text:
Selection marker for a cytoplasmic vector that works at low expression levels?
I need to express a selection marker on a plasmid in human cells (e.g. HEK293). However, I am using a cytoplasmic vector derived from a non-human virus with its own mechanism for transcriptional initiation. This means that the expression level of any protein marker will suck: low copy number, very weak promoter, unstable transcripts - these are things that I cannot change in this precise biological context.
Most selection markers (for instance KanMX) come with their own black-box promoter and so I do not know whether they rely on a high number of proteins being produced.
What would be a marker most likely to be selectable despite a very low expression level? I could not find any resource comparing the protein copy numbers of classic markers.
I need to be sure that the cells that cannot survive the selective pressure died because they did not have the marker, and not because the marker was too weakly expressed to protect  cells that have the marker. The standard approach would be to use a regular antibiotic selection and just work with lower concentrations of antibiotics but the number of false positives would most likely be too high.
I can manipulate the host cell to some extent, so I can use antibiotic selection but I can also complement a conditional deletion of an essential gene (auxotrophic marker or non-metabolic genes).

Are you trying to select for the plasmid or for expression of a gene from that plasmid (e.g. by a translational fusion of the gene with a marker)? Can you provide more information about the "technical constraints"?

@tyersome I would be just selecting for the presence of the plasmid after N divisions. Ultimately I would express other things (e.g. luciferase) from the same plasmid but before optimizing that aspect I need to know that the plasmid can stay there for a while. By technical constraints I mean that the plasmid comes with a pre-defined origin of replication and mechanism of transcription initiation, but is derived from a non-human mammalian virus, so it will most likely not "work" as well as in the original host (in which expression levels are already low)

@Mowgli If your plasmid does not have a strong promoter then how are you planning to use it for your later experiments with luciferase etc? Regarding whether the plasmid will stay: for how long would you be doing your experiment (HEK293 divides slowly)?

@WYSYWIG designing and testing better promoters on this platform is part of the ultimate goals. I expect luminescence (or other techniques based on signal integration) to be sensitive enough to detect even the very small expression level of the original construct. I am expecting the plasmid to be maintained for over a week - in theory it will stay "forever" like a genomically integrated lentiviral vector, if it has a replication mechanism (already built in) and a selection system (this question)

Based on your reply it doesn't seem clear why you can't use a standard promoter to drive your selectable marker. Why do you feel constrained to use a "very weak promoter"? Why do you think the transcripts for the marker will be unstable?

@tyersome this DNA does not go to the nucleus (something a bit similar to the HCV life cycle) so I cannot rely on validated host polymerase-driven promoters...

Oh, that makes a huge difference! I think this information would be very helpful to include in the body (if not the title) of your question — I'll make some edits, but feel free to change if you don't think they help. Can you also provide some links for information on this vector — I think that will increase the chance of getting an answer that helps you.

Flow cytometry looking for your plasmid.
These folks labeled their plasmid with a proprietary fluorescent marker, then used flow cytometry to detect cells which had taken up the plasmid.
A novel rapid and reproducible flow cytometric method for optimization of transfection efficiency in cells

An alternative and more direct method to using fluorescent reporter
  genes is to directly label nucleic acids with fluorescent dyes to
  track their intracellular delivery [16]...
  Using the non-enzymatic Label IT® Tracker TM Kits, any plasmid can be
  custom labeled in a simple one-step chemical reaction before
  introduction into mammalian cells [18]. Thus, both subcellular
  localization of the labeled DNA and expression reporter transgene can
  be monitored simultaneously following introduction of the labeled
  plasmid into mammalian cells [16, 18]...
Herein, we demonstrate the development of a flow-cytometric assay to
  determine transfection efficiency by labeling a reporter plasmid with
  Label IT® TrackerTM. This method does not depend on co-transfection of
  two different plasmids and simultaneously quantifies cell death,
  uptake of the labeled plasmid during transient transfection, and
  expression of the target protein.

Even if only a small fraction of your cells take up your glowy plasmid, you will sort those out from the rest with flow.

While the technique is interesting, it does not create a constant selective pressure like an antibiotic cassette or an auxotrophy marker, which means that I would have to sort the cells every few days to maintain a positive population... Additionally, chemical labelling prior to transfection cannot detect replication products.


text:
Breeder's equation and equivalent expressions for narrow-sense heritability
I am trying to model the phenotype of a trait as $X = G + E$, where $G$ and $E$ are the genetic and environmental effects. (I'll ignore the distinction between broad-sense and narrow-sense heritability in this question.) Wikipedia tells me that $$h^2 = \frac{\mathrm{Var}(G)}{\mathrm{Var}(X)}$$ The same page also gives the breeder's equation $R = h^2S$ but also says "Note that heritability in the [breeder's equation] is equal to the ratio [${\mathrm  {Var}}(G)/{\mathrm  {Var}}(X)$] only if the genotype and the environmental noise follow Gaussian distributions." So let $G \sim N(0, \sigma_G^2)$ and $E \sim N(0, \sigma_E^2)$ be distributed according to normal distributions. Then $X \sim N(0, \sigma_G^2 + \sigma_E^2)$ so $$h^2 = \frac{\mathrm{Var}(G)}{\mathrm{Var}(X)} = \frac{\sigma_G^2}{\sigma_G^2 + \sigma_E^2}$$
Now I want to perform a selection, choosing a parent with $X=a$. We can expect the child to have the trait $\mathbb E[G \mid X=a] + E'$ where $E' \sim N(0, \sigma_E^2)$ is some other environmental effect. (I don't want to bother with recombination and multiple parents, so we can just think of it as cloning the parent: given that $X=a$, we expect the parent's genetic part to have been $\mathbb E[G \mid X=a]$.)
To find $\mathbb E[G \mid X=a]$, note that $\mathbb E[X \mid X=a] = a$ and by linearity of expectation, $\mathbb E[X \mid X=a] = \mathbb E[G \mid X=a] + \mathbb E[E \mid X=a]$. To get the terms to cancel, we want to write $E$ as $\alpha E$ where $\alpha E$ has the same distribution as $G$. Since $\alpha E \sim N(0, \alpha^2 \sigma_E^2)$, we want $\alpha^2 \sigma_E^2 = \sigma_G^2$, so $\alpha = \sigma_G/\sigma_E$. Thus we have $$\begin{align}a &= \mathbb E[G \mid X=a] + \frac1\alpha\mathbb E[\alpha E \mid X=a] \\ &= \mathbb E[G \mid X=a] + \frac1\alpha\mathbb E[G \mid X=a] \\ &= \left(1+\frac1\alpha\right)\mathbb E[G \mid X=a]\end{align}$$ Hence $$\mathbb E[G \mid X=a] = \frac{a}{1+\frac1\alpha} = \frac{a}{1+\frac{\sigma_E}{\sigma_G}}$$
Since the parent was selected at $X=a$ and the child has mean $\frac{a}{1+\frac{\sigma_E}{\sigma_G}}$, we have $$h^2=\frac{R}{S} = \frac{1}{1+\frac{\sigma_E}{\sigma_G}} = \frac{\sigma_G}{\sigma_G+\sigma_E}$$
Now my problem is that the two expressions for $h^2$ don't match. They look pretty similar, but one of them has all the terms squared while the other one doesn't. What's going on/where did I go wrong?
ETA: To give a concrete example, suppose 80% of variance in the trait is explained by genes. Then the breeder's equation predicts the child to have $0.8a$. But computing $\mathbb E[G \mid X=a]$ gives $a/(1 + \sqrt{0.8^{-1} - 1}) = (2/3)a$. So the two approaches predict different things (although if it was 50% they would give the same prediction).

I found my mistake, which is where I said "To get the terms to cancel, we want to write $E$ as $\alpha E$ where $\alpha E$ has the same distribution as $G$." What we actually want is to find a constant $\alpha$ such that $\mathbb E[\alpha E\mid X=a] = \mathbb E[G\mid X=a]$. In my question, I assumed that this was the same thing as finding $\alpha$ such that $\mathbb E[\alpha E] = \mathbb E[G]$; hence I was trying to find $\alpha$ to make the distributions of $\alpha E$ and $G$ the same (the means are both 0, so I just needed to get the variances to equal each other). But actually, conditioning on $X=a$ shifts the distributions so the $\alpha$ I found in my question doesn't work.
Since my previous strategy doesn't work, I ended up skipping the step of finding $\alpha$ entirely. I realized that the random vector $(G, X)=(G,G+E)$ is a bivariate normal, because we can write $$\begin{pmatrix}G \\ G+E\end{pmatrix} = \begin{pmatrix}\sigma_G & 0\\ \sigma_G & \sigma_E\end{pmatrix}\begin{pmatrix}Z_1 \\ Z_2\end{pmatrix}$$ where $Z_1,Z_2$ are standard normal random variables.
Now Wikipedia gives the conditional distribution for bivariate normals, which in our case is $G\mid X=a$. We only need the mean, which is $\mu_G + \frac{\sigma_G}{\sigma_X}\rho (a - \mu_X)$. Both $\mu_G$ and $\mu_X$ are zero, and $\rho$ is the correlation which is $$\rho = \rho_{G,X} = \frac{\mathrm{cov}(G,X)}{\sigma_G \sigma_X} = \frac{\mathrm{cov}(G,G) + \mathrm{cov}(G,E)}{\sigma_G \sigma_X} = \frac{\sigma_G^2}{\sigma_G \sigma_X} = \frac{\sigma_G}{\sigma_X}$$ Thus we end up with $$\mu_G + \frac{\sigma_G}{\sigma_X}\rho (a - \mu_X) = \frac{\sigma_G^2}{\sigma_X^2}a$$ which is exactly what we want.

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Is any animal born adult-size?
Size growth after birth seems to be the norm in the animal kingdom (as well as among plants). This makes sense. It's evidently physically challenging for an animal to produce an offspring of its equal size, both if born through gestation or eggs.
But, is this always the case? Are there exceptions, i.e. animals that are born at their "normal", adult size? I don't seem to find any (nor that I am a biologist or expert on the topic).

You may perhaps want to more specifically ask whether, for instance, there are any animals (e.g. placental mammals) that do not grow in size after birth. There are terms for this, such as altricial babies (babies that are less developed in some ways, or require additional care) or precocial babies (those that develop less post-birth). You could ask for extreme examples of precociality! It may also help to read up on neoteny which is related but not directly linked; you may get some good ideas there.

Also, birth is something that we can interpret fairly easily for many vertebrates. However, what counts as birth for a moth or butterfly? The embryonic egg is certainly very small. The larvae grow. Then they pupate, and undergo eclosion (finishing metamorphosis) and come out of their pupa usually completely adult sized. It is not unusual for flies to eclose as very large imagos (adults) and then slightly shrink during the rest of their lifetime.

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Do we as humans develop tolerance to deodorants or antiperspirants?
Do we as humans develop tolerance to deodorants or antiperspirants? In particular when they contain isobutane, isopropyl, palmitate, isododecane, dimethicone, coconut oil, magnesium oxide, allantoin, dimethiconol, disteardimonium hectorite, propylene carbonate.

What do you mean by tolerance? This implies that by default we should have some reaction to these agents. What makes you think that?

I thought that these agents might modify the behaviour of sweat glands, which is itself some reaction.

deodorants don't modify sweat glands they just act to mask or absorb scents. some anti antiperspirants act to plug sweat glands.

Thanks for your comment John. Can you please restrict to the effects of the substances that I've listed? What about long term effects then? In other words, if I stop using deodorants/anti perspirants, does my body revert back to when I hadn't started using them yet? The answer to this is not obvious, in particular given your comment "some anti antiperspirants act to plug sweat glands."


text:
Can sleep be a barrier against aging?
I know that what I'm writing about may be a little strange, but as far as I know,when we are asleep, our human body is programmed to carry on biological functionalities in a really optimized way and we are less sensible to external stress.
So I wonder whether putting people in some state of induced coma for a long period of time (I mean for years) may reduce the effect of time and aging on their bodies to be able to awake them later ,almost as they were before undergoing the process ?
Note: I'm not speaking about the process of freezing bodies - only bare sleep.

Welcome to the site!  I've edited to clarify grammar and formatting; please feel free to [edit] if my edits conflicted with your intents.  Also, if you could show more of the research which you have already done, it would probably help us understand the context of your question.  Thanks!


text:
Bimodal frequency distribution of size of protein loops

The graph of number of amino acid (AA) residues in a loop Vs the frequency of their occurrence in proteins largely follows a tending-to-zero pattern. However, there appear to be some specific number of AAs where the frequency suddenly drops, leading to bi- or multi-modality in the plot. Is there some molecular explanation for this, or is it just an artifact?
I’ve attached the figure from a paper with a different research question but the same graph(Figure 2), albeit more detailed. (The same graph can be found in Brandon and Tooze (fig.2.8).) In the paper from which this is taken “A loop structure was defined as any region between two regular secondary structures that was at least three residues in length.”

Thank you for adding the graph. I have changed the wording to remove "oscillation" which has other connotations, and "probability", as what is plotted is frequency. I have also added a definition of a loop.

A curve of this type, showing a bi- or multi-modal distribution,
  suggests two or more constituent species
  in the population. In this case this is borne out by further analysis
  in the paper of different types of secondary structure components
  anchoring the loop, the peak at low numbers of amino acids reflecting
  the loops connecting β-strands in anti-parallel β-sheets.

The second frame (B) of Figure 2 is shown below (dashed line):

Anti-parallel β-sheets are abundant in proteins, and in many — although not all — cases adjacent strands are connected by short (four- or five-amino acid) loops such as the β-turn, the β-hairpin or the β-bulge loop.
Repeating small loops are especially well illustrated in β-sheets displaying β-meander:

The β-meander motif from the outer surface Protein A
Examples in larger domains of the β-barrel and immunoglobulin type also show some larger loops.

Beta barrel of green fluorescent protein, showing loops at end of strands

Immunoglobulin domain of PDB 5IML showing β-sheet with loops connecting strands


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How can one relate in vitro studies of caffeine (dose expressed as concentration) to dietary intake of caffeine (dose in mass)?
Having difficulty making the data in the below charts to apply to daily life. What is the right interpretation and implementation? How are the “in vitro” results of the below charts relevant to levels that cells would experience "in vivo" after the consumption of caffeinated beverages?

Link to the medical research article which the two above charts were taken from

Good - hope you get some useful answers. I could add that in the lab I work in, we often do in vitro experiments with cells or tissue in a dish, and it's a normal part of our daily business to ask questions exactly like this - it's a great question, though can also be difficult to answer sometimes. The science that figures out answers to these types of questions is called "pharmacology", by the way.

You're asking how skin growth rate is affected in vivo "confluent fibroblasts" by caffeine and it looks like that without the factors and matrix growth environment, that the caffeine metabolically stimulates the fibroblasts away from confluence in graph 1.

In the mentioned study, they tried to support the evidence from earlier studies in which caffeine consumption was associated with skin aging and slow wound healing:

Our research confirms our earlier observations that caffeine may have
  an adverse effect on the wound healing process, as well as on the
  aging process, of the human skin.

...and by "earlier observations" they mean another in vitro study.
In the study, they used 1, 2 and 5 mM caffeine solutions. 1 cup (~250 mL) of brewed tea can contain 95-165 mg caffeine (source), which makes it 2-3.4 mM, so much like the solutions used in the study. When you drink 1 cup of coffee (let's say, 2 mM caffeine solution), the caffeine, which is water- and lipid-soluble (StatPearls), will be dissolved in the body water and fat, which can together make ~50 kg in a 70 kg person. So, you would need to drink ~200 cups of coffee (~20 g caffeine) in ~2 hours (caffeine half-life is ~5 hours - source) to achieve 2 mM caffeine solution in the skin cells.
I haven't found any actual human clinical trial in which caffeine consumption would be associated with adverse effects on the skin. In a recent review: Coffee consumption and health: umbrella review of meta-analyses of multiple health outcomes (BMJ, 2017), they don't even mention skin or wound healing and regular drinking of 3-4 cups of coffee per day was not associated with an increased risk of various health conditions (except in pregnancy).

Since caffeine is water soluble, wouldn't you have to consume (approximately) 194 mg per liter of water to reach that concentration in skin?  That is above the LD50 for caffeine.

I edited the bold paragraph about the amounts. The concentrations of caffeine solutions used in the study and in coffee seem to be about the same, but when you drink a cup of coffee, caffeine would be dissolved in the whole body and would not be so concentrated in the skin cells any more. I think you would need unrealistic amounts of coffee to reach such concentrations.

The LD50 of caffeine is 150-200 mg per kilogram of body weight. So, the lethal dose for a 70 kg man would need to be at least 10 grams of caffeine (~100 cups of coffee) consumed in a short time.

Ah yes, weight not volume, so the 2 molar solution is about the LD50.

How can one relate in vitro studies of caffeine (dose expressed as concentration) to dietary intake of caffeine (dose in mass)?
Caffeine rapidly diffuses throughout the body's water, both intra and extracellular.
Therefore, since the caffeine will be relatively evenly distributed, you can calculate the amount of caffeine needed to reach a given molar concentration within any particular cell by knowing the total water in a person and the molar mass of caffeine (194.19 g/mol ).  A 72 kg person has about 40 liters of water in their body.
Combining those numbers, reaching 1mM requires 7.7676 grams of caffeine.  Reaching 5mM requires 38.838 grams.
How are the “in vitro” results of the below charts relevant to levels that cells would experience "in vivo" after the consumption of caffeinated beverages?
Wikipedia puts the LD50 of caffeine at 150-200 mg/kg, or 10.8-14.4g for our hypothetical 72kg man.  These numbers are likely very approximate as there isn't going to be a lot of well controlled clinical data on caffeine toxicity in humans, but someone reaching those concentrations stands a good chance of dying from caffeine poisoning.
For that reason I don't think these results are relevant to normal caffeine consumption.  I interpreted the high concentrations used in that study as a deliberate attempt to induce cell injury, not as a means to simulate normal caffeine consumption.


text:
Do air purifiers work against bacteria and viruses?
We would buy a mobile air purifier in our home.
Against the smoke of the city, etc.
It would have a HEPA + activated carbon filter. They are marketing it as:

"filtration process captures 99.97% of airborne particles down to 0.1
  micron in size."

and having also:

"encapsulated ion particle charging chamber"

But the question:
Would the mentioned filter+ion charger also help cleaning the air from bacteria and viruses?
Ex.: "Coronavirus/2019-nCoV" is about "Coronavirus virions are spherical with diameters of approximately 125 nm" - but I just Googled it, not from an official source. And 0.1 micron is 100 nm.
UPDATE: would it be more effective, if it would have UV-C light in the air purifier?

The aforementioned filter will filter microbes
Yes, it is routine practice to use microfiltration in labs to sterilize solutions from microbes. 0.2 micron filters will remove all typically-found bacteria most of the time, except for the odd bacteria here and there, though this is uncommon. 0.1 micron filters certainly remove all stray bacteria that may make it through upon a single 0.2 micrometer filtration. Here is a nice read on the appropriateness of 0.2 and 0.1 microfilters, which simply states that 0.2 micro filters are usually more appropriate since they additionally guarantee a better flow rate.
The aforementioned filter will NOT ensure filtration of viruses
These filters are not used, suitable nor effective for viruses, however. You ask specifically about the coronavirus. From a 2015 study:

Coronaviruses are members of the Coronaviridae group and contain a
  single-stranded, positive-sense RNA genome surrounded by a corona-like
  helical envelope (Ryan 1994). The SARS virus genome consists of 29,751
  base pairs. Approximately 41% of the genome is GC base pairs while 59%
  is TA base pairs. Coronaviruses have a size range of 0.08-0.15
  microns; with a mean size of 0.11 microns (see Figure 1).

This means 0.1 micron filters will not protect you from these viruses. They may help you reduce viral count in the air, which may of course be sufficient, but this would not be an adequate measure in a biological safety facility.
The cost-effectiveness of commercial air-purifiers for biosafety vs. pollution
On a advice-related note: I do not think air-purifiers are going to help you in a cost-effective manner to avoid viruses (e.g. Rhinoviruses that cause the common cold, for instance), lest you stay at home all the time. You expose yourself outdoors, and carry plenty of viruses indoors on your body and in your respiratory tract; these will bypass your filtration system on the daily. Being healthy and lucky enough to avoid exposure to viruses outside the house is still the best bet. I think an air purifier has a greater potential to help with smog and urban pollution, those particles are typically larger than the diameter of most microbes.

Wow, thx. I updated the question, UV-C popped in my mind :)

It would depend on the UV-C lamp and how it sits in the purifier. A quick google search copy pasta for you: "the average bacterium will be killed in ten seconds at a distance of six inches from a typical UV-C lamp". And from Wikipedia on microbe inactivation: "dosages for a 90% inactivation of most bacteria and viruses range from 2,000 to 8,000 μW·s/cm2". Air filtration units would have a flow-through, so the lamp(s) would have to illuminate a very thin cross-section of the piping; again, its efficacy would depend on the flow-rate, distance from the lamp, and illuminated area.

When thinking about using a HEPA filter for dealing with air-borne virus and bacteria, there are two important things one need to know:
1- While a sieve traps objects larger than a certain diameter and let the smaller ones pass through, this is not what happens in a HEPA air filter. In this case, due to the principles of fluid mechanics, and also because of brownian movement, there is a critical size (around 0.3 Micron, 300nm) for which, the filtration efficiency is minimum. This means that for both particles larger and smaller than this critical size, a HEPA shows very good filtration efficiencies. As you can see in the graph below, for a True HEPA, even for this "most penetrating" size, the efficiency could be still very impressive (higher than 99.7%).
This means that a good quality microfiberglass HEPA filter can be very good in eliminating nano particles the size of a virus.
2- The second point is that very small airborne microorganisms, are in many instances attached to bigger particulate substances in the air, whether liquid micro droplets or solid particles. I do not know so much about the nature of the bonds and whether this happens for the coronavirus or not, but this may be reason for higher risk of respiratory infectious diseases when PM2.5 air pollution gets high.
For these two reasons, I believe that HEPA air filtration could help a lot in indoor spaces, reducing the risk of infection, by reducing the number of particles of any size from the air.
In contrast, when comparing to the application of UV-lamps, there are to negative points:
1- UV lamps have lifetime and the radiation wavelength is so much affected by working hours of the lamp.
2- If air speed and exposure to radiation is not enough, complete degeneration may not happen and we can not be sure if we are not producing a new genetically improved virus!
All Together, I think we should generally be more careful with the active control methods. With passive control methods such as HEPA filtration, we are sure we are not adding anything new to the air!!!
As a reliable reference on the efficacy of HEPA filters on bacteria and nanoparticles you can see the Technical Memorandum of NASA Marshal space flight Center of May 2016:
Perry, J. L., Agui, J. H., & Vijayakimar, R. (2016). Submicron and Nanoparticulate Matter Removal by HEPA-Rated Media Filters and Packed Beds of Granular Materials.

Many thanks for the infos! :O


text:
Is it humane to kill fish by immersing them in very cold water or ice slurry?
I'm doing some research and advocacy for the humane treatment of wild-caught fish. Humane standards are more common on fish farms than at sea, so I am trying to identify some reasonable standards for what might be considered humane and also feasible for companies to carry out. One possible method of slaughter is killing fish through cold water exposure. Below is an exact quote from a representative at a commercial fishing company (which I won't name since I don't have the person's permission to share this quote yet). I would like to know if what the person describes might be considered humane. It's unclear to me whether these fish are actually dying of hypothermia, or if it's 'cold shock' or 'live-freezing.' I'm not even sure whether these three things are distinct phenomena, or different names for the same process.
"In regards to our fish, they are all dispatched in a method to reduce waste and limit stresses to the fish during it’s transition.  A fish left flopping on the deck ruins it’s meat and stresses the fish out enough to change the flavor of the meat.  We move the fish from the ocean directly into sub-freezing temperatures.  In the case of tuna, that means a refrigerated seawater tank, with the salmon it’s a slurry of seawater and ice.  Sardines are scooped out of the ocean in large nets and deposited into tanks of refrigerated seawater.   The cause of death is hypothermia and has been shown to have a calming effect on the fish for the brief seconds before they pass."

Hi, and welcome to the site!  It would be best if you could [edit] this with some more official sources than "a representative told me." Alternatively, an exact quote from the representative would be nice.  Thanks!

You should state if they cool the water slowly or if they change them to a freezing tank. my experience of fish is that their breathing ability would slow down in the first 5 seconds and that their muscles would start to slow down within 5 seconds, they would be confused and would have the energy to get further than a few meters, which would be the extent of their startled reaction, and then they would go rigid within about a minute.

I don't think this is an answerable question, except by (the ghost of) a fish that has undergone the process.  And then we'd have to compare that to the opinion of the ghost of a fish that has been eaten by a bigger fish...

@jamesqf — I'm not sure that is fair. At very least there is research on this subject such as this review about humane killing of farmed fish ...

@tyersome: But the point is that "humane" is a value judgement that can really only be made by the fish.

@jamesqf — Why do you say that? Humane is an english word that roughly means humans showing compassion ...

Thanks for the suggestions to clarify my question, I have edited above. Also, @jamesqf, I respectfully disagree with your line of thinking. Until the unlikely day when all animal products are abolished, humans will be slaughtering animals for consumption, and figuring out how this can be done in a way to limit unnecessary pain and suffering to the animal is of pressing importance. Surely we have some capacity to estimate and reduce the suffering of an animal.

I agree with @jamesqf that this is probably not answerable here. Biology can't answer questions about what is humane or not. It's possible that you could distill your question down to something answerable by biology, and that this could be used in an argument about humane methods, but it won't tell you whether something is humane or not.

An example of the sort of question you might ask would be to first do some research on methods of monitoring stress in fish, and then ask for a comparison of a couple different slaughter methods with respect to that measure of stress.


text:
DRAQ5 and PI incompatible?
I'm interested to analyse hemolymph cells from a marine mollusc. I wanna count only "alive" cells so my strategy was the following: DRAQ5+ (nucleated cells) and PI- (alive cells) and identify population in FSC vs SSC.
Staining independently with DRAQ5 and PI I found positive and negative populations for each one but, in the fully staining I lost DRAQ5+/PI+ population... (https://ibb.co/VpgcCTN)
Does anyone know if DRAQ5 and PI are incompatible?
Note:

DRAQ5: excitation with 640nm and emission filter 675/25.
PI: excitation with 488nm and emission filter 585/40

Rieger et al. 2010 seems to be relevant. -- "Gating on the population of PI+/DRAQ5+ cells, we used the similarity feature to determine the degree of similarity between PI and DRAQ5 stains in goldfish primary kidney macrophages (Fig. 3A). We found that there was a sizable proportion of falsely stained PI positive in these cells, as well as in all unfixed primary cells and cell lines tested (Fig. 3B)."

For my proposal, I prefer to have more false-positive than false-negative cases. The problem here is that I don't have double staining as you can see here. Independently, I have DRAQ5+ and DRAQ5- populations, the same happens with PI, I saw PI+ and PI- populations. But, adding both stains together I lost DRAQ5+/PI+ population...


text:
Will the sex ratio of chickens become favourable to females?
As male chickens are killed after birth in mass farming. Will being male become a negative evolutionary trait, that is to say will females become more likely as male death is more likely.

Also a follow up, does the chicken industry use selective breeding to increase the chance of females?

What do you mean by "the chance of females". I suppose you are still talking about sex-ratio. In all cases, please ask your follow-up questions on a separate post. Note that chicken are a GSD (Genetic Sex Determination) species. Just like other birds, they have a ZW sex chromosome system. There is therefore not much that can be done to bias the sex-ratio. Related post: Do males of all sexual species have Y chromosomes?

Any chick has a mother and a father. Hence, the contribution to the gene pool of the following generation comes at 50% from males and at 50% from females. As a result there is no selection for biasing the sex-ratio among its offsprings. The variance in reproductive success might be higher among males than among females but that does not matter for the sex-ratio.
This is known as Fisher's principle. In the terms of W.D. Hamilton (Extraordinary sex ratios), copy-pasted from wikipedia:

[..] given the condition that males and females cost equal amounts to
  produce:

Suppose male births are less common than female.
A newborn male then has better mating prospects than a newborn female, and therefore can expect to have more offspring.
Therefore parents genetically disposed to produce males tend to have more than average numbers of grandchildren born to them.
Therefore the genes for male-producing tendencies spread, and male births become more common.
As the 1:1 sex ratio is approached, the advantage associated with producing males dies away.
The same reasoning holds if females are substituted for males throughout. Therefore 1:1 is the equilibrium ratio.

To my knowledge, only kin/group selection can yield a sex-ratio different from 1:1 to be an ESS.

Let's assume all male chicks are killed, and all eggs are fertilised by some other population of males, not influenced by the farmed hens. Say for example a certain chicken (a female in this case) is more likely to produce females by some genetic mutation. Then chicks of said hen will also have a greater chance of producing females. This hen will have more female chicks than the average hen. Hence over time the sex-ratio tends towards females.


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Where can I find disease diagnosis datasets?
For an epidemiological study, I'm looking for datasets for any kind of vector-borne disease (i.e. West Nile Virus, Malaria, etc.), or any parasites that are dependent on intermediate hosts (i.e. Schistosoma spp., which have snails as intermediate hosts).
The data should include day or week and location of each diagnosis. I have been able to find diagnosis data for individual countries for each year, but I'm looking for daily or weekly data for city-wide resolution or at least smaller regions inside countries.
Additionally, it does not matter what country/continent the data is for, as long as there are many data points (i.e. at least 10,000). For example, if there is a lot of good data for Brazil, that's fine.
Does anyone know if such information exists, and if so, where I can find it? I've been searching for it for the past month but have had little luck with finding anything useful. Any help and guidance is appreciated!

Can you reveal some typical keywords to help with the search?

@Jan Maybe things like: "malaria outbreak dataset" or "malaria diagnosis dataset"? I'm not entirely sure what the best way to word this Google search is, either, which is severely limiting what I can find

I was thinking about synonyms for dataset and other keywords that help to find the type of data you are looking for. I'm very familiar with the medical terminology, but not with statistical one. Also can you show an example you've already found?

Is this close: https://data.gov.in/keywords/malaria ?

@Jan Hi again Jan, sorry for the late reply. That website's great! I didn't bookmark any of the sites I searched thorugh, so I'm having a hard time finding them again to share with you - but they weren't as good as yours; the best one contained monthly data for countries, not regions. Do you know if this kind of data is available for other countries (not just India)? I'm also looking for it, but in case you already have them. Lastly, add this as an answer :)

NIAID has released a new open data discovery portal and you can search or filter by disease, host species, etc. https://data.niaid.nih.gov/

CDC Wonder, a health database of the US Center of Disease Control and Prevention (CDC), has weekly data for Nationally Notifiable Infectious Diseases and Conditions, United States: Weekly Tables from 1996 to 2020 on the state level for antrax, brucellosis, dengue fever, leptospirosis, malaria, meningococcal disease, Q fever, rabies, etc.
Weekly tables since 2014 are available on Data.CDC.gov.
Weekly tables for 1952-2017 published in the MMWR are available at CDC Stacks MMWR and weekly tables starting in 2018 are available at CDC Stacks NNDSS.
HealthData.gov has two weekly datasets for malaria by US states - here is one.
Open Government Data (OGD) Platform India has data on a district or state level, for example, for malaria.
Keywords that can help in further search:

infectious disease
week or weekly report or data
MMWR (Morbidity and Mortality Weekly Report)
surveillance

Keywords, like diagnosis or outbreak, can limit your search too much.


text:
What’s this fungus growing in supersaturated salt solution
As a hobby, I’ve been trying to “grow” crystals of from supersaturated solutions of aluminium potassium sulphate.
I noticed that my solutions are also rather successful at growing a type of fungus.
The fungus grows bigger and bigger in the saturated solution and leaves behind yellow spores as the salt solution evaporated (see photos).
I’ve always thought that salt is antifungal and anti bacterial, and I’m surprised to see that there is a fungus actually growing bigger in a supersaturated salt solution.
I have tried boiling and filtering (with tea mesh filter so the spores probably got through) the salt solution, but the fungus keeps coming back, so the spores survive boiling too, unless there are spores floating around my room.
Is there a way to identify what sort of fungus it is? What sort of fungus is it likely to be? Have I bred a type of super fungus? Is my life in danger by allowing this to grow?
I live in Sydney, Australia if that helps with identifying the fungus.

It looks like an algae which of course grows very well in sea water. Possibly , in some respects your salt solution is similar to sea salt.

Welcome to Biology.SE! Do you have access to a microscope — I'm pretty sure your question is unanswerable without more information and (assuming sequencing is unavailable) a micrograph would seem to be the best bet. To test @blacksmith37's suggestion, see if keeping your experiments in the dark stops the growth. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

Thanks, I’ll keep them in the dark to see if that stops the growth.


text:
Has there ever been an approved viral infection treatment method based on the physical/mechanical properties of virus?
I imagined that typical cells and viruses could have very different physical properties or reactions to mechanical stresses, which makes selective targetting possible. For instance, some  major differences between viruses and animal cells:

Difference in size/mass
Difference in elasticity (lack of cytosol in virus)
Difference in structural composition results in a different reaction in response to different vibrational frequencies

Preliminary search found something related to microwave absorption induced oscillation mode fracturing airborne virus, taking advantage of the (structural) core-shell charge separation in virus (not sure if I described the principle right, to be honest). However, though looks exciting, it is more like a disinfection rather than a treatment method. So the question goes: Has there ever been an approved viral infection treatment method based on the physical/mechanical properties of virus?


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Is there any situation where bloodletting should be paired with transfusion?
Clearly, bloodletting only has benefits in a couple of rare instances —— for example promoting blood flow into reattached tissues1. But could it (or, should it) realistically be used along with transfusion for any purpose? Why or why not? (Based on Bradbury's Fahrenheit 451, where it mentions a blood transfusion/removal device)
1: Bennett-Marsden, M., & Ng, A. (2014). Hirudotherapy: a guide to using leeches to drain blood from tissue. Clinical pharmacist, 6.

Welcome to Biology.SE! This site tends to very exacting, so I would recommend you avoid statements like "bloodletting has been disproved", when you are really talking about its medical benefits. We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

I've made some edits that I hope will make this more acceptable to this community, but your question may actually belong on the [medicalsciences.se] site ...


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What happens when you cook tree spinach with aluminum?
The Internet is filled with warnings that you shouldn't cook tree spinach(Cnidoscolus aconitifolius) in aluminum, because it will react and create toxins that cause explosive diarrhea when consumed. However, I can't find anything more specific than that. Does something (presumably hydrocyanic acid(HCN)) from tree spinach react with aluminum? If so, how does the resulting product cause diarrhea?

If aluminium is present in a hot medium wtih cyanide, perhaps it can produce aluminium cyanide?   i had a look at aluminium use as a catalyst in organic chemistry, it could be anything, there is however something called...Cyanosilylation: Aluminum alkoxides, such as aluminum isopropoxide (Al(O-i-Pr)3), are employed as catalysts in cyanosilylation reactions, which involve the addition of a cyano group to a carbonyl compound plus another group.


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Long-term potentiations that last for a lifetime
One reads more often than not that

long-term potentiation has been reported to last for as long as several weeks
LTP is persistent, lasting from several minutes to many months

and most sources seem to explain mechanisms of LTP that just last as long - from hours to days to weeks to months. Only rarely it is explicitly mentioned that such-and-such LTP lasts for years or a lifetime, and most authors seem to hesitate to make such claims.
But there are memories (and learned skills) that can be retrieved many years and even decades later, even though not (consciously) used in the meantime.
I have no idea how this kind of "really long-term potentiation" is explained. Three options come to my mind:

The long-term potentiated synapses and the "memories" related to them have actually been used in the meantime (just "unconsciously" or in completely different contexts) and thus been re-newed and re-strenghtened every now and then.
They degraded but have been re-newed without having been used, but by some other mechanisms than "normal" LTP.
They actually did last for such a long time (i.e. didn't degrade) - and the authors just hesitated to claim it (because they could not prove directly).

Is one of these three explanations the correct one, or is there another one?

No time for an answer but some dendritic spines live long enough to sustain memories that can last for as long as the animal lives (Yang et al 2009). Each time a memory is recalled, it is also reshaped --potentially strengthened, attenuated, or otherwise altered.

@vkehayas. Hi, Vassilis, great  to hear from you again! The explanatory problem is that a memory or skill (as a holistic entity) may be un-recalled for decades and thus not reshaped. It's only the synapses involved in the memory that are re-strengthened, attenuated, or otherwise altered - just by being part of many other memories that were recalled. Does this picture make sense? (Alternatively one might consider that the memory itself actually was recalled, but unconsciously, maybe in dreams?)


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How to do research in bioinformatics without wet lab experiments?
I graduated in physics from Bangladesh and keen to work in the field of biology. Like, systems biology, computational biology, bioinformatics or systems medicine. I have not produced any research work in such fields as of now. I am studying sequence alignment and RNAseq and later plan to study flow cytometry bioinformatics. I have no affiliation with any institute now in my country as they don't accept students from other disciplines. Is it possible for me to do research on my own by using databases available? If so, I would be really grateful if anyone can suggest how to approach my research topic/work.

Doing actually valuable bioinformatics research completely on your own after graduating from university (I am assuming that this corresponds to a master's degree) is somewhere between impossible and very unlikely - even for someone who actually studied bioinformatics.
In order to really do research (in almost any field) you will have to become a PhD student first - and for that studying the relevant topics on your own, like you are already doing, is probably the best preparation.
If there are truly no 'cross discipline' applications possible where you are from, you'll probably have to apply for programs or positions abroad. It is, however, becoming increasingly common for bioinformatic research groups to hire people from various different backgrounds - ranging from wet lab biology to physics. I would advise you to actively look for such interdisciplinary research groups (ideally purely computational groups as a physics background will be more valuable there than in a mixed dry/wet-lab group) and potentially directly contact the group leader if the university/institutes don't offer any programs that would allow you to apply.

Thank you very much Nicolai

It seems to me that all you really need to do bioinformatics research is a computer. Of course it would be easier with formal training, but I don’t see that it is impossible without it. Sincerely, a wet lab biologist.

@canadianer I'm not saying it's completely impossible, but (as an analogy) all you need to do mathematical research is a pen and some paper - but honestly how many people who just graduated university can (nowadays) actually produce something worthwhile?


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why do our eyes not go red in response to body temperature?
I know that blood flow increases/decreases in response to temperature change, which is why (lighter-skinned) people go red when they are hot.
I know that the eye contains lots of blood vessels.
Why do our eyes not turn red when we are hot?

Skin turns red when light skinned people flush because it contains few absorbers, so photons diffuse through it long distances. During this time green and blue light is absorbed as photons encounter blood vessels. Red photons are not and so the skin appears redder.
The whites of the eyes are strongly scattering and have relatively few blood vessels, so changes in blood flow has a small effect on color.  The (wavelength-independent) scattering dominates over absorption.
The pupils open up on the approximately 22 mm gap between the cornea and the retina. You don't see changes in color here because the entire retina strongly absorbs all colors of light. The few red photons scattered by blood are very unlikely to be exactly aimed at the pupil. Instead most scatter back into the retina and are absorbed. This is compounded by the scattering anisotropy of blood, which causes most incoming red light to be scattered in the forward direction - directly into the strongly absorbing retina.


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Why are bats the source of dangerous coronavirus pandemics?
Why do coronaviruses come from bats?
I mean, why precisely coronaviruses and not (for instance) herpesviruses?
It looks like bats host more zoonotic viruses (per species) than rodents, although they don't develop any sign of disease.
The article above says that rodents host more zoonotic viruses than bats overall (68 against 61), but at the same time most of the latest pandemics originated from bats.
It also seems that bats could be involved in the maintenance of ebola viruses.
My question is: why did these major pandemics originate from bats and not from rodents, although rodents host more zoonotic viruses overall?
We should also take into consideration that human-rodent interaction is usually more likely than human-bat interaction, except for people who consume bats (like Chinese people; this would (partially) explain why both SARS and 2019-nCoV developed in China).

There is lots of discussion of this in the literature, but I think no solid answers: https://scholar.google.ca/scholar?hl=en&as_sdt=0%2C5&q=bat+virus+reservoir+physiology&btnG=

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, it is best to focus on a single question in each posting — this ensures you can get answers to each question and makes the results easier to find for other users. Thanks!

Why not bats?  .

I think your first link answers that question as well as anyone here can: they're highly mobile, have long lifespans that facilitate chronic viral infections, surpress their immune systems during hibernation, and often live in large groups that enable viruses to spread quickly between individuals.

Theory: When they fly, bats raise their body temperatures similar to those seen in other mammals that have a fever (100 to 106 degrees Fahrenheit)... Perhaps the viruses are primed to thrive in humans because bat fevers can overcome human fever temperatures. Perhaps a bat fever temperature is 110, if one of you has access to a feverish bat and a mini temperature gage.

keep in mind many of our viruses come from other many species, (dogs, birds, swine, bats, rats, cows), this particular one just happened to come from a bat.

@John I knew that, my question is why bats' viruses are deadlier than the others

they are not, viruses from bats are no worse than viruses from any other animal. Every spill over virus is a roll of the dice.

The preponderance of links between bat and human pathogens has led to a debate about whether bats disproportionately contribute to emerging viral infections crossing the species barrier into humans (26–30). Given the diversity of the Chiroptera order (Figure (Figure1),1), we may simply see more bat viruses because there are so many (>1,300) species of bats (31). However, even when accounting for the fact that they make up ~20% of extant terrestrial mammals, bats are overrepresented as reservoir hosts of pathogens with a high potential for spilling into human populations (32, 33). In fact, no known predictors that have been described to impact the likelihood of crossing the species barrier, including reservoir host ecology, phylogenetic relatedness to humans or frequency of reservoir-human contact, explain this pattern (32). Thus, why bats are such a frequent source of pathogenic human viruses remains a tantalizing mystery.

--Going to Bat(s) for Studies of Disease Tolerance
Other references that debate whether bats are special, generally conclude that they might somehow be, and argue about causes, include

Brook CE, Dobson AP. Bats as ‘special’ reservoirs for emerging zoonotic pathogens. Trends Microbiol. (2015) 23:172–80. This may be the best of the group, going into more detail and including more recent data
Dobson AP. Virology. What links bats to emerging infectious diseases? Science (2005) 310:628–9.
Wang LF, Walker PJ, Poon LL. Mass extinctions, biodiversity and mitochondrial function: are bats ‘special’ as reservoirs for emerging viruses? Curr Opin Virol. (2011) 1:649–57.
Olival K, Epstein JH, Wang LF, Field HE, Daszak P. Are bats exceptional viral reservoirs? In: Aguirre AA, Ostfeld R, Daszak P, editors. editors. New Directions in Conservation Medicine. Oxford, UK: Oxford University Press; (2012). p. 195–212.
Luis AD, Hayman DT, O'Shea TJ, Cryan PM, Gilbert AT, Pulliam JR, et al. . A comparison of bats and rodents as reservoirs of zoonotic viruses: are bats special? Proc Biol Sci. (2013) 280:20122753.

The following paper proposes that the bat borne viruses evolve to rapidly-transmit as a response to their robust immune systems:

We carried out virus infectivity assays on bat cell lines expressing induced and constitutive immune phenotypes, then developed a theoretical model of our in vitro system, which we fit to empirical data. Best fit models recapitulated expected immune phenotypes for representative cell lines, supporting robust antiviral defenses in bat cells that correlated with higher estimates for within-host viral propagation rates. In general, heightened immune responses limit pathogen-induced cellular morbidity, which can facilitate the establishment of rapidly-propagating persistent infections within-host. Rapidly-transmitting viruses that have evolved with bat immune systems will likely cause enhanced virulence following emergence into secondary hosts with immune systems that diverge from those unique to bats.

Accelerated viral dynamics in bat cell lines, with implications for zoonotic emergence, eLife Sciences (2020)


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Why does hair turn white but not skin?
From my understanding melanocyte stem cells (McSCs) stop being produced and we have a finite reserve that gets depleted with time. They're at the origin of melanocytes that create hair and skin pigments. Our hair turns white when we don't have any more McSCs. So why does our skin stay the same color with aging?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, please add some more details with references to reliable sources (e.g. You say MeSCs stop being produced and are depleted with age. Where did you read this? At what age do they stop renewing themselves? How long do they typically live?) Thanks!

I've made some edits that I think will improve your questions reception on this site. Please make additional edits to add more details when you can.

Nice question. Will write an answer later, when I have some time.

I thought it was common knowledge among biologists that melanocyte stem cells don't get regenerated. I could throw this link where you can read: "After just a few days, all of the pigment-regenerating stem cells were lost. Once they're gone, you can't regenerate pigment anymore. The damage is permanent."

whether they get depleted or not, the question remains. Hope  @Chris gets some time for a basic answer

Biology includes a huge range of disciplines including many specialties (e.g.ecologists and plant biologists) the practitioners of which have no particular reason to know this kind of information!  ——— I think you may be taking that quotation out of context — I think it is saying you don't make more McSCs once they've been killed. Also note that it is best to reference primary literature rather than secondary sources. Finally, if you can find a good reference, please [edit] that information into your question since comments are ephemeral.

@borilla I haven't forgot it, but there is too much work...

The answer to this question has its reason in the hair cycle. Our hair goes through a cycle of growth. At the end of this cycle, the cells in the hair follicle die and have to be replenished before a new hair cycle starts, also the hair falls out eventually. See the figure from reference 1:

The replenishment process is done by to two cell types: Epithelial stem cells which replenish the hair follice itself and melanocyte stem cells (MCSC) which replenish the melanocytes in the follicle and produce the pigment of the hair.
The MCSC are located in the bulge region of the hair, to be able to successfully replenish the pool of pigment cells the MCSC need to do things: proliferate and also differentiate. Proliferation makes sure that there are enough cells in the bulge region to repeat this process in further hair cycles, while the differentiation generates the cells who actually produce the pigment. When the MCSC are lost, no further pigment producing cells and hence no pigment can be made.
It has now shown that with age this pool of MCSC is not replenished completely anymore, eventually resulting in the loss of the melanocyte stem cells. The reason that our skin does not become gray at some point is that this process doesn't happen there, so pigment cells are not depleted. Reference 1 summarizes this topic nicely, while reference 2 is the original paper.
References

Melanocyte Stem Cell Maintenance and Hair Graying
Mechanisms of Hair Graying: Incomplete Melanocyte Stem Cell
Maintenance in the Niche

If I understand correctly, after a certain age hair follicles are not replenished with MCSC. But MCSC are still present somewhere in the skin to differentiate into the melanocytes of the basal layer . And these basal layer melanocytes don't last forever so they need to be replaced.
If this is correct then my question is:   where are those MCSC that still create melanocytes for the basal skin layer?

MCSC need to proliferate before they can differentiate into melanocytes. This happens to rise the number of cells present in the bulge region and to avoid the depletion of the stem cell niche. If the would only differentiate, then there are no cells left after a few hair cycles. So actually the stem cell niche is empty when you have no pigment anymore.

humm I still don't understand where the melanocytes in the basal layer of the skin come from after all your hair have turned gray. I read both articles and I can't find an explanation on the net. Maybe I am misunderstanding the whole process...


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Statistics: How are protein species distributed over cell types?
There are roughly 10,000 to 20,000 protein species in the human proteome (while I've seen also numbers of 500,000 to 1,000,000). Furthermore, there are roughly 200 different cell types in the human body. My question is:
How are the protein species distributed over the cell types?
This means specifically:
How many proteins are expressed by n cell types?
How many cell types express n proteins?
Probably these numbers are not known exactly because not all the proteins may be known that a given cell type expresses.
But there might be evidence which general form the two distribution curves do have. Are they Poisson distributions and do look more like this?

Or this?

Or that?

Or some other kind of distribution, e.g. Gauss or even multi-modal?

You can refer to this website - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4889822/ This website gives a wide view of protein species distribution. So you can correlate it with the statistics.

You may be able to find some relevant data at this site: https://bionumbers.hms.harvard.edu

@Dirigible gives an excellent answer with some good literature-  you may also find this recent paper to be of interest "Analytical distributions for detailed models of stochastic gene expression in eukaryotic cells" - includes proteins (Fig 5): https://www.pnas.org/content/117/9/4682

From my searches, there is no single resource that includes an atlas of all human proteins produced across all human cell types.  However, there are several recent mass spectrometry studies that look at cell-type-resolved proteomes for specific human and mouse tissues that provide some insight into the distribution of proteins across different cells.
A Cell-type-resolved Liver Proteome
This study identified between 6200 and 8500 mouse gene products in each of four cell types -- hepatocytes, hepatic stellate cells, Kupffer cells, and liver sinusoidal endothelial cells -- and a total of 10,075 gene products across all four cell types.  Figure 1D shows that there is significant overlap between the proteomes; 5,246 proteins (52.1%) are shared by all four cell types, and only 1,451 proteins (14.4%) are cell-type exclusive in this set.  Besides cell-resident proteins, the authors also report secreted proteins unique to hepatocytes and Kupffer cells.  These results by-and-large corroborate an earlier publication, Cell-Type-Resolved Quantitative Proteomics of Murine Liver, where the authors reported 8,338 of 11,520 (72.4%) proteins were common to the five hepatic cell types tested.
Cell type- and brain region-resolved mouse brain proteome
This study looked at four types of isolated neurons from specific regions of the mouse brain as well as five types of primary cultured neurons.  Of 13,061 total proteins, 10,529 (80.6%) are common to the five cultured cell types tested, and only 194 (1.4%) are unique to a single cell type.  Figure 2D makes clear that protein abundance across cell types - not just binary presence/absence - is important to cell identity.  (More on that below...)
Region and cell-type resolved quantitative proteomic map of the human heart
Getting to the human proteins mentioned in your question, this publication analyzed three cardiac cell types and adipose fibroblasts across 16 anatomical regions, giving both spatial and functional perspectives on protein type distribution in the human heart.  Figure 5A, like Figure 1D for the mouse liver proteome paper, shows a great amount of overlap of proteins between cell types:  of 11,163 total proteins, 7,965 (71.4%) are common to all cell types (including adipose fibroblasts), and 617 (5.5%) are unique to one type of cell.  Interestingly, and perhaps not surprisingly, the subsets of proteins unique to specific cells are enriched for cell surface markers. (Related:The in silico human surfaceome)
Social network architecture of human immune cells unveiled by quantitative proteomics
These authors identified more than 10,000 different proteins across 28 primary human hematopoietic cell populations, with three or four biological replicates per cell type, including 17 distinct types of immune cells.  They identified an average of 9,500 proteins per cell type, and, for the immune cells, generated both "steady state" and "activated" proteomes, giving insight into how the proteome changes both across cell types and within each type between states.
To directly answer your question,

How are the protein species distributed over the cell types?

I took the data from Supplementary Table 6, averaged the replicates, converted protein copy-number values to a binary presence/absence matrix, and computed the number of immune cell types (1 - 17) represented by each unique protein ID.  The inset graph combines cell type and activation state labels to ask whether the effect of activation dominates over cell-type differences in proteome divergence.

Presence/Absence, no threshold -- Unique protein distribution across 17 primary immune cells types.  A protein is considered "present" in a cell type if average copy-number value is greater than zero.  Data from Rieckmann et al. Nat Immunol. 2017.

Because the inferred protein copy-numbers from the mass spectrometry data cover a high dynamic range, I also looked at the distribution of proteins that had average copy-number values at least double the zero-depleted cell-type-specific median copy-number value.

Highly abundant proteins -- Unique protein distribution across 17 primary immune cells types.  Protein-cell pairs are only counted if the average protein copy-number is at least double the median protein copy-number for each cell type.  Data from Rieckmann et al. Nat Immunol. 2017.

Taken together, these distributions suggest a few things:

for this diverse set of immune cells, a majority of proteins are present in all cell types when looking at strict presence/absence data
after subsetting for highly abundant proteins, a bimodal distribution appears, suggesting that protein abundance is a better metric for functional comparison of proteomes than a simple binary metric
the proteomes of one cell type between different activation states are more similar than the proteomes of different cell types in the same state

For anyone interested, I've made the cleaned-up data available on Dropbox.
A more complete answer might combine the data from the immune cell and heart cell publications to get a sense of proteome concordance across tissues, but, just from a cursory analysis, differences in protein labels between the datasets would make comparison tedious, so I'll leave that to someone else!


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How do bats survive their own coronaviruses?
How do bats survive their own coronaviruses (without showing any symptoms)?
Or, more generically, how can viruses keep reproducing inside healthy carriers without inducing any pathogenic effect?
Are coronaviruses able to replicate themselves without harming bats, or maybe these viruses are just latent like herpesviruses in humans?

Related question: Why are bats the source of dangerous coronavirus pandemics?

Perhaps bat immunity is a result of their crowded living conditions needed to survive cold winters.  The bat that gets sick and dies does not breed.

It's common for the reservoir host of a zoonotic virus to be tolerant of it. MERS coronavirus appears to cause mild or no disease in dromedary camels ( source ), but kills about 35% of confirmed infected humans. ( CDC ) Sin Nombre hantavirus seems to be mild in the deer mice that spread it, despite ~36% fatality rate in humans. ( source ) Mosquitoes are efficient vectors for flaviviruses like dengue and zika in part because they have adaptations we lack that protect them from the virus. ( source ) Also, human communities are host to several viruses: about 90% of people have a herpesvirus infection ( source ) with similar numbers for polyomaviruses. ( source ) Very few of these infected individuals show symptoms.
The wide prevalence of these asymptomatic infections shows that the virus is successful when it can replicate while the host remains healthy. In general, virus reproduction kills cells, and when cells die faster than the host can replace them, this causes symptoms up to and including death. The host's immune system supresses virus activity, and a virus that can't evolve ways to avoid immune supression will be wiped out. But if the virus gets so good at avoiding the immune system, it will kill the host, which is bad for the virus. So both host and virus tend to evolve to a point where the immune system wins most, but not all of the time. There is a lot more to it, but I'll stop here.
In conclusion, we don't really need to look for special properties of bats to explain their tolerance of coronaviruses, even though, as iayork points out, there are reasons to expect bats might be more resistant.

this is why I added these lines to my question: "Or, more generically, how can viruses keep reproducing inside healthy carriers without inducing any pathogenic effect?"

Excellent answer. As Lewis Thomas said: "Disease usually results from inconclusive negotiations for symbiosis"  The question is less one of why the bats don't get sick and more why we do.

@Zafalija I've added another paragraph which I hope answers this part of your question.

@timeskull I was rereading your answer: "There is a lot more to it, but I'll stop here" Could you link me something about virus-host evolution?

@Zafalija Here's the best review I could find: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207818/

It's been tentatively proposed that bats are often unusually able to tolerate long-term infection with a wide range of viruses (though this hasn't been formally shown to be true). A specific cause for this (possible) phenomenon isn't known, but many possible explanations have been put forward. It's likely that if it's true, there's no single cause but rather a combination of multiple causes to add together.

Bats have an array of unique life history characteristics that not only allow them to be particularly good reservoirs for viruses that are highly pathogenic in other species, but also appear to have shaped their immune systems. Although research on bat antiviral immunity has focused on only a few species to date, at the genomic level, selection on genes is concentrated on the innate immune system across both suborders of bats. However, while these studies have provided a rich source of hypotheses, the majority remain to be tested at the functional level and many questions remain that cannot be answered from comparative genome studies. Experimental studies to date have demonstrated some functional differences between bat species, with the common emerging theme that the overall antiviral response appears to converge on a lower inflammatory profile, with tight regulation of the cytokine and inflammatory response key to clearing viral infection without the pathological outcomes typically associated with infection.

--Going to Bat(s) for Studies of Disease Tolerance


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How many metabolites are in the metabolome of (almost) all eucaryotic cells?
Which small biomolecules (up to the size of amino acids) are present in (almost) every eucaryotic cell and thus part of its biochemical network, constantly and inevitably being produced and metabolized?
Is there either a comprehensive list (e.g. being a sublist of this one) or at least a number: How many are there (roughly)?
To ask it differently: How many small molecules are in the metabolome of (almost) all eucaryotic cells?
Side question: Does the famous Metabolic Pathways poster contain all of them, or which percentage (roughly)?


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Virus cannot survive on surface after certain time period, but why and how?
I'm not a biology student at all, but I'm trying to get a clearer picture on what is meant by "virus cannot survive after a certain period".
To my understanding, a virus cannot be killed it can only be inactivated (for example, by means of heat and lowered pH).
So I really don't understand how can virus get inactivated by just being on a certain surface for an extended period.
I've come across numerous articles which told me virus won't survive on a surface. They usually focus on comparing the survival time between different types of surfaces but never touch on how the virus gets inactivated.
Can someone help me understand the "how"?

Related: 2019 Novel Coronavirus (nCoV) lifetime outside an organism

"To my understanding, virus cannot be killed" This is just because they're generally deemed not to be alive in the first place.

It does depend on the surface, and the virus, different ones are destroyed in different ways. A virus survives in the same way an antique car survives, as in it still exists in good enough shape to function.

I am thinking virus can be degraded by lots of extracellular enzymes (e.g. proteases) which microorganisms are constantly secreting. That's how elements locked up in "biomass" cycle again. And that explain why virus survive more poorly in moist and hot environment where microbial activity is the highest. I could be wrong but just saying.

Many important viruses are coated with a lipid envelope and rely on this to enter the host cell. This envelope is fragile - it's similar to a soap bubble - and it can be disrupted in many ways. Lipids will oxidize in air over time and this will degrade their ability to maintain an envelope. Surfactants such as soap or solvents such as alcohol will disrupt an envelope quickly. Even if the genome inside survives, if the envelope is disrupted the virus won't be able to infect cells.
The exact mechanism of inactivation likely varies a lot from virus to virus, and hasn't been studied extensively.
This paper found that Hepatitis C virus RNA survived alcohol treatment, but lost infectivity, presumably due to envelope disruption. In contrast, heat treatment (80°C) destroyed both the envelope and the RNA.
Another paper found enveloped viruses survived being dried out a shorter time than non-enveloped viruses. (5 days vs. weeks)
Speaking generally, the environment outside a body is hostile! If you were taken out of your home and dropped somewhere in the wilderness, there's many different ways you could die, and it's more remarkable if you survive. A similar situation arises for viruses.

+1 To be fair I don't think the last paragraph is a good comparison, as a virus is just a bunch of molecules and not a living thing. And I think it's from this understanding that the original OP asked his question. If you put a table outside on a surface it won't get destroyed either. Obviously the answer is "viruses are relatively fragile, because evolutionary the advantages of surviving away from organisms that could replicate them was fairly pointless" . Does make me wonder whether with the increased population density of human organisms there will be a point where it's worth surviving.

The point I was trying to make is that viruses are complex systems that have many potential points of failure. In that regard, they are closer to a living thing than a table, which can take a lot of damage and still function as a table. Maybe a better comparison would have been to some electronic device like a PC that you'd expect to stop working if its left outside. But, I expect rain would destroy it before anything else 99% of the time so it doesn't work the same way.

@DavidMulder: To give a better analogy, a virus is like a car that functions well in the city but will break down gradually if left into the wilderness, rapidly if it is thrown into a pond or the sea. Similarly, viruses 'survive' well in their hosts, but will gradually break down if left outside, and rapidly so in certain environments.

@DavidMulder Even with the table, leaving it outside under the sun / rain / snow etc. versus leaving it in your home over a long period of time means different rates of degradation.

@DavidMulder I would argue that there's a fine line between a "bunch of molecules" and a "living thing". The death of a "living thing" is just what happens when a sufficient number of internal systems of the thing (which are themselves "bunches of molecules") are placed in hostile scenarios for a sufficient time for them to cease function. I would think the comparison of a virus on a surface to a human in a desert is apt (if incredibly simplified) - the concept of "death" might be different from a micro to a macro scale, but the ultimate result is the same for the subject.

thanks for the response, it helps me to better understand how Virus break down in the wild.
I can understand how solvents and heat can disrupt or destroy the envelope or even some structure within the virus.
The point about oxidization seems to explain mildly.
So if a virus is being filtered by a mask, and then if I put a mask inside my home for extended period, oxidization will gradually disrupt the stability of the virus envelope, does my understanding correct?

yes, oxidation will eventually degrade viruses stuck in a mask, and speed up inactivation by other processes like drying out.

Ultraviolet (UV) light emitted from the sun has enough energy to break chemical bonds in DNA and RNA.
Some frequencies of UV light can cause damage in the DNA in skin cells that can lead to replication and expression errors, which lead to cancer (melanoma).
Similarly, UV can break up and inactivate the genomic payload of a virus:

Sunlight or, more specifically, solar UV radiation (UV) acts as the principal natural virucide in the environment. UV radiation kills viruses by chemically modifying their genetic material, DNA and RNA. The most effective wavelength for inactivation, 260 nm (55), falls in the UVC range, so-named to differentiate it from near-UV found in ground-level sunlight, i.e., the UVB and UVA portions of the spectrum, 290 to 320 nm and 320 to 380 nm, respectively (51). Nucleic acids are damaged also by UVB and UVA but with lower efficiency than by UVC radiation (64).

Surfaces exposed to sunlight would see partial to complete inactivation of virus particles over time.
There is a paper here that discusses using a safer frequency of UVC radiation as a biocide:

The biophysical reason is that, due to its strong absorbance in biological materials, far-UVC light does not have sufficient range to penetrate through even the outer layer (stratum corneum) on the surface of human skin, nor the outer tear layer on the outer surface of the eye, neither of which contain living cells; however, because bacteria and viruses are typically of micron or smaller dimensions, far-UVC light can still efficiently traverse and inactivate them13,14,15.

So your saying natural sun light is enough to kill viruses. though it can take days/ hours dpending on the surface? Also that it only kills the viruses that are on the surface, and not behind something/ embedded deep inside? So a moist though thin hankie, would take longer to disinfect than a similar dry one?

You'd need to measure how different UV frequencies get through layers of fabric, but people wear clothes and hats to protect against sunburn. This should perhaps give an intuitive sense to what extent a hankie can be sanitized.

Well I have used a hat and a hankie. A hat worked well. But a hankie made me feel hot very soon. I'm bald. I don't trust my intuition here. Was curious to know your knowledge or best guess? :-)

I don't know the answer, but I suspect keeping a handkerchief in your pocket will allow it to accumulate a lot of bacteria and viruses. You could put your handkerchief on a clothesline to expose it to the sun, but then there are pollen and mold spores in the air, which are allergens for some people. I hope you find an answer.

okay thank you. hopefully multiple researchers will do a bunch of studies and answer these question in the coming months

Like other forms of life, viruses are composed of fragile molecules susceptible to damage from the environment.  They may oxidize in the air, suffer mechanically stresses, be hit by UV light, etc.  Metabolism in cellular life combats this effect by actively making repairs and by forming and maintaining protective barriers.
Viruses don't do that.  Outside of a cell, they don't do anything.  They don't have a metabolism.  They can't make repairs.  The damage accumulates until they can't work anymore.

Welcome to Biology.SE! Your point about viruses not be able to make repairs is a good one, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!

For the record, I would like to place here a response that was received for How do viruses die outside of host cells?, which was deemed to be a duplicate of this post and closed.

This isn't very professional, but there are the basics. Viruses are obligate parasites, which means they can't live outside a host (in this case, a cell) for long. Viruses get damaged as everything else, the damage taking many forms, such as hydrolysis, photolysis, free radical damage, reaction with other molecules (like detergent), conformation changes, dehydration, maillard reactions, and changes induced by heat of labile molecules (like decomposition). All types of damaging processes happen at an increased reaction rate with increasing light and heat. Viruses have rudimentary repair mechanisms if any, so it's a matter of time before they become inactivated. A damaged virus entering the body wouldn't be able to do much harm if any, as their genetic information would be damaged beyond repair, and so, not able to be replicated to make more viruses. Their proteins and genetic bits would still trigger an immune reaction and immunize against intact and not very damaged viruses (which is why damaged viruses are used in vaccines). Those damaged viruses that remained outside just become microbe food.

Virus as complex ordered system, without actively maintaning the order, the order will lose after time and finally lose the ability to infect the host.
Even the virus in a host body that is not destroyed by the immune system will "die" (means not functioning any more). It doesn't matter a single virus live or die, the important thing is the pupulation - if virus get replicated is more than that is dead in a period, the population will increase in the host body.
Infection is also about statistics, you need enough virus to get into the host body for them to successfully start the pupulation increasing process before they all become dead (killed by immune system or degraded in other ways)
We are not sure whether the virus particales outside host are all dead or not, only sure about the chance they infect the host after a time is low.
So another reason (besides detailed mechanisms) is that they are not replicating to sustain the population that is dense enough to easily infect the host.


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How would blocking Na/K ATPase affect the ability of a neuron to exhibit a series of action potentials?
Neural firing usually occurs in the form of spike series. Several action potentials are happening in a quick succession. Whereas Na/K pumps (and other pumps) restore ion gradients to allow processes that take place during an action potential.
Now my question is, what would happen if we completely blocked these pumps and immediately after, we started exciting a neuron? Would the neuron be able to fire a few times before losing the gradients? Or, would one single spike completely diminish the gradients and without restoration by pumps, a second AP would be impossible?

For those who might wonder about the same problem, I've found an answer to my question. During a single AP in the soma, transmembrane currents are so brief in time that only small fractions of the ion gradients are being used up. Theoretically, the cell should be able to exhibit numerous APs before exhausting its ion gradients to the point where it can no longer fire.


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Why does smoking change the human voice?
What happens to the biology of the voicebox of smokers?
Women's voices can change to croaky men's voices, and vaper's voices develop "white noise" content, like a TV set to static, compared to their original voice which is closer to an oboe reed. I am curious why the white noise content and What happens to the voicebox and what happens to the sound of humans that smoke?

Smoke is hotter than air and passes through your vocal cords (before getting to your lungs), irritating them.
Irritation produces inflammation and inflammation produces mucus and general edema that could affect the biomechanics of your vocal cords, especially if you're a seasoned smoker.
The edema of the vocal cords is called Reinke's edema, which is classified as a benign polyp and will definetely make your voice more low-pitched.
I just saw that you added vaping in your question.
Since vape contains irritating chemicals too, I think its effects wouldn't be much better than smoke..obviously it depends on how often you smoke/vape.
Also, check this article:

Significant research has been conducted about the effect of cigarette smoking on the larynx and vocal cords. Several studies also suggest that exposure to electronic nicotine delivery systems can cause cellular hyperplasia (growth of cells) and metaplasia (change in cells) in mucosal lining in rats. It is theorized and likely that the same would occur in human tissue. Another experiment assessed the toxicity of vegetable glycerin, which is known to be harmless in liquid form. Its effects change in aerosol form. The experiment concluded that the substance led to squamous metaplasia of the epiglottis epithelium. Other research shows that nicotine in cigarettes is likely to lead to cancer, including in the mouth and larynx.
If the delicate lining of the vocal cords are exposed to hot, vaporized chemicals, the tissues are likely to undergo change and lose their ability to behave normally. This may produce hoarseness, loss of vocal range, voice fatigue, or vocal injury.

and finally:

These diseases and their effects on the voice can deeply affect singers and other people who use their voice for  a living. The only option to avoid these is to abstain from vaping completely.


text:
Can Coronaviridae mutate into something as dangerous as Flioviridae?
Can coronaviruses mutate to an extent to get as dangerous as fliovirusues such as Marburg viruses, Ravn or Ebola Zaire?

I would say this is rather unlikely. The virus would have to change everything from the cells it infects, probably the way it enter the cells and infects new cells to the mode of action and the genetic material responsible for that.

Please do some research on viruses  (eg read the Wikipedia pages) before posting here. Has the possibility of flu mutating into Ebola virus also been bugging you? Or dogs mutating into wolves?

Corona and filoviruses are far more different than cats and dogs. They are more different than humans and bacteria. If you're concerned about corona mutating into filo, you should worry about your children being single-celled thermophilic archaebacteria. I voted to close this question as lacking in basic research.

@David - Unless the poster edited the post, then the question specifically asked whether Coronavirus could mutate into something 'as dangerous as Fliovirus', not 'into Fliovirus'. This is a perfectly valid question to ask.

@4agalaxy7 — The question is not perfectly valid here because it is ambiguous in this respect and shows no evidence of prior research on virus (molecular) biology. Your literal interpretation is possible, but the lack of response of the poster to my comment suggests otherwise. It is more likely a scare scenario type question demanding reassurance rather than explanation.

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. It is possible, therefore, that some questions about coronaviruses relating to the recent 2019-nCoV outbreak may not receive a satisfactory answer. You may therefore wish to consult this list. of reputable external sources of such information.

As a matter of simple numbers, the current coronavirus is FAR more deadly than the Ebola virus.  At a rough estimate, under 20,000 people have died from Ebola since it was discovered.  So far, almost five times that many have died from Covid-19 in the US alone, and the count is increasing.

Each existing virus can mutate until it becomes ready to affect new species, organisms, cells or whatever.
Coronaviruses too are capable of mutating, so they could become more dangerous.
But can coronaviruses (which cause respiratory tract diseases) mutate into filoviruses (which cause hemorrhagic fevers)?
Of course not.
Filoviridae and coronaviridae are two different families of viruses, like felidae and canidae are two different families of mammals, in the order carnivora.
And you would never ask if cats can mutate in dogs!

'Dangerous' is quite a subjective term, and can be defined in different ways.
Viruses vary in their pathogenicity, which is essentially the ability of the virus to cause a disease in a single individual. This can influence other factors, such as the case fatality rate, which is the proportion of people who die from the disease once they have contracted it. For example, the Ebola virus has a very high case fatality rate of up to 90%.
However, those aren't the only ways in which you could define 'dangerous'. We might also consider the total number of people that the virus can kill. This often isn't a linear relationship with the case fatality rate. Often, viruses with a high case fatality rate 'burn out' before than can inflict a global pandemic, because people die before they can spread the disease on to others. Vice versa, viruses with a relatively low case fatality rate, such as the Spanish Flu (2-3%) can be extremely 'dangerous' and kill millions of people.
But there is no hard and fast rule, as the propensity of a virus to cause a global pandemic is influenced by many, many other factors.
So to answer your question: is it possible for the Covid-19 to mutate into something as dangerous as Ebola? Well, if we are thinking about it's pathogenicity - Influenza A H5N1 (bird flu) had a case fatality rate of about 60%, which is pretty high for a flu virus. For context, the seasonal flu which has a case fatality rate of about 0.1%. I'm not an expert in Virology, so it would be great if someone with more knowledge could confirm this, but it seems very unlikely that the Covid-19 virus could acquire mutations to the degree where it would kill as high as 90% of the people who acquire it, like Ebola does. Ebola is a hemorrhagic virus, which is a totally different mechanism of pathogenicity to the Coronavirus family.
It's plausible that Covid-19 could obtain mutations which allow it to transfer more quickly between humans. For example, we know that the Spanish Flu acquired mutations in hemagglutinin subtype which allowed it to be more transmissible between humans. Generally, Coronaviruses have relatively lower R0 rates than other disease (~2/3 compared to Measles which is 12-18). The total number of people killed by the Ebola outbreak was about 11,000. Covid-19 has already killed ~3000 (although the exact figure is hard to quantify), so it seems like on the global level, Covid-19 will be more dangerous than Ebola, if we consider the total number of people killed.

This does not in any way answer the question.

I don’t think you understand the question.

As I understand it — correct me if I am wrong — your statement that "the Spanish Flu acquired mutations…" means that this strain of flu virus differed from previous or reference strains in containing certain mutations, rather than during the course of the pandemic it underwent mutations that increased its transmissability. i.e Spanish flu differed from the previous year's flu in the way flu does each year. This is important because my reading of the question is that the poster wishes to know whether the currently circulating virus could suddenly become more virulent: now, not next year.


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Evolution history of virus tracing
How do biologist trace evolutionary history of virus, is there any article on this issue,
e.g. how scientist got to know that coronavirus evolved from bat or camel or pig?

The identification is done by sequencing virus samples and comparing them to reference genomes of viruses. By doing this, you can analyze how closely related an unknown virus is to the references.
For the nCoV this method shows it is 96% identical with a known bat coronavirus (see reference 1 for details).
As viruses accumulate mutations due to errors during replication, this method is also used to generate genetic trees of the virus to analyze how it spreads, map routes of infection and also if the virus has been introduced to humans more than once (reference 2 has a nice overview on this topic).
The problem here is: You need to have some known references for comparision, if you have a completely new virus which has never emerged before, this will not help. For this reason there are projects ongoing which collect samples to identify yet unknown viruses (see reference 3)

Discovery of a novel coronavirus associated with the recent
pneumonia outbreak in humans and its potential bat origin
DNA sleuths read the coronavirus genome, tracing its origins and
looking for dangerous mutations
Virome analysis for identification of novel mammalian viruses in
bats from Southeast China


text:
Do mycorrhiza only form with angiosperm?
if not than with which Phylum it forms

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

Mycorrhiza refers to any fungi that forms a symbiotic relationship with a plant. There are many different species, and they are necessary for healthy plant growth in ~70%-80% of vascular plant species with representatives from more than ~90% of plant families. Needless to say, mycorrhiza associations with plants are very common.
What you may be thinking of is rhizobia, which are not as ubiquitous.  Rhyzobia are soil bacteria associated with legumes (peas, soybeans, clover, lentils, etc.). Rhizobia fix nitrogen for the legume, and the legume forms root nodules where the rhizobia live. The nodules provide an ideal location for the rhizobia to live and thrive. This relationship has only been observed in legumes (scientific name: Fabaceae).
In summary:
Both mycorrhiza and rhizobia form Symbiotic relationships with plants. Mycorrhiza are fungus that form relationships with most species of plants. Rhizobia are bacteria that form relationships only with plants in the legume family.