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What would happen to the membrane potential if a cell didn't have developed relative refractory period?
If the Na+ voltage gated channels remain open instead of getting deactivated during the re-polarization period, would the membrane potential become 0 since the Na+ ions would be constantly bringing into the cell while K+ is transported out of the cell, which makes them cancel each other out in a sense? However, I feel like there is something wrong with my reasoning but I don't know which part.

Welcome to Biology.SE. You are dealing with an electrochemical potential, but only thinking about charge. Are you familiar with the Nernst potential and its extension to multiple ions? This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer.

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" If the Na+ voltage gated channels remain open instead of getting deactivated during the re-polarization period, would the membrane potential become 0 ? "
No, if Na+ channels remain open then the repolarization period would never happen.

Mathematically we can prove the above with the Goldman–Hodgkin–Katz voltage equation

where

approximate relative permeability values at the peak of a typical neuronal action potential are pK : pNa : pCl = 1 : 12 : 0.45 calculator

and thus we can see that the membrane potencial is much higher than the opposite for example

For a typical neuron at rest, pK : pNa : pCl = 1 : 0.05 : 0.45 calculator

and the only variable that we have changed was the  relative membrane permeability for Na+

Hypothetically speaking if [K+]i = [K+]o = [Na+]i = [Na+]o = [Cl-]i = [Cl-]o the membrane potential in that case in fact would be zero.

However that is impossible because at rest, Na⁺/K⁺ ATPase constantly moves 3 Na+ ions out and moves 2 K+ ions in, and thus these gradients are maintain, so they cannot ever be the same.

Regarding your other question
What would happen to the membrane potential if a cell didn't have developed relative refractory period?
In that case the probability of repolarization and hiperpolarization to occur is diminished and thus it's possible to assume an extreme scenario of convulsions with death associated.
Example: Strychnine is a neurotoxin which acts as an antagonist of glycine and acetylcholine receptors

on the other hand, an excessive relative refractory period scenario, would result in a difficulty to achieve the threshold and depolarization
Example: mechanism of action of local anesthetics

by applying the principle above it is possible to reversibly decrease the rate of depolarization and repolarization of excitable membranes

As a side note (or curiosity), based upon that equation we can also modify Cl- values, and in that case we can speak about the mechanism of action of hypnotics and sedatives (such as benzodiazepines)

Thank you so much of your detailed answer, I really appreciate it! If you don't mind, could you tell me why it's illogical to think that the membrane potential would become 0? I get that mathematically it changing the permeability of Na+ causes the membrane to stay depolarized but I still don't know why hypothetically speaking, in an environment where only Na+ and K+ are present inside and outside a membrane, the membrane potential wouldn't just be 0 when both voltage gated K+ and Na+ channels remain open and the total concentration of K+(inside+outside) = concentration of Na+(inside+outside).

if and only if, at rest, the Na+/K+ pump failed, then it would be possible such scenario.. but it has nothing to do with ion channels, because ion channels only open and close.. if there is no gradient then ions dont move.
Sorry in advance, I think that i got a little off topic with my answer.. I've also edited it

Thank you..I gained a better understanding now! Just to make sure, is it right to think that if both Na+ & K+ voltage gated channels just remain open, depolarization wouldn't occur, and the membrane potential would decrease (compared to ~ +45) but it wouldn't become 0, because there is always a gradient. In this hypothetical situation, Na+ would keep coming in and K+ keeps going out, but the membrane potential doesn't depend on the opening/closing of voltage-gated channels, but rather the concentration gradient of different ions. Thank you again for answering my poorly worded question


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What is the latest consensus on the causes of sexuality?
In 2019, scientists concluded that there is no gay gene. Epigentic markers of homosexuality have been disproven. The Exotic becomes Erotic Theory is an ancient decrepit idea that holds no water. Yet, scientists think that it may have a genetic component. However, we simply cannot find it. I find this very odd and was wondering if there were any studies (as of December 2021) that could shed some light on why some people are gay, straight, bisexual etc.
https://www.pbs.org/newshour/amp/science/there-is-no-gay-gene-there-is-no-straight-gene-sexuality-is-just-complex-study-confirms

Rather than sexuality which definitely has a genetic basis - without which the species would die out, are you perhaps referring to sexual orientation? Could you point to the studies that you claim "disprove" a genetic or epigenetic connection to show us evidence of your prior researches as per our requirements laid-out in the  [help]. Please also take our [tour].

Certainly. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0014821

Comments are intended for discussions that lead to improvements in a post. They are ephemeral and often overlooked; consequently they should not be used to convey information important to the post. Instead please [edit] your response into your post. ——— 2) Please give full reference information not just a link as links break. This is a good example of how to format references. ——— 3) Note that the paper you linked isn't about sexual orientation and their failure to find epigenetic markers is not proof that such markers don't exist!

It was cited as such. I didn’t read the full article.
I think you are being a little draconian. This is my first time posting on stackexchange biology

For what it's worth, there is never such a thing as a "something gene", that's just not how it works. All humans have the same complement of genes and this is a classic misconception in media reports on genetic issues. Can you explain what it is you say that "scientists" concluded in 2019? Can you also explain how the paper you linked to is relevant? That seems to be a study on ageing, and specifically how epigenetic modifications change with age, so I don't see the connection to your question.

Added source. The source uses the term gay gene.

As currently written your post suggests you lack the background to understand a real answer. Your source says "There is no gay gene" — what do you think you are supporting by adding that source? Science is a process not a body of "facts" — you will have a much better experience here if you do some additional reading and make sure you understand the basics of genetics (or if you do have that background, then make that clear by not using pseudoscientific terms like "gay gene"). In addition, you really must provide references for strong claims such as your second sentence.

there is no one gene controlling X, and X has no genetic basis are two very different things. height has no single gene but it certainly has a genetic component. there is also such a thing as triggered genetic elements, a male has all the genes to make a female and a male, but only one set of genes gets triggered. many genes are like this, everyone may well have the genes for every sexual orientation just as they have the genes for testes and ovaries.

Take a look at Greg Cochran's hypothesis.

On the epigenetics of sexual preference, please see the following:

Balthazart, J. (2020). Sexual partner preference in animals and humans. Neuroscience & Biobehavioral Reviews, 115, 34–47. https://doi.org/10.1016/j.neubiorev.2020.03.024

Balter, M. (2015). Homosexuality may be caused by chemical modifications to DNA. Science. https://doi.org/10.1126/science.aad4686

Wikimedia Foundation. (2021, November 2). Epigenetic theories of homosexuality. Wikipedia. Retrieved December 11, 2021, from https://en.wikipedia.org/wiki/Epigenetic_theories_of_homosexuality.

First article is great. Thank you very much!

You are correct. The Nature article to which you refer does contain the line, "There is no gay gene." But that can't be, and is not, the conclusion. In context:

The largest study to date on the genetic basis of sexuality has revealed five spots on the human genome that are linked to same-sex sexual behaviour — but none of the markers are reliable enough to predict someone’s sexuality.
The findings, which are published on 29 August in Science and based on the genomes of nearly 500,000 people, shore up the results of earlier, smaller studies and confirm the suspicions of many scientists: while sexual preferences have a genetic component, no single gene has a large effect on sexual behaviours. “There is no ‘gay gene’,” says lead study author Andrea Ganna, a geneticist at the Broad Institute of MIT and Harvard in Cambridge, Massachusetts. Ganna and his colleagues also used the analysis to estimate that up to 25% of sexual behaviour can be explained by genetics, with the rest influenced by environmental and cultural factors — a figure similar to the findings of smaller studies. “This is a solid study,” says Melinda Mills, a sociologist at the University of Oxford, UK, who studies the genetic basis of reproductive behaviours. [Emphasis mine; punctuation changed for formatting reasons.]

In stating, "There is no gay gene", you commit the offense that many journalists do when quoting scientific study results: you cherry-picked the sensational sentence, which misrepresents the entire paper.
The second paper you use as a source simply summarizes the original paper, which states,

Same-sex sexual behavior is influenced by not one or a few genes but many. Overlap with genetic influences on other traits provides insights into the underlying biology of same-sex sexual behavior, and analysis of different aspects of sexual preference underscore its complexity and call into question the validity of bipolar continuum measures such as the Kinsey scale.

People cherry pick for several reasons, some innocent, some less so. In 1999, Gur et al published a study on white and gray matter distribution in men vs. women doing certain tasks, revealing a difference. The result: headlines shouting that men really were different than women, and that men had more of the matter associated with logical processing than women. This was a complete misrepresentation of the findings, ignoring that this only pertained to brain usage during certain tasks. Some people used this oversimplification to support their bias that men were smarter than women.
Interpreting scientific articles is sometimes very complicated. Any attempt to boil it down to one take away - other than "it's complicated" - is usually wrong.

I read most of the article. Yes it’s more complicated than just saying “there is no gay gene” but when you are done reading; to sum it up; yes, sexuality cannot be determined by one singular genetic component.

@Aaron Of course the important context is that very, very little can be determined by one singular genetic component, beyond the molecular level. The examples that can are quite unusual and highly notable; that's what the authors are expressing: they have not been able to identify one of those notable, unusual exceptions.

@Aaron - It takes more than 100 genes to determine hair color. So, I would be correct in saying, "There is no single gene responsible for hair color." That is very different than saying/proclaiming, "There is no hair color gene!"

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What is the normal flora in Respiratory Tract (Upper and Lower)?
I opened my notes and it stated :

pharynx, trachea, bronchi : << flora normal
bronchioli & alveoli : steril

which I doubt because many papers I read stated that the lower-respiratory tract is not as sterile as we thought. However, the normal flora in the respiratory tract in all of these papers have different kind of bacteria. For example: one paper stated that the upper respiratory tract has Corynebacterium spp., Dolosigranulum spp., where other papers stated that viridans group streptococci, Staphylococcus epidermidis, etc. were found.

Welcome to Biology.SE. Can you please [edit] your question to add more detail including: 1) references & links to the papers you've consulted (example of how to format references; and 2) the organism is question (I'm guessing you probably mean for humans, but this is [Biology.SE] not [MedicalSciences.SE]). As written this may not be a great fit for this site since it seems to be asking for a list of microorganism names, so please also tell us why you want to know this. That may influence what kind of answer is appropriate.

I've done some copy editing on your post, but please make sure I've not altered your intended meaning. In addition, note that the abbreviation of genus names (e.g. you originally wrote S. epidermidis) should only be done after the full name has been written out. In the future please check your posts for spelling and readability before posting. Finally, please clarify what your question is — are you asking whether the lower respiratory tract is normally sterile or are you interested in the composition of the normal flora — each post should only have a single question.

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What is the limiting factor for algal growth in the oceans?
As far as I can tell, pelagic algae require four main things to live: sunlight, carbon dioxide, trace minerals and physical space. What is the limiting factor?
Note this is kind of a deceptive question, because although it might seem straightforward, it can be tricky to figure out the limiting factor. So, in fact, there may be no definitive answer, but nevertheless I am sure there are people out there who know more about this than me, and I am hoping to get some expert insight.

Sunlight varies by the depth and lattitude so it can be the limiting factor.

Maybe other animals eating it?

According to Liebig's Law of the Minimum, such organisms as algae will grow until they are limited by anything that they need. So unless we start from the absurd position that all marine environments are effectively identical, the limiting factor must vary from microenvironment to microenvironment.
A trivial example would be sunlight, as suggested in the comments. The photic zone of the ocean is only 200m deep, such that when you get deeper than that is is nearly impossible for algae to grow, due to the lack of sunlight. This is only one such limiting factor.
Another limiting nutrient that has gotten a lot of press is iron. In fact, there are people who think (or have thought) that we could reverse trends in atmospheric carbon dioxide concentrations and thus global warming through iron fertilization of the oceans. (I have not been following the literature on this but I believe there is reasonable to be skeptical of the claim.)
In other cases it appears that the limiting nutrient is phosphorus, or nitrogen, etc. There are obvious correlates to the problems of algae blooms, eutrophication, marine dead zones, etc.
There is a significant amount of academic work on this that I would recommend reviewing, to see if you can figure out the answer to your underlying question:

https://aslopubs.onlinelibrary.wiley.com/doi/pdf/10.4319/lo.1988.33.4part2.0796
https://www.jstor.org/stable/1352354
https://www.srs.fs.usda.gov/pubs/chap/chap_2019_grace_001.pdf


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How to use karyotype notation?
I'm looking at two karyotypes, one for a person with Klinefelter's Syndrome and another with Patau's. What is the karyotype notation for them? I don't understand what I looked up online. Any help is appreciated. Thanks!

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

At a minimum, posting the notation that you found when you looked them up would be helpful.


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How much of TLR 7 agonist is safe for human beings, as it is both linked to development of autoimmune diseases but is also used as Vaccine adjuvant?
This question is motivated by the fact that TLR 7 agonists have been linked to development and acceleration of Lupus-like disease both in animals and human beings. But at the same time, TLR 7 agonist at lower doses is also being used as vaccine adjuvant (in covid vaccine- Covaxin, for example).
I will quantify the what I know. The study on murine model shows that a dose of 100 microgram of TLR 7 agonist, 3 times a week, for 8 week, is lethal for mice and triggers Lupus-like disease. On the other hand, a single dose of covaxin has 15 microgram of TLR 7 agonist. That is, for two doses 4-8 weeks apart will give total 30 microgram dose to human beings.
Now human beings are about 3000 times heavier than mice. So, the lethal equivalent to human beings should be frequent doses of 300 milligram. What Covaxin gives is a total of 30 micrograms.
My question is, does this imply that Covaxin is safe for human beings? How do we interpret these numbers? Is there better understanding available in the field that can throw some light on what level of dosage of TLR 7 agonist is safe and when does it backfire?


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Is the response to a vaccine correlated with the reaction to the disease?
I was wondering if the response to a vaccine correlates with the reaction to the disease.
For example, if someone had a strong reaction to a vaccine, this person would also have had a severe course of the disease.
It is clear that it is hard to test a hypothesis in this case, but maybe someone could answer this question based on the biological mechanisms at work (receiving a vaccine vs. getting infected).
A similar question was already asked in Medical Sciences SE (for Covid vaccines), but was closed without an answer.

I see some theoretical potential that the general virulence of a bug (virus, bacterium..) to the human host could be (negatively) correlated to the immune-response caused by diverse vaccination methods against same bug.
While the ability of a bug to evade the hosts immune system e.g. by minimizing easily recognizable epitopes could establish a logical connection to the hosts immune reaction against vaccines presenting same epitopes, vaccine adjuvants diminish the correlation.
However, practically the bugs evolution against antibody recognition aims at preventing neutralization, while the prevention of immune-system activation is achieved via other mechanisms:
A common bacterial strategy, which is entirely uncorrelated to vaccination responses, is to produce proteins (virulence factors) that bind host antibodies to inhibit the host's immune system defenses. Another example that indicates poor correlation is  production of virus-induced anti-inflammatory cytokines that may suppress T cell outgrowth.
Such suppressed cytokines include: Interleukin 10 (IL-10) or transforming growth factor β (TGF-β), or reduced production of inflammatory cytokines, such as IL-12 (Marshall, Urban, Welsh; 2011).
However, you seem to approach this question from a different standpoint:

For example, if someone had a strong reaction to a vaccine, this
person would also have had a severe course of the disease.

Here, you you seem to define the correlation as a function of different people as opposed to different bugs, while assuming constant vaccines and other factors.
Also, you define the "reaction to a disease" as the severity of the course of the disease. In contrast, the vaccination response quite unambiguously must be interpreted as the immune response.
As a persons good immune response against a vaccine should be correlated with a good immune response against the bug itself (independent events; no temporal order) and a good immune response against a bug (necessarily) has to negatively correlate with severity of caused diseases (as you passively define all other factors to be constant), the severity of disease should theoretically be negatively correlated with immune response to the vaccine. This also assumes that the recognized epitope(s) of the vaccine, that define the "vaccination response" are the same that define the immune response against the bug. Also, please mind that existence of a negative correlation per se does not state degree of variance coverage (compared to other factors).

I appreciate the answer! But I still can't deduce whether having stronger side-effects (fever, fatigue vs. say pain at injection) to the vaccine (say, mRNA covid?) would imply a stronger reaction to infection (death vs fever). You said "vaccination response ..must be interpreted as the immune response.", but I do not know if immune response (number of antibodies?) is proportional to "symptoms". I also do not know how much of a role the absence of adjuvant would play when infected. If I had strong / weak side-effects to vaccination, would I be more likely to die from / survive an infection?


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What mechanism causes the presence of photosensitizers in mitochondria to change membrane ionic currents?
In the original question, the article in question was talking about specifically about this compound, Benzoporphyrin:
Characterization of Perturbing Actions by Verteporfin, a Benzoporphyrin Photosensitizer, on Membrane Ionic Currents
From my original understanding, the addition of a photosensitizer to the mitochondria of a cell and the presence of appropriate light causes a change in the ionic membrane current. Nonetheless, from knowledge of photodynamic therapy, using the benzoporphyrin would create reactive oxygen species, which would wreak havoc on the mitochondria.
Yet this is not the case and it also changes the membrane potential.
I originally wondered what was the mechanism behind this and I still do, however the article goes on to describe a multitude of varying research papers on the similar topic on various types of photosensitizers as if it were common knowledge, yet I could still not find an underlying explanation for this application's.
I will link the other papers which the original article refers to, but this seems to be a wide topic and not reserved solely to this paper. I hope this makes it easier to answer.
-Papers-: 1
2
3

Would the changes in currents show the direction/specificity expected by unspecific damage to mitochondria? Generally there are more ways to break something rather than to improve functionality (https://www.nature.com/articles/nrc.2017.32). Some photosensitizers seem to cause damage to the mitochondria trough reactive oxygen species (https://www.frontiersin.org/articles/10.3389/fphar.2020.557429/full).


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If x amount of a chemical starts to become harmful for a mice, then will 3000x amount of it start to get harmful for a human (3000 times heavier)?
My reasoning is simply that since human beings are 3000 times heavier than mice, the safety threshold for exposure to a chemical should be approximately 3000 times higher for human beings as compared to mice, assuming similar biology for both the organism.
Is there reason to believe this to be true? Or is this too naïve an assumption? If so, why?
As a concrete example, I am trying to understand what a study involving the harmful effect of 100 micrograms of TLR 7 agonist exposure to mice, can qualitatively say about its effect on a human being. Can we roughly assume that 300 milligram of the same TLR 7 agonist will have similar effect on human being?
Edit: Some people have shown concern that this question of mine is duplicate of another question that I asked - How much of TLR 7 agonist is safe for human beings, as it is both linked to development of autoimmune diseases but is also used as Vaccine adjuvant?
I think this is not the case. The earlier question is about a puzzle- TLR7 agonist is both helpful as an adjuvant and also triggers autoimmune disease in the same organism when the organism is exposed to different amount of the agonist. The question is, what amount of TLR7 exposure in human beings is hence safe?
On the other hand, this question is about how the toxic effect of any toxin scales with the body size of the victim? An answer to this question can partially answer the earlier question if there are murine models that have studied safe exposure levels to TLR7 on mice. But a proper answer to my previous question will involve how TLR7 agonist acts on human body, and why it is helpful at some concentration and why it backfires at some other concentration. The question, on the scaling of effect of a toxin, on the other hand, asks for a general scaling law.

This is seems to be a duplicate of your previous question How much of TLR 7 agonist is safe for human beings, as it is both linked to development of autoimmune diseases but is also used as Vaccine adjuvant?.  Posting multiple similar questions comes across as spamming the site and is not going to be well received. Please delete this post and focus on improving the previous version.

There is a scaling factor, which used to be (body_weight)^0.67 (see here), but I have no idea what the currently accepted value is, or even if body_weight (rather than, say, surface area) is the currently accepted criterion.

@tyersome I think the two questions are totally different. The TLR 7 question is about a puzzle- TLR7 has been shown both as harmful and useful at different concentration. The question is- when does this phase transition happen? The question in this post, on the other hand, is about how the effect of a toxin scale with the size of the victim? The first question is about transition point from helpful to harmful in the same organism. The second is about effect of the same amount of chemical in organisms of different size. Totally different questions. Just inspired from the same thing- TLR7.

I think you need to learn some terms - look up things like LD50, MIC (minimum inhibitory concentration) to start with. Compare those between different species.

It need not necessarily scale with body weight. Body weight (volume) does have an effect on the pharmacokinetics but drug/xenobiotic/toxin metabolism can also differ between different species.

This isn't exactly comparing apples to oranges, but it is like comparing peaches to nectarines. Humans and mice are not exactly the same except for size. As an example of metabolic differences between animals, adults can ingest 50 g of xylitol without problems (maybe diarrhea). Fifty percent of dogs weighing 50 pounds will die given 2 grams.

@anongoodnurse Does this kind of scaling effect of toxicity with body weight exist for two organisms of the same specie, between a newborn and a 5 times heavier adult, or perhaps two healthy adults with same BMI who naturally have different weights?

This isn't a "scaling event of toxicity". It's a physiological difference in metabolism. The comments are quite clear.

@anongoodnurse I am not sure if I understand you. This is not my field, so maybe I am missing something. I asked you a different question altogether in my last comment. Intuitively, it feels to me that an x amount of toxin will do more harm to an healthy average child than a healthy average adult (larger in size). Can this assumption be scientifically justified? Both are same species. Can we use something like (body weight)^0.67 scaling factor to judge the effect of the toxin, as suggested in the comment by user338907 ?

@TLR78agonist - Intuition isn't science. Scientists don't give human beings of differing weights toxins to test their ability to metabolize/survive. Also, not all toxins are created equally. If toxins must be administered (e.g. some chemotherapeutic agents are quite toxic), they are given in the lowest dosage shown to be effective. That's based on trials, not intuition.

@anongoodnurse My point was, whether such a scaling effect exists within the same specie, human or non-human. Scientists test effect of stuff on animals all the time, so I thought someone may have tested this. Agreed that intuition is not science, but is often the guiding principle in science. Surely a scientific method will determine whether this thing that appears intuitive to me is actually true or not. I just wanted to know if it is scientifically known to be true.


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Why does distention of the veins not decrease their resistance in the first case but decrease it in the second?
Here are two quotes from Guyton and Hall Textbook of Medical Physiology, Chapter 20 (emphasis mine):

Why is venous resistance so important in determining the resistance to venous return? The answer is that when the resistance in the veins increases, blood begins to be dammed up, mainly in the veins themselves. However, the venous pressure rises very little because the veins are highly distensible. Therefore, this rise in venous pressure is not very effective in overcoming the resistance, and blood flow into the right atrium decreases drastically.

A sudden increase in blood volume of about 20% increases the cardiac output to about 2.5 to 3 times normal. An analysis of this effect is shown in Figure 20-15. Immediately on infusing the large quantity of extra blood, the increased filling of the system causes the Psf to increase to 16 mm Hg, which shifts the venous return curve to the right. At the same time, the increased blood volume distends the blood vessels, reducing their resistance and thereby reducing the resistance to venous return, which rotates the curve upward. As a result of these two effects, the venous return curve of Figure 20-15 is shifted to the right. This new curve equates with the cardiac output curve at point B, showing that the cardiac output and venous return increase 2.5 to 3 times and that the right atrial pressure rises to about +8 mm Hg.

The quotes are from different sections of the chapter, so I believe they are unrelated. It seems that the distensibility of the veins doesn't cause their resistance to decrease in the first case, but does in the second case. Why?

Resistance clearly changes in the first case, as the paragraph is describing what happens specifically when resistance increases, which in turn leads to changes in venous volume. The second case is completely different, it is describing what happens when volume increases. Please think about it a bit and clarify your question.

@BryanKrause I've changed the title to make it better correspond to the question in the body of the post.

It still doesn't make sense, though. In the first case the scenario is that the resistance is increased. You seem to be asking "Why doesn't resistance decrease when resistance increases?"

@BryanKrause I'm asking why it doesn't decrease despite the high distensibility of the veins. Look at the second quote: the increased blood volume distends the blood vessels, reducing their resistance. I assume the blood also distends the veins in the first case, but why doesn't that cause the resistance to decrease, as in the second case?

Because the scenario there is that the resistance is increased... that's your given. Think if you were solving an electricity problem using I = V/R - if I said "R is increased" you'd know that either I must decrease or V must increase for the equation to hold. If you were then told that also "I is unchanged" you would then know that V must have increased; you would not ask "why isn't R decreased" when that happens.


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How does the first organism infected by a disease get infected?
How does a micro-organism causing some communicable disease infect the first organism it infected?
I was reading about HIV, when I found that HIV has jumped from chimpanzees to human beings. But, how did the first chimpanzee affected by HIV get affected?
In other words, is it possible (without artificial means) for a new infection to get started? How?
NOTE:
I am not aksing about the origin of pathogens, rather, about how they infect the first organism infected from it, and thus, become a disease causing microorganism.

Does this answer your question? How did viruses come to be?

Another related question. Please note that you are expected to do prior research (including, but not limited to searching on this site) before posting. In addition, micro-organisms includes many pathogens that are not viruses, so your question is unfocused and poorly worded as well as under researched. Please take the [tour] and consult the [help] starting with [ask] for details about what is expected.

@tyersome sorry, but I didn't mean only viruses, its just while reading about HIV, this question came in my mind

and @tyersome, I did not want to know how viruses or other microorganisms are "formed", instead, my focus was on how it "infects" the first organism it infected. For example, Rhinovirus (causes common cold) may have formed from dna fragmemts, or whatever. I was asking that how did the first rhinovirus-infected organism get infected?

The key term to find information pertinent to this question is Zoonosis (link to the Wikipedia article).
However, one should not generalize zoonotic origin to all the diseases affecting humans - in fact, the relationship between humans, diseases, and other organisms carrying these diseases is rather complex.

Some diseases are uniquely human: their origin is unknown - they might have evolved together with humans or were transmitted to humans or their predecessors millions or billions years ago. Smallpox is one example - it became eradicated as soon as it was eradicated in human population.
Other diseases have evolved to be transmitted between different types of hosts, e.g., such as humans and mosquitoes. Flaviviruses, such as Zika, Yellow fever, dengue, west Nile virus are examples of such pathogens, adapted to two different types of hosts. In fact, some of these are adapted to mammals other than humans, but capable of infecting humans due to sufficient similarity. Some of these might not be able to effetcively replicate in humans, even though being a serious health hazard.
For some diseases insects (or other organisms) serve as mechanical vectors, merely carrying disease from one human to another or from a human-like animal to humans, while not infecting the vector.
There are animals that can be infected by both animal and human viruses. E.g., the types of influenza affecting many birds are not dangerous for humans, and these birds do not get infected with human influenza. However, pigs and paultry may get infected by both. The influenza viruses coexisting in a pig then undergo gene reshuffling, producing new viral strains infectious to humans, that humans get from pigs.
Finally, what the OP probably had in mind is the transmission of viruses such as Ebola, SARS/MERS, and HIV which exist in nature as animal viruses and suddenly transform to become human viruses. This is an evolutionary process, which is rarely successful.

HIV
E.g., the bushmeat consumption has probably on many occasions introduced SIV to human population - perhaps thousands or millions times during the history of this virus. However, not being adapted to humans, the virus didn't cause pandemics - until the moment when this transmission as accompanied by a fortunate mutation (or mutations) that allowed it successfully replicated and be transmitted in human population. It is quite possible that it took some time for this virus to further adapt to human population before it became as lethal as it is.
Ebola
Ebola is an example of virus that seems to be poorly adapted to human population - although successful in replicating itself, it fails to keep enough hosts alive to assure its permanent existence in the population. Last century has seen multiple Ebola epidemics, all successfully contained by quarantine measures. There have been probably many more spillovers over the course of human history, but they all ended with virus becoming extinct in the human population by eliminating available hosts.

Can you tell me how: 1) Uniquely human diseases got into the human population? 2) Multi-host disease causing pathogens infect the first host it infected? 3) Pathogens which use insects as vectors infect the first human it infected? 4) Pig influenza virus get into the first pig it infected? 5) HIV/ Ebola viruses (before mutation) infect the first animal they infected?

The two threads linked (here and here) have some information, but no one knows for sure, since it happened long time ago. HIV, Ebola, Zika, SARS/MERS are well studied, since they happened recently. Some other disiseases are merely mentioned in historical records from a thousand or two thousand years ago (see also this thread), but we cannot look back any further than that. Unlike dinosaurs, viruses and bacteria have not left fossil records.

okay.. thanks:)

Viruses evolve like all other biological species. The family of SIVs that gave rise to HIV goes back millions of years across many hosts.
Just like you can build a "family tree" out of related plant or insect or mammal or bacterial species, you can do the same with viruses. The family tree of HIV and SIV goes back to a broader classification of lentiviruses that includes some affecting non-primate mammals.
Viruses affect all types of life: bacteria and animal, plant and protist. They've likely existed as long or nearly as long as cellular life.

Oversimplified, your answer means new infectious diseases are caused by evolution of already existing micro-organisms?

If that's true, then I got it, thanks.

@AsmitKarmakar Yes, that's accurate.


text:
Why is the genetic code so heavily conserved?
Except some organisms, most organisms follow the same Genetic Code
tRNAs, tRNA synthetases, ribosomes, etc. comprise the translational machinery for converting nucleotide codons to proteins.
My question is:
Why is the genetic code so heavily conserved across life, given that the genes for the translational components noted above presumably vary significantly across evolution?

Can you cite any sources or point to anything that indicates where you got your information? Note that the genetic code is not the same for all organisms: https://en.wikipedia.org/wiki/Genetic_code#Alternative_genetic_codes

It looks like you might be looking at this or something like it: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783965/ Note that while tRNA genes sometimes go into the nucleolus, they do not leave the chromosomes. It is just that the tRNA part of the chromosome goes to hang out in the nucleolus for a while!

@MaximilianPress my bad, I didn't google alternative genetic codes, because I thought only one existed. Still, the vast majority of organisms (Except mitochondrial genes of some organisms) follow the same genetic code. I will add edits to my question.

@MaximilianPress You mean that tRNA are synthesised from chromosomes the same way mRNA are (by transcription)?

Even if they are synthesized from DNA, what if that specific part of DNA (which codes for tRNA) undergoes variation?
Wouldn't that lead to large diversity of genetic codes, possibly one for each species?
Why is it not the case?

I suggest that you read more about the evolution of translation and transfer RNAs, they are not stable in their sequence (e.g. https://www.frontiersin.org/articles/10.3389/fgene.2014.00303/full). While in general the genetic code and the translational apparatus is remarkably conserved (and therefore a good argument for a single origin of life), it is by no means "frozen" or identical across all organisms.

tRNAviz is a neat tool from the Lowe lab that allows you to visualize the structure and sequence variation of tRNA isotypes across the tree of life.

looking at update to question: what do you mean by "vast diversity of genetic codes"? I am sure that the nucleotide sequence variation underlying the genetic code is "vast", but that is probably not what you mean. I am not sure what "vast" diversity of a qualitatively-defined multidimensional construct looks like. If you are confused about evolutionary stasis, why it's hard to get "better" than the existing code, that would be a more answerable question.

@acvill that link seems to be broken, this one works: http://trna.ucsc.edu/tRNAviz/summary/

@MaximilianPress Thanks!

I  suggest you reflect on what happens if a single mutation occurs in a gene during evolution. There is a chance that it can be lethal, beneficial or neutral. Now, how many mutations would occur in a bacterium of 1000 genes if a mutation of the anticodon of a tRNA caused the wrong amino acid to be inserted everywhere it occurred? And what effect would that have? So the question — which is not easy to answer — is really, how did the alternative genetic codes ever evolve?

@MaximilianPress >what do you mean by "vast diversity of genetic codes"< Explaining in detail: Think that all living organisms evolved from a single cell which had some DNA. Now, without variation, that single DNA would get replicated exactly as it is, and all that would exist on earth today would be single celled organisms. Because of variation, that DNA changed to large diversity of genomes unique to each organism.

@MaximilianPress My question: If tRNA is formed from DNA, then it should be subject to mutation and crossing over. That, in my opinion, should lead to an unique genetic code in each organism, which is not the case.

@David, do you mean "there obviously may have been mutations of tRNA anticodons, and that would effectively kill the organism in which that mutation occured."? If that is what you mean, what if a human zygote undergoes such a mutation? If that isn't what you mean, please explain more.

Comments are not places to answer questions but to suggest improvements in them or ask for clarification. Improvement (or withdrawal) of your question can, in my opinion, be made if you think a little more about the consequences of your proposition. I say nothing about what "obviously" must have occurred, only ask you to think of the consequences. How many mutations would a mutation in the anticodon that changed the amino acid specificity potentially cause in the case I mentioned? One, 1000, 5000? Could an organism (zygote or whatever) survive the larger numbers?

And you might edit your title to express what your idea properly. Transfer RNAs of all organisms are not "the same" — the relationship between anticodon and cognate amino acid conforms to the standard genetic code in most cases.

@MaximilianPress — Whether or not your edit makes it a good question, it clearly does not reflect the concern (albeit misguided) of the OP. And ribosomes and tRNA synthetases are red herrings. A more interesting case study would be of the original amber and ochre mutations that led to the identification of stop codons.

@David Following this over-long comment discussion, I see OP as being principally concerned about stability of the genetic code across evolution. From this point of view, I see the edit as directly reflecting the concern of the OP. I believe that a fixation on tRNAs is an over-reductive view on this very complex problem. If you or OP would like to roll back and propose a more appropriate edit, I invite you to do so.

@MaximilianPress thanks for the edit. It exactly is my concern.

@AsmitKarmakar Thanks for confirmation. I have now attempted an answer, as I think that this is easier to answer.

There are a variety of posts on this site already that address related questions:

History of ideas about the form of the genetic code
Why 20 amino acids instead of 64?
Is there recent info about the hypothetical ancient two-codon genetic code?
How did the genetic code evolve?

I don't believe that any of these answers specifically address the high conservation of the code, except as implicit (though I could be missing something).
A useful paper
However, one such post links to this paper that discusses the evolution of the genetic code.
Part of the introduction restates the question's motivation rather well, I think:

The fundamental question is how these regularities of the standard code came into being, considering that there are more than $10^{84}$ possible alternative code tables if each of the 20 amino acids and the stop signal are to be assigned to at least one codon.

In other words, why has this space of $10^{84}$ codes not been more widely explored than we observe in nature?
The first part of the paper's abstract seems relevant (I have bolded a few sections that might be taken as explanatory hypotheses):

The genetic code is nearly universal, and the arrangement of the codons in the standard codon table is highly non-random. The three main concepts on the origin and evolution of the code are the stereochemical theory, according to which codon assignments are dictated by physico-chemical affinity between amino acids and the cognate codons (anticodons); the coevolution theory, which posits that the code structure coevolved with amino acid biosynthesis pathways; and the error minimization theory under which selection to minimize the adverse effect of point mutations and translation errors was the principal factor of the code’s evolution. These theories are not mutually exclusive and are also compatible with the frozen accident hypothesis, i.e., the notion that the standard code might have no special properties but was fixed simply because all extant life forms share a common ancestor, with subsequent changes to the code, mostly, precluded by the deleterious effect of codon reassignment.

They then review a variety of evidence for each theory, from which I will present one example.
Is the genetic code optimal?
They note a 1991 paper that used biophysical properties of amino acids and estimated that a randomly selected genetic code was ~0.01% likely to be at least as robust as the existing genetic code. In other words, the code seems to have at least somewhat minimized possible errors. So, the existing code is at least well above-average in terms of possible codes, and it's possible that the reason no better codes have been explored is that it's trapped in a local minimum of the code landscape (see Figure 3 from that paper here).

They go on to discuss this in more detail. I personally find other evidence about the "coevolution" and "collective evolution" theories interesting, but obviously it is hard to repeat a multibillion year experiment.


text:
Using the law of independent assortment, why can't heterozygous parents make identical twins?
In a case where two parents are heterozygous, why can't any pairs of their children be identical twins? As the question asks, I tried to explain this using the law of independent assortment, which states that alleles a gamete receives for one gene do not affect alleles for the other. I don't get how this relates to identical twins. When I searched this up, I found that identical twins come from when an egg splits into two, but if it's one cell, why would the law of independent assortment matter? Same with the heterozygous part - why would that affect the formation of identical twins when it's copies of the same cell? Any help is appreciated, thanks!

They do it all the time, because identical twins come from one (fertilized) zygote splits into two embryos instead of remaining one. You and I understand this, but I don't understand the rest of your question. The independent assortment already happened before that split. :/

what do you mean when you "heterozygous" exactly? all humans are heterozygous (or rather, the probability of complete homozygosity of a human genome created by sex is astronomically small)

Are you sure the question is about twins? or just identical children from separate gestations? If the latter - then you can explain it using independent assortment. The former - as already mentioned - happens all the time for reasons already explained.


text:
Scientific word for organisms that can regrow themselves
Is there any term for living organisms or more specifically animals that can regrow a whole from small components (assuming sufficient quantity of cells or specific organs are present)?  For example - as I understand - worms can regrow from a relatively small part of a worm - fragmentation?  Some creatures can regrow limbs.  Many plants can grown from small cuttings or root segments (fragmentation) as well as by budding.  I wonder if any term exists to describe all of these processes, either for the respective kingdoms or more generally.  In other words is there a class of life that is definitely not like mammals, which cannot reproduce limbs let alone survive the loss of any major organ function?

Yes, there is a term: This process is called regeneration.

…and you might describe the organisms as self-regenerating.

OK regeneration is clearly a related contept, but reading up on the term it's about biological processes rather than classification of organisms. Plus humans have some regeneration abilities. Perhaps my question is asking for a false dichotomy.


text:
Do lobsters demonstrate any problem solving capability?
I was watching this video where a man takes a grocery store lobster and raises it in a salt tank, the lobster exhibits curious behavior that looks like intent.  In the comments there was a claim that lobsters were intelligent animals on par with the octopi, one user claiming they could perform complex tasks related to problem solving and cooperation and that they have experienced this behavior first hand.  Looking it up I could only find a single article from peta discussion, which vaguely hints at cephalopod like intelligence.  I've not seen any supporting evidence or even discussions from reputable sources to back up anything further.
What's more is that I've looked up the neuron count for lobsters, my understanding was the smartest arthropods were things like ants and bees, and that most ocean arthropods had significantly less neurons than even ants.  I understand that you shouldn't use neurons as a proxy for intellect, and arthropods often don't have "brains", but this should apply to both lobsters and cephalopods.  In other words, using neuron counts may be applicable in comparing rough cognitive capabilities of cephalopods and arthropods, especially with several order of magnitude gaps between the two (100,000 vs 500,000,000) and because the way in which neurons are used in their body is similar.
I have huge skepticism that lobsters can demonstrate any significant problem solving capability, let along problem solving capabilities on par or comparable to cephalopods.
Are there any reputable pieces of evidence or experiments that demonstrate lobster problem solving skills?

They are curious creatures (in the can-I-eat-it-or-fight-it sense), but I doubt they have much problem-solving capacity. I seriously doubt they're as smart as cephalopods, but they probably can learn, at least a little.
They don't use a high intellect to hunt and ambush their food or to avoid predators like octopi because they largely rely on their armor and claws for defense, and they're mostly omnivorous so they'll eat plants and algae until prey wanders into their space on so they wouldn't evolve the brain for complex thinking.
I watched the video and that particular species is territorial (hence the rubber bands on their claws) so much of that intentional behavior has to do with how it maintains and protects it's territory (moving waste away from it's sleeping space to avoid attracting predators, moving the substrate around, grabbing foreign objects in it's space etc.).
I also tried to find articles on lobster intelligence, but as far as I read they don't exhibit problem solving behaviors anywhere near as complex as octopods and other cephalopods, at least not from any scientific articles that cited their sources. That doesn't mean they're not interesting though, I found this really neat article on the effects of serotonin on certain crustaceans aggressive social behaviors.
I hope that answers your question.

Welcome to Biology.SE. We're looking for answers that provide explanation, context, and include references to reliable sources. Your post appears to be mostly opinion/speculation, which is not appropriate for this site. You will get a more positive response if you explain why your answer is right and support assertions with appropriate citations. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] or delete your answer accordingly.


text:
Any evidence that getting a covid booster works for omicron?
I've been hearing colloquially that the booster helps for immunity to Omicron, but haven't actually found any evidence supporting this. Does anyone know of any studies that look at the efficacy of the vaccine for Omicron cases?

Does this answer your question? Why are scientists saying that the Omicron COVID-19 variant is a reason to get a booster?

The Omicron variant of SARS-Cov-2 is still so new, that until the last few days there has been no statistical raw material on clinical experiences and patient-data to show what protective effect is given against it by the original covid-19 vaccines.
In default, therefore, of patient data, laboratory tests have been made on antibody serum samples from boosted vaccinees, and these have indicated the likelihood of much better protection against Omicron by boosted doses (i.e. a 3-dose schedule) of the original vaccines rather than the original two, which have shown themselves effective against the original form of this coronavirus and its kown previous variants before Omicron.
Naturally of great interest is actual clinical patient data, and within the last week, the original laboratory data have been supplemented by publication of a (preprint) report of a UK-based case-control study surveying actual patients.
The report itself can be found at (https://khub.net/documents/135939561/430986542/Effectiveness+of+COVID-19+vaccines+against+Omicron+variant+of+concern.pdf/f423c9f4-91cb-0274-c8c5-70e8fad50074),
and its results are described and excerpted in this answer:
(Why are scientists saying that the Omicron COVID-19 variant is a reason to get a booster?) .
(The link here is to a 'second/supplementary answer' at tab /105626#105626 .)
In brief, these are early patient data, the identifiable Omicron cases are predominantly of milder infection, and the patient statistics in the case-control study, so far as they go, confirm the laboratory test data in showing a markedly enhanced vaccine effect against Omicron when a booster dose of the Pfizer/Biontech vaccine is used.
The report's conclusions include that

"our findings support maximising coverage with third doses of vaccine
in highly vaccinated populations".

For more, see the earlier answer.


text:
How can stat major get into bioinformatics?
I'm in my first semester of phd in information science and
I want to work with bioinformatics professors.
As a stat major, what should I prepare for before contacting some of them?
I thought about completing some coursera courses in bio but will they count?

I know little of the subject, so not an answer, but you can take a look at our dedicated sister site: [bioinformatics.se], they might be able to give you a few pointers. Please take their tour and have a look at their help centre before posting to ensure that your query is on-topic.

I suggest moving this question to Bioinformatics or Academia communities.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and delete or [edit] your question accordingly. In particular, please note that opinion based questions such as this are not appropriate — questions should be about biological processes or mechanisms and have factual answers. This is neither and thus is likely to keep accumulating down and close votes.

Thank you Rogue and Roger.

In addition to what I said above, you now seem to be crossposting this on Bioinformatics SE. Cross-posting is impolite and your post is off-topic for the same reasons there as it is here.

People, you cannot on the one hand tell a new OP that something should be moved  to another SE and then call them out for crossposting. That is toxic behaviour. Better just recommend to switch to a completely different community such as Reddit and Biostars where opinion-based answers are accepted and make a closing vote.

@ATpoint: There is no toxic behavior here only standards and the SE model in action. 1) The first user who suggested moving also said to check the help before posting — if the OP had done so they would have found that this post is off-topic here and there. 2) I never suggested moving this post (and would have mentioned not crossposting if I had) and directed the OP to appropriate resources for details about how to use this site, which they do not appear to have consulted. 3) If you wish to discuss this site and how it works then please use [meta].

Bioinformatics is still rather open to people with various backgrounds - biologists, mathematicians, statisticians, physicists, computer scientists. Solid base in math and/or software development is greatly appreciated.
The usual entry paths are:

Doing Masters in bioinformatics after having done previous studies in another field (usually biologists learn a bit of math and programming, while computer scientists learn a bit biology)
Doing a PhD in bioinformatics - this seems to be your case. So it may be a good thing to contact potential supervisors for doing a thesis in bioinformatics.
Doing a postdoc in bioinformatics (similar to the previous option, but later in the career and with less opportunities outside of the academia).

Remark: In English-speaking academia one more frequently talks about Computational biology rather than bioinformatics - it is a broader term, encompassing many useful areas of research (see this thread). It has however limited use outside of academia or in other languages.


text:
Phenotype of a possible gene mutation
I have noticed multiple cases where patients had similar body characteristics :

decreased ability to gain weight (slim)

they are capable of sleep only 6 hours or less with normal functioning (although they prefer long sleep)

increased susceptibility to ligaments and connective tissue damages

CVS morbidities: example angina

I think its a good opportunity to ask here what could this mutation be and how would someone search for such characteristics in gene mutation databases.
I searched a lot using ordinary way and found a possible match ( ADRB1 receptor mutation) it causes the affected person ability to sleep less hour and CVS symptoms but i can't confirm if that's the case with the first and third characteristics.

Sounds a lot like the symptom of Marfan syndrome.

@bob1, marfan syndrome would have a different presentation  (you will notice their long extermities and eyesight problems ) not quiet like this case.


text:
Bug Identification: Black Insect with Red/Orange dot on back
I lifted the cover off my push bike today and discovered 15-20 of these insects all along one of my brake cables.
A few were tending to "egg" like structures that were stuck to the cable and stood out (I've since wiped these away).
I've never seen these before and haven't had much luck Googling or reverse image searching.
They have black "ant" like bodies with orange/red dots on their back. The same orange/red is present on the tips of their "feelers".

Video of one walking down my tyre; https://i.stack.imgur.com/LTm5b.jpg
This was in Queensland, Australia.

It's difficult to judge scale from the pictures, could you give us some rough idea of size at all?

@ARogueAnt. it was about the same size as a large ant.

Possibly young harlequin bugs.

The narrow black body, long bent legs, red abdomen, and red-tinted antennae all make me think this is the nymph of a hemipteran called an assassin bug (Family Reduviidae).
The nymph of the Bee Killer Assassin Bug (Pristhesancus plagipennis) looks similar to yours and is found in Queensland. [Source: Queensland Museum]

 Source: Queensland Museum

This is definitely what I saw! Thanks!


text:
Owl identification. Winter in Haliburton, Ontario, Canada
Is this owl a 'Great Grey Owl' or 'Barred Owl'? I'm thinking a Great Grey because it was quite huge - about 1.5 to 2 feet tall.

Cross-posted on The Great Outdoors

That is a nice picture of a Barred Owl. The heavy well-separated streaks on the breast and eye color (dark vs. yellow) are both distinctly different from that of the Great Gray. The markings in the facial disk are also distinctive — e.g. the fine even lines in the Great Gray vs. the blurry, more disordered pattern in the Barred. (Also Great Gray Owls are even bigger: 60-80+ cm long vs. 40-50 cm for Barred Owls.)
An excellent resource for identifying North American birds is the Cornell Lab of Ornithology's All about birds site. That link is to their comparison between these two species.

I agree. Strix varia (barred owl) vs larger, greyer, Strix nebulosa

Cornell has a great phone app, too, btw, to identify birds by sound. Its recognition accuracy is impressive.


text:
How would a virus “evolve” if someone is infected with both the omicron and delta variants at the same time?
If someone is infected with both variants (let’s say within a day or two), what are some of the likely outcomes with respect to the virus “evolution”?

is it most likely that only 1 of the 2 variants survives?

if both survive, is it likely that the 2 strains “mix” with each other to produce a 3rd strain?  Obviously 2 viruses don’t have “sex” per se, but I read https://www.cnbc.com/2021/12/05/omicron-variant-may-have-picked-up-a-piece-of-common-cold-virus.html  that the omicron strain actually has a gene that is found in the common cold virus.

By what mechanism could that have happened?  Somehow a common cold gene got inserted into the virus, or did that just happen by random mutation?
My primary question is by what mechanism would a virus insert a snippet of RNA from another virus into its own RNA?
On further study, I found this link to an OSF preprint which talks about “template switching”.  https://osf.io/f7txy/
Here is the text:

This highly mutated Spike variant harbors a novel insertion mutation ins214EPE. Although the position 214 appears to be an insertion hotspot10the EPE insertion in Omicron appears to be novel. Previous analyses of sequences deposited in GISAID suggested that insertions in the SARS-CoV-2 genome likely arise from polymerase slippage or template switching.10,21Template switching is a normal event during RNA synthesis for coronaviruses, as this process is used to generate sub-genomic RNAs (sgRNAs).22,23In this process, also known as copy-choice recombination, the RNA-directed RNA polymerase (RdRp) and the nascent strand dissociate from the template RNA strand and reassociate with a new template (or the same template at a different position), and then RNA synthesis continues. Typically, such recombination involves templates with high sequence similarity (“homologous recombination”), although non-homologous (or “illegitimate”) recombination between dissimilar sequences can also occur.

Could someone boil down the meaning here in simpler terms?  For starters, I don’t understand how recombination applies to viruses?  Isn’t recombination a DNA process?  How does it relate to viral RNA?

Welcome to the site. Please take a [tour] and visit the [help]. In particular this SE values questions that show some prior research (and attempts to answer it themselves) and scientific backing for claims. Please provide a reference for the flu gene insertion, and demonstrate what you have found out about this topic.

how rhinovirus swap RNA is not understood but we are fairly confident they do. https://www.nih.gov/news-events/nih-research-matters/understanding-common-cold-virus

Ok.  It makes sense that we just don’t know the recombination mechanism(s) yet.  I had been reading a lot of sources that seemed to gloss over the details.  I guess we just don’t know the details.

Basically your options 1 and 2 are the the only likely outcomes from a co-infection with two SARS-CoV-2 viruses. There is a 3rd option, which is that there is a co-infection, producing some amount of both viruses.
Total competition (i.e. one being completely gone, the other 100% output, your option 1) is unlikely unless one of the co-infecting strains has low initial input (i.e small amount infected), and low replicative ability compared to the other strain. In this case, you might see that one of the viruses doesn't survive the competition. However, this would be hard to detect with current technology and hard to prove experimentally as well unless the strains had sufficient differences (i.e. not just single base mutations) and you could survey the entire viral population to look for levels of output.
One of the reasons for these difficulties is that viruses, particularly RNA viruses exist as what is known as a quasispecies, this is where there is a pool of virions with variant genomes as the output from any particular infection. This is caused by errors in replication of the genome (RNA polymerases tend to be more error prone than DNA polymerases and/or not have a proof-reading mechanism, though SARS-CoV-2 (RNA virus) does have a proof-reading RdRP1 (PDF)). Because of this, and because of the way we do most sequencing - by chopping the genetic material into small bits, then assembling a consensus sequence computationally - it can be difficult to tell if there is a population of virions that are one strain or not, as the computation methods lead to missing of the non-dominant sequences. There are methods (computational and new technological) to look at these sorts of things, so we may have a better idea soonish.
For option 2: Recombination is common where-ever there is a genome, be it DNA or RNA. RNA polymerases are particularly prone to recombination events, and this is a major driver of evolution of RNA viruses2. Indeed it seems that this is a common feature of Coronaviruses in general3. Basically what is happening here is that there are multiple strands of RNA present at replication and the RNA pol can jump from one to another, often in a sequence dependent manner (i.e. at regions of high similarity) or sometimes where there is secondary structure of the RNA that causes the polymerase to jump from one location to another based on proximity, skipping the bits in-between.
Now, there's a bit of complexity here - there are multiple different genera of coronavirus called Alphacoronavirus to Deltacoronavirus (nothing to do with the SARS-CoV-2 variants, just unfortunate naming choice from someone(s) when dealing with this virus). The different coronavirus types have the same overall RNA structure (i.e. encode the same genes), but have quite diverse sequences, so an Alphacoronavirus has a different sequence to a Gammacoronavirus, meaning that homology based recombination is less likely than within the genus. Having said that, there are still highly conserved parts of the genome within the family as a whole, so those might be sites where recombination could occur.
1: Robson et al., Molecular Cell  2020; 79(3):710-727.
2: Tackas et al., Plant Virus-Host Adaption: Molecular Approaches and Viral Evolution. 2014; 385-394 (paywalled?)
3: Kek et al., Adv Exp Med Biol. 1987; 218:99-107.

Thank you for this answer.  Interesting.  So can RNA polymerase “jump” from one strand to another at any point on the strand?  Or are there only a few well-known points where jumps can occur?

Yes they can jump. Generally this seems to be done at certain regions within the RNA and these sites are consistent across a genome type. I think it can happen at any location, just is much more likely to happen at specific places.

bob1's answer describes the general mechanisms very well.
One must not forget that the emerging recombinations still underly the pressure of evolution: They need to survive and to spread with a rate at least comparable to the original strains.
Nature has done this big experiment and now we can see several small clusters of Delta/Omicron recombinations, see pango designation issues #473, #439, #444—now assigned pango lineage XD, #445—pango lineage XF, and #446 for details.
It is interesting that the successful recombinations follow some pattern: The Spike gene is completely or at least to the greatest part from Omicron, ORF1ab is completely or partly from Delta. Most interesting is the recombination described in #444: It has just an Omicron spike in a Delta backbone.
EDIT: More than half a year later, more Delta/Omicron recombinants have shown up(XAW, XAY, XBC, and XBD), some of them with considerable spread. For an overview of the current state of affairs (27-NOV-2022) see this article by C. Roemer et al. on virological org.

If you were to speculate on how omicron has a gene found in the common cold, would you speculate that this happened by random mutation, or by actual interaction with a common cold virus?  I understand this is pure speculation, but what odds would you give?

This is a different question and should be asked as a question, not in the comment section. But any acquisition of a complete gene, i.e., something with >100 nucleotides or >33amino acids needs a cause. Since common cold viruses are still coronaviruses, and two of them even betacoronaviruses, I would say that acquisition by interaction is almost secure and random mutation is precluded. But we have not seen this in the wild upto now.

Yea it is a different question, but this site frowns on speculation (understandably).  This is why I framed my original post the way I did :)


text:
How should I measure the oxygen dispersed during photosynthesis in pondweeds?
I am to conduct a lab investigating how different wavelengths of light affects photosynthesis in Egeria pondweeds.
The idea is to put color filters on light bulbs and shine them on the pondweed in a sodium hydrogen carbonate solution. Then to measure the oxygen, I have an oxygen sensor which measures dissolved oxygen (mg/L).
Now, what I have a trouble with is if measuring the dissolved oxygen is the right way to measure the rate of photosynthesis depending on color of light? Will it work?

One experiment I saw online, was that during 5 minutes you measure the oxygen dispersed, and it will show you the mg/L depending on time.

That solution might just kill the plants.

Why not do it in a standardised pondwater, unless you don't mind the results being for only that sodium bicarb solution?

A couple thoughts.  The plant is undergoing cellular respiration too, so I am not sure that there will be a net oxygen out.  I assume that the sodium hudrogen carbonate is going to provide a source of carbon dioxide to a closed system, but even then the plant will release carbon dioxide from respiration from sugar that it has made and burned.

Is the atmosphere sealed and airtight?  You could possibly have Sodium Hydrogen Carbonate in a water reservoir in the container, but not in the water that the pondweeds are growing in.

what margin of error is acceptable in the result of your tests,light bulbs and filters might not be the best way to produce the different parts of the electromagnetic spectrum you want(i guess you want to keep the energy level fixed so only the color changes).different LED`s might be a better solution for your experiment.

Bubble formation might be easier to measure than oxygen concentration. Bubbles can be measured optically Or acoustically.
A sealed container with a little carbon dioxide gas might work.
See below article.
“Acoustic effects during photosynthesis of aquatic plants enable new research opportunities”
Helmut G. Kratochvil and Michael Pollirer
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349586/

You can also work out via displacement - pondweed underneath an inverted container, traps bubbles that escape (gentle agitation might help) and measure volume .

The experiment means anything only if different "colors" (wavelengths of light) affect the rate of photosynthesis. A good experiment requires that you "keep everything same/identical*, to the extent possible, save the color of the light the plants are exposed to. If you detect any changes in the concentration of oxygen, you can plot the color of light to the oxygen concentration.
Photosynthesis is a chemical reaction:
$6CO_2 + 6H_2O \rightarrow C_6H_{12}O_6 + 6O_2$
At the very least, the concentration of $CO_2$ and amount of $H_2O$ must be constant for different colors, as they can alter the rate of photosynthesis, and are therefore confounding factors.


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What has a more negative impact: Having only a partial deletion of a specific gene or the having entire gene deleted?
I am looking through a genomics database to see whether patients who have intellectual disability have deletion of only a specific gene of interest and no other mutations (e.g. deletions or copy number variations of other genes).
I have seen that some patients have deletion of the entire gene whereas other patients have deletion of only part of the coding region of the gene. However, even if part of the gene is deleted, patients have intellectual disability and other abnormalities.
I was wondering, in general, is it more serious for a person to have a deletion of an entire gene in contrast to having part of the gene deleted? Can having part of the coding region of a gene deleted be just as serious as having the entire gene deleted?
Thanks.

Highly gene dependent I suspect - delete an important motif in one gene then yes, delete one repeat in a highly repeat rich gene (e.g. Ankyrin repeats) and it might not be.

I strongly agree with bob1, a particularly clear example is that some partial deletions will result in a dominant negative allele — these will have a stronger effect than a complete deletion. ——— Consequently, this is only answerable for specific deletions of specific loci. As written this isn't a question with a useful answer, so I've voted to close.

The answer depends as @bob1 says on the gene and the mutation probably.
For a simple analogy, think of a gene like a chainsaw or other piece of machinery.
To break it down a little:
Full gene deletion
We expect a full gene deletion to be associated with a loss of function. This is very bad if the gene is essential to life
If you lose your chainsaw, you can't cut anything, which is bad if you need to cut things e.g. for your job.
Partial gene deletions
Are more ambiguous. They might cause:

Full loss of function of the gene (equally bad to full deletion).
A crucial piece of your chainsaw is broken, so you can't start it.
Partial loss of function of the gene ("hypomorphs", less bad than full deletion).
There's something wrong the chain on the chainsaw, so it's slower than usual, but you can still cut some wood.
Gain of function of the gene (could be better or worse than full deletion!)
There is something wrong with the gas tank, and the chainsaw might explode and hurt you!

Gain of function is the most interesting but probably the rarest. Here is one example, where a partial deletion of the tumor suppressor gene p53 switches its function so it turns into an oncogene (a tumor promoter), effectively switching its function from protecting against cancer to making cancer more likely.
Here is a powerpoint from a class that goes over gain-of-function and loss-of-function in a little more detail.


text:
What specific interaction between methylphenidate and quetiapine causes toxicity concerns?
A number of reputable sources on drug interactions posit a potential interaction between methylphenidate and quetiapine, described on Medscape as follows:

quetiapine increases toxicity of methylphenidate by pharmacodynamic antagonism

I'm trying to understand the pharmacodynamics of this supposed interaction, and where the elevated toxicity concerns come from. I've been unable to find a direct source for it that describes the exact mechanism of toxicity.
I'm coming at this without a whole lot of background in the topic, but I do understand the basics of binding profiles, dissociation constants, agonists/antagonists, binding affinity, etc., which has at least allowed me to do a bit of preliminary digging. This is what I came up with, based on the reading I've done so far:
Quetiapine's binding profile differs from its primary active metabolite, norquetiapine. Both have a fairly long list of receptors to which they can bind: SERT, NET, 5-HT receptors, α receptors, σ receptors, dopamine receptors, histamine receptors, and muscarinic acetylcholine receptors.
The most frequently theorised hepatotoxicity concern for methylphenidate apparently involves an interaction with β-adrenergic agonists. However, quetiapine does not appear to have any particular binding affinity for β1 or β2, and the description above says antagonism rather than agonism.
Methylphenidate mostly affects DAT and NET, along with a couple of 5-HT receptors.
5-HT1A seems unlikely to be involved, since methylphenidate has a fairly low binding affinity for it, and quetiapine / norquetiapine are agonists.
Quetiapine is an antagonist for 5-HT2B, but only dexmethylphenidate is known to have any affect on 5-HT2B, and even then it doesn't appear to have a particularly strong binding affinity.
Quetiapine, unsurprisingly, has a strong effect on SERT. Levomethylphenidate has a mild effect on SERT, but other forms are not known to (both Ki and IC50 exceeding 10000).
This left me with the most likely interaction: methylphenidate is an NDRI, so it fairly strongly blocks the norepinephrine transporter (NET), and norquetiapine also has a strong blocking effect on NET. This seems like a strong candidate for being the source of concern - they're both antagonists on the same receptor. Two drugs blocking the same receptor is usually a recipe for problems.
Reading more of the literature, it seems like α2A probably also plays a role here. From what I've read it controls norepinephrine production in a negative manner, since it's an autoreceptor. If inhibited, it may increase the amount of norepinephrine in the brain. Quetiapine is an α2A antagonist, so that's a secondary mechanism by which quetiapine would affect norepinephrine levels. α2B and α2C may also be involved here but I couldn't follow the literature well enough to figure that part out.
This is where I start to lose track of things. What I suspect the interaction is referring to is that both drugs increase norepinephrine through one or more mechanisms (e.g. by inhibiting reuptake and/or increasing production) leading to a potential scenario where a person who takes both drugs may end up having far too much norepinephrine. However, it isn't clear to me where the toxicity comes from. The symptoms of excess norepinephrine mimic that of stress, which can lead to increased blood pressure, but it seems odd to refer to that as "[increasing the] toxicity of methylphenidate"  - that phrasing implies that some aspect of methylphenidate is already inherently toxic, and that quetiapine somehow specifically amplifies that. I'm struggling to reconcile that with my understanding of the pharmacodynamics. It also seems odd, to me at least, to refer to those symptoms as "toxicity". I guess it's technically correct, in the sense that anything that damages an organism is toxic, but it seems like a stretch.
Can someone provide a clearer explanation of this theorised toxicity? Am I missing something obvious? Is my (admittedly armchair) analysis fairly close, or am I way off?
 Medscape reference: quetiapine (Rx) or Methylphenidate. Both have identical statements.

Could you cite some of those reputable sources? It’ll help other people give a good answer. Thanks!

Medscape and Drugbank were the primary two. WebMD's interaction checker repeats the same interaction description as Medscape, although I wouldn't necessarily consider that to be quite as reputable. NICE BNF didn't list an interaction, but that list doesn't tend to include less severe interactions when they're only theorised.

Something potentially relevant that I just spotted: Drugbank mentions increased seizure potential from methylphenidate use, but doesn't have many details. Their page for bupropion, on the other hand, goes into more detail. However, that only serves to confuse me further - it states that norepinephrine has anticonvulsant properties, then goes on to say that bupropion (and, by inference, NDRIs in general) are thought to have proconvulsant properties that arise from their norepinephrine reuptake inhibition. That seems backwards to me.

If you're going to quote something, you need to reference the specific source of that quote. In this case you should do that with an [edit]. Ideally other specific information should also be tied directly to a specific source with a reference for that specific item.

You're already ahead of the curve on your research into this question. Doing a quick Google Scholar check (after the usual drug info/interaction sites), I haven't found the exact antagonist mechanism of quitiapine. I suspect you might need a PharmD to answer this. I'm not sure the problem is hepatotoxicity; are you? What, exactly, is your concern? I would have guessed (I'm not a pharmacologist) the interaction referred to is an increase the adrenergic property of methylphenidate, but I don't know. Please edit to make clear your concern.

Also, if this is a personal thing - as in, you're taking both meds (no judgement here) - this is the wrong place to get your information. You should be talking to your pharmacist/pharmacologist or your psychiatrist; I'd recommend a PharmD. If your primary doc put you on the combo, forget about asking them (I'm a doc, so I can say that with confidence.) The Pharmacist can give you an idea of the incidence/severity of interactions; the PharmD can give you the pharmacodynamics as well.

@BryanKrause It wasn't possible to directly link to the interactions on those websites. The search function is implemented through in-page XHRs and didn't give me a unique URL. Hence the lack of a direct cite.

@anongoodnurse I appreciate the concern, but I'm not asking for personal medical advice. I am taking both medications, but due to the dosages and dose timings the pharmacokinetics add up to a very minimal crossover, and both my doctor and pharmacist are OK with it. I asked the question out of curiosity and a desire to better understand the relevant pharmacology; I don't think it'll ever affect me personally.

@anongoodnurse Re: "I'm not sure the problem is hepatotoxicity; are you?" - No, I'm not sure it's hepatotoxicity. I suspect it's not. My current best guess is they're concerned about a scenario akin to serotonin syndrome but with norepinephrine instead, with seizures as a potential primary complaint. But I've been unable to discover a good source for this, although, admittedly, likely in no small part due to my lack of formal training in this field.

Drugs.com doesn't display any interaction between methylphenidate and quetiapine. You should be sceptical while reading articles and drug instructions. Sometimes the things people write there are nothing more than guesses and loose thinking, and you can debate them (even the claim that quetiapine is useful for "schizophrenia" is debatable).

quetiapine increases toxicity of methylphenidate by pharmacodynamic antagonism

Pharmacodynamics refers to the study of drug actions, for example the affinity for different receptors is pharmacodynamics. In contrast, pharmacokinetics is concerned with the fate of a drug: how does it spread/how is it distributed after administration, how is it metabolized.
An antagonist is something that blocks/reduces the effect of a drug/ligand.
By stating "pharmacodynamic antagonism" we can infer that there is not a pharmacokinetic concern. A pharmacokinetic interaction could include, say, drug A impacts the absorption of another drug B: that could lead to lower or higher concentrations of B when co-administered with A rather than alone. It could involve interference with the metabolism of the drug, like by inhibiting or activating liver enzymes, causing more or less of B to be in an active form for longer/short periods of time.
Okay, so how can pharmacodynamic antagonism increase toxicity? That seems to be the primary question here. How can blocking the effect of a drug make it more toxic, without having any pharmacokinetic effects?
First, it seems like this Medscape reported interaction is mostly a theoretical one. I do not see reports of this being a substantial interaction of concern, and Medscape gives it a rather low "monitor closely" guideline.
I believe the concern they are raising is that because quetiapine may reduce the effectiveness of methylphenidate, higher doses of methylphenidate may be necessary to get the same effect. That could increase the potential for hepatotoxicity, particularly in combination with other drugs. I think this warning is meant to advise providers to think about this and consider all the combination of drugs given.
It's difficult to build a database of all possible higher-order combinations of concern, and that's why this sort of information is meant to be interpreted by a physician (particularly a primary care doctor who acts as a central point of care) or pharmacist to decide what level of concern is relevant for each specific individual case.

i'm absolutely surprise that in the most supposedly famous forum about biology sciences, that no one knows what pharmacodynamic antagonism means... with all the respect, (and for god sake..) its right on the name they are antagonic: one is an antipsychotic the other is a CNS stimulant.. thats the problem, they have opposite mechanisms of actions and thus the side effects (or toxicity.. like medscape calls it,, drugbank says side effects.. who cares honestly they are antagonic and thats the problem)

Think I should first start by mentioning that I am not a physician nor I am trained to make any clinical or diagnostic reasoning.  With that in mind, let me try my best to clarify most part of the question.

regarding a somewhat theoretical point of view, pharmacodynamic interactions

are those in which drugs influence each other’s effects directly source

drug to drug interactions often are classified as synergistic, additive, or antagonistic in nature reference
and thus when the effect of one drug is impeded by another, the effects of these drugs are antagonistic
Back to the point,
methylphenidate, in a nutshell, acts by blocking the reuptake of dopamine and noradrenaline which leads to the increasing levels of dopamine and noradrenaline in the synaptic cleft
on the other hand, quetiapine (is almost the opposite) a second generation antipsychotic has antagonist actions on 5-HT2A/D2 receptors (serotonin receptor/dopaminergic receptor) but are also partial agonists at 5-HT1A receptors (another serotonin receptor).
as I've mentioned quetiapine is a second generation antipsychotic (which is still, at present time, synonym for "not so clean drugs", what I mean by that is that they bind to almost everything that is receptor.. ) and thus the other receptors that you have mentioned (H1 and alpha 1 antagonism) are linked to side effects source
as one can see

This table shows Ki values for quetiapine at different neurotransmitter receptors. Ki is inversely proportional to affinity. This means that high Ki numbers suggest low affinity at a given receptor, while low Ki numbers are associated with high affinity.

they like to bind.. (a lot..) and thus the side effects.

Now, once established some background, lets go to the main part of the question: Why some literature reports toxicity interactions between the two?
in fact drugbank.com also reports similar

The risk or severity of adverse effects can be increased when Quetiapine is combined with Methylphenidate. Drug Interactions section

that has to do with the pharmacodynamic properties of both, since one has the opposite mechanism of action of the other (pharmacodynamic antagonism) it is expected to notice some increase of side effects.

Finally I would like to address, once again, to the fact that I'm not a physician and that therapeutically it has been reported with some relative success the combination of those two drugs

Conclusion: Quetiapine addition to methylphenidate was effective in reducing ADHD and aggression in individuals who did not respond sufficiently (based on CGI-S, RAAPP, and ADHD-RS-I criteria for significant improvement) to OROS methylphenidate alone at a 54-mg/day dose. study

The quote is under methylphenidate on this page: https://reference.medscape.com/drug/seroquel-xr-quetiapine-342984 - "quetiapine increases toxicity of methylphenidate by pharmacodynamic antagonism. Use Caution/Monitor. Closely monitor for signs of altered clinical response to either methylphenidate or an antipsychotic when using these drugs in combination"

founded, my apologies, couldn't find the reference at time. I'll edited my answer.

nevertheless, what i wrote remains true and applicable to the subject; toxicity in that sense regards to the fact that since one drug is antagonizing the other mechanism of action thus leaving adverse effects as major result for the organism, that's the meaning of toxicity in this context. there's no CYP450 interaction (which means that an increase of the steady state concentration of one of the drugs will not happen) nor toxicity due to pharmacokynetic factors such as metabolization.. hence the main meaning of that phrase contextualized is that side effects can be increased

I've upvoted your answer, but the last part was disturbing. Sure quetiapine "was effective in reducing ADHD and aggression", because it makes you sleepy and apathetic. It's ridiculous to claim that it "treats" ADHD.


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Transcript without a start codon in mouse genome?
I am looking at the mouse reference genome in combination with ensemble annotation and am finding many transcripts that have no start codon.
For example, the transcript ENSMUST00000193149 at position 165503943-165567747. The first CDS has a frame number 1. In the UCSC genome browser, I see that in one of the tracks ADCY10 gene starts at this location, but in the protein sequence, there is an X under the first base, followed by a T under the next three (which indeed correspond to T).
I am puzzled: why does the transcript start at something other than the start codon? Why does the annotation indicate its start position as 165503943 instead of 165503944 where the actual codon starts?

The entry in ensembl has a "CDS 5' incomplete" tag
http://uswest.ensembl.org/Mus_musculus/Transcript/Exons?db=core;g=ENSMUSG00000026567;r=1:165331512-165395316;t=ENSMUST00000193149


text:
Colonizing Mars: Is research being done to find the most radiation-tolerant plant species?
Due to Elon Musk's stated objectives to colonize and live on Mars in his lifetime, is there research occurring to determine what plants would be the most hardy to survive in the extreme environmental conditions of the planet?
Direct surface growth appears to be impossible due to strong ultraviolet rays reaching the planet's surface due to the lack of an ozone layer, and also the direct unimpeded cosmic ray bombardment leads to surface radioactivity, due to the lack of geomagnetic field protection.
But are there any research studies being done to try to determine what plants if any would be most tolerant of partial or minimal shielding from these otherwise life-ending and mutation-forming environmental conditions?
It is well known that initially all colonization support materials are going to have to be transported to the red planet from Earth. It will be a long time before the initial colony would be capable of mining, sorting, processing, and producing anything useful from surface materials already on the planet.
If it would be possible to design a reduced-shielding Mars greenhouse roof material that is lighter and thinner than one that provides the full filtering needed to produce safe Earth-like solar irradiance for common food crops, then it would be possible to build larger and more expansive in-ground / underground greenhouses for hardy slow-growing but radiation tolerant plants, to help support slow-but-steady oxygen production for the more fragile parts of the rest of the Mars survival mission.

There is a Space Exploration SE

I was not aware of that. Should I vote to delete and then repost there, or can it be moved by a moderator?

this question have been asked over at https://space.stackexchange.com/ before and you can find some good links there.https://space.stackexchange.com/search?q=plants+on+mars

No need to flag your own post – just click on the 'Delete' button (grey text at the bottom of your question).


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qPCR - different results total RNA vs mRNA
I have performed qPCR on a tissue, where I have extracted total RNA and also purified mRNA. I ran the qPCR samples together, and have therefore been exposed to the same conditions except the purification step from total RNA -> mRNA. In my results, a gene is down-regulated in the total RNA, but it is not in the mRNA. What could be the reason for that?

What is the mean magnitude of cycle number difference between the treatment and control in each case? I would favor the total RNA results since mRNA enrichment has different biases for different transcripts.

@acvill the mean magnitude difference of the RQ values for the total RNA is 6.63, and for the mRNA -0.8957 - I have subtracted the treatment from the Control

There are a few possibilities.

For whatever reason, your transcript of interest is poorly captured by your mRNA enrichment such that, in both the control and the treatment, mRNA enrichment selects against your mRNA. This would be evident if the CT value for the mRNA control is much higher than the total RNA control, assuming that the mass of total RNA you used in your mRNA enrichment is the same as the mass of total RNA used in each qPCR replicate.
If your primers / probes are nonspecific, your total RNA qPCR results could be the result of downregulation of some off-target noncoding RNA. If your mRNA enrichment protocol is non-destructive (i.e. relies on positive selection of mRNA and not degradation of non-mRNA), you could test the specificity of your primers / probes by performing qPCR on your non-mRNA fraction. Though, interpretation of these results could be confounded if point #1 is also true.


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What is this large, lively barnacle?
Yesterday I found this creature in a rocky cove in central California, around mid tide (+ 3 feet). It's about 3-4 inches long. At first I thought it was dead, but it closed its mouth when I removed the tiny white pebble, and rotated the operculum rapidly when I poked the bit of exposed yellowish flesh underneath. I think it's some sort of acorn barnacle, but haven't been able to identify a species with the white shell and distinctive red-and-white color and texture differences on the opercular plates. What could it be?

Update: this is a giant acorn barnacle, Balanus nubilis. Between Pacific Tides mentions that they can vary widely in coloration, and there's a picture of a similarly colored one here.
We had our ID confirmed by email by a representative of the Monterey Bay Aquarium, who added this info:

You beat me to it.  That is indeed a giant acorn barnacle (Balanus
nubilus).  Unfortunately, barnacles can’t survive long after being
detached from their rocks and they’re unable to reattach on their own.
Rocky intertidal zones are harsh environments and animals living in
these areas must deal with both water and air, rapidly changing
temperatures, exposure to sunlight, desiccation, high wave energy, and
predators from both land and sea.
The stringy threads attached to the barnacle in your photo are the
byssal threads of California mussels.  Mussels secrete these threads
to anchor themselves to rocks, each other, barnacles, etc.  It’s very
common to see mussels and barnacles clumped together in high surf
zones.

I think it's a thatched barnacle (Semibalanus cariosus). The iNaturalist app would also be a helpful tool in which to ask this question.

Welcome to the site. This is a good answer, but can you tell us why you think it is the thatched barnacle, and perhaps provide some links with information about these animals? It would really improve your answer.