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Where can I get info about A. thaliana proteins' locations?
I have a list of A. thaliana proteins and I'd like to know their location in the cell. I've found SUBA but they seem not to share their dataset and only allow queries through their website. It's inconvenient for me, because I need to locate 1.6k of proteins and process the results further. Is there a dataset or an API I could use instead?
PS. If this is not the right forum to ask this, please notify me.

cross-posted https://bioinformatics.stackexchange.com/questions/18111/where-can-i-get-info-about-a-thaliana-proteins-locations

You can also try using The Arabidopsis Information Resource (TAIR).
It is the database specifically created for model higher plant Arabidopsis thaliana.
You can download the files in .fasta, .gz, .txt, .csv formats from their DOWNLOAD WEBPAGE. The website also provides links to other A. thaliana information resources.
PS:  The database is weekly updated.
Edit 1: Try this or track to download_files/Proteins/Properties/AtSubP_results

That's where I looked first but I haven't found any file with protein locations. In an NCBI article about SUBA I've found a link to some .csv files used by the website, although they have to be cleaned to be usable.

can you point to where on TAIR specifically these localisome data reside?

@micoay, I have added a link to my answer. Please let me know if it works for you. I'm assuming you already have the protein-ID list.

Thanks, I missed this file. For people searching for the file on the website: Downloads/Proteins/Properties/AtSubP_results.

@micoay, If that has solved your problem, then please accept my answer by clicking a tick button on the left side of my answer on your forum. I would appreciate that.

If you click through to the actual SUBA4 publication, you can see in the data availability section that they have reposited source datasets from which their predictions are derived, at http://dx.doi.org/10.4225/23/581055ddcb1ce.
These appear to be standard e.g. CSV files of various data layers, such as here. It may take some effort (e.g. their algorithm) to integrate these data sources, I am not familiar with these datasets.
It is of course inconvenient that they don't choose to advertise this on the server itself.

Thanks, I found it too, after posting here. I was hoping there was a link on their website I missed.


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What is the probability for an offspring to inherit schizophrenia?
If an European male (i.e. white) is diagnosed with schizophrenia, but an European female (also white) 2-3 years younger than the male is healthy, what is the probability that their first child will:
a) be diagnosed with schizophrenia later in life?
b) have some other mental condition?

I'm not referring to any studies and do not have background in biology/medicine. All I'm trying is to get an answer for my case, because other forums remain silent.

I'm glad that you've made it a tiny bit more specific. The site requirements are that you should show the results of your prior research - perhaps use as a springboard for your researches something like this, this or this. There are indications of a genetic link, but it's far from cut and dry, more like a genetic susceptibility which might get triggered.

https://pubmed.ncbi.nlm.nih.gov/27872260/

Personal medical questions and health advice are off-topic on Biology.SE. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice.

But if scientists don't know an answer, how can a doctor know?

It may not be about "don't know" so much as "don't want to be legally responsible for" - in fact, the medical Stack Exchange is sometimes reluctant to answer personal questions about the questioner's own health (or in this case their child's), too.  But also, there is a specific medical Stack Exchange (I don't remember what its exact name is, but it'll be in the list), which may be more applicable to a question about human health than Biology.SE (which covers everything, from tomatoes to amoebas to fish), though I'm not sure.

Doesn't that probability depend on the father's age?

Haven't directly answered this
I found a recent literature review that is relevant to this:
"Gene-Environment Interactions in Schizophrenia: A Literature Review"
by Marah H. Wahbeh and Dimitrios Avramopoulos *Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Academic Editor: Sarah Tosato
Genes 2021, 12(12), 1850; https://doi.org/10.3390/genes12121850 (registering DOI)
This article notes that the chance of schizophrenia is more likely to arise if one of a group of conditions is present.
Conditions such as prenatal maternal exposure to some infections, childhood adversity, and cannabis use.
As far as increased chance of other disorders, the below article only uses the measure of first or second degree relatives - not chance of heritability from a parent only. This study uses the entire population of Taiwan.
"Familial Aggregation and Heritability of Schizophrenia and Co-aggregation of Psychiatric Illnesses in Affected Families"
I-Jun Chou,  Chang-Fu Kuo,  Yu-Shu Huang,  Matthew J Grainge,  Ana M Valdes,  Lai-Chu See, Kuang-Hui Yu,  Shue-Fen Luo,  Lu-Shuang Huang,  Wen-Yi Tseng  ...
Schizophrenia Bulletin, Volume 43, Issue 5, September 2017, Pages 1070–1078, https://doi.org/10.1093/schbul/sbw159
"The RR (95% CI) in individuals with a first-degree relative with schizophrenia was 3.49 (3.34–3.64) for mood disorders and 3.91 (3.35–4.57) for delusional disorders."
(RR is relative risk.)

Seems that the first article gives 80% genetic chance for a child to inherit a disease?

@mercury0114 that's the heritability - i.e. how much of the variation between individuals in having schizophrenia is caused by genetics. This isn't the same as the probability of getting it with a first-order relative has it.

source: Stack Exchange

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

sort: votes


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What is the upper limit for 'active' vaccinations
As far as I know the effect of vaccines is caused mainly by creating Memory Cells specific to a single pathogen.
As there is obviously a lower limit of memory cells needed for immunity ( at least one), and an upper limit for the number of memory cells (they have to fit inside a human)
there is a an upper limit of about a trillion diseases against one can be immune at the same time. But I guess this limit is much lower. Has it ever been studied? And can it be relevant in practice, or could I get a new vaccination every day without loosing previous ones?

"...could I get a new vaccination every day without loosing previous ones?" Previous what? Previous cells that can react to the antigen? Immunity isn't at a fixed level, like memory in the Cloud, which starts kicking out older information to make room for the new if you exceed what you've paid for. "Has it ever been studied?" Not in the way you present. How would that be useful to know? Also, I don't think it would pass the ethics committee. ("OK, what can we expose this guy to next? Should we try dengue virus?")

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


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Can the SARS‑CoV‑2 virus mutate in people who have been fully vaccinated?
I am curious to know if the original SARS‑CoV‑2 virus, or any of its variants, can mutate in people who have been fully vaccinated. I am referring to those people who have received all the recommended vaccinations and booster vaccinations since the worldwide outbreak of COVID-19 back in November 2019.
Can SARS‑CoV‑2 mutate in people who have been fully vaccinated?

I wonder if we also can say something about expected mutation rates between vaccinated and unvaccinated, or even the kind of mutations that are likely to happen in each case.

Most likely there is little effect. See last (new) ¶ of my answer.

@leftaroundabout: Please see my comment on Ben's post.

I don't know "anything" in mutation, but if a virus is not "killed" (with or without vaccination), mutation can occur and can be transmitted ... It is a logical "defensive" reaction. Do we know all about "virus"? No, and in reality, about "nothing".

Since vaccination is not 100% protective against infection (i.e. the virus can sometimes succeed in establishing and replicating in a vaccinated host's body), the answer is yes. Furthermore, since vaccination is also not 100% protective against transmission — although it does lower the probability of transmission from infected individuals — such mutations could also be transmitted to other hosts.
However, vaccination greatly reduces the probability of infection and onward transmission. It might also be expected to reduce the duration and intensity (viral load) of infection, which would further reduce the probability that a mutation arises in an infected person (because the total number of mutations is proportional to the population size of the virus within the host).
Singanayagam et al. (2021) found that the peak viral load was not greatly reduced in infected, vaccinated people infected with the delta variant (relative to unvaccinated people), but that the decline from the peak was faster; with more effort/re-analysis of these data, we could estimate the magnitude of the change in the expected total number of viral replications over the course of an infection, which would in turn tell us the expected proportional difference in overall mutation  probability due to changes in the within-host dynamics of the infection. (Also see this answer for more detail on viral load in vaccinated vs. unvaccinated individuals.)
Responding to a comment: the mutation rate (i.e. per base pair per viral replication, or per genome per viral replication), and the mutational spectrum (i.e. what kinds of mutations occur) are not expected to change much under vaccination - these are determined by the biochemistry of viral replication, and are probably not affected by what the host's immune system is doing.
(Disclaimer: my background is in ecology/evolution/epidemiology, not virology or immunology or biochemistry.)

Singanayagam, Anika, Seran Hakki, Jake Dunning, Kieran J. Madon, Michael A. Crone, Aleksandra Koycheva, Nieves Derqui-Fernandez, et al. “Community Transmission and Viral Load Kinetics of the SARS-CoV-2 Delta (B.1.617.2) Variant in Vaccinated and Unvaccinated Individuals in the UK: A Prospective, Longitudinal, Cohort Study.” The Lancet Infectious Diseases 0, no. 0 (October 29, 2021). https://doi.org/10.1016/S1473-3099(21)00648-4.

+1 - Of course you are aware of this, but it seems like the OP may not be - but it may be worth clarifying that viruses mutate whenever they replicate, entirely independently of whether they are in a host that has been vaccinated - the vaccine doesn't precent mutations, just (as you said) reduces the opportunity for them to replicate and mutate.

If someone wants to leave a reason for their downvote I would be happy to try to respond.

My background is chemistry but your answer seems pretty logical. I would resume it with the fact that vaccination results in a faster decay of the number of virus particles within one's body. How many enter the body and their business within should be independent of our immune response.

I did not downvote but I do not agree with your claim that "the mutational spectrum [...] are not expected to change much under vaccination - these are determined by the biochemistry of viral replication, and are probably not affected by what the host's immune system is doing.". That is completely false; because of course the mutational spectrum depends on the immune system; if it is good at destroying a certain viral strain then of course the virus population would mutate away from that strain!

@user21820, what you are describing is within-host selection, not a change in the mutational spectrum. Perhaps that process should be included in my answer, but it's not technically mutation.

@BenBolker: Yes, within-host selection is not mutation, but I didn't say that it is. What I said is that the mutational spectrum is affected by the host immune system characteristics. It would be best if you fix that issue with your post.

@user438383: Sorry, but I don't think you know what you are talking about. The only way we can scientifically determine mutational spectra (to within a given confidence level) is via population-based statistical sampling. For example, each carcinogen leads to certain spectrum of frequencies over the various kinds of mutations, on a statistical basis. Comparing with a baseline spectrum lets us statistically deduce the mutational spectrum of a particular carcinogen being tested.

@BenBolker: It occurs to me that you may have a differing interpretation of "spectrum". No doubt the immune system is unlikely to directly affect the actual mutation process, but the resulting spectrum is all we can observe; we can never observe the actual mutations, and it is largely irrelevant to the topic at hand. Even in the case of carcinogen mutational spectra, some spectra are due to error-correcting mechanism failures. Are you going to say that those are not the true spectra just because the carcinogen didn't affect the actual mutations or DNA-breakages?

Of course vaccination in an ongoing pandemic influences what can spread out more. I think you are both right but taking different aspect. Modesty, I am not specialist at all, I have interpreted the question as for what happen "inside". So the virus can mutate but it has less time / less population. Anyway my interest is mostly dictated by the time being. Unfortunately.

@user21820: The mutational spectrum isn't affected by the characteristics of the host's immune system.  The ways in which the virus mutates are totally unaffected - the only thing that changes is which of those mutations are selected for or against once they appear.

@Vikki: That's what you assume. You, like all the others making your claim, have not a single bit of evidence, because the virus uses the host's cellular mechanisms in order to replicate, and those mechanisms are affected by the immune system.

@user21820: The cellular mechanisms which the virus uses in order to replicate (basically just the cellular translation machinery and the cell's supply of high-energy nucleoside triphosphates) are not affected by the immune system, and you have yet to provide a single bit of evidence that they are.

@user21820 : I really hesitate to get into this, but those of us you are arguing with (me, Vikki, user438383) have the weight of convention and standard definitions on our side. Yes, you could define "mutational spectrum" as "the set of alterations in gene sequence observed between the infecting genome and the genomes transmitted to new hosts", but that's not how it is defined in the literature. While it's not physically or biochemically impossible for immune processes to affect the process of viral replication and thus change the mutational spectrum ...

... it's not a phenomenon that, as far as I know, has ever been observed or speculated to be a plausible outcome. Feel free to post an answer of your own if you like -- I'm going to disengage from the debate now.


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Can a less fit strain of a virus impose over a fitter one?
According to this link, the Dominant Delta Variant may mutate itself into destruction.

The Delta variant in Japan was highly transmissible and keeping other
variants out.
But as the mutations piled up, we believe it eventually became a
faulty virus and it was unable to make copies of itself.

I was told that evolution was about survival of the fittest, and that in the case of virus strains, a more contagious strain would likely increase in frequency relative to a less contagious one. So how can a mutation of the strain Delta which can't replicate or replicate less, increase in frequency relative to the original Delta strain?
Can a less fit strain of a virus impose over a fitter one?

Could you clarify what you mean by impose?

the original coronavirus strain was displaced worldwide by other strains called alpha, delta, etc. The delta, alpha, etc. imposed over the original coronavirus strain

How are you quantifying 'displaced'? The original strain still exists, presumably, but the other variants are found at higher frequencies. Are you interested in whether it's possible for a less fit strain to reach a higher frequency than another? 'Imposed' doesn't seem to be the correct biological term. I think 'outcompete' is better to use. Sorry if I sound pedantic, but having the correct terminology often is the best way to understand something.

If I can simplify the question: “Why would a ‘faulty’ mutated strain of the delta variant increase in prevalence relative to the wild type delta variant?” The answer is probably “it’s complicated” and “more information is needed.”

That's a discusion of semantics, not biology. Displaced can also be used to the Situation you describe. If you partially mover someone from a position you can use the word displaced

Btw, there are a Lot of researchs using the word displacement to describe the displacement of alpha by beta

Also note that the term “fitness” has a specific meaning in biology. For a given genotype, relative fitness is the proportion of that genotype in the population gene pool of the next generation. So, by definition, a “less fit” strain cannot overtake the wild type.

correction, I meant "there are a lot of researchs using the word displacement to describe the displacement of alpha by delta*". typo or corrector

@acvill "Why would a ‘faulty’ mutated strain of the delta variant increase in prevalence relative to the wild type delta variant?” Even though the question arised with sars-cov-2, I would like to know if there was ever a known case with any virus where a less contagious strain of the same virus could overtake a more contagious one. Because if there wasnt, that means this is also impossible for sars-cov-2

If one strain of a virus displaces another, or even becomes more prevalent, isn't that strain the fitter one, BY DEFINITION?

@jamesqf  the question is, how can a strain that's faulty to replicate to the point is going to disappear (cleary not the fitter) impose over another. If a strain replicates little, or not at all, the hosts are going to be taken over by other strains. But the japanese man claims (indirectly) that a faulty to replicate strain took over the non faulty ones.

@Pablo a less fit strain may outrun a fitter one due to genetic drift, if the infected (sub)population is small... although in this case measuring fitness is problematic. It seems that the variant introduced in Japan, although classified as Delta, had actually low fitness (there is some genetic variation within each variant). Also, a fitter strain may simply become extinct by exterminating all its hosts - not the case of sars-cov-2, but not something unheard of.

@Pablo: But if a strain mutates in such a way that it can't replicate, or doesn't replicate as well, that mutation has made it less fit.  Conversely, a strain that replicates so well that it eliminates its hosts (perhaps by causing collateral damage), is likewise not fit.  The ideal would be for the virus to reproduce and spread without adversely affecting its host.  Or even benefitting the host, as many of the microorganisms in your microbiome do.

@jamesqf agree. That's why what that japanese researcher said doesnt make sense to me, and I came here to ask if there is an explanation for what he said.

@RogerVadim I'm not familiar with the concept of genetic drift, for what I read it would seem randomness play a role, but here we are talking about 10 millions viral particles per mililiter per infected person, so it's a population of trillions.

@Pablo we are not talking about competition within a single host, but about being transmitted to another host and successfully establishing a new infection. The number of people in the cited article is rather small.

"I find it incredibly difficult to believe that all Covid-19 in Japan has simultaneously and more-or-less in unison, evolved to be a dead end, that seems like a bizarre suggestion.  " I think this sentence means the first man believes all sars-cov-2 particles independently (not from the same parents) mutated in the same direction. Is this even possible?


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Do mutations in a fundamental structure of a virus [Omicron Variant] make it more transmissible?
I am not a microbiologist, nor a virologist so I had a question - in the new Omicron virus variant, a large number of mutations were reported for the protein spike.
From my naïve understanding, the spike is an integral part of how the virus replicates inside a host - thus, does it mean that changes in protein spike structure would lead to a more transmissible - therefore deadly variant?
And if so, won't the effect of vaccines reduce drastically since there's a fundamental change in the virus' structure which the immune system might not anticipate? Or the antibodies be able to handle?

Omicron as an escape variant might be a good example for  questioning  a rule that says "... more transmissible - therefore deadly variant". Any changes the success of which depend on immune escape  bear a chance that pathogenic factors are reduced and relinquished for the sake of transmissibility.

(Converted from a comment.)
We have no idea at this point. Mutations are worrisome because they could indicate changes in transmissibility or virulence or capability for immune evasion, but it's almost impossible to predict.
efficacy of vaccine/natural immunity
The easiest aspect to measure (approximately) will be immune evasion, by measuring the affinity of antibodies raised by existing vaccine to virus of the new strain in vitro ... transmission and virulence are much harder to quantify (or quantify proxies for) in the lab.
Antibody trials to evaluate efficacy are what a lot of immunologists will be spending their time doing over the next week or two: for example, from this article

[Prof Penny Moore at the University of the Witwatersrand will engineer] “pseudoviruses” – harmless, non-replicating viruses used to model coronavirus variants ... to carry Omicron’s mutations. These will then be exposed to antibody-carrying blood plasma from vaccinated people and those who have recovered from Covid infection to see if they neutralise the virus.

[Prof Alex Sigal from the African Health Research Institute in Durban] is growing batches of live Omicron from people who became infected in the recent surge in Gauteng in South Africa. Once he has enough to work with, the variant will be tested against blood plasma from vaccinated people and those with some natural immunity after a Covid infection.

transmissibility
Again, it's hard to predict what will happen to transmissibility simply from knowing the genetic sequence. It is possible to do in vitro studies with cell lines to try to estimate changes in transmissibility, although these do not perfectly predict how much a real live infected person will transmit (for example, these tests are done without any involvement of the immune system). e.g.: Hou et al 2020, Plante et al. 2021.
virulence
Virulence describes the severity of illness in a person infected with a given strain. This is probably the hardest of the three characteristics to measure in the lab; we may just have to wait until the omicron strain has spread and observe the fraction of cases that need to be hospitalized or sent to the ICU (although this still won't tell us what fraction of people who are infected have very mild or asymptomatic cases and are never even recorded as COVID cases ...)

Hou, Yixuan J., Shiho Chiba, Peter Halfmann, Camille Ehre, Makoto Kuroda, Kenneth H. Dinnon, Sarah R. Leist, et al. “SARS-CoV-2 D614G Variant Exhibits Efficient Replication Ex Vivo and Transmission in Vivo.” Science 370, no. 6523 (December 18, 2020): 1464–68. https://doi.org/10.1126/science.abe8499.
Plante, Jessica A., Yang Liu, Jianying Liu, Hongjie Xia, Bryan A. Johnson, Kumari G. Lokugamage, Xianwen Zhang, et al. “Spike Mutation D614G Alters SARS-CoV-2 Fitness.” Nature 592, no. 7852 (April 2021): 116–21. https://doi.org/10.1038/s41586-020-2895-3.


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Could Sars-CoV-2 vaccines make the immune response less effective against new variants?
Some viral diseases (e.g. influenza and dengue fever) are thought to exhibit original antigenic sin.
The immune system remembers viruses that it has been previously exposed to, allowing the body to mount an effective defense if the same virus is seen again.  However, in some cases, this immunological memory can be overly specific.  When the body is exposed to a new variant of a familiar virus, it produces antibodies against the old variant rather than the new variant.  If these antibodies are less effective against the new variant, the infection can be more severe than it would have been in a person with a naive immune system.
Is there reason to believe that the same phenomenon could occur for Sars-CoV-2 and its variants?  In particular, could people who were infected by or vaccinated against the original strain be more vulnerable to Omicron or other future variants?

here is a good place to learn about the imune system https://www.youtube.com/watch?v=LmpuerlbJu0

"If these antibodies are less effective against the new variant, the infection can be more severe than it would have been in a person with a naive immune system." What is the reasoning behind this statement?

The wikipedia article for Original Antigenic Sin (OAS) oversells it a bit, in my subjective analysis. While the effect is experimentally verified - e.g. patients with a Dengue type 4 infection will produce antibodies that bind type 1 much more strongly than 4 if they were first infected with type 1 (source) - there is no evidence I'm aware of that proves the resulting immune response is less effective than a naive immune system of the same age would mount. From Original Antigenic Sin: How First Exposure Shapes Lifelong Anti–Influenza Virus Immune Responses:

Although OAS has often historically been depicted as a problematic response, recent data have demonstrated that, in certain contexts, eliciting OAS may also be beneficial.

It's not obvious that the poor match of OAS antibodies to the second infection is enough to make up for the much more rapid response compared to that of a naive immune system. Mismatched antibodies generally still neutralize other strains, it's just that a higher concentration is required.
A big confounding factor here is another mechanism, Antibody-Dependent Enhancement. ADE is most infamous in Dengue, which causes mild disease the first time but can be deadly after that if later infections come from a different strain than the first virus. ADE arises in this case because Dengue virus can infect the white blood cells that envelop and attempt to destroy antibody-bound particles. This results in accelerated virus production and a dysfunctional immune response. Despite the fact that immune cells do not display the ACE2 receptor that their spike protein needs to bind before it can fuse with the cell membrane, both SARS and SARS2 have been found to also infect macrophages when spike-binding antibodies are bound. Unlike Dengue, though:

Macrophages infected with SARS-CoV, however, did not support productive replication of the virus.

and

SARS-CoV-2 infection thus produces antibodies that elicit ADE of infection, but these antibodies do not contribute to excess cytokine production by macrophages.

Which, together with the protective effect observed for SARS2 vaccination and prior infection, we can conclude ADE isn't an issue for COVID severity, even if variations arise that can escape antibody neutralization.
Finally, there is some important context here that is not obvious to the casual investigator. The new omicron variant of SARS2 has been described as "highly mutated" because it has more than 30 mutations in the spike protein, out of 1250 amino acids in the full sequence. In other words, the other ~97.6% AA are identical. For comparison, I looked up and ran a BLASTp analysis of hemaglutinin (analogous receptor binding protein in influenza virus) from H1N1 and H3Nx strains of influenza. (uniprot accession nos. P03452 and F1KLX3, respectively) These two antigens have only 42% identical amino acids. So they are far more dissimilar than different variants of SARS2. COVID is not likely to reach similar levels of differentiation anytime soon, and we can expect any potential OAS effects to be mild for a long time as well.

No.
Let's approach this issue from the beginning. At first, we have what is called innate, nonspecific or natural immunity... many synonyms to say that it is

" the body's first line of defense against germs entering the body " quote

Now, one important feature that this mechanism has is that it will be the first to contact with the target antigen and thenceforward do another specialty of them that is Antigen Presentation (dendritic cells are the most famous for that)

APCs may interact with two classes of lymphocytes: the B or bone marrow-derived lymphocytes, but especially with the T or thymus-derived lymphocytes.  quote

From here adaptive immunity appears which includes everything you have refereed.
In that sense, all that will matter here and related to the subject is that if Ig's will have affinity for the antigen.

Let's assume they have cellular immunity, which is

a protective immune process that involves the activation of phagocytes, antigen-sensitized cytotoxic T cells and the release of cytokines and chemokines in response to antigen. Cellular immunity is most effective against cells infected with viruses, intracellular bacteria, fungi and protozoans, and cancerous cells. It also mediates transplant rejection nature

Let's assume they don't have affinity to the antigen

In that case (that could be due to a mutation of virus surface...) your immune system will  not recognize that epitope (fancy word to say antigenic determinant, it's the fragment that the immune system will recognize).
As a result of that a new Antigen Presentation must be done. In parallel HIV is a good example of that, the virus that infects a person at first is continuously suffering mutation after mutation (due to the inefficient reverse transcriptase enzyme), and thus when the body has Ig's to attack the infection, there's already another virus to attack, and so on, and so on..


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Why are apes so poorly adapted for walking upright?
Non-human apes are quite poorly adapted for walking upright, in terms of their anatomy. I have found many sources that explain how their anatomy is so unsuitable for an upright life, yet none have given reasons why they evolved like this in the first place
It seems like most adaptations for bipedalism would work well enough in other apes, and there should be at least some pressure to move well on the ground
Given this, why are the other apes so poorly adapted for walking upright?

You could ask 'why are humans so well adapted for walking upright' or 'what was the benefit to humans for walking up right' and then consider why those reasons may not apply to apes

@user438383 I get that humans had more reason to be upright, but it still seems like these reasons would apply to the other apes, at least to some degree

Maybe in a few million years given the right environmental pressures... yes. But what're their habitats like at present? Admirably suited to them being how they are (barring loggers cutting down the local trees).

This might be a useful starting point for thinking about comparisons between humans and other apes: https://nationalhumanitiescenter.org/on-the-human/2010/02/the-challenge-of-comparisons-in-primatology/

When you write:

It seems like most adaptations for bipedalism would work well enough in other apes, and there should be at least some pressure to move well on the ground

Based on our understanding of how bipedalism arose in ape-like human ancestors, I don't believe that this is true.

There are significant constraints that can make bipedalism disadvantageous (at least in the case of humans, see below), and thus apes would have to either find a substantially different bipedal strategy (likely difficult, given the path taken by human ancestors), or accept the tradeoffs of the human approach to bipedalism.
Do we know that moving around on the ground on all fours is a poor strategy for these primates, to the extent that they need to do so?

Constraints of human approach to bipedalism
Pelvic adaptations to bipedalism significantly restrict the size of the birth canal (see image), among other changes. This imposes a significant tradeoff between walking upright, maternal/neonatal mortality, and other parameters.
Quote from the linked article:

Pelvic anatomy impacts human performance. To walk upright in an energetically efficient manner with a minimal risk of injury, the pelvis must be robust and have a shape that maximizes muscle lever arms and minimizes load [5–11]. The ability to regulate body temperature is affected by the width and depth of the pelvis, which plays a crucial role in determining overall body proportions and the body's surface area-to-mass ratio, thereby influencing heat loss through the body's surface [12,13]. Finally, and most critically from a selective standpoint, pelvic shape must allow the delivery of a healthy infant without harm to the mother [14]. These goals are not all achieved by the same pelvic morphology, yet all three demands must be met. Therefore, selection has favoured compromises between these often contradictory pressures [15–17].

I think this is more about HOW humans are adapted to walking upright, while the question asks why apes aren't so adapted.

@jamesqf that is fair, I will update to directly address this (to the limited extent possible given the vagaries of evolutionary reasoning).


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Evolutionary pressure of vaccines towards a virus
I am trying to understand the following quote from one of the Twitter threads
:

A change in the spike protein which allows the coronavirus to enter and infect human cells that is radical enough to make our vaccine completely ineffective would also, almost certainly, be so extreme as to make the virus non-functional. -- Sara Gilbert, Oxford Team.

What are the underlying principles that backs this claim?

In biology, especially molecular biology, a common and important principle is that the structure determines the function. If the structure of spike protein changes so drastically that antibodies cannot recognize it anymore, this would very likely mean that the part of the spike structure responsible for infecting the cells (by binding to cell receptors) has also changed, making it unable to bind to the cell receptors. Therefore, it would become "non-functional", as the author put it.

See also: https://www.sciencedirect.com/science/article/pii/S2666379121000410 (on non-evolution of vaccine escape mutants in measles)

@Domen - That would make a good answer.

Does the quote refer to and include a situation where mutation is improvement of function, not deterioration?


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Was the Harcourt COVID-19 isolate paper ever published?
One very interesting paper concerning COVID-19 was the paper describing the first isolation of the virus by Harcourt et al. However, this paper as far as I can tell was only published as a preprint in May of 2020 describing research done in January and February of 2020. I used Google Scholar and other web searches and I cannot find any indication that the paper was ever peer reviewed and published in a journal. Since it is such an important paper, it seems kind of surprising to me that after a year and half the paper seems to still be unpublished. Am I missing something here?

https://pubmed.ncbi.nlm.nih.gov/32160149/ You could have found this by hovering your mouse over the author's name in the preprint link, which offered you the choice of seeing other papers by Jennifer Harcourt.

This is of course not the first isolation of the virus so what do you mean with "important paper"? Many other papers described the same thing, though with less details and cell lines.

@reuns Well, by "first" I mean the first verifiable isolation. The only ones I know of prior to it were unverifiable claims by researchers who never submitted their isolate to a repository. If you read the Harcourt paper, you can see that was a major goal of their research ("We also deposited the virus into two virus repositories, making it broadly available to the public health and research communities.").

What? The virus was first isolated in China around Jan 5. Did you read the WIV (RaTG13) and China CDC papers? https://www.nature.com/articles/s41586-020-2012-7 https://www.nejm.org/doi/full/10.1056/NEJMoa2001017

And their WA1 isolate has been used in USA only. Most countries did a isolate from one of their first patients and made a stock from it. I am not aware of much international strain sharing.

@reuns As I said in my comment, the Chinese claim to have produced isolates was that: just a claim. They did not submit their isolates to a virus repository as is standard practice when discovering a new virus. Are you even reading my comment? My question refers to the first verifiable isolate. It is important that viral isolates be verified because many types of errors can occur in a de novo genomic analysis, so it is critical that other researchers verify the results. This can only be done if the virus is submitted to a repository--hence the remark in the Harcourt paper.

Useless to discuss with someone who thinks that those papers are just "claims". A virus sequenced several times independently doesn't need to be "verified".

@reuns As I said before, an isolate is supposed to be submitted to a repository so that the genomic analysis can be verified. Also, there are experiments and checks of various kinds that can only be carried out on a live virus. A published genome is not a substitute for an isolate. The Harcourt isolate was to my knowledge the first isolate which was made available to researchers.

No, virology doesn't work like this.

It was published in June of 2020 by Emerging Infectious Disease under a slightly modified title. (It's not uncommon for journal editors and/or peer reviewers to require changes to the title of a manuscript prior to publication).
Found as the top result under "Similar Articles" on PubMed page of the bioRxiv pre-print. PMC link and full citation below.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7258473/

Harcourt J, Tamin A, Lu X, Kamili S, Sakthivel SK, Murray J, Queen K, Tao Y, Paden CR, Zhang J, Li Y, Uehara A, Wang H, Goldsmith C, Bullock HA, Wang L, Whitaker B, Lynch B, Gautam R, Schindewolf C, Lokugamage KG, Scharton D, Plante JA, Mirchandani D, Widen SG, Narayanan K, Makino S, Ksiazek TG, Plante KS, Weaver SC, Lindstrom S, Tong S, Menachery VD, Thornburg NJ. Severe Acute Respiratory Syndrome Coronavirus 2 from Patient with Coronavirus Disease, United States. Emerg Infect Dis. 2020 Jun;26(6):1266-1273. doi: 10.3201/eid2606.200516. Epub 2020 Jun 17. PMID: 32160149; PMCID: PMC7258473.


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Could Omicron be the variant of a variant?
I read that the newly discovered variant of Covid-19 has a higher number of mutations than the other variants. Isn't it more likely that it is the variant of a variant? It would be absolutely normal, after all, viruses of this family mutate so frequently that they are continuously evolving.
There would be a missing point though, is the intermediate variant a known one or is it a variant that passed under the radar?

It's pretty straightforward (in theory) to determine whether a new variant is a sub-category of an existing variant, or a new variant on the same level as e.g. Delta, by building a phylogenetic tree and looking at where the new samples fall.

Useful resource: https://cov-lineages.org/lineage.html?lineage=B.1.1.529

From what I've read (which isn't much beyond a few synopsis articles), despite containing some genetic features of some previously identified variants of concern, Omicron genomes are not directly descended from any of these other variants. Apparently the closest ancestor is from a mid-2020 lineage that hasn't been of much concern. There's a twitter thread from Trevor Bedford (Fred Hutch faculty member)  here breaking it down into a pretty digestible chunks and citing some cool interactive resources.

At the point of its discovery, Omikron wasn't a "variant of a variant", but goes down directly to the Pango lineage B.1.1.
Now we know something more, with the discovery of the outgroup now named BA.2 and the original Omikron being BA.1: There was a common ancestor to the two sister lineages, now named B.1.1.529.
Note that this still does not make it a "variant of a variant" because for being named a variant, a lineage must fulfill some additional criteria, such as becoming dominant or at least a notable fraction of all cases in some region, or being in other terms different and interesting enough to be worth additional attention.


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What are marine fungi like?
Particularly, what is their mycelium like and where exactly do they grow it?
I imagine that their spores travel though water same as terrestrial fungi travel through air until they stumble upon solid food (a carcass, a living host, sea floor rich with organic remains etc), at which point they begin growing mycelium network though that object. While I understand that there are many species of marine fungi, is my understanding generally correct?
Also, are there any fungi plankton: that constantly float in the water column and extract nutrients right from it, without ever having to "settle down"? If yes, do such fungi grow some special, "floating" version of mycelium?

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.

In addition, this site works well for focused questions rather than broad overviews of a subject. Have you read the most relevant wikipedia page? Note that also has an extensive references section that you can get into. Also, how about one of these freely available review articles?

@tyersome, I thought that the specificity of my question details should be evidence enough that I've looked and given quite some thought to the question myself. I even provided my understanding of what the the answer could be and asked for confirmation. I've read some articles and the wiki page: while they give a lot of specific detail (like habitats, distribution etc), I didn't quite get the impression of what they are like. Especially in terms of mycelium: because it's the key feature of terrestrial fungi, but at the same time doesn't quite make sense to have in open water.

As currently written your question seems to be asking for a review of an entire kingdom in multiple habitats across ~70% of this planet. I hope you can see that that isn't a reasonable question for this site, which is why your post has two close votes for "Needs more focus". If your primary question is about the growth form of planktonic fungi, then please [edit] your title and body to focus on that. It is important to clearly ask a single question (per post) as this ensures that you get a clear answer and that others can find this by searching. It will also helps you search more effectively.


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What is, (and what isn't) "kinetic replication" as it applies to molecules and to living organisms?
CNN's World's first living robots can now reproduce, scientists say describes "xenobots"; clusters of stem cells that move around and by this motion occasionally push enough free stem cells together such that they form a new one, at least that's my understanding.
The article says:

"Most people think of robots as made of metals and ceramics but it's not so much what a robot is made from but what it does, which is act on its own on behalf of people," said Josh Bongard, a computer science professor and robotics expert at the University of Vermont and lead author of the study.
"In that way it's a robot but it's also clearly an organism made from genetically unmodified frog cell."
Bongard said they found that the xenobots, which were initially sphere-shaped and made from around 3,000 cells, could replicate. But it happened rarely and only in specific circumstances. The xenobots used "kinetic replication" -- a process that is known to occur at the molecular level but has never been observed before at the scale of whole cells or organisms, Bongard said.

Interestingly the CNN article actually links to the new paper in PNAS Kinematic self-replication in reconfigurable organisms which uses "kinematic" rather than "kinetic".
There is no easy to find Wikipedia article titled "kinetic replication" and the phrase does not appear here in Biology SE nor in Chemistry SE.
I found the 2009 PLOS Computational Biology article Investigating the Conformational Stability of Prion Strains through a Kinetic Replication Model which relates the structural stability of the prion aggregates to the rate of replication.
I also found the 1996 Biophysical Chemistry paper Prionics or The kinetic basis of prion diseases.
And in Journal of Physics A: Mathematical and Theoretical (2015) there is Hidden percolation transition in kinetic replication process.
Nothing jumps out to me as a clear definition.
I found searching for the term to be somewhat confounding because the word "kinetics" relates to the measurement of reaction rates as well as to focus on the actual physical interaction between individual molecules (or organisms) which I think is what's being referred to here. Lots of search results including "kinetic" and "replication" but very few on the combined term.
So I'd like to ask for an answer that explores the term "kinetic replication", hopefully cites a formal definition or at least outlines a generally accepted one, and offers a way to distinguish when the replication of a molecule or an organism is "kinetic replication" and when it isn't.
Question: What is, (and what isn't) "kinetic replication" as it applies to molecules and to living organisms?

I chose the replication tag but it automatically switches to dna-replication which I am not sure applies here.

I upvoted because: nice find. I suspect the answer may lie in a whimsical comment coining the term made to a journalist more than a hard-science definition. Google Ngram shows 0 results.

@ARogueAnt. I updated a few minutes ago to add the link to the PNAS article which uses "kinematic self-replication" (a robotics term) rather than "kinetic replication". I'm surprised Ngram didn't at least pick up the two papers I've linked to, do they only search in books or do they also check journal articles?

I'm not certain. The reference which leapt out at me was to the superpower of one of the X-Men, hence the whimsey.

It seems to me, having watched the video in the CNN link, that what is being referred to might be autocatalysis: the concept that the product of a reaction can catalyze the same reaction.  Auto-proteolysis is a great example. Despite what Wikipedia says, autocatalysis as an explanation for the origin of life long predates 1995. See this video for a great explanation by Manfred Eigen, who received the Nobel prize in 1967

@user338907 excellent video and explanation, thanks!

@user338907 nobody has posted an answer yet, perhaps that link and a very brief summary of a few key points will work an an answer?


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Occurrence of the theoretical thymine enol::guanine base pair in DNA
DNA polymerase has a proofreading exonuclease activity that can remove incorrect tautomers in the DNA template or incoming base. In theory the enol form of thymine can form three hydrogen
bonds with guanine. Why is this base pair not favored in nature?

This is surely just a chemistry question — "why is the keto form of thymidine more stable than the enol form?" If there is almost no enol form there can be almost no base pairing involving this form.  In which case your question should be migrated to SE Chemistry. Or do I misunderstand you?


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What is the definiton of repertoire shift in B cells?
I am new to biology and trying to understand this term.
Couldn't find a comprehensive defintion.
Thank you

Welcome to SE Biology. Please finish reading the [Tour] and the Help on asking good questions where you will read that you are required to show the research you have done before posting. In biology we deal more in explanations and usage than formal definitions, and if you search for "B cell repertoire shift" you will find many papers on this topic. Read their introductions and if you still can't understand post a sentence or two and explain what it is specifically that is causing problems.


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Why would it be unsafe to eat spoiled, but heated, food, but safe to drink spoiled, but chlorine purified water?
To my understanding, spoiled food is not supposed to be consumed even after cooking it, since the heat may eradicate germs, but their toxines may be heat-resistant and thus still active. However, there are some purification tablets which are marketed as making spoiled water potable, apparently containing chlorine or iodine usually. Such tablets seem to be recommended also for water purification by the WHO. In the description of such tablets, their effect on toxines is never mentioned, and I wonder why toxines surviving the eradication of germs seem to be no problem here. Do water borne germs usually not synthesize toxines, or to a much lesser extent than food borne pathogens? Or do such tablets somehow inactivate their toxines?

I've never heard anyone refer to water as spoiled. But water doesn't provide a lot of materials/nutrients from which to produce toxins, I assume. It's difficult to metabolize furiously  in plain water.

Water really doesn't "spoil".  The various purification methods are to kill microorganisms living in the water, which if ingested could reproduce and cause illness.  There are usually not significant amounts of toxins in water.

Thank you both for your comments. I see now that "spoiled" is not the correct term in water. I would have assumed that a body of water (let's say a pond) would still be rich in nutrients, but it seems plausible that nutrient density is low in comparison to items of food, and therefore very low toxin synthesis may occur even in a static body of water.

Water can be more dangerous than you know. Dogs swimming in ponds or lakes with blooms of cyanobacteria have died within minutes. Chlorine or iodine wouldn't affect that water's toxicity. There are plenty of toxins in water, but they tend to harm marine organisms that accumulate them and the animals that eat them.

@EpicBroccoli Yeah, water isn't like...agar or fruit juice.

To some extent you can eat heated spoiled food (the point of cooking really). I recall a concentration camp in France where inmates received sporadically tuberculosis infected dead cows, which they ate following a 24h boiling in water. Water is quite often contaminated but more rarely infected in the sense of supporting active multiplication of pathogens (with notable exceptions in cases of flooding with cholera epidemics for instance). In addition on most of the chlorine tablets it is specified it should only be used on clear water (filtered or not, but no turbid water).


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Gene Sequencing
The human genome project took an effort of around 15 years, billions of dollars and thousands of scientists working together.
So how is that the genetic sequencing of covid variants could be done at such a faster rate?

Welcome Tarique. We are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on and see our homework-question policy. Enjoy the Stackexchange network. (The human genome is over 130,000 times bigger and then there's Moore's law too).

Practice, practice, practice. The technology required is now in place.

The sequencing techniques have evolved, notably with spread of the next generation sequencing (NGS) and more recently nanopore. Sanger sequencing used in the first human genome project is a rather slow technique, although still widely used (especially in clinical setting).


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Do spike-protein-based vaccines undermine the DNA repair system?
I ain't no biologist, but I came across a paper recently and tried to understand it:
SARS–CoV–2 Spike Impairs DNA Damage Repair and Inhibits V(D)J Recombination In Vitro
My question: Is it a correct takeaway that vaccines that are based on the full-length spike-protein such as the one from BioNTech may possibly be undermining our DNA repair system, rendering our immune system more vulnerable in general than it was before?

For those interested, chemist and blogger Derek Lowe has published a post on the article in question.

Note: in the time since writing my answer, the paper in question has been retracted. Here's the text of the retraction notice provided by MDPI in collaboration with the authors:

The published article has been retracted. Following publication, the first author contacted the editorial office regarding an improper experimental design with the potential to significantly affect the integrity of the resultant experimental data.
Adhering to our complaint procedure, an investigation was conducted. Both the chosen construct of the spike plasmid that contained a C-terminal fused with 6xHis tag and use of a GFP reporter system under overexpression conditions in the protocol were identified as having the potential to introduce significant ambiguity regarding the nature of the reported observations. The reliability of the results and conclusions presented have therefore been undermined. Furthermore, statements regarding the effect of the spike protein on the adaptive immunity are misleading as in this article no experiments related to the adaptive immunity were performed, and the full-length spike-based vaccine was not studied. Therefore, conclusions related to vaccine safety are not validated and lacked experimental support. This article is retracted and shall be marked accordingly. This retraction was approved by the Editor-in-Chief of the journal Viruses.

While the linked paper presents interesting results, the conclusions must be interpreted in context of their in vitro methods and cannot be readily extrapolated to understand the in vivo effect of SARS-CoV-2 mRNA-LNP vaccines. Here is their important caveat:

Although no evidence has been published that SARS–CoV–2 can infect thymocytes or bone marrow lymphoid cells, our in vitro V(D)J reporter assay shows that the spike protein intensely impeded V(D)J recombination.

They show that spike protein expressed in human embryonic kidney cells (HEK293) can localize to the nucleus and inhibit non-homologous end-joining (NHEJ), which is a vital process in the generation of diversity in the antigen-binding regions of antibodies. However, the way the human adaptive immune system works is such that the cells responsible for generating antibody diversity never internalize the antigenic protein. Once injected, the mRNA-containing lipid nanoparticles are endocytosed by dendritic cells. The mRNA is then translated and the spike protein is presented to T- and B-cells in lymphoid tissues to elicit an immune response. These T- and B-cells are the cells that carry out V(D)J recombination, but they are not the cells that are engulfing the nanoparticle load.
Two good reviews that cover this process in-depth:

Teijaro JR, Farber DL. COVID-19 vaccines: modes of immune activation and future challenges. Nat Rev Immunol. 2021 Apr;21(4):195-197.
Angeli F, Spanevello A, Reboldi G, Visca D, Verdecchia P. SARS-CoV-2 vaccines: Lights and shadows. Eur J Intern Med. 2021 Jun;88:1-8.

The authors explicitly suggest the first part of your question in their discussion section:

indicating that full–length spike–based vaccines may inhibit the recombination of V(D)J in B cells,

However, for this to have a meaningful effect on the immune system as a whole requires that a significant portion of B cells uptake the vaccine and express spike protein, which isn't demonstrated. The paper also, frustratingly, doesn't indicate if their results showing an effect of spike protein on DNA-repair occur in the presence of the non-structural proteins Nsp1, 5, etc., which as they mentioned are known to transport themselves to the nucleus. If spike protein can't get to the nucleus without these other viral proteins which are not included in the vaccine, then there's no reason to suspect the vaccine-produced spikes would have this effect.
With regards to the second part, "rendering our immune system more vulnerable in general than it was before", the spike-based vaccines have been demonstrated to generate a robust B-cell response, so we can rule that out. The immune functions full-length spike protein is suggested to impair are measurably functioning well in vaccinated individuals. In the cytoplasm of cells, mRNA of vaccines and the spike protein they produce can be expected to be recycled after a day or two, so long term effects of this nature are very unlikely.


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What is the effect of anti-fungal soap?
As I understand, most popular anti fungal soap/shampoo has Ketoconazole as an active ingredient. Ketoconazole stops the growth of fungi, but as it does not kill it, but halts division, how can soap/shampoo stop fungal infections? Not all fungus will reproduce at the same time during 5 minutes after soap/shampoo is applied on the skin, so is soap just pseudo medicine?

Ketoconazole is a antifungal drug. How I understand many antifungal drugs, specifically ketoconazole, work, is through inhibition of the sterol biosynthesis pathway which forms ergosterol. Similar to how cholesterol is necessary for the stabilization or regulation of a mammalian lipid membrane, ergosterol works similarly in the cell membranes of fungi. Without ergosterol, it is most likely true that the fungi are incapable of survival.
The sterol biosynthesis pathway is incredibly long and complex, but ketoconazole works specifically to inhibit a key enzyme in the pathway known as CYP51A1. This inhibits the synthesis of ergosterol, as previously noted, which is necessary for most fungi for cell survival - so I do believe that ketoconazole does work to directly kill the fungus. As such, it is an appropriate treatment for fungal infections - the proof of which can be found in the fact that it was clinically approved to do so.

Welcome to Biology.SE. This looks like it could become a good answer, but answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer appears to be speculative opinion and is thus inappropriate for this site. This is a good example of how to format references. ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site for details.


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Transformation and PCR in molecular cloning
After obtaining the recombinant DNA, it is common to transform into E. coli to screen for recombinant DNA and amplify it. But I would like to ask can we amplify it using PCR?
I think there will be 3 DNA molecules after restriction-ligation:

recombinant DNA 2. self-ligated plasmid 3. unligated fragment containing the gene of interest (GOI)

To amplify recombinant plasmid only, can we design primers that span through the insert fragment and the vector, which can only pair well with the recombinant plasmid, but other types?
However, I don't know whether this restriction in primer design will affect GC%. So I am thinking whether we can do phosphatase treatment to prevent self-ligation, then add exonuclease to digest all linear DNA i.e. only retain recombinant plasmid eventually, so the restriction can be overcome (since we can design primer on suitable location on recombinant plasmid now), may I ask is this valid?
After PCR, the recombinant plasmid is linearized (2 blunt ends created by forward and reverse primers if I understand correctly?), which becomes less stable since it can be degraded by exonuclease. Therefore, can we add ligase to circularize the plasmid? Can ligases ligate 2 blunt ends?
I don't know whether this method can be done but I am thinking if we just want the amplify the DNA (don't need the protein product) after generating recombinant plasmids, won't this be more efficient than bacterial transformation?
Thank you and please correct if I made any mistakes.

why would someone go through the hassle of cloning a fragment into a plasmid if you have no intention to use the plasmid for anything?

I’m voting to close this question because it is unclear, seems to contain multiple questions, and shows no evidence of the expected prior research. Please note that each of those is sufficient reason for closure on this site. Please see the [help] starting with [ask] for details. It also appears to be based on a misunderstanding of how and why molecular cloning is done.

I'm not at all sure that you recognize the process here. Generally the bacteria are used for amplification of the plasmid to levels at which you would use it. Doing this by PCR is technically possible, but much much more expensive, has a higher error rate (due to error prone DNA polymerases), and requires extra steps. You also won't get as much DNA out as you would from a bacterial culture. Culture is also scalable - you want more DNA, just grow more bacteria. Once you have a plasmid transformed into a bacterial strain, you can store stocks of this at -80 in glycerol form. You can then scrape a small bit, grow overnight and perform a <2h procedure the next day and end up with several micrograms of very clean DNA.
I highly recommend you read a good cloning protocol, such as those found in Sambrook et al., Molecular Cloning: a laboratory manual or Current protocols. Cloning has been around for >50 years now, I think the process is more or less optimized.
The usual process of generating a plasmid goes like this:

Generate insert (often by PCR, but maybe from another plasmid or via a library generation)
Digest insert with appropriate restriction enzymes
Digest backbone with the same enzymes
Ligate backbone and insert
Transform into bacteria
Pick colonies
Screen colonies for insert (See below)
Grow up colonies with successful clones
Prepare plasmid DNA from successful clones
Use that plasmid in experiments.

The bacteria will generally digest the linear DNA through production of exogenous DNases, and linear DNA often doesn't transform well, so your exo-nuclease step is unnecessary.
Usually when you are screening colonies you use primers specific for the insert, or, if wanting to determine if the insert has been inserted in a specific orientation, then one primer on the backbone and another on the insert. Only amplification from both primers producing a band of the correct size is a positive insert. In this case it is possible to produce primers that only recognize those plasmids that have an insert.
There are a few cases where you might generate primers that span the whole insert - sequencing of the whole insert might be one. Plasmids often have these sorts of sites already incorporated. If you see something labeled M13 or BGH, these are common sites for sequencing primers. Another common usage is if you want a range of inserts (e.g library preparation), and you don't know how big the inserts might be, then you can use the insert spanning primers to identify plasmids which have self-ligated (no insert) as these will only produce very small products on a gel. It is not possible to make insert spanning primers that only recognize the recombinants. No need for ligation or exonucleases.
Another possible scenario is where you want to change a base (or more than 1) in an already constructed plasmid. This is called Site Directed Mutagenesis. In this case you do want the PCR to go all the way around the plasmid, and parental DNA (from the plasmid) is damaged by digestion with the methylation specific restriction enzyme DpnI (PCR products are not methylated, but bacterially grown usually are), and the nicked circular product repaired by the bacteria after transformation.
Primers will not affect the GC content of your product. If you don't like the GC content of your primers, move them to a more amenable location.
It used to be that everyone did an alkaline phosphatase (APs) treatment of the digested DNA to prevent self-ligation. In practice, APs are very hard to get rid of or inactivate and tend to remove the necessary phosphate from your insert when you mix the products together at ligation. This leads to inhibition of the ligation and lowers your chance of success.


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Is it possible to make a vaccine against cancer?
If we can make RNA vaccines against COVID-19 and we know which errors in our DNA leads to different kinds of cancer, can we make a vaccine that will teach our immune system to detect and destroy cancer cells?

The question is akin to "is it possible to make vaccine against viruses?" - for some viruses the answer is yes, for others no.

@RogerVadim Currently the vaccines agains HIV and Hepatite are testing. That vaccines bring to your body the constant parts of viruses that are not mutate

what I am saying is that there are throusands of kinds of cancer, just as there are thousands (or millions) of viruses... in fact, many of them we don't even know yet. A claim that all viruses/cancers can be cured  is impossible to prove, but easy to disprove. See also Faulty generalization.

This is not a direct answer to your question, but perhaps an interesting comment: Cancer has many different underlying causes. One of those are viral infections, such as certain types of HPV (human papillomavirus), which are known to induce several different types of cancer (cervical, anal, vaginal ...). HPV vaccine already exists, and it does indeed provide protection against HPV-induced cancer. Therefore, this is – as your title asks – a type of vaccine against cancer :-)

@RogerVadim It is not only true for the cancer caused by viruses, it is also true for the treatment of other cancers. I will expand my answer tomorrow.

@Chris I did not mean specifically the cancers caused by viruses, but I see now how my phrasing could be confusing.

@RogerVadim Ok, but I didn't include these and at least mentioning them is probably a good idea.

Like vaccines for viruses, wouldn't vaccines need to be targeted to each type of cancerous cell? Also for a number of cancers, there is a vaccine-ish solution. Want to lower your risk of lung cancer, then don't smoke or work with dust without a respirator. Want to lower your risk of melanoma, wear a hat and sunscreen.

@DWGKNZ "then don't smoke" - if technology gives us ability to smoke without hurt, why not?

@Robotex Your reference to faulty generalization is itself an example of faulty generalization. You have reached your conclusion that "a claim that all viruses/cancers can be cured is impossible to prove" by implied reference to proof by example but that is just one type of proof. It is not impossible to prove the claim (albeit very difficult) using proof by exhaustion. One can, in principle, examine every inch of the earth and gather every known virus and test them all.

It is not only possible, these vaccines are in active development. Biontech (the company which developed the Comirnaty Corona vaccine) was founded to develop vaccines against cancer, Moderna is developing similar approaches. It was the research on the cancer vaccines and the development of the mRNA vaccine approach in general made the fast vaccine development for the SARS-CoV-2 vaccine possible.
Biontech has published results of a mRNA based cancer vaccine against melanomna in the summer of 2020 (reference 1) which shows promising results, Moderna has shown data from a phase I study on head and neck squamous cell carcinoma (reference 2). See references 3 and 4 for an overview over the topic.
References:

An RNA vaccine drives immunity in checkpoint-inhibitor-treated
melanoma
Moderna Announces Clinical Updates on Personalized Cancer Vaccine
Program
mRNA vaccine for cancer immunotherapy
mRNA vaccines — a new era in vaccinology

Might not be the answer you're looking for, but there's already a vaccine for one particular type of cancer - cervical cancer. Cervical cancer is largely caused by a virus though (HPV, Human papillomavirus). See Wiki.

Three HPV vaccines (Gardasil, Gardasil 9, and Cervarix) reduce the risk of cancerous or precancerous changes of the cervix and perineum by about 93% and 62%, respectively. The vaccines are between 92% and 100% effective against HPV 16 and 18 up to at least 8 years.

Note that, if I understand correctly, this is not a vaccine against cancer. It is a vaccine against a virus that can cause cancer but not against the cancer itself.

@terdon, one of the users argued the same in his (now deleted) answer. However, would you then by the same arguing say that "COVID-19 vaccine" is not a vaccine against COVID-19 because it is a vaccine against the virus SARS-CoV-2 that causes COVID-19?

@Domen The question specifically asks "can we make a vaccine that will teach our immune system to detect and destroy cancer cells?". If these HPV vaccines attack the virus, rather than the cells, then this is not what the OP wanted to know. Which is why this answer starts with "Might not be the answer you're looking for", I guess. It's still a useful answer, but the distinction that terdon pointed out is important.

@Domen: COVID-19 is a syndrome that's a direct result of infection with SARS-CoV-2. You don't get COVID-19 without SARS-CoV-2 infection, and if you have SARS-CoV-2 infection, you have COVID-19; the distinction is semantic hairsplitting. HPV causes genital warts (sometimes), but it's lingering damage from HPV that sometimes leads to cancer (of various forms) down the line (years after you've cleared the HPV itself in many cases); you can still get those cancers without HPV, and you can get HPV without getting those cancers. The vaccine stops HPV, it only indirectly protects against cancer.

@domen that is a false analogy. Cancer is not caused by pathogens per-se, it is caused by aberrations in the cell's DNA sequence. The link between a virus and the disease it causes is far more direct and the vaccine that targets the virus is actively targetting that virus and, by extension, the associated disease. However, the HPV vaccine will have absolutely no protective effect from developing cervical cancer through random mutation (as is usually the case with cancers) and not as a result of HPV infection. [cont...]

[...cont] So this is a vaccine against HPV, and by protecting you from HPV infection it can protect from HPV-induced cancer but it will not have any effect on non-HPC induced cancer and HPV is not the only way of developing cervical cancer. You can still develop the cancer if you are unlucky enough to develop the same mutation through other means.


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Were fall foliage leaf colors in Canada also delayed in autumn 2021?
English is not my first language. I didn't fully grok this National Geographic article published November 24 2021 by Sarah Gibbens. But it discusses just the eastern U.S.A., NOT Canada. How ever what about fall foliage in Canada in 2021? Also delayed?
The sub heading is

Throughout the eastern U.S., fall colors arrived behind schedule, which scientists say is a sign of things to come.

In the middle

From Vermont to North Carolina, fall foliage appeared behind schedule this year—continuing a long-term trend that, according to one recent study of maples by researchers at George Mason University, has pushed the appearance of fall colors back more than a month since the 19th century.

Anecdotally, I thought they were.

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Could the EDTA coating of tubes kill blood fed mosquitoes?
Problem is as follows: culex pipiens fed with freeze-thawed cattle blood sampled in 9ml EDTA tubes enjoy their meal and thrive. Same population fed with freeze-thawed human blood sampled in 4 ml EDTA tubes die. 4ml tubes are overall quite less filled, hence hypothesis is remaining EDTA is more concentrated possibly leading to the death of the mosquitoes. Is this something plausible?
Thank you !

Have you tried using other sample tubes? For example heparin or citrate coated?

Not yet, i'd like to solve that mystery of cattle versus human blood

Put them in the same sized tubes?


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The almost extinct dinosaurs
Dinosaurs split into "lizard-hipped" and "bird-hipped" dinosaurs. Of these two groups, only the "lizard-hipped" (Saurischia) survived (these names are backwards).
Of Saurischia, only Theropoda survived. The diverse Sauropodomorpha clade died out fully.
Of Theropoda, only Tetanurae survived.
Of Tetanurae only Coelurosauria survived. And so on. By the time we got to Aves (birds) we are (according to wikipedia) 46 levels deep (if I counted correctly) with most levels unnamed. Aves is defined as the smallest clade that includes all living birds. In addition, we can go several levels outward to Avemetatarsalia and still have birds the only living group thereof (why we don't consider everything in Avemetatarsalia a "dinosaur" is unclear to me).
In contrast, the evolution of mammals does not follow such extreme pruning, starting from Synapsida (the sister clade to Reptila), there are 17 steps to take us to Mammalia according to wikipedia. Of course, there are probably many more branches along the lineage of birds and mammals than is known form the fossil record, but a 2.5:1 ratio in known branches is still intriguing.

Is it true that the tree leading to birds had more "pruning" extinctions than most other clades such as mammals?
If so, why would this be?

Note that "steps" or "levels" in the phylogeny have no biological reality. They will vary depending on the level of details humans get access to and care to describe. Comparing the shapes of different branches of the tree of life is a legitimate question, but relying on such steps or levels might be a problem. That said, I don't have a better proposal.

@bli: That is what my first question gets at, is the difference in depth "real" or just because humans happen to have more details about the evolution of birds than of mammals?

keep in mind dinosaurs were successful for a LOT longer than mammals so it is not surprising there was a lot more diversification. T-rex is closer to the present day than it is to the first dinosaur by a large margin. we also have a LOT more dinosaur fossils than early mammals. also think about how severe the KT extinction was, 75% of all species, that alone is responsible for most of the pruning.


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Is there any methods to avoid the pcr control contamination?
Why do I use the primers in the D1-D2 region to amplify the fungus, and using water as a negative control has a weak band that is the same size as the target fragment? When using the ITS primer, using water as a negative control in the ITS region, there is no band. why does this happen?

Can you add some more information on the regions and also your protocol? What do you do for the PCR and how do you do your controls.

I use the NL-1F and NL-4R primers to amplify the D1-D2 region of fungi, using the Thermal cracking method to obtain the fungi DNA template. Control does't add DNA template. PCR program is 95℃ 5min, 95℃  30s, 51.5℃ 30s,72℃ 1min,72℃ 5min, 4℃.36 cycles. The electrophoresis result is that the control has a weak band. I use the ITS1-F and ITS4-R primers to amplify the ITS region. Only change the annealing temperature to 55℃。The control doesn't have band. why does this happen?

It would be great if you could use the edit function to add this information to the question. To understand this right, if you amplify the D1-D2 region and use water as a negative control you get a weak band, when you do the same blank control on the ITS region (with the ITS primers of course) you get a blank negative control?

yes, i use water as a negative control has a weak band that is the same size as the target fragment, when amplifying the D1-D2 region? When using the ITS primer, using water as a negative control in the ITS region, there is no band. why does this happen? thank you very much.

I think you have a contamination problem. Most likely the primer used to amplify the D1-D2 region are contaminated with your DNA. This can happen easily and underscores the importance of proper negative controls.
Since your negative control with another gene is clean, this points against a contamination of your other reagents (dNTPs, water) or even your pipette (yes, this can happen and I have seen this in the lab). Otherwise the negative control of this reaction would show a band as well. I suppose that all reagents except the primers are the same for both reactions, so this clearly points to a contamination of the primers.
This is easy to solve: Make a fresh dilution of your primer working stock - preferrably at another working space where you do not work with your fungal DNA. If possible use filter tips when doing PCR work to avoid cross contamination of samples.

I don't think you can say where the contamination is and would treat all reagents and pipettors as potentially contaminated. The contamination could be  D1-D2 PCR product which would explain the other control being OK.

@Michael_A I would agree, if the negative control of the other gene would also show a band. Since it doesn't (and I suppose that all reagents except the primers are the same between these two reactions) this is highly unlikely.

I agree with Chris. You don't want to have handled amplified PCR product at the same workstation (or with the same pipettes) used for setting up reactions or diluting primer stocks. Filter tips are strongly recommended. And I'd also consider decontaminating all of your work stations and pipettes with a diluted bleach solution or something like DNAzap (check pipette user manual for cleaning instruction first to make sure it won't cause damage, but shouldn't).


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Why are O-antigens and H-antigens on (certain) bacteria called O and H?
Somehow, despite extensive searching, I cannot find an answer....
Does O stand for oxygen and H signify hydrogen?

The "H" and "O" identifiers first appeared in German-language publications around 1920 to describe different forms of disease-causing bacilli. Thankfully, Arkwright and Goyle provide an English explanation of the terms in their 1924 review.1

These writers called the two forms, which they described, the "H" and the "O" form, because in the case of B. proteus, the first bacillus investigated, the "H" form was represented by the normal, which grew with a spreading film (Hauch) on the surface of agar, whilst the "O" form, which occurred as a variant, grew in isolated colonies without any film (ohne Hauch).

The literal translation of Hauch is "breath", and ohne Hauch is "without breath", though some sources translate Hauch as "thin layer", which is probably the intended meaning.

References

Arkwright JA, Goyle AN. The Relation of the “Smooth” and “Rough” Forms of Intestinal Bacteria to the “O” and “H” Forms of Weil and Felix. Br J Exp Pathol. 1924;5(2):104-114.

As a German speaker, "Hauch" idiomatically means something like "a touch of ...", so "thin layer" is indeed an appropriate translation in this context.


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Is it OK to use predicted protein sequences from RefSeq for protein sequence alignment?
I'm doing a project, and my goal is to do alignments of a particular gene product to see if there is any conservation of secondary structures across different species.
So far, I have found a few from UniProt that are reviewed. I want to add more from different species, but the sequences were all created via AI prediction from a genome sequence.
Can I use those at all or no?

Welcome to Biology.SE! So, you are aligning protein sequences from some species with a known function, and you want to know if it's ok to include proteins from other species that are computationally predicted to have the same function? This is pretty standard practice, though you should expand on what you mean by "AI prediction". HMMs are common tools for searching for proteins with similar structural motifs, is that what you used?

not quite, I am aligning the same gene product from different species. The gene of interest is a human gene and I am searching for homologs. I have found homolog sequences in rat and mouse, which were reviewed and backed by experimental data. If i blast this human gene against xenopus tropicalis, I get a protein sequence that is "predicated by automated computational analysis...derived from a genomic sequence...annotated using gene prediction method: Gnomon, supported by mRNA and EST evidence." I am confused by the wording here...does this protein exist or?

Thanks for the clarification. I suggest editing your question to add the information you've provided in your comment. Concerning your question -- does this protein exist -- you should read up on how Gnomon works.

I did read that link before posting here...and I got the idea that the the answer is highly likely...I also have read the Refseq FAQ regarding the xp prefix (most of my sequences' accession number starts with that since they were all predications)...but I am still unsure...


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What is inside digestive system while it's empty?
Up to this point, all my life I assumed that stomach and intestines are filled with air. I got this impression from all the anatomic drawings in schoolbooks and encyclopedias that show empty stomach and intestines like a big sacks, with only small amount of digestive fluids in stomach at the bottom of it.
But getting some in-depth knowledges of scuba/free diving, it seems that it was a lie, all along! If it would have been filled with air, divers would need to "equalise" it, like they do with middle ears, sinuses, mask and lungs. Otherwise, they would face pretty serious barotrauma.
So, if it's not filled with air... Is it filled with liquid? I don't think it's likely, in this case we would always feel "fullness" and it would add too much weight.
My current hypothesis is, that stomach and intestines are so stretchy (distendable?), that it just collapses naturally, when empty, and maybe only contains small amount of mucus on it's walls to decrease friction of the walls. Is this correct? I couldn't find this information anywhere on the internet, strangely. Maybe it's so obvious that nobody writes about it?
I can imagine intestines shrinking, but stomach? It's kind of hard to imagine how such a big "bag" can shrink so much to not contain any gas/liquid in it...

When empty there is almost nothing in them. However one is frequently swallowing sinus mucus and saliva.  My doctor told me a couple gallons in 24 hours; but I have no internet source so not an answer.

"Is it filled with liquid? I don't think it's likely, in this case we would always feel "fullness" and it would add too much weight" How would you know this if it's the normal state of being? If it were this way since infancy or before? You would feel "normal". Which is normal. Also, your urinary bladder shrinks when empty. Why not your stomach?

As far as barotrauma goes, how distensible are the sinuses, the middle ear, the lungs and the diving mask? Not very. But the intestines? Very. If you're absolutely full of gas, you'll get gas pains (not the bends) on ascending, but you don't need to equalize something that you can't possibly equalize. Barotrauma of the GI tract is rare; much more commonly, the lungs are involved. I wrote a full answer including Xrays, but got the erroneous message that your Q was deleted, so my answer was discarded. Sorry.

@anongoodnurse That's true, I meant filled with liquid to the extent that is shown on all the anatomy pictures in encyclopedias.

@anongoodnurse NP, your comment is good enough for my understanding! I think that probably one possibility of barotrauma is when diver swallows some high pressure breathing gas on very deep depth, so that it would greatly extend when coming back to surface quickly (for example in an emergency assent).

As I said, barotrauma to the GI tract is rare. Even when there is free air in the abdominal cavity, and the GI tract is imaged for perforation, it usually is found to come from trauma to the lungs and damage to the diaphragm. "I think that probably one possibility of barotrauma is when..." Imagining something doesn't make it so.

There is nothing. The tissue compresses together.
The entire digestive tract, including the esophagus, is pressurized by muscles.
Gases do get produced by digestion (and disfunctionally by air swallowing) and those gases must be removed from the body.
A small amount of air and carbon dioxide can naturally exist in the stomach, but if this increases it will rapidly cause disomfort or other symptoms, such as burping.

A rapid transit time is 24 hours; more normal is 36-40, and even 72 hours is still considered normal. Unless you're NPO for >72 hours or you've undergone a rigorous bowel prep (ugh!), there's almost no time that the entire GI tract is empty. Also, I can't recall ever seeing an upright abdominal film where there wasn't an air-fluid level in the stomach. Air (and saliva) in the stomach is the norm.

@anongoodnurse The OP is asking about gases, not fluids. Obviously the digestive tract has fluids.

It's not obvious from your answer. "There is nothing." That's not quite the extent of it.

If by "nothing" he meant air, then I'm fine with it!


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Could someone explain how chromosomes are counted here?

I'm not sure how chromosomes are counted in this picture. I would reason that there would be 8 chromosomes in the diploid cell, but that doesn't seem to be the case. Could someone explain?

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Where did the diagram come from?  I'd say it is flat-out wrong, as the left shows 8 chromosomes. It shows 4 types of chromosomes or 4 pairs of chromosomes, but a total of 8 chromosomes.

Like @mgkrebbs commented, the left poster shows a total of 8 chromosomes, but only 4 pairs of chromosomes. I would dare say that you are right and that the poster is wrong. The left has 8 chromosomes, and 4 pairs of chromosomes. The right has 4 chromosomes, and they are not paired up, so the number of pairs is insignificant.

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In the absence of natural enemies, does evolution eventually create natural enemies?
I wonder if there is experimental evidence on this (either from computer simulations or perhaps cases of isolated species like on the Galapagos Islands).
Imagine the hypothetical situation of a group of individuals of the same species that becomes isolated from all others. I know it's not a very realistic scenario because life is pretty much everywhere on Earth, but maybe experiments could be done in the laboratory.
So we have, for example, 100 or 1,000 or so individuals of the same species (any species, from any domain and kingdom of life) that is isolated from all other life. I know this group would undergo several speciation events (I think I've read about experiments like this and I think it's not really debatable, but is likely to be universally agreed upon by evolutionary biologists), but would this group eventually evolve natural enemies (e.g. a predator-prey or host-parasite or similar relationship)?
I think limited resources would certainly result in different competitors evolving, with some competitors fitter than others, but I'm not sure about enemies. I'm thinking that given adequate time, full-blown enemies would be almost certain to evolve, but that's just a guess.
A more specific example might be to take a single ant colony or honeybee colony and isolate it in a laboratory and study it over hundreds of generations or more.
I did some searching on this, but didn't find anything closely related to this question.
For more context, I started thinking about this question while reading this article.
Thanks in advance for any thoughts on this.
Edit: assume in a lab experiment that non-living nutritional sources (e.g. sugar water) were supplied in a measured way.

I’m voting to close this question because unfortunately this is a speculative question, even if the answer is likely yes, it is still speculative and unable to be answered with evidence from the literature.

I'll add a comment here to partially answer this question - if you take reductio-ad-absurdum as an argument: Imagine the beginning of life on this planet - at some point there must have been 1 animal species, assuming all animals are descended from this species, now there are thousands, some of which are predators... so, yes?

True that, but I'm seeking experimental evidence (either in silico or in vitro) published in the last 20-40 years or so. For example, the 1952 Miller–Urey experiment was in vitro & although it didn't involve life, it was in vitro & insightful in that only water, methane, ammonia, and hydrogen started the experiment. But at least 3 amino acids were identified in the resulting solution: glycine, α-alanine and β-alanine. In 1996, Miller said: "Just turning on the spark in a basic pre-biotic experiment will yield 11 out of 20 amino acids." So they've been doing experiments like this for ~70 years.

Also, here's an oversimplified experiment in silico where some experimental parameters do not lead to natural enemies, no matter how many generations are allowed to pass: https://ncase.me/trust/


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Why are Anisakiasis infections relatively rare in Japan?
In Japan raw fish are routinely eaten in the form of sushi and sashimi, and frequently no freezing or other preservative treatments have been applied. Even so, incidence of illness due to the common parasite Anisakiasis is reportedly only about 1000 cases per year. Given that very high concentrations of Anisakiasis and other nematodes are found in many types of food fishes, like mackerel, why would parasitical illness be so low?

Can you edit your question to include a source for the "1000 cases per year" figure? In fact, a source I found states that Japan accounts for 90% of global cases, which would suggest that such infections are relatively common in Japan.

When a question includes the word reportedly, the question that follows is “reported by who?” It is expected that askers include sources for their claims, especially those as specific as a number of cases. Concerning your assertion that cases are relatively rare in Japan, relatively is the operative word, there. I took that to mean “relative to other countries”, hence my comment.

Regardless, the crux of your question is essentially “Why are cases in Japan lower than expected?” I believe the answer is “it isn’t”. What is the base rate of Anisakis-containing fish consumption in Japan and other countries? What is the per-capita incidence of Anisakiasis in Japan and other countries? What is the likelihood of Anisakiasis given parasite ingestion? Each of these questions needs to be answered before you can assert that Anisakiasis is “rare” in a given population.

What do you consider rare? Japan accounts for more than 90% cases of Anisakiasis globally. The rest 10% coming from other countries like Netherlands, Spain etc. So, you need to consider those countries.

I read the freely available article:
“Anisakidosis: perils of the deep”.
It mentions that Japanese chefs are skilled at detecting Anisakis, hence infection is less likely.


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Drinking salt water
I have been told that one should never drink sea water no matter how much thirsty
It turns out that drinking saltwater adds lot of salts to the body that need much more water than the amount consumed to be removed leading to dehydration
A few questions arise in my mind

Why can't our kidneys excrete a little more concentrated urine than usual to remove excess salts (sea water is not saturated unless perhaps the Dead Sea water)
At maximum a more concentrated urine will damage the bladder or some portions of the kidney but that will not kill us as fast as dehydration.
Anyway the kidneys should know that the body is already having a shortage of water (that is why we are thirsty enough to drink salt).

Also should not absorption of salt stop in the intestine after enough has diffused passively
And if it is being(in case concentration is high but not than of blood) being actively absorbed it should stop after desired amount has been absorbed

If it too concentrated and threatens to cause plasmolysis the intestines should actively absorb water right?

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"Why can't our kidneys excrete a little more concentrated urine than usual to remove excess salts" Things have limits and sea water is beyond that limit. Just because I can run a bit faster than usual doesn't mean I can continuously speed up forever. "Also should not absorption of salt stop in the intestine after enough has diffused passively" Think about what you're saying here. When does diffusion stop? When concentrations are equal. Is that too salty for the body? Most definitely. I'm pretty sure you already know both those things but you do not seem to be adding 1 and 1 together.

This has been asked and answered before. Search for "drinking sea water" in the search function at he upper left of the page; you will find some answers.

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Chemiosmotic hypothesis
During the transport of electrons, some H+ are removed from the chloroplast stroma, which causes a proton gradient to build up inside the thylakoid lumen. But what's the source of H+ in stroma at the first place?

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I suggest you do some research before posting here. Try reading Lehninger's Biochemistry book. They have explained it very well. If still any confusion, you come back and rewrite your question.


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Exoskeleton Bug Identification
I found these bug shells / exoskeletons / casings in the corner of my room and I am wondering what they could be. They are about 1-2 cm long. The light colored spots on the floor are likely related. I was thinking they might be from pill bugs, but this is a second-floor room so I am unsure. Located in NW Washington, USA.
Thank you!

They are all wrapped in spider web, so you have a nice spider keeping your bugs down. If you could unwrap a few, then you might be able to get an ID. I suspect several different types of insects. The bottom middle (darker one) is likely a cranefly or something similarly leggy.

Welcome to Biology.SE. Looks to me like a spider has been feeding on a mixture of things including something pill bug like — I suspect the spots are spider droppings. Can you try opening up some of the little sacks and getting clearer pictures of the contents? Also, you might want to  check above where you found the bodies for webbing or a spider.


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Illustrating Action Potential Conduction and Ion-Gated Channels

I can separately illustrate action potential and ion-gated channels along an axon.  However, I am not sure if I did the right thing on the picture below.  What I'm trying to show are the simultaneous processes of (1) the flow or propagation of action potential along the axon length, and (2) the position of ion-gated channels along the axon length.
The blue figures are for sodium. The red figures are for potassium. The arrows show the propagation of action potential.
Was I able to depict what I'm trying to show properly?  If not, how can I correct this?

For clarity - this is entirely your own diagram? Or you've modified someone else's?

@BryanKrause this is my own diagram.