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If bacteria with recombinant DNA molecules do not survive in gene cloning, how they can be grown into a colony after being isolated?
This is as far as my understanding of gene cloning goes. Let's say that the plasimd (vector) in the bacteria contains an ampicillin resistence gene. Through restriction enzymes, the ampicillin resistance gene is cut through and foreign DNA is inserted. This creates a recombinant DNA molecule.
Once many bacteria are introduced to a medium that contains ampicillin, only ones that have no recombinant DNA and functional ampicillin resistance genes will survive and those with the recombinant DNA won't. Through the addition of some chemicals, the surviving bacteria will turn blue and those with the recombinant DNA will turn white. Thus, bacteria with recombinant DNA can be taken and grown in their own culture, the recombinant DNA can be isolated, and research goes on.
However, if all the bacteria with recombinant DNA have been killed because they have no functional ampicillin resistance genes, how can they be 'grown' in their own colony? They're all already dead, aren't they?

This topic has been covered in previous questions, e.g. https://biology.stackexchange.com/questions/69141/selection-of-recombinant-host-by-color-selection-method.

You are mixing up too many things: 1) the ampicilin gene is normally not cut out to make recombinant DNA. Instead 2) cutting/pasting into a vector is usually performed at a multiple cloning site (MCS) independently of the ressitance gene. 3) The blue/white screening uses a beta-lactamase gene and is also unrelated to ampicilin.

@Nicolai yep I realized how off it was and answered my own question. I would've deleted the question because of how confusing it was but wasn't able to because it already had an answer.

The question confuses too many things. The process being described, Lac Z Blue-White Screening, doesn't involve cutting the ampicillin gene, nor do the bacteria with the recombinant DNA or without the recombinant DNA die in the process of the experiment.
The plasmid contains a Lac Z gene involved in creating enzymes that break down galactose. In a test tube, the vector plasmids take up the gene of interest and the recombinant DNA is produced. The recombinant DNA is then added to the medium of bacteria, but only some of the bacteria will be transformed and take up the plasmid vector. In these bacteria, restriction enzymes will 'cut open' a space for insertion in the Lac Z gene, and DNA ligase will seal it up. The insertion of the gene in a bacterium disrupts the Lac Z gene and make it unable to produce the required enzymes to break down galactose. Then, the bacteria are applied to a Petri dish that contains growth media with a derivative of galactose, X-gal in it. When X-gal is broken down by the bacteria able to create the necessary enzymes from their functional Lac Z genes, the bacterial colony will turn blue. So, when you add these bacteria into the Petri dish, only the bacteria without the recombinant DNA will break down X-gal and turn blue, whereas bacteria with the recombinant DNA will not be able to break it down and remain white. This allows the researcher to distinguish between the bacteria with and without the recombinant DNA, and allow them to isolate for the ones with it.

I answered my own question because I learned in the time since I asked it just how off it was.

Your description of how blue/white staining works is (essentially) correct, however the generation of recombinant DNA does not happen in bacteria. Recombinant plasmids are generated by researchers in vitro (meaning in a test tube) using restriction enzymes (and more like DNA ligase). Note that in most cases even a plasmid that did not receive the gene of interest would still be recombinant, since the even the base plasmid used is usually not found in that form in the bacteria used.

@Nicolai I've updated the answer given your remarks. Do you think it's good now?

I’ll elaborate on this answer in the future but, in the meantime, blue/white screening is used to differentiate between bacteria that were transformed with the vector and gene of interest and bacteria that were transformed with an empty vector. An empty vector still confers antibiotic resistance and thus allows the bacteria to grow, but it does not contain the gene of interest and is therefore useless to the researcher.


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Difference between aerosol and droplet transmission for airborne diseases
I've been doing some pandemic reading and can't find why there is a distinction between transmission by aerosols and by droplets. Some articles give a size cutoff of 5 microns; how is that important?
Aerosols were also mentioned to be either wet (small droplets) or dry (dry remains from an evaporated droplet). Does that mean droplets can evaporate enough to count as an aerosol?

An Aerosol is a suspension of droplets or particles in air. A "suspension" means that the droplets or particles are suspended in the air and do not just fall down with gravity. Very tiny droplets can be suspended in this way by the Brownian motion of the air molecules: The air molecules move around randomly (their speed indicates the air's temperature) and hit these tiny droplets back and forth and prevent them from falling down as they would normally do because of gravity. But larger droplets are too big, the air's Brownian motion is not powerful enough to keep them suspended against gravity, so larger do fall down and do not create an aerosol.
So, if the coughed-up droplets are big, they will quickly fall down - and as a result the disease will be hard to transmit (the healthy person needs to stand close enough to the infected person to inhale the droplets before they fall down). However, if the droplets are smaller than some size, they form - as I described above - an aerosol. Such an aerosol can be suspended in the air for a long time, which can mean that a person who walks into a room where a person previously sneezed will get infected. It can also mean that the aerosol can float around the room, and infect a person standing pretty far away from the source.

source: Stack Exchange

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

sort: votes


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What arthropod is this?
Location: Johannesburg, South Africa
Colour: Brown/Grey
Legs: 6 or 7 pairs
Size: ~10mm
I've been finding these guys in my bath tub the past two mornings. I've caught and released them. I'd like to know what they are so that I can decide whether pest-control measures are needed.

That is an Isopod crustacean, in the suborder Oniscidea https://en.wikipedia.org/wiki/Woodlouse. These are harmless, so I would not worry about contacting pest control. They are also known as "pillbugs".

It should be mentioned that they are a good indicator of moisture problems as they only like very damp conditions, if you are continuing to see them you may want to start looking for leaks, rot, and mold. they also indicate easy access for other insects so you may want to start sealing cracks. https://pestcontrolcanada.com/sow-bugs-pill-bugs/

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


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Lizards Undergo Rapid Evolution: Please, tell me this is not a lie
This article states that transition from eating insect to eating plants is called and caused evolution.
The article neither provides images nor swears that they are telling the truth.
Has someone else tried the same method as the article's author? Those lezards were still eating insects in nineties in Algeria.
Can somebody living in Pod Mrcaru provide us with images of the same lizards?
Could this transition which is preceeded by human [... not nature] be compared to evolution?

Comments are not for extended discussion; this conversation has been moved to chat.

The article is referring to an actual series of studies, the divergent evolution is caused by the population being introduced to a small island free of predators. It is well known that small isolated populations can evolve quickly, change can spread much faster in small populations. Note the lizards still eat insects it is just the island population also eats some plants, they have other noticeable differences as well.
To answer your question Yes this is evolution, likely a combination of natural selection and genetic drift. Evolution is just a change in allele frequency (basically a heritable change) a group of organisms over time.
Like many news sites they do horrible job of sourcing their information, but is referring to actual science.

just to be clear, the comment in my answer does not refer to your answer but the one OP has marked.

[It is well known that small isolated ...] is this a law? I'm sorry it's not well known. [lizards still eat insects...] why wasn't this stated in the article? P.S answer me is this evolution?

Thank you John for your knowledge, time and energy. I'm accepting your reply as an alternative only because I trust you. I'll see and come back later. Thank you so much NatWH

@John In the well known link, (1) the author says "If you do it an infinite number of times, it will be 50%.". This is a fallacy, isn't it?

I can't find that anywhere in the paper, do you have a page number?

Since the existing answer barely even tried, I will give one. Rapid adaptive evolution on ecological time-scales is pretty much non-controversial, and has basically been understood since Haldane. The paper that this report is derived from is here (amongst others, see John's answer), and does appear to show morphological evolution over the course of some 37 years in response to different resource availability.

I really appreciate your answer and your time.

In Fig. 4. of the article, how can I convince myself that this is evolution rather than a normal morphological change (e.g. between two persons)?

Fig. 4 is a demonstrative example; I would look at the quantitative evidence in the earlier figures.

I swear of God, I could not be convinced. I'm sorry for your time. I'm going have a look at https://evolution.berkeley.edu/evolibrary/article/evo_01 and find some free glossaries

and please NatWH do not blame me. As you may admit, today's internet is full of lies. the Arabic article that targeted the object article was also full of (let say lies) falsification and information that neither exist in the object article nor in the official one you provided. I will study the article you provided. Here is the link http://www.ahewar.org/debat/show.art.asp?aid=346856


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Evolution - The ability to control ear muscles
Among animals the ability to control ear muscles is pretty common, but only a few humans have the ability. Is it because we in general lost this ability ?

Yes, humans have lost the ability to move their ears toward sounds like many other animals such as cats and rabbits.
It is thought that our ancestors lost the ability to move their ears around 30 million years ago when

Ear size decreased and the associated musculature changed 1 (Steven Hackley).

A review from Steven Hackley outlines the evidence that the neural circuit remains in modern human brains. Apparently, the neural circuit still responds to directional sounds and may cause our ears to curl slightly (2 - 3 mm).

This adaptation would have very little pressure on gene pool selection, as it provides little to no advantage other than slight, likely negligible, hearing improvement.
As survival fitness in terms of hunter-gatherer qualities, such as those of keen hearing and sight, are today meaningless in terms of reproductive viability, this phenotype would not persist over time, in my opinion.

Welcome to SE Biology. I think you've only alluded to an answer for the question, which I read as Do we have an ancestral group that lost the ability to control their ear muscles? Your answer concerns why we could have lost the ability to control our ear muscles.

Hi, thanks for having me. He's asking 'is it because we in general lost this ability'. I'm saying 'yes, we as a species have lost this ability due to lack of genetic selection for the trait, although it still likely shows up in some gene pools sporadically'.  See definition of vestigial.

No worries. Editing to include what you have summarised in your comment would improve the answer.


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Control for Bisulfite sequencing
I am wondering how can I control my converted DNA!
I converted my DNA with bisulfite then I amplified the converted DNA with specific primers of BSP and purified my product and finally sequenced the product!
In which step should I control my DNA? And what is the protocol?
thanks for any advice.

Wait, so you're looking to retroactively add controls (not feasible) or add controls for future processing? If you already went through the entire process with no controls, I'd be uncertain as to how you're convinced the process went smoothly to begin with.

To initially optimize PCR conditions: Mix 50% methylated bisulphite-converted DNA (50 M)
and 50% bisulphite-converted unmethylated DNA (50 U) to test for proportional PCR amplification with bisulphite conversion specific
primers and PCR master mix.                                                                                This is from nature protocol,I dont know how should I control the PCR product because we just have one paired primers and there is no difference between methylated  and unmethylated product! should I design another primers that bind to CPG Island?


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Having a lot of trouble identifying this insect

It was found in central Alabama

This is a true bug nymph; it may be an Assassin Bug (Reduviidae), but I'll admit to uncertainty there.

A friend of mine, ecologist, also suggested that it's a young Reduvid bug, and that it's supposed to suck blood.

Its legs are too thin, ain't Reduviidae supposed to be more robust? Maybe it's from an herbivore group.

I'm inclined to think it's not a Reduviid - those flared legs remind me more of something plant-eaterish; maybe something in the Coreoidea.  The problem is that Heteropterids are a bugger to know well, and that's just the adults.  The juveniles are a real pain.  Better to submit it to one of the ID sites like Bug Guide.

cool it looks like a cousin of the golden egg bug.

This is a true bug (Heteroptera) larvae as the dorsal scent glands and the wing pockets show (see image below).
I suspect it to be a member of the family Coreidae as it exhibits typical (larval) characteristics of this family: a rhomb shaped body and long legs and antenna.
A reduviid larvae, as some of the commentators suggest, would have a strong, often bow-shaped rostrum (proboscis) that I assume should be visible from the perspective of the photographer. Also, reduviid bugs usually have a relatively long head composed of a long neck and nose.

Compare more images of coreid (knowyourinsects.org) and reduviid bugs (knowyourinsects.org).

Image sources (in reading direction):  Mictis profana Graham Wise CC-BY-2.0 | Coreus marginatus AfroBrazilian CC-BY-SA-4.0 | Arilus cristatus Judy Gallagher CC-BY-2.0 | Rhynocoris annulatus Slimguy CC-BY-4.0


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For long term survival of a species in a harsh environment which is more important-mutation or evolution?
The environment is the ultimate cause of population stabilization. Considering the environment to turn harsh for the survival of a species.How to adapt better to this change-by evolution or by mutation?

Considering mutation is part of evolution this question does not make a lot of sense.

maybe because i am not related to this field

One of the central requirements of evolution is that individuals of a species vary. Natural selection acts on variants. Mutation is the source of variation upon which evolutions works. Variation is then increased through sexual reproduction and recombination. Variation in the environment is the reason that variation among individuals is so important for the long-term survival of a species. Otherwise, it would be best to fix on a single optimal genotype. But with variation in the environment, the optimal is a moving target. So your question is complex. Variation in the environment requires a mechanism for species to adapt to change. That mechanism is mutation, amplified by sexual reproduction and recombination.

To operate for many generations evolution needs a process that adds variation (mutation) and a process that removes it (natural selection). Evolution can operate without mutation but not for very long the process will exhaust the available variation rather quickly.


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Can monoclonal antibodies work only if the target of it is located in the cell's surface?
Can monoclonal antibodies work only if the target of it is located in the cell's surface?
or it can be used to targeting a protein located inside the cell?

You have been in this site for some time so probably you are aware of our site policy of expecting research effort from the user. Your question is very basic. Did you try to find out anything at all?

Your comment is probably related to your other question.

Monoclonal antibodies (or antibodies in general) are large proteins (around 150 kiloDaltons according to Wikipedia), so cannot cross the plasma membrane. So monoclonal antibodies target extracellular molecules or cell surface molecules. However, there are techniques to target proteins inside a cell, like lysing the cell, or using gene modifications, or otherwise a technique covered in this paper: https://www.tandfonline.com/doi/abs/10.1517/14712598.5.2.237


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Does evolution select against genetic diversity?
Only the best genotype in a species will win. So it sounds like evolution selects against genetic diversity.

I would not close this post as duplicate of "Evolution of diversity and extinction resistance".

selection of any kind reduces diversity almost by definition, without mutation to offset it evolution would quickly run out of diversity to work with. keep in mind however it a rarely a single genotype that is successfully but rather a set complimentary genotypes coexisting.

TL;DR
In a population, directional selection reduces genetic diversity.
Simple scenario
In a population, directional selection reduces genetic variance (at the loci that are under selection and other linked loci). Selection selects for variants that are associated with the highest fitness. Hence, selection reduces the number of variants (or at least the frequency of the variants that are associated with a lower fitness).
Note that, by reducing genetic variance, selection also reduces heritability (see this post for definition) for the selected trait.
Note that, for a correct terminology, you should not say that selection "selects for" low genetic diversity. Selection "selects for" variants associated with high fitness which causes a reduction in genetic diversity. Selection indeed does not "select for" any population-wide statistic but only for specific variants in the population which affect those population-wide statistics.
Selection vs evolution
You say

Does evolution select against genetic diversity?

Please do not confound "evolution" with "selection". There are a number of "drivers" of evolution other than selection (e.g. genetic drift, mutation, migration). Both selection and drift reduce genetic diversity, however, mutation and incoming migration will typically increase it.
Balancing selection
Note also that there are types of selection that maintain genetic variance such as negative frequency-dependent selection, or heterozygous advantage for examples. Those types of selection that maintain genetic diversity are called balancing selection.
Multiple populations
Imagine a scenario where two populations are present in two different environments. If there is directional selection going into opposite direction in each environment (aka local selection), then selection will still reduce within-population genetic diversity but will increase the among-population genetic diversity.
Definitions of genetic diversity
Genetic diversity is a concept used in population and evolutionary genetics. The term genetic diversity is typically defined as the probability of non-identity by state of two alleles. In a single population, this is identical as the definition of expected heterozygosity. Let $p$ be the allele frequency in a population, the genetic diversity $\pi$ at this locus in this population is defined as $\pi = 2p(1-p)$.
More info about these definitions and their relationship to $F_{ST}$ (a widely used statistics of population divergence) in Nei (1973) and Charlesworth (1998).
Definitions of genetic variance
Genetic variance is typically a term used in quantitative genetics. One could say that genetic variance is defined by the phenotypic consequences of genetic diversity. See this post for the definition
For simplicity, above, I used the terms genetic diversity and genetic variance correctly but without highlighting that they take different definitions.
Intro to evolutionary genetics
Your question is a very introductory question in evolutionary genetics. You might be interested in some intro books (have a look at the post Books on population or evolutionary genetics).

Heterozygote advantage, multiple population, balancing selection etc merely delay the problem or break it down into smaller pieces. There is no way to get around the fact that the best genotype in a population will win for the vast majority of traits.
The practical consequence is
https://www.natureworldnews.com/amp/articles/16388/20150907/endangered-species-genetic-diversity-explains-decline.htm

Some species may face extinction when they are not able to adapt as easily to changing environments or defend against new diseases. To better identify or rank threatened and engendered species, researchers from Purdue University suggest using the animals' rate of genetic diversity loss.

Of course this is attributed to more proximate causes and not evolution.

Heterozygote advantage is a type of balancing selection. Your quote is completely unrelated to the rest of the question (and comes from a non-peer reviewed source). The sentences merely delay the problem or break it down into smaller pieces. and the best genotype in a population will win for the vast majority of traits are unclear and possibly wrong.

Are you the same user as user43230 (the OP)? It is totally fine to post an answer to your own question. You do not need to create a new user for that. Changing user for that can be seen as spamming (esp. when the answer is wrong).


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How does cancerous tissue break down radioisotopes faster than normal tissues?
Apparently, many medical practitioners use radioisotopes to detect cancer in patients. From my textbook (McGraw Bio 12, pg. 10);

Using a method called radioisotope tracing doctors can inject
  radioactive material into a patient and trace its movement in the
  body. For example, cancerous tissues in the body are characterized by
  a much higher level of activity than healthy tissues. Consequently,
  cancerous cells take in more glucose—a common cellular energy
  source—than healthy cells. Injecting a patient with radioactive
  glucose and then performing a positron emission tomography (PET) scan,
  such as the one shown in Figure 1.1, is one method to diagnose a
  cancerous tumour

Apparently, cancerous tissues break down radioisotopes at a much higher rate than normal tissues. But how?

In addition to the detailed info in the answers, it's important to understand that nothing in biology breaks down radioisotopes.  They decay at a rate determined by nuclear physics (half life), regardless of whether they're in the body, or in a bottle sitting on a shelf.

Cancerous tissues break down glucose faster, not radioisotopes. Doctors use PET technique to detect breakdown of glucose, and "hot spots" are investigated as potential tumors.
Glucose can be labeled with radioisotope to show up on PET scan. Normal glucose is "invisible".
Hence, candidate for tumor will breakdown any glucose, but radioactive glucose will show up on scan.

In other words, radioactive glucose, as a product of being coated in radioisotopes, will show up on our diagnostic machines, correct? This is why it's useful?

@Korvexius it is not covered with anything, but contently bound with radioisotope of fluoride. See first link

Cancerous tissue is growing faster than most other tissue in the body. That is the nature of the disease. This growth will must assimilate nutrients, so any traceable nutrient will be seen to concentrate where the cancer is.
Radioactive isotopes are a useful tracer because they can be composed into chemically normal nutrients, and concentrated accumulations can be imaged noninvasively to infer where the cancer is. A possibly bonus is that the cancer gets preferentially irradiated.


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Do some plant proteins have no domains?
I've always been under the impression that all proteins consist of at least one domain (with the exception of intrinsically disordered proteins). However, I've come across some things which challenge that while reading some papers and I'm not sure how to understand it. From one paper (https://doi.org/10.1016/j.tig.2006.09.003);

We determined the tendencies for individual protein functional (Pfam)
domains to occur among duplicates or singleton genes (see the
supplementary material online) resulting from independent GD events
that occurred 60 and 70 MYA in the lineages of Arabidopsis (a) [15]
and Oryza (r) [16], respectively. Analysis of Pfam domains as the
experimental unit also permitted us to compare these angiosperm events
with GDs in yeast [20] and Tetraodon [21]. Between 1334 and 1704
domain types were found in the four organisms, with duplicated genes
containing an average of about one domain and singletons averaging
0.15–0.40 domains (see Table 1 in the supplementary material online).

If the average singleton in the genomes of the organisms under study here have 0.15-0.40 domains, that means the majority have no domains. Checking the supplementary material confirms this. In a second paper (https://doi.org/10.1016/j.gpb.2016.06.003), Figure 6 shows that both rice and humans have a substantial number of proteins without any domains.
What is the meaning of this? How can these proteins have no domains? The best explanation I can come up with is simply that this data is a possible artifact resulting from simple lack of detection by domains were based on the specific database being used (Pfam in one case and InterPro the other), but I'm not sure if this is the correct understanding of this.

I suspect you are confusing two different things — from your quote it seems likely that the paper is talking about the subset of domains that are defined in the Pfam database. My understanding is that most proteins have never been studied and their existence is inferred from DNA sequences. This means that unless the inferred proteins have detectable homology to a characterized protein they won't have a defined domain. This is not the same thing as them not having one or more structural domains ...

Makes sense. So, in this context, is there a clear significance to that singletons have a lower defined domain frequency than duplicated genes?

Hard to see what it might mean, but since I don't have time to read the paper I'd be unwilling to say that it didn't mean something. Could be just that duplicated proteins are by definition more common and thus more likely to have been studied, but there may be something deeper like them being (on average) less essential (due to the duplicate) and so easier to study/recover mutations ... if you are sure (based on rereading the paper) that the interpretation in my first comments is correct, you could [edit] this question to focus on what you just asked and see whether anyone has an answer ...


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DNase annotations of Drosophila melanogaster
I am familiar that the RedFly database provides annotations for 1,458 sites in the genome of Drosophila melanogaster subject to cleavage by DNase I. It seems the vast majority of those annotations come from the original FlyReg database originally reported in 2005, which merged with RedFly early on. I have looked, but not found any additional sources of annotations of the Drosophila genome of DNase cleavage sites. I wanted to ask, to be sure, if there are no additional studies / experiments which record DNase annotations in the Drosophila genome outside of the ones recorded by RedFly.

I think that DNAse-seq is no longer the favored assay for chromatin accessibility.
These days, I believe ATAC-seq is favored, or even single-cell variants of ATAC-seq. (links to drosophila papers)
I can't comment on a general Drosophila regulatory database beyond what you already know about, beyond what's obvious via google (here, here).

Very useful answer but are you sure it's no longer favored? 2021: "DNase I is still the reagent of choice for TF footprinting, which can determine the location of TF binding sites due to the protection of the site by the TF itself." https://doi.org/10.1038/s43586-020-00008-9

@arara interesting, I don't have access to the review unfortunately so it's hard for me to evaluate. I suspect that there is a subtle distinction between "TF binding sites" and "chromatin accessibility". Chromatin accessibility is a rather more generic phenomenon. What I would bet is that ATAC-seq is more common these days in large part because it's easier methodologically. But I could readily accept that DNAseI is a more diagnostic, less biased reagent at the single molecule level (or for e.g. one locus probed on a Southern blot). But I'm also not an expert in the field!


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How can we use the number of crossovers per chromosome to calculate the recombination rate in cM / Mb?
I was reading a paper titled "Tetrad analysis in plants and fungi finds large differences in gene conversion rates but no GC bias" (2018). According to this paper:
"The between-species differences in CO rates reflect in part the fact that each chromosome needs at least one chiasmata. Indeed, the CO rates are more uniform when expressed as CO events per chromosome with about an order of magnitude difference in cM Mb-1 per chromosome: from ~5.3 COs per chromosome in yeast (= 22 cM Mb-1 per chromosome, N = 16) to ~2.3 COs per chromosome in Neurospora (= 2.8 cM Mb-1 per chromosome, N = 7), to ~2.2 COs per chromosome in Arabidopsis (= 0.9 cM Mb-1 per chromosome, N = 5) to ~1.4 COs per chromosome in Chlamydomonas (= 0.7 cM Mb-1 per chromosome, N = 17)."
Here, the authors give 1) the number of crossovers per chromosome in each of these four species and 2) the equivalent recombination rate in units of cM / Mb. However, I don't understand how the conversion was reached in each case.
Take Chlamydomonas reinhardtii for example, with 1.4 COs per chromosome. There are 17 chromosomes, so that's 23.8 total crossover events. (Roughly agrees with Table 1.) The whole genome is ~110 Mb, so that's 0.216 CO / Mb. And ... I am unsure how to proceed. It's just not clear to me how to complete the conversion for any of these organisms. How can I calculate the recombination rate in cM / Mb, as the authors of this paper did, from the number of crossover events?


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What is the X-chromosome responsible for?
I understand that the X-chromosome is responsible for certain disorders, like red-green colorblindness; but besides disorders, what do the genes on the X-chromosome determine?

The number of genes on the X chromosome approaches 1000 and thus your question is too broad for this site.

@canadianer Could just give some general things that these genes would be responsible for, or is it too broad?

"besides disorders" - it's not a complete answer, but for info it's not really helpful to think of genes as 'coding for' a disorder. Any gene that does anything useful can get broken, and when it does the severity of the consequences depends on how important its normal function is.

Can you explain a bit more of your thinking here, and show what research you have done before asking?

@arboviral I agree with what you have said. I phrased the question that way because I had only known that genes on the X-chromosome were responsible for certain disorders until that point.

@CMK My point was more that it's more accurate to think of them as responsible for whatever's broken in the disorder. So the lack of a properly functioning gene for [...] results in a disorder. Otherwise some people are bound to think "hey, why don't we just delete the gene and then nobody will get the disorder".

@arboviral Thank you. That makes a lot of sense.

Here is the list! There are about 900 protein coding genes and about 500 non-coding transcribed sequences. It is not going to be feasible to explain you the function of every single one of those genes. Your question is hence too broad.
You will find here on wikipedia a small subset of those ~900 genes.
If your question was

Are all genes that are on the X chromosome related to sex?

Then, the answer is "no". Most of them have nothing to do with gender specific traits.

Where did the quoted section in your answer come from? (I agree it sounds like that is the misapprehension that prompted the question, but I don't see it anywhere.)

Thank you for your answer and for the links, although I would he lying if I said that I understood what they were saying. However, concerning the genes involved with sex determination, what do those genes determine, in fact?

I have changed "sec determination" with "gender specific trait". That was a typo. In humans, there are only one gene affecting sex determination, it is SRY (coding for TDF) present on the Y chromosome. I don't know much else about eventual gender specific beneficial genes on the X chromosome.

Somewhat related: Do males of all sexual species have Y chromosomes?

@Remi.b Thank you for your response. What is your opinion on this article, which says that there is more than one gene that affects sex determination? https://genderedinnovations.stanford.edu/case-studies/genetics.html#tabs-2

I only just read the first few sentences. I am not so surprised that with severe medical intervention such as a gonadectomy or large injection of male hormone in females, you can masculinized or feminize the individuals. In principle, it is completely possible that several loci affect sex determination (it is the case in many species), I just had never heard such claims in mammals.

I would like to start the answer by mentioning that I was fortunate to attend a lecture by Jenny Graves, a scientist working on X chromosomes recently.
In her lecture she mentioned the genes on X-chromosomes as "brain and balls" genes. As Remi.b has already added a list you can go through it to find a few of these genes. I am highlighting a few of them as follows:-

Androgen receptor (AR) - Required for prostrate formation in males. Mutations may lead to muscular degeneration and loss of motor control (Kennedy's syndrome).
AIFM1 - An inhibitor of apoptosis. Mutations may lead to neurodegenerative conditions like Charcot-Marie-Tooth disease 4.
MeCP2 - Heterozygous female MeCP2 mutants suffer from Rett Syndrome. It is almost exclusively seen in females because male mutant embryos die during pregnancy.
BEX1, BEX2 and BEX4 - Brain-expressed X-linked (BEX) proteins

Also regarding sex determination - the mammalian XY sex determination is Y centered i.e. the SRY gene on the Y chromosome is the gene responsible for determining maleness. Interestingly some species not using the XY system have evolved female specific sex determination genes. I will add relevant citations when I have time.

I added a few relevant citations because someone downvoted without providing a reason.

Thank you for your answer. So, does this mean that the X+chromosome contains genes that direct the formation of part of the male reproductive system?

Yes. Since, the size of the Y chromosome is much smaller than X chromosome it does not contain many genes. Most of the genes on Y are only involved in early determination of sex. Information regarding organ development is still encoded by X.

@CMK Also consider upvoting if the answer satisfies your curiosity.

Thank you. I would upvote, but my reputation isn't high enough. I'm sorry about that. But, just to be clear, the X-chromosome does direct The formation of the male reproductive in part?

@CMK Yes, it does. The androgen receptor (AR) being on the X is a clear indicator of the fact. If you take a look at the list Remi provided i am sure you will find a few more genes involved in male development. I will go through the lis and let you know if I find a few as well.

Okay, thank you for this. It has been extremely helpful. Would this, then, mean that female is not the default gender as many people say, or is this conclusion gratuitous based on this fact? Thank you.

Female is called the default gender because in absence of SRY gene all embryos develop to be females. Loss of function SRY mutant XY genotype gives rise to female babies. Although these individuals require hormonal supplements for proper development during puberty. Link for syndrome - https://en.wikipedia.org/wiki/XY_gonadal_dysgenesis

I understand. However, I read elsewhere that there are genes which required to suppress male development and promote female development. It's found in this article. https://genderedinnovations.stanford.edu/case-studies/genetics.html#tabs-2

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Low-cost simple water testing for faecal contamination
I live in Indonesia and there are lots of sewage pipes discharging directly from homes/restaurants/etc directly into the river. It's also common to wash clothes and so on, so there is likely detergent in there as well.
Some water courses that people bathe in seem to be more s**t than water, if you see what I mean, in that it starts off in the river, then diverts into various smaller canals which often end up with trash, diapers, and so on.
I'm wondering what I could do to test/measure this in simple & low-cost fashion, so that I could test in different places and on different dates, and possibly to include quantative values such as 'how much dirtier' the river is when there are many people bathing in it, or when it is dry season, or whatever.
I think I don't need to test for every pathogen so it might be sufficient to just test for E coli? [I think S. aureus is also common, as skin boils tend to occur after bathing in dirty water.]

I don't have a good answer for you, but I'd note that this sort of thing is often a target of international health organizations.

You could start by reading about the presumptive coliform count: https://microbeonline.com/probable-number-mpn-test-principle-procedure-results. I'd also recommend reading a textbook of microbiology/public health for more detail, because this is a standard topic in those fields. An example is: https://www.universitiespress.com/details?id=9789389211436.

The best and most common would be the "multiple fermentation tube” or “most probable number” technique. Rather than testing for all pathogenic bacteria, it uses indicator microorganisms to assess the potability of the water. You'll need a lab to do this but if you have access to one, I'm sure that all the needed materials are common there. Here's a copy of the method: https://www.who.int/water_sanitation_health/resourcesquality/wqmchap10.pdf


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what is the active ingredient in cymbopogon citratus that repels mosquitoes?
We are doing a project about mosquito repellants using lemongrass, cymbopogon citratus. But, based on our researches online, it stated that it was all a hoax and a better alternative is its cousin cymbopogon nardus.So, is the hoax actually true??? And please tell about the active mosquito-repelling ingredient.

I think the problem isn't a hoax; it's just that people are overly excited about 'natural' as opposed to synthetic remedies.
C. citratus might be hazardous - the active ingredient is citral α-pinene.
C. nardus might be hazardous, too - the active ingredient is citronellal or citronella. [There's confusion, in the article, about whether citronella has other plant chemicals in addition to citronellal.]
They're both partially effective as insect repellents.
"It is commonly assumed that plant-based repellents are safer than DEET because they are natural. However, some natural repellents are safer than others, and it cannot be assumed that natural equates to safe."
This info all comes from a 2011 scientific article about plant-based insect repellents:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059459/
Here's a link to a table with the results, summarized below:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059459/table/T1/?report=objectonly
And a table with possible toxicities:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059459/table/T2/?report=objectonly
Citronella has found its way into many commercial preparations through its familiarity, rather than its efficacy. Citronella was originally extracted for use in perfumery,..."
C.nardus is at least somewhat effective in 3 lab studies; citronellal    is the active ingredient.
C. citratus - the active ingredient is citral α-pinene.  Again, it's at least partially effective in 3-4 studies, e.g., "74% protection against An. darlingi for 2.5h"
Here's a scientific article from 2011 about the scientific basis for the therapeutic use of Cymbopogon citratus, stapf (Lemon grass):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3217679/
But it doesn't mention 'insect repellent' among its possible uses!:
"Studies indicate that Cymbopogon citratus possesses various pharmacological activities such as anti-amoebic, antibacterial, antidiarrheal, antifilarial, antifungal and anti-inflammatory properties. Various other effects like antimalarial, antimutagenicity, antimycobacterial, antioxidants, hypoglycemic and neurobehaviorial have also been studied."

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Prove that the worms are unicellular
In Biology class our teacher divided the class in two groups. Our group(i'm in) has to prove that the worms are unicellular(although it is not true). The other group has to prove that we are wrong. The plan for the debate for our group is to have a list of characteristics that are equal both for worms and unicellular. I wrote that they both have organelles and like the rain worm,  unicellular parthenogenesis. But now i'm out of ideas. Give me some suggestions.

You could start by contrasting the cell type and compare the structures which are found in exact type of cell. You could then go on to talk about cell division and structures that are present to enable cell division.
You could refer to sheer size, a visible worm clearly cannot be unicellular as we are in the wrong order of magnitude- unicellular organisms being measured in microns reparler them visible to the naked eye. You could use this as your opener, to them talk about the differences you would see under the microscope.
You could talk about body plans and how they have evolved differently.


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How did researchers find out that it was only the maternal chromosome that underwent deletion in Angelman syndrome?
It is known that in Angelman syndrome, the chromosome 15 undergoes deletion in the maternal chromosome while in Prader-Willi it's in the paternal.
I understand it can be detected by FISH or other chromosomal staining methods (which would have been used those times), the chromosome number which underwent the deletion.
How could they figure out which chromosome (maternal or paternal)  had undergone the change. My question is, which technique allows the chromosome to be marked maternal or paternal? Which technique was originally used?

Don't have time to make a proper answer so just leaving a comment. As far as I know there is no way to specifically stain either the maternal or paternal chromosome. It was basically genome analysis of Angelman and Prader-Willi patients to find a correlation with both diseases and a deletion on chr15 (same in both). Genome analysis of parents showed that the inherited deletions showed that Prader-Willi patients always got the deletion from their fathers, and Anelman patients from their mothers. Source: https://www.ncbi.nlm.nih.gov/pubmed/2564739

This was further corroborated by the fact that the key player, the gene Ube3a, was an imprinted gene that had parent-of-origin specific (namely maternal) expression. Source: https://www.ncbi.nlm.nih.gov/pubmed/8988171 . It would be expected that a gene expressed this way would only cause disease disease when a deletion was inherited from the parent whose chromosome the gene will be expressed from. A parental deletion would be irrelevant to Angelman syndrome because Ube3a is silenced on the paternal chromosome in the relevant tissues regardless.

The kicker would be a mouse model where maternal Ube3a deletions always cause the phenotype in progeny, and paternal Ube3a deletions never do. This probably exists but I'm too lazy to look. Such breeding experiments would confirm causality as all variables except the maternal deletion would be controlled for, although I'm convinced enough by the genomic correlations with specific parents.

If that's enough of an answer please let me know.

Thanks! Just the first comment was enough for my answer. I wqs assuming this to've been pretty old sruff when genome analysis and all hadn't yet arrived. Thanks.


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Evolutionary explanation of the bicuspid on the left and tricuspid on the right
The left heart handles more pressure and logically it would make sens to have a valve with three leafs on the left (If I had got to choose, I'd have put three on both sides).
Other than being more susceptible to valvular disease (also because the pressure is higher on the left), the bicuspid having 2 leaves don't do any good (To my knowledge).
Since this is not the case, there might be some evolutionary constraints that might have caused this difference.
Any explanation according to valvular evolution along the phyla?

Logically it would be better to have less number of valves as pressure to be handled increases.

I agree more valves makes it structurally weaker.


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Why are valves preferentially affected in endocarditis?
The inside of the heart is covered by endothelium throughout. Why are valves predisposed to endocarditis? I know it can affect other structires like the septum, chordae etc. But why the valves? Especially bacterial endocarditis.
Wouldn't a place on the ceiling of the atria be quieter and have less turbulence?
Robbin's Pathology says that valves derive nutrition from the surrounding blood and there vessels but mostly on the proximal side. So it might not be due to nutrition.
Are there theories for this?


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How does hyperthyroidism cause diarrhea?
According to Robbin's Pathology, hyperthyroidism leads to an overactivity of the sympathetic system.
It also goes on to mention that this sympathetic hyperstimulation in the gut leads to increased motility leading to diarrhea and malabsorption.
How would sympathetic stimulation cause hypermotility? Isn't the parasympathetic system responsible for it?
Also, how does hyperthyroidism increase the sympathetic tone?

Can you please give a reference to the article?

@another'Homosapien' Its from Robbin's. A textbook for path.

Okay, I thought there would be an online version too...

https://studentconsult.inkling.com/store/book/robbins-cotran-pathologic-basis-disease-kumar-9/

Not that actually, I meant online version (PDF) of the book.

I believe these are the relevant pages (p.1083-1085) https://bit.ly/2C5Rdpu

Hyperthyroidism leads to an overactive sympathetic nervous system, hypermotility and diarrhea (Culp and Piziak 1986) (Geffner and Hershman 1992) (Maitra 2015, p. 1084) (Thomas et al. 1973). A demonstration of this is the patient presenting with the sole symptom of intractable diarrhea. It was found to be secondary to hyperthyroidism, and was treated successfully with β-adrenergic antagonists (Bricker et al. 2001).
Was the hypermotility due to excessive β-adrenergic activity, or insufficient α-adrenergic activity?
An article by Silva and Bianco (2008) states that β-receptor expression is under transcriptional control of a thyroid response element, and is upregulated by increased thyroid signalling. There is much less research on α-receptor expression, I would be much obliged if anyone can provide me with access to the following article:

*Bilezikian, JP, Loeb JN 1983, ‘The Influence of Hyperthyroidism and Hypothyroidism on α and β-Adrenergic Receptor Systems and Adrenergic
  Responsiveness’, Endocrine Reviews, vol. 4, no. 4, pp. 378-388.*

In any case, they add that increased β-receptor expression is rather modest, often overestimated, and cannot account for the magnitude of amplification in responsiveness induced by thyroid hormone (TH). Rather, thyroid signalling increases cAMP levels associated with a2 and β-receptors to a degree which could account for these changes.
Increased cAMP occurs during normal β-receptor function but is significantly potentiated by TH in several ways: increases in adenylyl cyclase; downregulation of β-receptor G-protein subunits, Gai and Gβ; and downregulation of phosphodiesterases which degrade cAMP. This explains the effectiveness of the β-adrenergic antagonist noted above, as propranolol decreases cAMP levels, thus decreasing hypersensitivity of the hyperproliferated β-receptor (Silva and Bianco 2008).

“The reduction of the sympathetic activity associated with
  hyperthyroidism outflow (via increased rate of norepinephrine
  metabolism to decrease overall levels) is likely overridden by the
  increased sensitivity, as suggested by the clinically significant
  amelioration of the adrenergic symptoms with β-adrenergic blockage and
  the consistent observation of elevated cAMP production.” (Silva and
  Bianco 2008).

What are the effects of preferential/hyperactive β-receptor function on gastrointestinal motility?
The β1-receptor increases ghrelin secretion from the stomach – a peptide secreted when the stomach is empty to increase hunger, increase gastric acid secretion and gastrointestinal motility. The β2-receptor promotes smooth muscle relaxation (decreased GI motility) but contracts sphincters of the GI tract (Adrenergic receptor 2018).
β-adrenergics also promote the secretion of gastrin – a peptide which increases antral muscle mobility and promotes stomach contractions; relaxes the pyloric sphincter, which increases the rate of gastric emptying; is involved in the relaxation of the ileocecal valve; induces pancreatic secretions and gallbladder emptying; and contributes to the gastrocolic reflex (Gastrin 2018) (Katzung and Trevor 2014, p. 143-144).
What are the effects of relative α-receptor deficiency on gastrointestinal motility?
Considering that β-receptor antagonism causes a relative increase in α-receptor activation we should consider them also. The α1-receptor causes smooth muscle contraction. The α2-receptor causes negative feedback on norepinephrine signalling, relaxes the gastrointestinal tract when activated on presynaptic terminals and contracts of sphincters in the GI tract. It does this by decreasing levels of cAMP (whereas β-receptors work by increasing cAMP) and so it will become less active as TH becomes more active (Adrenergic receptor 2018) (Silva and Bianco 2008).

What are the adrenergic-mediated effects of hyperthyroidism on gastrointestinal motility?
Under prolonged conditions of excess TH overall peristalsis will
increase due to mixed effects on smooth muscle contraction primarily
via α1, and β2. There will be an increase in hunger and gastric acid
  secretion via ghrelin (Adrenergic receptor 2018). Hyperphagia and
hypermotility are both suggested to play a part in steatorrhea
  (Culp and Piziak 1986).

How does hypermotility cause diarrhoea?
In addition to the mechanisms above, it has also been suggested that excessive fatty food intake contributes to the steatorrhea seen in patients with hyperthyroidism. This is compounded by a reduction in time that digestive secretions can act on chyme, ultimately leading to a reduction in absorption and an increased liquidity of the stool (R Santra, Calcutta School of Tropical Medicine, 2016).
Finally, it is important to note at this point that not everyone with hyperthyroidism will show hypermotility - some hyperthyroid patients show delayed gastric emptying (Pustorino et al. 2004). Indeed, constipation has been reported in patients with hyperthyroidism (Culp and Piziak 1986). Nonetheless, it is held that dysthyroidisms alter the motility of the gastrointestinal tract, and we do not completely understand how this works (Pustorino et al. 2004).

References to come, if desired.

search that article at gen.lib.rus.ec ,its there


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How does the ATPase stain for muscles revert on changing the pH?
Muscle sections are stained with ATPase to differentiate between types of fibres and to display the ckecerboard pattern. But it is done at two different pH. The staining is reversed at acidic/basic pH.
To quote this site

Acid preincubations inhibit the myosin ATPase activity in fast (mammalian type 2A, 2X, and 2B) fiber types, but not slow (mammalian type 1, see Figure 1A). Conversely, basic preincubations inhibit myosin ATPase in slow fiber types only (Figure 1B).

Why is this so? Isn't the ATPase same in both the fibres?

No, they contain different myosin ATPase isoforms. The myosin ATPases of slow fibers are more acid-resistant in their activity.

@pbond thanks! Could you pls elaborate your answer so that I can mark it answered. I've understood it. Once the genes expressed changes, as you have mentioned in your previous answer, anything can change!


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What is the state of actin-myosin in my biceps after I have flexed my arm?
When I'm starting to flex my arm, the myosin and actin slide over each other in a ratchet like mechanism. When I've totally flexed my arm, are the actinomyosin left in this contracted state? Since there is a visible decrease in length of the muscle, muscle fibres should have contracted.
So do they remain in this contracted state? Does the myosin head attach to the actin all this time? If it leave the actin, does the myosin snap back to its original position and relieve the tension/comeback to original length? Does it require any energy expenditure? Because I can keep my arm flexed throughout the day without getting fatigued. Also, What is the state of the actinomyosin if left in a half flexed state?
By state, I mean, the stage of the cross-bridge cycle

When I've totally flexed my arm, are the actinomyosin left in this contracted state?
Yes, the sum of the length of all sarcomeres in series determine the length of the muscle.
So do they remain in this contracted state? Does the myosin head attach to the actin all this time?
Yes, it stays attached.
If it leave the actin, does the myosin snap back to its original position and relieve the tension/comeback to original length?
It doesn't really 'snap' back, it 'walks' back over the actin.
Does it require any energy expenditure?
Yes, the myosin heads require ATP to 'walk' back as well. If ATP is depleted cannot walk back, as is the case with rigor mortis (https://en.wikipedia.org/wiki/Rigor_mortis).
What is the state of the actinomyosin if left in a half flexed state? By state, I mean, the stage of the cross-bridge cycle
Myosin will partly overlap with the actin, but not completely. But this has nothing to do with the cross-bridge cycle. The myosin heads need to complete several cross-bridge cycles to fully contract the sarcomere.
For further reading, the Wikipedia page on the sliding filament model is a good start: https://en.wikipedia.org/wiki/Sliding_filament_theory

Thanks! Once it is contracted, ad you say, the myosin remains attached to the actin, is ATP required then??


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What is the evolutionary advantage of having polymorphisms in MHC?
The MHC genes are widely polymorphic and hence cause an issue in tissue matching pre-transplantation. Why is there such a polymorphism?
I know that different polymorphisms in MHC can lead to variation in the immune response to the same offender. But then, if there is a difference, shouldn't there be a selection for those that mount a better response?
So, why the polymorphism?


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How is the site of administration of a vaccine decided?
Vaccines can either be given intramuscular or subcutaneous or intradermal. I know the technique used is specific for each organism. What decides this?
I understand the reason for oral vaccines in polio but, why should a vaccine that is given s/c not be given im?
If there is a logic to this (which I am sure there is), it would be a lot easier to remember the same.

When the effectiveness of subcutaneous is comparable to intramuscular, then the choice is made based on the degree of discomfort and adverse reactions.
In many situations intramuscular will outperform subcutaneous delivery due to subcutaneous fat having poor vascularity which may result in slow mobilisation and processing of antigen(source).
Disclosure: I am not a biologist so this is outside my field of expertise.


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How is TB harmful in HIV patients?
The mycobacterium of TB doesn't secrete any toxins. The cause of disease in the immunocompetent is the collateral damage due to the immune response against disseminated infection. But then, when HIV patients are immunocompromised, why should TB do any harm to them? There is an absence of the typical granuloma in HIV cases.

@always confused I  mean that. I meant that the immune response is doing more damage than the pathogen per se. For example in cholera, it is the bacteria that secretes a toxin which does the harm. In TB, theres nothing like that. It is immune cells destroying surrounding tissue.

Mycobacterium tuberculosis is the bacterial species which causes tuberculosis. Many people in the world (~1/3 of the population) have an M tb infection. However, an immunocompetent host is able to prevent the bacteria from causing disease (tuberculosis). In the case of an HIV patient, there is no immunity, and thus the bacteria is free to cause disease.

You still have innate immunity, which is the biggest perpetrator of immune-mediated tissue damage, IMO, when supplied with constant stimulation.

This is an interesting an useful question about host-pathogen interactions. For a general reference (for both hosts with and without a competent CD4+ T-cell response) see Cecil Medicine, Ch.332, and Murray Medical Microbiology, Ch. 28. There is also a decent review in Lancet Infectious Disease that discusses the pathophysiology in immunocompromised hosts.
Overview / tl;dr
Tuberculous mycobacteria may not secrete any toxins or replicate quickly, but they are clever and persistent. Without an effective immune response, they will eventually overwhelm the lungs, spread to other organs, and kill the host through organ failure and/or embolization.  In these cases, infection is universally fatal if not treated. This is what happens in HIV patients with a low CD4+ T-cell count.
In hosts with a competent CD4+ T-cell response, infection is sometimes fully resolved and sometimes held at bay for many years without major organ damage.  In other cases, the immune system's methods are too powerful for the infected organ. Tissue damage in these cases is the direct result of prolonged activation of large fused groups of macrophages. Importantly, this is not an overactive immune response, it just happens to be too much for the local organ. You cannot treat TB by shutting down this immune response. If you block TNF-$\alpha$, for example (a major player in the cross talk between CD4+ T cells and macrophages), you end up with disseminated TB. The solution here is elimination of the pathogen with direct anti-mycobacterial treatment.
Initial Infection
In either an immunocompetent or immunocompromised host, tuberculous mycobacteria enter, e.g., alveolar macrophages through phagocytosis and, initially, prevent fusion of the phagosome with lysosomes, while allowing fusion with other vesicles. This allows the bacilli to live, access nutrients, and replicate within the macrophage.
Immunocompetent host
In the immunocompetent host, the interaction between the infected macrophage and CD4+ helper T cells leads to formation of an activated macrophage and either elimination of the mycobacteria or compartmentalization of the infection. Either of these outcomes are generally good for the host. Clearance of a pathogenic bacteria is obviously good. Latency in a walled off compartment is a close second.
The typical disease syndrome of pulmonary tuberculosis involves a brief, often unremarkable respiratory infection, followed by a long period of clinical latency. In many cases where the primary infection isn't fully cleared, latency may be lifelong, only to be discovered incidentally at autopsy. The brief illness followed by clinical latency corresponds to the infection of alveolar macrophages with an immune response that successfully walls off the infection.
In a host with generally capable CD4+ T cell / macrophage cross talk, if disease develops, it typically occurs after years or even decades of latency, through reactivation. Reactivation may be the result of a temporary failure of the compartmentalization strategy, with short term or partial immunosuppression due to age, some other illness or drug. It is sometimes the result of re-exposure. In severe cases, the result is a massive and damaging, but relatively slow immune response. This is not toxic shock syndrome or gram-negative sepsis. It occurs over month to years, with night sweats and weight loss. Fever may or may not be present. Tb is a slow burn. The OP is correct here, that the tissue damage seen in these cases (caseous necrosis, cavitary lesions, sometimes followed by hemorrhage), as well as the night sweats and weight loss, are all caused by the immune response, not directly by any toxin produced by the mycobacterium.
This lung (image from wikimedia commons) was chewed up by giant, angry macrophages, spurred on by CD4+ T-cells:

Immunocompromised host
This lung (image from a public slide set through the University of Utah), on the other hand, was not chewed up by giant angry macrophages, but was lethally infected with M. tuberculosis all the same:

In an immunocompromised host, the clinical syndrome is different. For an HIV patient with a low CD4+ T cell count, alveolar macrophages are not sufficiently activated. There are no large cavitary lesions, but they are also unable to clear or quarantine the replicating bacilli. This results in disseminated tuberculosis, sometimes with spread through the bloodstream to the brain, kidney, and bone, and devastating illness that is universally fatal without treatment. Death may result from organ failure (e.g., of the lung), infectious or non-infectious embolism.
Interestingly, in an AIDS patient with disseminated TB, when you combine TB treatment with HAART (highly active antiretroviral therapy), you can sometimes see a paradoxical worsening of symptoms. This is called immune reconstitution inflammatory syndrome, or IRIS. It may look like worsening TB, with fever and worsening lung function. The solution for TB-IRIS is not immunosuppression, but supportive care and, again, direct treatment with antimycobacterial therapy. Here again, the problem isn't an overactive immune response, it is the pathogen.


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State of voltage gated sodium channels in depolarised potentials
Case 1
We learn in Physiology that during the depolarization phase in the membrane, more sodium channels tend to open as the membrane potential increases i.e., less negative. This is a kind of positive feedback which leads to the action potential and explains the threshold of depolarization that is required for action potential.
So in short, as the membrane potential becomes less negative sodium channels tend to open.
Case 2
On the other hand there is famous graph from Bertram Katzung, Susan Masters, Anthony Trevor-Basic and Clinical Pharmacology, Edition 12. which shows the dependence of the sodium channel function based on the membrane potential preceding the stimulus.

To quote,

The fraction of sodium channels available for opening in response to a stimulus is determined by the membrane potential immediately preceding the stimulus. The decrease in the fraction available when the resting potential is depolarized in the absence of a drug (control curve) results from the voltage-dependent closure of h gates in the channels.

Both these cases look pretty contraindicating to me. But I attempted to explain this by the three stages of the Na+ channel.
Case 1 - may be addressing the transition from closed to open channels, i.e., opening of the m gate. (I'm just hypothesizing here so correct me if wrong)
Case 2 - as mentioned in the book, talks of closing of the h gate leading to inactivated gates at higher membrane potentials.
Do case 1 and case 2 happen one after another? Are the voltage ranges for each different? Is my explanation for case 1 correct?


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Help me identify the following insect
This is my first post in this forum. I found the following insect at my kitchen in my apartment in Kolkata, India. Could you please help me identify the insect.
Thank you.
Best regards,
Saugata

Might be a red palm weevil
Rhynchophorus ferrugineus
https://en.m.wikipedia.org/wiki/Rhynchophorus


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Evolution of the (phenotypic) facial features of the indigenous people of (west/central) Africa
I am not even remotely an expert in this field; I just got curious, so help me.
First of all, let us remove all human sentimental attributes from this question (such as connotations of scientific racism or emotional reactions thereof) and ask it from a purely scientific point of view. The typical facial feature of a West/Central African person (the so-called broad African type) exhibits a wide nose, a lack of nasal bridge projection (similar to many Asian noses) and a prognathous skull shape that resembles more closely to our ancestor Homo Heidelbergensis than many other indigenous phenotypes from other parts of the world do.
I agree that this claim sounds anecdotal, and is certainly not true of all Africans (for example, Ethiopians), but one cannot dismiss it simply on grounds of ethical policing. I cannot help but notice that many of my African friends remind me of our shared ancestry (with no disrespect meant whatsoever), as is clear from the photographs below, one of a supposed Homo Heidelbergensis and one of a random African Homo Sapiens of today.

My question is the following. What is the reason behind this seeming resemblance? Is this appearance an illusion and possibly a construct of a prejudiced mind, or does this have a valid scientific answer? For example, are most Africans closer to our ancestors than the rest of humanity is? How does evolution answer this question?
Thank you for your help.

Note that I had never heard of the expression "broad african type" and could not find much reference to this term when googling. But anyway, I'm happy to use it to refer to a particular set of typical facial features.

What is the reason behind this seeming resemblance?

Note that the Homo Heidelbergensis image is not a picture (obviously) and much of what is being depicted was open to artistic interpretation. It is possible that some of the feature you are thinking of are not real. Have a look at the post In reconstructions, how are various shapes of facial features determined from skull only?.
You list several phenotypic traits and it would be too broad of a question if you were expecting an explanation about the evolution of each of these traits. I will just pick one classic trait; the nose.
One of the role of the nose is too even up the temperature of the air that we're inhaling. As such, the shape of the nose is under differential selection pressures depending on the environment. So if the nose of Homo Heidelbergensis looked alike (assuming it really looked like on the facial reconstruction) today's "broad African type", it is probably because of shared environment. Note however that nose shape vary a lot among african lineages and also among non-african lineages. You might want to have a look at this popular article.
A big point of ressemblance is the skin color that you don't talk about. Have a look at the posts Why do we assume that the first humans were dark-skinned? and How did some humans evolve to be white? to learn more about skin color

Is this appearance an illusion and possibly a construct of a prejudiced mind, or does this have a valid scientific answer?

First, see my above point about facial reconstruction.
H. Heidelbergensis lived in Africa and in this resepct shared an environment that is like the environment that modern african are encountering that what modern Han Chinese are encountering. In this respect, we could expect some ressemblance.

For example, are most Africans closer to our ancestors than the rest of humanity is?

No, they're not and they cannot be. The MRCA of all humans today is more recent than the MRCA between any human and H. Heidelbergensis. You should have a look at this intro to phylogeny to understand a little bit better how different lineages relate evolutionarily speaking.

Thank you for this wonderful answer. Could you also briefly comment on why a prognathous mouth is better suited in central Africa? Thank you again!

I never meant that all features that one would identified with the so-called "broad African type" are adaptive. I said some might be and went on talking about skin and nose. I don't know if prognathous jaws would be in any way adaptive and I don't know if H. Heidelbergensis (and other hominids that lived in Africa) had such jaws. I can't think of a hypothesis for why they would be adaptive either.

Prognathous mouth is believed to be related to diet during childhood not anything genetic. It is the norm and the underdeveloped jaw we see in industrial populations is due to living off of soft processed foods their entire lives. Wisdom teeth issues are linked to this as well.


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Why is gene finding in Eukaryotes such a difficult task?
Why is gene prediction in eukaryotes such a difficult task? Every gene starts with a codon and the non coding regions in between a coding region also has some specific base sequence(which are used by enzymes to recognize non coding regions during splicing). A computer program could simply search for start codon and then for stop codon. In between it could also search for those non coding regions since they start with specific base sequences. Why does gene finding need such complex things such as HMM?

What research have you performed to try to answer this question yourself?

The main problem is that while most of the things you describe are necessary to have a protein coding gene (introns, the non-coding regions within a coding region, aren't actually per se, even though they're common), they are not sufficient. Additionally there are also genes for non-coding RNAs (including tRNA and rRNA), which obviously don't have a 'coding region' (and also usually no introns).
In order to classify something as a functional gene we usually require that is actually made into (at least) RNA, which requires regulatory sequences that lead to transcription of the gene, these are called promotors. In eukaryotes there are many different promotor sequences, so its very hard to predict them computationally, additionally there are evolutionary remnants in our genomes, which are called pseudo-genes, and while they still have the general structure of a gene, they are not actively used any more.


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Advanced Higher Biology 2017 - EPT Index
I was recently completing a biology past paper the Scottish SQA 2017 Advanced Higher Biology Qualifications. The question is as follows:

To solve this, I did:
EPT Index = 100*(striped stonefly + net spinning caddisfly + flathead mayfly)/(total number of taxa) = 100*(6+6+3)/(44)=34.09%
So, I answered C, however, the answer is B. What mistake have I made?

Do not post questions as graphics. They are unindexable and unreadable by people with sight problems.

The point of the question was to determine if you know what taxa are.  You don't; remedying that might give you the right answer.

Well, you made a mistake: The numbers in the second table are irrelevant to the question as it is not about taxa but about individuals. And the ETP number is calculated from number of EPT taxa (and not individuals).
The correct answer was 3*100/7 = 42.9% ==> B good quality of water.


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Is a nature possible where animals do not kill each other?
like the title suggests, i always wondered if its possible that nature would work without animals killing each other. Where they just eat plants. Like one special plant for each animal. If they eat to much of them away they also will stop multiplying to much, so there will never be too much of one species etc, terefore balance. I am sure there could be other controlling mechanism for balances.
:)

I suppose your question could be rephrased, "how could predators never evolve?" This type of question should be asked on worldbuilding.SE, not on a science website. Note that plenty of points are unclear in your question. How about cells phagocyting? Is this allowed in your imaginary world? How about competition leading to death of other individuals?

Somewhat related: Are there any multicellular forms of life which exist without consuming other forms of life in some manner?

I'm voting to close this question as off-topic because it is unclear and in essence is not open to empirical testing and is therefore unsuitable on a scientific website.

No. Because a spiderwebs can't catch herbs.

I'm not sure how a spider would catch herbs in its web.

No, even herbivores will eat other animals, and predation goes down ot the cellular level.  Also something has to be ating your dead and will have a huge evolutionary pressure to evolve toward predation with no predators present.
Animals by definition have a much better profile of nutrients for other animals.
Deer routinely kill and eat birds, eggs and even dead rabbits. In nature food is food and evolution does not care where you get it from. Carnivores will and have evolved from an herbivorous ancestor when no carnivores are present.


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Bacteria utilize short chain fatty acid as energy source
I'm doing research about the short chain fatty acid producing bacteria. I studied 7 short chain fatty acid (acetic propionic butyric isobutyric valeric isovaleric and captionic). and I found that the bacteria produced all acid in 8-12 hr incubation time  and after that all short chain fatty acid rapidly decreased, except acetic acid slightly decreased. How can I explain this results?  and I did my experiment under anaerobic condition.


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What is the purpose of Prostaglandin F2-alpha and the Prostaglandin F receptor in the melatonin cell signaling pathway?
I've been doing a lot of research recently on the melatonin cell signaling pathway for an extra credit project at school. I've included an image in this post, which is a diagram of the MT1 pathway. It seems to be a fairly standard GPCR sequence. I can identify all of the elements depicted in the diagram, but unfortunately I don't understand why some of these elements are present at all.
The portion of this pathway that stands out to me the most is the presence of a Prostaglandin F receptor (FP) as well as the presence of Prostaglandin F2-alpha (PGF2α). From the research that I have done, I've gathered that PGF2α is a prostaglandin found naturally in the body that can been used as an abortifacient in medical applications. I have not found any research that covers exactly why these two elements are present in the MT1 pathway.
Here's what I know: the Gi beta-gamma complex (Gβγi) and the Gq alpha subunit (Gαq) both activate Phospholipase C (PLC), which in this reaction causes the hydrolysis of PIP2 to create IP3 and DAG. My current hypothesis is that FP carries PGF2α into the cell, and PGF2α helps to activate PLC in some way. Unfortunately, I haven't been able to find any information online supporting this. Has anybody done any research regarding this topic, and if so can you provide any insight? I really, really appreciate it.

I don't have an expertise on this topic but check out the google scholar search. The top hit is this article: Melatonin blocks in vitro generation of prostaglandin by the uterus and hypothalamus. Apparently (from the google scholar hits), this relationship has been observed in vivo too.


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Is rabies virus infectious outside host?
Can rabies virus remain infectious on environment i.e on soil, grasses, leaves and water?

Cross posted question on medical.sciences.SE

First off all we need to be 100% sure what does be infectious mean. According cambridge dictionary meaning of the word infectious is be able to past from one host organism (multicellular/cellular) from another. So this is actually biggest hole in your question.

But i think you mean something else then word infectious. In my oppinion you wanted to know if rabbies can survived outside of its host. The rabbies virus as many other viruses cannot live outside of its host. Rabbies is exists in "public reservoir". This fact only confirm its variety of hosts such as bat, bears, dogs etc. (technicly all warm blood species) and its long incubation period (for example 1-3 months in humans.

According this site:

Rabies virus is transmitted through saliva and brain/nervous system tissue. Only these specific bodily excretions and tissues transmit rabies virus. If contact with either of these has occurred, the type of exposure should be evaluated to determine if postexposure prophylaxis is necessary.
Contact such as petting or handling an animal, or contact with blood, urine or feces does not constitute an exposure. No postexposure prophylaxis is needed in these situations.
Rabies virus becomes noninfectious when it dries out and when it is exposed to sunlight. Different environmental conditions affect the rate at which the virus becomes inactive, but in general, if the material containing the virus is dry, the virus can be considered noninfectious.

To sum this:
Rabbies viruses need to have contact with host, typicly by biting. It is possible to be infected by other contacts such as kissing, licking not dry saliva, but still the virus cannot live long outside of body. So long incubation and variaty of possible host (most infected is bats) makes the true killing combination.

Yes I was referring to survival outside host. As in if a rabid animal drools on grass or soil, can it survive in those?

Also. Has there been any cases of rabies infection from virus outside of host rabid animal?

https://www.elsevier.com/connect/8-things-you-may-not-know-about-rabies-but-should good article

I didn't find anything relating to virus survival outside host

Because there is not such a case. This is only the possibility. You know, i dont think that any person (not including little children) be so mindless to implated the saliva to his wound.

Btw you can easialy go threw the sites like WHO and you will find deffinitly some information on this topic.

So infection from outside host is a theoretical possibility but there has never be a real case?

I've only read about the virus transmitted from bite and scratches. But wanted to know if it can be transmitted from saliva from a rabid animal thats on the environment.

So i hope this answer is enought for you.

Thank you for your answer. I am just paranoid I may come into contact with rabid animal's saliva without knowing it. So wanted to know if the virus can infect like this.


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What is my pet tortoise' species?
I got this tortoise from my uncle. He said that it wandered into his yard. Found in Khon Kaen, Thailand during the summer.

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Have a nice stay!

It is a Burmese brown mountain tortoise - Manouria Emys Emys
 I differentiated it from a burmese black mountain turtle by this method.


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Do plants experience the following feelings
I am not a student of biology,in other words I have not read biology much.
But I read that plants have life and so my question is the following:

Suppose I take two saplings of two different varieties of hibiscus(or any other tree variant) and I put them in the same pot and allow them to grow up.
  Suppose they grow up and become well grown plants after say 4-5 months.
  My question is:
Will the two saplings experience any feelings for each other,in other words will they become friends or share any relation with each other.
  Suppose one of them is attacked by insects and its growth gets shunted,will the other plant also experience some feeling for it.
If I uproot one plant will the other one feel lonely or any other kind of feeling as if its counterpart is missing.

If someone cares to answer the above questions,I would be very grateful.
Thank You

Wikipedia defines emotion as "any conscious experience characterized by intense mental activity and a certain degree of pleasure or displeasure."
Plants do not have a central nervous system and therefore no mental activity so they certainly don't have emotions in the sense that humans and animals can have emotions. However plants feel/detect being eaten and they can communicate this to other (related) plants by releasing volatile organic compounds.

But a large component of animal emotion is hormonal, e.g. the "fight or flight" effect of adrenaline.

well according to the wikipedia page on emotion an "emotion is any conscious experience characterized by intense mental activity and a certain degree of pleasure or displeasure." And while plant are aware of their surroundings I would argue that they have no mental activity, and thus no emotion. Or do you argue that animal emotion is defined differently than human emotion? But I should define emotion in my answer for clarity.

I would guess that that Wikipedia article is discussing human emotions in the context of psychology, and so is missing rather a lot.  It is perfectly possible to experience the hormonal component of emotion without any sort of intense mental activity.  A common example is the injection of adrenaline given after allergy testing: it produces the physical fight/flight symptoms without a significant mental component.  (Of course in humans it's impossible to entirely separate the physical causes/reactions of emotion from the thoughts about the reactions.)


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Can multiple antibodies bind the same antigen?
Given the size difference between small molecule antigens and antibodies is it ever possible for multiple antibodies to bind to the same antigen if they recognize different domains on that antigen? When the antigen is a protein rather than a small molecule is it more likely that multiple antibodies can bind?

Does this answer your question? Can more than one antibody bind the same antigen

Not only is it possible for multiple antibodies to bind a single antigen, when that happens, it's more likely to trigger a full immune response.
Here's a description of the concept from a company that sells antibodies for research. To help understand the quote, you'll need to know that the portion of an antigen that an antibody binds is called an epitope.

Because an antigen can have multiple different epitopes, a number of antibodies can bind to the protein. When two or more antigen binding sites are identical, an antibody can form a stronger bond with the antigen than if only one of the antibody’s sites is bound. Antigens with multiple identical binding sites are called multivalent, and antibodies are able to bind it more strongly.

Here is an article that describes, among other things, the importance of clustering in B-cells when multiple B-cell receptors bind to a single multivalent antigen.

Thanks! Does that only work for large antibodies though? I'm worried that the relative size of a small molecule compared to the antibody means that even with multiple epitopes only one antibody will be able to bind it. I reached out to novus and they were unable to give an answer

@ike that's going to depend on the antigen. Is this for something you're working on in a lab?

Yes--We're looking to work with aflatoxin, a small molecule produced by Aspergillus flavus that has multiple antibodies which recognize it.

Oh yes, that's an intercalating agent. I wouldn't be surprised if you got more than one antibody binding to one molecule of aflatoxin, but you'd have to test it. Are you trying to measure a quantitative signal?

it's more of a binary on/off as to whether both bind or not.


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Minimum hardware and knowledge to study effects on live cells
I'm very interested to study the effects (or reactions) of different forces (magnetic fields, electric fields, etc) on living tissues/cells.
I know I have to have a living cell, the force applied and a microscope to study this but I do not know what kind of microscope will do and what kind of living organism to use (and how).
Any help to get me started will be of a tremendous help.

This is too broad of a question. You might wish to research first and come back when you have a specific question. Basically you are asking how to study cellular responses to physical stimuli - much broader than that in the field of cell biology is next to impossible. You might wish to visit our help center. Note that each stack has its own unique help center.

Quite contrary - this is a very beginner question in a vast domain. All I need is a simple/basic guidance for it. If every time you ask a question in a new field you are invited to take a walk (aka "search the internet") then we will never advance or start to become cautious with the people from that field.

A beginner question, yes, and that's fine. It's just too broad. It's an open-ended question and pob

I want to start with magnetic and electric fields only to see if it works and then to move to the more mysterious "qi" energy field....but I need to start from something...

The "minimum hardware" you need consists of, at least:

a microscope, as you said (which one exactly depends on what you want to do with it);
whatever device you need to apply physical stimuli to cells (again, it depends on what you want to do exactly);
a cell culture incubator;
a cell culture hood to be able to work under sterile conditions;
a dedicated cell culture room where to put the previous two items;
a cell line to perform experiments on (actually, more likely several different cell lines).

Your question sounds like you are thinking about a personal project, but consider that none of these items is cheap. Add them up, and this project is really not affordable with the finances of an average individual.
The "minimum knowledge" you need consists of, at least:

knowing how to do cell culture (mostly working under sterile conditions, which not only requires proper equipment but also very specialized technical skills);
knowing (at least some of) the scientific literature about cellular responses to physical stimuli, because no lab is going to hire you as an intern if the project you have in mind has already been done and its results published years ago. You can search the biological scientific literature using PubMed.

So, to me it seems that your best chance of starting this project is to find a cell biology lab with this equipment and expertise, and do an internship there. You can start by looking this up on the website of the university closest to you.

Thank you for your comment - at least you split the problem into many more manageable ones. I think the basic start for me is to get the "basic kit" for this kind of experiments. For example minimum microscope specs, most basic cells (that are easy to grow and handle) and easy to observe.


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Protein folding
I've two questions
1. Is free ATP available in the cytoplasm of the cell?
2. In the protein folding funnel, prions and other misfolded proteins are located at the local minima of the graph. If ATP was freely available, it could possibly give a kick to the misfolded structure to cross the energy barrier and this should help the structure to fold along the idealistic path. But such a thing does not happen in reality. Why?

Yes
The energy released by ATP hydrolysis must be coupled, by enzymes, to some other reaction or process in order to be useful. It isn’t magic. There are ATP-dependent chaperones that assist in protein folding.

It seems ATP by itself can also solubilize misfolded proteins (http://doi.org/10.1126/science.aaf6846)

@WYSIWYG Very interesting, thanks.


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Apoptosis related
I have two questions
1. Is it possible for a cell undergoing apoptosis to induce apoptosis in
     a surrounding cell?
2. If we induce apoptosis in a normal cell surrounding a tumor.
     Is it possible for the molecules released during apoptosis to
     differentiate between normal and cancerous cells?


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Are insects really strong or just small?
It's a common statement that insects are stronger, faster and jump higher than almost anything by mass.
However, this leaves out that compared to their mass, all large creatures are actually pretty weak and small creatures are usually strong.
Have there been any studies where the strength of insects and mammals, for instance, is compared directly rather than by this ridiculous "per mass" method? I'd like to have comparisons between creatures that are similarly heavy.
My goal is to figure out the differences in strength between insects, reptiles, amphibians, mammals, fish, etc while actually considering that strength doesn't scale as easily as mass.

How do you define "strength" ? You call the "per mass" method ridiculous, but what's a "direct" comparison? The most direct one I can think of is "how many grams can this creature lift", and I don't think you need a comparative study to find that hundreds of kilograms (what an elephant can lift) >>> hundreds of milligrams (what an ant can lift). Strength scales with mass, so a direct comparison of strength comes down to a comparison of mass. Strength does not scale linearly with mass, hence the flaws of "per mass", so the question is finding a better scale. So: "how do you define strength"?

The issue is that strength and mass are not in a direct relation. Increasing mass by 10x does not increase strength by 10x. The most direct one you linked is exactly what I want to find out, but for comparisons between different creatures.
The key is that the comparison has to be apples to apples. No comparing creatures of very different masses and assuming that they are equivalent.
Strength is pulling, pushing, lifting. Any application of force really, as long as it can be generalized enough that we can compare many different creatures on the same benchmark and that has studies.

Finding a better scale would perhaps be a result of this question. As long as we have good comparisons we can just plot them out on a graph and it should be quite informative about the exact relation between size and strength. Also about how they vary by type of creature.

"it should be quite informative about the exact relation between size and strength." We already know that: strength varies roughly as the square of linear size. Are you asking for an explanation of how this was determined?

Please quote a source with link for the "common statement" you refer to in your question, especially the "strong" aspect. Or else take responsibility for it yourself — e.g. "I believe that…" because otherwise it sounds as if you are setting up a straw horse to knock down.

As in the original question, what I'm looking for is actual measurements. I'm aware that the strength of muscles is proportional to their cross-section. The question is more specifically about how strong animals of different kinds are compared to each other, at the same weights. Clearly there are huge anatomical differences between insects and reptiles - how do they affect strength?
This is why I want to know about any experiments or other ways that creatures of similar mass have been compared in strength.


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Can gut flora affect what we can eat and what we cannot?
Back many years ago, I've read a mushroom guidebook, which I don't have anymore. I was unable to find the name of a particular mushroom. The book comprises listing of edible and poisonous mushroom species. One particular mushroom was said to be "poisonous to some people". the effect is not allergy-based, but rather straightforward poisoning. What drew my attention was the phrase:

If you haven't tasted it before, do so in small doses first. Each family member has to do it regardless of how other family members responded, because the condition is not genetic

This has lead me to think, that if condition is not genetic, then it may depend on which gut flora you have. Gut flora is very helpful in digesting many substances in our food, and possibly even toxins. This has lead me to ask the question Can a human be inoculated with gut flora from another animal and thus be able to eat food otherwise poisonous to humans?
Supporting evidence:

I have read that pronghorns can browse on sagebrush, a herb that is poisonous to ordinary cattle. The toxins kill the cattle's gut flora, that is supposed to aid in their digestion. It is not, however toxic to the pronghorn's gut flora, which can digest the toxins.
Changing your diet abruptly may result in embarrassing stomach upsets. These upsets are transient, however. This may reflect a change in the ratio of bacterial species which reflects optimal adaptation.

Putting that theory to the test:

Attempting to inoculate Pronghorn's gut flora to cattle -- Will the cattle be able to feed on sagebrush?
Diversity of gut flora in humans: One may expect some difference in gut flora between that of city dwellers, such as in Europe, and that of tribes in the rain forests of the Amazon and Africa. Can a city dweller in Europe eat anything the forest dweller may eat? Does he/she need some bacteria inoculation to adapt to certain foods?

Limitations
Not all poisoning cases may be avoided by introducing gut flora that is supposed to digest the toxins. Failures to avoid poisoning may include:

Poisons that are absorbed by the body and the animal eating the plant or mushroom is not affected by it. Floral gut from the animal will not avoid that type of poisoning in a human eating the plant/mushroom.
Poisons that are digested by the animal's own digestive enzymes.
Environmental incompatibility: The introduced bacteria must be compatible to the type of food the host feeds on, as well as the chemical environment of the guts. For humans, this limits us to gut flora extracted from animals with diet similar to ours (Not counting processed food and cooked food). Ruminants and predators are out, Omnivores are in.
Poisons that an animal avoids by excreting it rather than absorbing it, and the bacteria does nothing in digesting it.
Host compatibility: The introduced gut flora must do its job in the guts, and not turn against its host. In turn, the host's immune system must "leave it alone".

DISCLAIMER -- a somewhat-related breakthrough research is underway at the Weizmann Institute of sciences. Conditions such as diabetes, Krohn's disease, obesity, resistance to infections, behavioral and psychiatric tendencies among others were once considered issues on their own, and unrelated to gut flora diversity (or lack of). This research shows otherwise. The research even includes a custom diet which is unlike common diets. Rather than counting calories, your diet is tailored to suit the type of gut flora you have. You may assume that some bacteria may secrete toxins which cause organ damage, such as kidney, liver or pancreatic failure. The healthy gut flora may keep those harmful bacteria in check. On the other hand, it is possible gut flora may digest some of these toxins before they are absorbed by the body.