the typical flu symptoms. But the body does not tell us, that it's a virus infection right now.
Rather hard example: we experience pain the left arm and feel uncomfortable around the heart area, and we can only assume that it's a heart attack. But the body does not tell us that the heart is having issues right now.

Why, from a biological perspective, can't we "listen" to our body to find out the real causes for our issues, and not only experience some symptoms? What would our body need to actually be able to tell us what's wrong?

As cooperative entities (cells) form a larger body, the larger body takes up functions that are beyond the scope of an individual cell. This involves storing and processing information at a higher level of abstraction and quantity. Your blood cell wouldn't be able to understand what a computer is, in the same way your blood cell doesn't expect you to understand how it recognizes a virus, because as a large body, you cannot see the virus.
This is very similar to how a Prime Minister may not be able to understand all the complexities of building a rocket, but he/she can direct a space agency to build one. If there any problems, the space agency can convey that to the Prime Minister without going into detailed explanations, because he doesn't need to know anything about the equations of the rocket's trajectory. He just needs to know information at a larger scale.
So the answer to your question is that we can't "listen" to our body because everything is happening on a microscopic scale, while our large body is tuned to have senses which "listen" to macroscopic phenomena.

You give good examples, but they are a bit one-sided.
The short answer is: these alarm signs you list were not crucial for our collective survival.
Pain with CTS at least makes you stop using your hands, and if you use your brain, you might find the specific cause (without doctor or warning from your keyboard vendor).
I once had a bad blow to both my shinbones - walking was no problem, but as soon as I came near a table with chairs, it was red alert - for weeks, automatically. It was so tender, I just did not want to bump into something. My shinbones were screaming: let us heal! Without the (fear of) pain, I would have exposed my legs to normal bruises, and it would not have healed.
Your virus/flu example I don't understand. You mean being able to differntiate between if and which virus?
Infections make fever, and fever changes your behaviour - good for your group if you skip a hunt and stay at home. Today you can get scanned at the airport. Same idea.
The vitamin D example has to sides: tired and dizzy is neither sensitive nor specific. More often than not, it has other reasons (sleep,hunger,rotation,low blood pressure), and bone problems are the usual "symptoms".
In a way, our hunger and appetite leads us to get enough (too much) of the good stuff. After salty food we drink, without thinking (actually we think, leave out the salt, think again and drink and then we think we didn't drink enough, probably)     But then again, you can't have a precise warning sign for every vitamin, essential amino acid, element and metabolite. You can, but then it is a machine.

Thank you for your answer. Seems very reasonable, that such a system would not really have any benefits.


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heart rate vs pulse strength when exercising
I have noticed, depending on the exercise I am doing, two different patterns (and probably every combination in between):

if I do an exercise like biking, I can feel I have a faster heart rate but the pulse (touching my neck) doesn't feel very strong.
in opposite, I have noticed that if I do an exercise like push-ups, the heart rate is not as high, but the pulse feels stronger.

why the difference?

Get a portable BP  tester, they are inexpensive and accurate ( those I have used).

I used to have one, but I don't see the link as to why some exercises seem to favor a high heart rate and others seems to elicit a stronger pulse.

Position matters. You are sitting upright when cycling, but are horizontal with pushups, affecting the way the blood volume moves. Also, when cycling, no Valsalva maneuvers are done, whereas with pushups, weightlifting, etc., people tend to do Valsalvas, which makes the blood volume 'stuck in your neck', so to speak, larger, so the pulse "pressure" will seem greater. Other factors also apply, and it depends when you check your pulse for "pressure".


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Long-term viability of induced parthenogenesis
Short version:
Some parasitic bacteria, such as Wolbachia, cause hosts from sexually-reproducing insect species to reproduce asexually instead, with an all-female line. Sometimes, all members of the species end up reproducing in this way - see e.g. Encarsia formosa wasps. How many generations can this remain viable before the effects of

reduced genetic diversity/inbreeding
possible reduced parasite resistance
etc.

take their toll?
If that's too vague a question, what is the longest time/no. of generations that induced-parthenogenetic species have been known to survive?
NOTE: This only applies to induced parthenogenesis resulting from e.g. parasitic bacteria infections. Not to naturally-occurring parthenogenesis.
Full version:
Certain parasitic bacteria, such as Wolbachia can induce thelytokous parthenogenesis in their haplodiploid insect hosts. The infection is passed on down the generations, from mother to daughters. Eventually, this can lead to speciation.
(In non-technical language... the effect of this is that infected female insects lay unfertilised eggs, which hatch exclusively into females, which later on lay unfertilised eggs which hatch into more female insects...
Members of a species which previously reproduced sexually now reproduce asexually, and the asexually-reproducing members of the species may eventually diverge so much from the others genetically that they become a separate species.)
All Hymenoptera (ants, wasps etc.) are haplodiploid.
One would expect that this would reduce genetic diversity in the infected population. A species which previously reproduced sexually, and now reproduces entirely asexually, might be expected long-term to lose biological fitness as a result of inbreeding depression. See also: "Muller's ratchet"
However, a 2001 paper investigated the effects of Wolbachia-induced parthenogenesis on Trichogramma wasp species, comparing such wasps to those that reproduced sexually and to those that were naturally parthenogenetic. Fewer of the infected wasp embryos survived to adulthood, but this was due to direct effects of the infestation on embryonic growth. Inbreeding depression was not a factor.
A 2000 paper also noted that Wolbachia can be horizontally transmitted through the sharing of a common food source, and stated:

horizontal transfer of parthenogenesis-inducing Wolbachia among offspring of infected females offers the potential for recombination between different Wolbachia variants and thus for circumventing Muller's ratchet.

Though I think that would only apply to the bacteria, not its host.
A notable example of Wolbachia-induced parthenogenesis is the chalcidoid wasp species Encarsia formosa. I don't know how long this has existed as a distinct species. Antibiotic treatment to kill the Wolbachia can restore their ability to give birth to males.
Is there a theoretical limit on the number of generations an induced-partheogenetic species should be able to survive? And what is the longest amount of time that any such species has been observed to survive?
Sources:
Tagami, Y., Miura, K., & Stouthamer, R. (2001). How does infection with parthenogenesis-inducing Wolbachia reduce the fitness of Trichogramma?. Journal of Invertebrate Pathology, 78(4), 267-271. (Paywalled, unfortunately.)
Huigens, M. E., Luck, R. F., Klaassen, R. H. G., Maas, M. F. P. M., Timmermans, M. J. T. N., & Stouthamer, R. (2000). Infectious parthenogenesis. Nature, 405(6783), 178-179.
Stouthamer, R., & Luck, R. F. (1993). Influence of microbe‐associated parthenogenesis on the fecundity of Trichogramma deion and T. pretiosum. Entomologia Experimentalis et Applicata, 67(2), 183-192. (Paywalled.)

What a good question!I think that Wolbachia infections could be sustainable on the long term.Lots of species are currently infected by Wolbachia (looks like at least 25% of all insects species could host Wolbachia) and some scientists call it a symbiosis rather than an infection.In other words, I think Wolbachia doesn't lower the evolutionary success of its hosts.

@Zafalija Bear in mind that Wolbachia infection affects different hosts in different ways. In some areas, there are species with 100% of the population infected, but no apparent symptoms. (Not even Wolbachia's famous biasing of sex ratios.) For example, in the Carpathian Basin, three of my favourite butterfly species - the Large Blue (Phengaris arion), Alcon Blue (Phengaris alcon) and Mountain Alcon Blue (Phengaris rebeli) are all 100% infected. And in the UK, 19 populations of another butterfly, Euphydryas aurinia, also have 100% Wolbachia prevalence, without any apparent effect!

Sources for the above: https://www.researchgate.net/publication/276509070_Controversial_patterns_of_Wolbachia_infestation_in_the_social_parasitic_Maculinea_butterflies_Lepidoptera_Lycaenidae and https://en.wikipedia.org/wiki/Euphydryas_aurinia

@Zafalija OK. I just wanted to get across that my question is explicitly about host species that it induces parthenogenesis in. It doesn't do that in any of the butterfly species with 100% infection that I mentioned.

And Wolbachia can be lost of course, e.g https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6493766/
Loss of cytoplasmic incompatibility in Wolbachia-infected Aedes aegypti under field conditions

I knew about entire populations infected by Wolbachia.I was trying to say that Wolbachia infection doesn't have any negative impact on the survival of the species due to lack of genetic variability; lots of species have been infected for centuries without becoming extinct, so I guess their altered sex ratio is not an important factor for survival, at least until some male survives: having a unisex population is obviously a serious evolutionary threat.

Since wolbachia infections can be "entirely cleared" as stated by @PolypipeWrangler, you won't have entire species with no males at all.Maybe you could find some populations totally infected by wolbachia, but since wolbachia infections are 'reversible' some male could appear here and there, restoring a little genetic variability in our pool.Please notice that parthenogenesis could be beneficial in some cases: it seems that lots of invasive species are parthenogenetic (https://scholar.google.com/scholar?hl=it&as_sdt=0%2C5&q=parthenogenetic+invasive+species&btnG=&oq=parthenogenetic+i)

@Zafalija You mention "species infected for centuries". Did any of these become parthenogenetic as a result of the infection? If so, could you tell me the names of these species? Thanks!

@PolypipeWrangler Thanks. But that scenario relied on the high temperatures in the locality, and not all species with Wolbachia will live in regions that get that hot.

Check this: https://www.karger.com/Article/Abstract/104228                                     Wolbachia was discovered in 1924.It is likely that it has been around for centuries, if not millennia, before its discovery.Also, @PolypipeWrangler's comment pointed out that wolbachia can be lost.We surely do know that it can be lost due to high temperatures, but you can't exclude that wolbachia could be lost due to other environmental factors.Please notice that wolbachia could actually improve the fitness of certain species!

@Zafalija I've looked at the abstract (I can't read the full article due to the paywall). It mentions Culex pipiens (but misspells it "pipientis"). Wolbachia induces cytoplasmic incompatibility in that species, but that's not the same thing as parthenogenesis.

That abstract was meant to be a reference to the fact that wolbachia has been discovered in 1924, not to parthenogenesis induced by wolbachia.If it's true that wolbachia has been around for centuries, if not millennia, there could be lots of species infected by wolbachia on the long term, with its effects being parthenogenesis or cytoplasmic incompatibility (which could lead to rapid speciation events), but I don't think there's enough literature about this.These are only my speculations, but keep in mind that centuries and millennia are nothing in evolutionary time, hence I think

that lots of species have been hosting wolbachia for long periods of time (maybe losting it after some environmental change), and the fact that we currently know about species infected by these bacteria means that it isn't awful in evolutionary terms.This theory is probably true if wolbachia is really old, while it's totally erroneous if wolbachia is recent.


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How to obtain raphides from plants?
I recently found out that certain plants produce needle-shaped crystals called raphides. I am a physicist and I have an experiment in mind that could use these needles, but I would need to extract them from the plant and keep them in a liquid solution somehow.
How can I do this? Is this possible/hard to do? Does anybody know how to do this or have any experience?

Searching for raphide purification I came up with a paper where they isolate these crystals from kiwi fruit:
Konno, K., Inoue, T. A., & Nakamura, M. (2014). Synergistic defensive function of raphides and protease through the needle effect. PloS one, 9(3).
Does that help?
Note, however, that while according to this paper these large crystals can be kept in suspension that isn't the same as a solution ...


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How exactly does alcohol solution kill or neutralize viruses?
To reduce the risk of infection by viruses (including 2019-nCoV) the CDC suggests:

Wash your hands often with soap and water for at least 20 seconds. Use an alcohol-based hand sanitizer that contains at least 60% alcohol if soap and water are not available.
Avoid touching your eyes, nose, and mouth with unwashed hands.
Avoid close contact with people who are sick.
Stay home when you are sick.
Cover your cough or sneeze with a tissue, then throw the tissue in the trash.
Clean and disinfect frequently touched objects and surfaces.

To my knowledge most alcohol-based hand sanitizers use ethanol. In clinical settings sometimes isopropanol is also used.
Question: How exactly do alcohols, especially ethanol and isopropanol provide some disinfecting action against viruses? Are the virus particles simply dissolved? What happens?

I've added the sterilization tag for lack of a better option. Hand sanitizer does not sterilize, but we don't have a sanitization tag.

Coronaviruses are enveloped viruses, so I would assume that the alcohol disrupts the membrane and thus strips away the molecules used for host cell recognition ...

I'm voting to close this question as off-topic because it concerns medical hygiene and is not about a specific biological problem in the terms of SE Biology.

@David No, it's specifically about the mechanism behind the effect of a particular chemical on a specific type of organism, and not about public hygiene. I've written the question carefully to make sure of that, I'm not certain you've read it through, or perhaps you are distracted by the background information.

@David If stripping away the molecules used for host cell recognition is the answer, then that is the answer and closing simply blocks people from posting it.

How artificial procedures kill living organisms is off-topic here imho and I have always taken this attitude to questions of this sort — this must surely have been asked before. An analogous question would be on the mechanism of death by the guillotine, or (we had a spate of these) by astronauts’ helmets coming off in outer space. This site is for questions about actual biological problems you are faced with.

@David If someone with a "biologist's ID card" asked about how a bleach solution was actually sterilizing the inside of their hood, would you close their question as well?

I don’t close questions, but I would vote that a question of that sort be closed. In my opinion a methodology question on how to adopt sterile procedure in a non-clinical situation would be on-topic if it showed research and raised a point of difficulty. Questions on the mechanics, no.

I think this is an absolutely valid question in my opinion. I disagree with David in that the mechanism is irrelevant; of course the way in which life is vulnerable to organic solvents is a biological question. However, to be fair I think the answer is rather simple and easy to google; ethanol lyses cells by rupturing the plasma membrane (which is made of ethanol-soluble lipids) and additionally denatures proteins. Alcohols can also dehydrate cells (substitute the water contents of a tissue) and have been as such used as fixatives.

This type of question is certainly on topic here since it's asking about how a chemical impacts a biological particle. There is no doubt about it, and the question should not be closed. @David this site is not just for questions related to a professional biologist's lab setting, but it's meant for (and certainly is used for) asking a wide range of biological questions. This includes questions about everyday people /situations such as hand sanitation, as long as they are asking about the biological characteristics, mechanisms, or impacts of that situation. Which is the case here.

@theforestecologist — basic chemistry then?

@SPr I see the goal of Stack Exchange as being the generation of good answers to on-topic questions. Not all viruses have envelopes and no viruses that I know of are cells. Having a well-written, well-sourced and well-received answer to this question is a net plus for the site, and learning that alcohol is only effective against some kinds of viruses and not others wouldn't necessarily always come from a quick googling.

Alcohols dissolve lipid bilayers
Many viruses have an outer lipid bilayer. Ethanol lyses cells, and in the same fashion damages membrane-bound viruses by rupturing the bilayer (which is made of ethanol-soluble lipids).
Alcohols misfold the protein coats of viruses
Additionally, alcohols denature proteins, which misfold in non-aqueous conditions. Some viral surface proteins are important for adhesion and attachment, and misfolding these renders the virus inactive. The total breakdown of viruses is essentially due to the misfolding of their protein coat (the capsid).
The same goes for bacteria
With the additional effect of dehydrating cells
Alcohols substitute the water contents of a tissue and have been as such used as fixatives. Common laboratory examples include methanol and ethanol.
Typically, 70% (140 proof) ethanol is used for bench wiping to kill or inactivate microbes. This includes viruses.
This is all standard, common, easily and readily accessible knowledge. Here's a bonus source.

(1) Read closer, I've addressed viruses. Admittedly it is a short answer, but I don't think it can be made substantially better. I could format the viral part to bold font if you really think it will help... (2) All that applies for ethanol and methanol apply for isopropanol too. Isopropanol is used in cleaning work surfaces; methanol is too toxic to humans for that purpose.

We expect you to show a minimum attempt at your own research, and explain where you remain unclear about something. This is the most standard textbook, easy-to-search query. You have clearly not thought to use a search engine, and you have also not consulted the search bar on this stack yet. You'll find an answer anywhere if you look. I also urge you to read this. I'm sorry you are so hurt about my inclusion of membrane-bound microbes; viruses too sometimes harbor membrane envelopes. Alas!

From wikipedia: A capsid is the protein shell of a virus. It consists of several oligomeric structural subunits made of protein called protomers. Viruses don't have a lipid layer. In addition, I am removing your last comment S Pr - be nice svp.

Thanks for the edit, it looks great!

A comment on the question suggests that several infectious viruses (including 2019-nCoV) are envelope viruses and that alcohol can "strip away the molecules used for host cell recognition". Viral envelopes (are), typically derived from portions of the host cell membranes.
A key component of these envelopes are of course lipids.
From Antiviral activity of alcohol for surface disinfection:

Antiviral activity and the viral envelope
Because of the structure and composition of the different virus families, viruses react differently to the action of disinfectants. From a disinfectant point of view, the presence or absence of an envelope is the most important trait of a virus. Lipid-enveloped virus families are, generally, susceptible to many disinfectants, alcohols included. The higher the lipid content and the larger the virion itself, the more susceptible the virus is.
Many (but not all) of the so called small `naked' virus families (e.g. adeno, parvo, picorna viruses causing a.o. poliomyelitis,hepatitis A, hand foot and mouth disease, common cold) that do not possess an envelope are quite resistant to common disin-fectants, alcohols included (6, 7).
Fortunately, the herpes viruses (herpes simplex I and II, 5-8,varicella, Epstein Barr); paramyxo viruses (measles, mumps);retro viruses (HIV, AIDS); hepadna viruses (hepatitis B); coronaviruses (SARS) are lipid-enveloped virus families that are, generally, susceptible to the disinfectant activity of alcohols(5, 8).
5 JuÈlich W-D, v. Rheinbaben F, Steinmann J, Kramer A. On the virucidal efficacy of chemical and physical disinfectants or disinfection procedures. Hyg Med 1993; 18: 303-26.
6 Tyler R, Ayliffe GA, Bradley C. Virucidal activity of dis-infectants: studies with the poliovirus.J Hosp Infect 1990; 15:339-45.
7 Mbithi JN, Springthorpe VS, Sattar SA. Chemical disinfection of hepatitis A virus on environmental surfaces. Appl Environ Microbiol 1990; 56:3601-4.
8 Croughan WS, Behbehani AM. Comparative study of inactivation of herpes simplex virus types 1 and 2 by commonly used antiseptic agents.J Clin Microbiol 1998; 26: 213-5.


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What are the environmental conditions for SARS-CoV-2 to survive?
What do we know about the environmental limits for nCoV to survive outside the body? For example, in:

In open air
On surfaces
In water

What are the limits for temperature, humidity and air pressure, where the virus, can or cannot survive?

Because "any" Coronavirus is so dangerous, much research have been done on viruses with similar properties. They are called "surrogates". Because nCoV is new, we don't have any studies, so we need to estimate it's behavior from previously studied similar viruses.
Here:
RH   = Relative Humidity.
Tr   = Room Temperature
TGEV = Transmissible Gastroenteritis (surrogate)
MHV  = Mouse Hepatitis (surrogate)

Viral survival for the TGEV/MHV surrogate:

on stainless steel:      4°C @ 20% RH:  28 days
in water/sewage (TGEV):  25°C: 22 days
in water/sewage (MHV):   25°C: 17 days
contaminated water is a potential vehicle for exposure if aerosols are generated

For airborne Human Coronavirus 229E (HCV/229E):

Optimal survival:  6°C @ 50% RH:
Poor* survival:     20°C @ "High" relative humidity (RH)
(* "poor" in terms of 20°C but varying RH.)

For SARS CoV-P9:

Serum: 96 h = 4 days
Sputum & Feces: 96 h = 4 days
Urine: 72 h = 3 days

For SARS-CoV (GVU6109):

in diarrheal stool (at low pH): 4 days
in respiratory/air droplets:  >7  days @ 20°C (Tr)
in respiratory/air droplets:  >20 days @ 4°C

"The main route of transmission of SARS CoV infection is presumed to be respiratory droplets. However the virus is also detectable in other body fluids and excreta. The stability of the virus at different temperatures and relative humidity on smooth surfaces were studied. The dried virus on smooth surfaces retained its viability for over 5 days at temperatures of 22–25°C and relative humidity of 40–50%, that is, typical air-conditioned environments. However, virus viability was rapidly lost (>3 log10) at higher temperatures and higher relative humidity (e.g., 38°C, and relative humidity of >95%)."
"We and others have reported that infectivity of SARS CoV (SARS coronavirus) was lost after heating at 56°C for 15 minutes but that it was stable for at least 2 days following drying on plastic."

UPDATE: 2020-03-13
From [7]:

"We found that viable virus could be detected in aerosols up to 3 hours
  post aerosolization, up to 4 hours on copper, up to 24 hours on
  cardboard and up to 2-3 days on plastic and stainless steel. HCoV-19 and
  SARS-CoV-1 exhibited similar half-lives in aerosols, with median
  estimates around 2.7 hours. Both viruses show relatively long viability
  on stainless steel and polypropylene compared to copper or cardboard:
  the median half-life estimate for HCoV-19 is around 13 hours on steel
  and around 16 hours on polypropylene. Our results indicate that aerosol
  and fomite transmission of HCoV-19 is plausible, as the virus can remain
  viable in aerosols for multiple hours and on surfaces up to days."

For SARS-CoV-2:
Experiments were performed @ 40% RH and 21-23°C.

Copper (Cu):      4 hours
Stainless (Fe):   48 hours (2 days)
Cardboard:        24 hours
Plastic:          72 hours (3 days)
SARS-CoV-2 is most stable on plastic and stainless steel.

References:

[1] 20xx https://aem.asm.org/content/76/9/2712.short
[2] 1985 https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-66-12-2743
[3] 2005 https://academic.oup.com/cid/article/41/7/e67/310340
[4] 2009 https://www.sciencedirect.com/science/article/abs/pii/S0043135409000785
[5] 2010 https://www.hindawi.com/journals/av/2011/734690/
[6] 2003 https://www.ncbi.nlm.nih.gov/pubmed/14631830
[7] 2020 Aerosol and surface stability of HCoV-19 (SARS-CoV-2) compared to SARS-CoV-1


text:
Why are P and T waves curved and not straight (ECG)
The P and T wave are in shape of a curve while the QRS complex is in straight lines.
What is the reason this is happening?

P wave represents atrial depolarization (hence atrial contraction).
Atrial depolarization takes only a split second, therefore its corresponding wave will be smooth and rounded.
Variations from this shape could be consequences of various heart diseases: for example,a spiked P wave is called P pulmonale and suggests right atrial enlargement.
T wave represents ventricular repolarization: a normal T wave looks like an

upright low amplitude broad hump following the QRS complex.

Abnormalities in T wave could be the signs for multiple heart diseases, varying from myocardial ischemia to hyperkalemia.
In particular, peaked T waves suggest an hyperkalemia diagnosis.
T wave abnormalities are well documented here
The QRS complex corresponds to ventricular depolarization, which is faster and more intense than atrial or ventricular repolarization: hence a normal QRS complex is peaked.
In conclusion, P wave and T wave are rounded because these correspond to low-intensity electrical events while the QRS complex is provoked by an intense electrical event.


text:
Small Black Fly Identification
Could anyone help to identify the following small black fly please?

Here is some relevant information which may help:

Location: London, UK
Length: ~5mm
They are slow to react and drift lazily & silently around a room

After my own research, I thought it might be a fungus gnat, but I'm uncertain.
Hopefully, if the species can be reliably identified, I can then look to find out what attracts them and how to deter them.

We need a photo with the wing venation in focus for a reasonable chance at family-level identification; if on getting such a photo the family is Sciaridae (which does seem likely given the animal's color), good luck (species level identification in that group is firmly in the "some disassembly required" camp).


text:
What kind of mushroom is this? Found in SF
We found this on a trail in San Francisco. Could someone please tell me what kind of mushroom this is?


text:
What does lymph actually look like?
I have scoured Google and a number of my anatomy textbooks for a picture of lymph. However, I cannot find any such photo (or video) showing its actual appearance.
Can someone provide a reputable image or source where a photograph of lymph can be seen?
What I do know:

Tortora & Derrickson (14th) A&P textbook mentions it consists of a "clear liquid extracellular matrix that is similar to blood plasma but with much less protein."

A photo purporting to be lymph does exist on Wikipedia, but lacking any further corroboration leads me to remain uncertain of the photo's authenticity.

Context:
I'm preparing a lecture for my 100 level college A&P course, and I was hoping to include a photo for my students to see and compare.
NOTE: I am hoping for a photo of lymph that is not classified as lipid-containing Chyle, for which I can find photos. However, a comparison photo would be ok :)

http://www.ijcasereportsandimages.com/archive/2014/012-2014-ijcri/CR-10458-12-2014-osman/ijcri-1045812201458-osman-full-text.php

This seems to be one of rare actual photos of lymph online (suggested in the comment above):

Image: Lymph (source: IJCRI - Case Reports Journal)
This particular lymph (or "lymph fluid" or "lymphatic fluid") was aspirated from a "lymphocele", which is an abnormal collection of lymph in the body (appearing outside of the normal lymphatic system).
While a lymphocele is not normal, the lymph in it, such as in this photo, looks quite normal: it is a clear (translucent) and yellowish liquid.

The lymphatic (lim-FAT-ik) system is a network of tubes that collects
  lymph (LIMF). This clear, pale yellow fluid drains out of blood
  vessels all over the body. (KidsHealth.org)

The froth is from proteins as they normally appear in the lymph.
The image of lymph in Wikipedia is not a clear lymph, but obviously a chyle (a milky fluid containing the lymph and chylomicrons due to thoracic duct injury).

Thanks for this! I'm not familiar with the International Journal of Case Reports and Images, but this is certainly better than I found (and, if I determine it to be reputable -- which I don't doubt -- it's a great new source for clinical images to infuse into my course lectures!)

@theforestecologist, if you need more medical images: https://biology.stackexchange.com/questions/38774/open-database-of-medical-images/79533#79533

Now this is the type of Q&A/discussion that this site is supposed to emphasize! I love learning new resources. Thanks again for your informational responses and help :).


text:
How to calculate the quantification of qPCR to the equivalent of the number of nuclei in fungi?
I have a question about the quantification through qPCR. The my question is: if I made the qPCR of a fungal functional gene, how is possible to obtain from the quantification number (in nanogram) the equivalent number in number of nuclei?

To clarify: you're asking about converting between copy number (which may be expressed in moles, molarity, or just a raw number) and nanograms of DNA?

If I obtain the quantification between nanogram to covert this number in number of nuclei. Because in one paper I found this sentece: "As few as 148 fg of Verticillium dahliae DNA were detected and quantified (through qPCR), which is equivalent to five nuclei". How is possible to make this convertion? @Punintended

From your comment:

"As few as 148 fg of Verticillium dahliae DNA were detected and quantified (through qPCR), which is equivalent to five nuclei". How is possible to make this convertion?

The Verticillium dahliae JR2 genome is 36.2 Mb.  Assuming this organism is haploid and dsDNA has an average mass of 660 g/mol per base pair, that means the molar mass of the genome is 2.40 × 1010 g/mol.  Therefore, 5 nuclei will contain 8.30 × 10-24 mol of your genome.  Multiplying the molar mass by the number of moles gives us a mass of 1.99 × 10-13 g, or 199 fg, which is close to your cited value.


text:
Why would a 2019-nCoV protein sequence in the NCBI database match a protein submitted in 2018?
There seems to be a bit of a conspiracy theory brewing over some data in the NCBI database, and I don't have the necessary knowledge to make sense of it.
It basically goes like this:

Go to NCBI BLAST
Click on the big Protein BLAST button
Enter AVP78033 in the main search box and click BLAST
Click on the first result that shows a 100% match and click "See 5 more title(s)" in the first entry

This shows that the search is a complete match for a Bat SARS-like coronavirus protein from a 2018 research paper, for Wuhan seafood market pneumonia virus (which the NCIS site indicates is an alias for 2019-nCoV), and for Bat coronavirus from 29 Jan 2020.
My question is - why would a protein from Bat SARS-like coronavirus and 2019-nCoV be showing up as a perfect match for one another? Does this mean that 2019-nCoV might actually be a previously-discovered coronavirus that very recently started infecting humans? Or could it be that a recently collected sample from Wuhan was mis-identified as 2019-nCoV when it is actually the same coronavirus from the 2018 submission?
Clicking around the links on that site seem to bring up dozens of similar but different pages that I don't have the knowledge to distinguish, but the Accession column from the search results described above contains a link to this page, which says that it is a provisional refseq and acknowledges that it is identical to the bat coronavirus:

PROVISIONAL REFSEQ: This record has not yet been subject to final
              NCBI review. The reference sequence is identical to QHD43418.
              Annotation was added using homology to SARSr-CoV NC_004718.3.

Can somebody who actually understands these things please make sense of this?

How does a previously-discovered virus being identical to the coronavirus, indicate any sort of conspiracy in any way shape or form?

@IanKemp It's not identical to a previously-discovered virus. Only the envelope protein is identical. The claim is that someone took an existing virus and gene-swapped part of it to weaponize it while leaving other large parts intact. This is built on a false premise, but I think most laypeople (including my self prior to asking this question) would not know this.

Can you post screenshots of what we should click on? I'm not able to find it with your instructions. There was no result with "5 more titles", only 2, 4, 14, etc. Maybe a link to the final result would help as well.

2019-nCoV is a virus that originated from the bat (at least this is the current hypothesis). It shows 96% squence similarity to the BatCoV RaTG13 sequence (see reference 1), showing its origin.
It still is 87,99% identical to the "Bat SARS-like coronavirus", which explains the hit you found and is not unexpected, as these viruses are very closely related (see reference 2).
These viruses are closely related, so I wouldn't expect too many differences at all. Then envelope proteins can be critical for function/structure of the virus, so mutations there might occur less frequent. And if they occur, I would only expect few changes over time, so with this little time gone, probably no mutation is seen yet. Additionally, due to the redundancy caused by the codon degeneracy, not every mutation in the genomic material translates into changes in the protein.
References:

Full-genome evolutionary analysis of the novel corona virus
(2019-nCoV) rejects the hypothesis of emergence as a result of a
recent recombination event
Genomic characterisation and epidemiology of 2019 novel coronavirus:
implications for virus origins and receptor binding

Thank you for your answer. What is the meaning of the apparent 100% match between the respective envelope proteins? Is it common for distinct viruses to have identical envelope proteins?

@JLRishe It is not common for viruses from different virus families to have identical envelope proteins, except probably when they emerged from each other through evolution. But the case here is to compare the genome of chimp and man and then find identical proteins. Only that these viruses are much closer together from an evolutionary point of view.

What I'm trying to ask is - I'm surprised that two viruses with ~88% sequence identity would have identical envelope proteins. Is there a reason for this? Do envelope proteins evolve a lot more slowly than other parts of a virus?

@JLRishe These viruses are closely related, so I wouldn't expect too many differences at all. then envelope proteins can be critical for function/structure of the virus, so mutations there might occur less frequent. And if they occur, I would only expect few changes over time, so with this little time gone, probably no mutation is seen yet. I adapted the answer, is this clearer now?

Thank you again! I just found this paragraph in Wikipedia that seems to address the different rates of evolution between DNA and proteins: https://en.wikipedia.org/wiki/Molecular_evolution#Relation_to_nucleic_acid_evolution

Nitpick: coronaviruses do not have DNA. They're RNA viruses. The virion, IIRC, includes an RNA-to-RNA transcription enzyme.

@CarlF You are absolutely right, thanks for reminding :-)


text:
Tryptophan side-chain structure, how should it be orientated?
I would like some clarification on whether it matters where the NH and double bond are placed in these two structures of tryptophan (W) that I drew. I marked the right side as correct and the left side as the incorrect one, but suddenly I am thinking that where you place the double bond and NH don't matter as long its placed in either orientation of the structure it should be tryptophan right?
Simply put, I took my chemistry classes a few years ago and don't remember if this changes the structure if I changed the position of the NH and double bonds, that is all, and would some clarification on it.

EDIT / UPDATE:
I noticed a mistake and re-drew the structure, but am still not clear about the so called "trivial" rotation mentioned. Does the new picture reflect whether or orientation not mattering? I am still confused if I drew it correct.

Care to explain why that is the case?? Don't really understand why this question is so poorly received I am genuinely trying to learn about amino acids.

Some suggestions about why this is being poorly received. 1) This qualifies as a "homework" question since it "addresses a basic biology concept that may seem trivial to biology professionals". For such questions, you are required to use the "homework" tag. 2) It is actually a (trivial) chemistry question in disguise, since you are just asking whether a chemical compound is still the same after rotating a bond. ——— Have another look at a correct structure for tryptophan — you have the placement of the aromatic ring and the nitrogen wrong.

But its not a homework question, how do you want me to prove this? I'm not taking any classes and am studying for the MCAT exam, I wanted to memorize the amino acids, but am confused if switching or rotating the orientation of the NH and double bond would make it a different molecule other than tryptophan

I have looked at the structure beside what I drew at least 100 times over and I cannot spot the difference between what I drew (incorrectly) and the correct structure. If I were asking a homework question, how come I did not reference a problem or something, I'm not trying to pick this molecule out of a list or anything like that, it is for my own personal understanding, not a homework related question, not sure how you would like me to prove this.

Did you read the page I linked to that describes what "homework" means on this site? I quoted the part that is relevant to this question. ——— You appear to have forgotten that sigma bonds freely rotate and thus that the two structures you drew are just different representations of the same molecule. Consequently, I encourage you to refresh your understanding of basic chemistry before taking the MCAT. ...

I have found that starting with a relatively accessible and reliable source like Khan Academy can be very helpful, however they aren't perfect for chemistry. 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.

Hi Tylersome,
Thanks for attempting to put on the right pathway. And no I did not see "homework", and have since read that in your new posts. I guess a follow-up question I have is how would I be able to discern what is a "trivial" question is for one person and not for another? Questions I ask whether they are trivial or not, are intended for my own personal understanding, not for homework purposes as I have already graduated from university and am currently trying my best to refresh my knowledge. However, I would still like somebody feedback on the second image I uploaded of the structures

since I still don't know if I drew them correctly (in the second image). I even tried inputting my drawing into chemspider and it comes out either as zero results.

Just to clarify are you referring to my 2nd picture or the first? And yes, the NH is supposed to be part of the 5 member ring, sorry if my drawing isn't clear enough for this indication. I think I now see the bond rotation, especially in the 2nd picture I drew.

I dont think this is a trivial question, it is rather a core biochemistry question regarding the positioning of amino acids side chain in proteins. The various positions are called rotamers, and it is important to understand this in structural-biology and enzyme catalysis

Good question, this regards rotamers!
Basically, the side chain of amino acids can rotate as shown in the figure below for glutamate (Glu; E). The various option for side-chain rotation is called rotamers! Some amino-acids side chains have the potential of many rotamers (such as glutamate) while some can only adopt a few (such as tryptophan) due to steric restraints. You can read about it here on FolditWiki or in the article 'Rotamers: To be or not to be?: An Analysis of Amino Acid Side-chain Conformations in Globular Proteins'.

The set of amino acid side-chain conformations in globular proteins
cannot be considered as normally distributed around some rotamer
points. Outliers occur systematically. The rotamericity of an amino
acid depends essentially on the different environments the amino acid
meets in real protein structures. Factors such as the backbone torsion
angles of the residue itself, the secondary structure and tertiary
contacts influence the rotamericity. (...)

When solving a protein structure, scientists spend a lot of time on placing the amino-acid side chains into their correct rotamer position. Which rotamer a particular side chain should adapt, depend on the surrounding environments. Some amino acids side-chain are also very flexible and will move around the various rotamer position that they can adopt. In the example of glutamate (figure above), it would most likely adapt a rotamer position pointing either out towards solvents (if the the side chain is on the surface of the protein), or perhaps towards a positively charged amino acids side chain such as Arginine (R) or Lysine (K) to form salt-bridges or H-bonds.
In the case of Tryptophan (W), it is often involved in pi-stacking and would therefore be found in a rotamer position that stacks with other aromatic amino acids side chains. It is also a very bulky amino acid, and might therefore only have space in one particular conformation. Note that tryptophan (W) only has two rotamers, which are similar to the two that you drew in the updated figure, and again shown below. Note that both of these are correct, and that my hand-drawn bond angles are a bit off. These two rotamer options for tryptophan are even found in enzymes catalytic site, where the 'flipping' from one confirmation to the other is the key-mechanisms the allows substrates into or out of the active site!

These structural arrangements are a lot easier to understand in three-dimensions, if you are still struggling then it could be a good idea to use a visualisation program (e.g. PyMol or Coot) and take a look at tryptophane's and other amino acids side chains by downloading some protein structure from the PDB database.
Here are also some related questions

Protein Structure Parameters
How to convert PDB file of Amino Acids to rotamer tuples list of all AAs instances


text:
A question about dicumarol
I know that dicumarol was discovered in moldy sweet clover as it caused hemorrhage in cattles, but if someone had thromboembolic disorders causing uncontrolled thrombosis,would it be fine to eat moldy sweet clover (in case of absence of any means of modern life) especially that it contains other microorganisms?