Does DNA contain information beyond protein synthesis? It's well known that genetic information is stored in DNA.  As far as I know, DNA only has information at the protein level.  What about higher levels, such as organelles, cells, tissue, organs? Is there any known carrier of information at that level? If not, what guides those levels of structure?

Hypothesis: Above the protein level, there is no real genotype/phenotype.  Instead, it's all done through cell division.  So, there is no split between information and embodiment.  Instead, it's through a prototype-duplication model: cells grow and split, creating more cells.  As for differentation into different types of cells, and organization into tissue and organs: the information and control systems for that are currently unknown.

What a timely question.

  Does DNA contain information beyond protein synthesis?

Yes. In fact, protein-coding genes only constitute a tiny part – less than 2% – of the whole DNA. There are of course many other genes which aren’t protein coding: there are genes for ribosomal RNA and we find more and more genes which code for small RNAs, such as tRNA. But even if we count all those genes we won’t come above maybe 10% of the total DNA.

Most of the DNA is instead devoted to the regulation of gene expression, most importantly via the binding of transcription factors (but the picture is much more complex than that). With the conclusion of the ENCODE project, a whole slew of papers were published which show that in fact most of the DNA is actively implicated in the binding of various factors (although it’s not known how much of that actually contributed to the cell’s fitness).

But I’ve hijacked your question a bit here. So let’s come back to what you’re actually interested in:

  What about higher levels, such as organelles, cells, tissue, organs?

There is no known mechanism (beyond the already mentioned regulation) which would encode such information in the DNA. Excluding its existence categorically may be hard but given that we haven’t found any machinery which would be necessary to read such information, we can be pretty confident that it doesn’t exist.

  If not, what guides those levels of structure?

The higher levels of organisation are to all appearances emergent. That is, they are a consequence of the lower level organisation. For instance, take the cytoskeleton which carries much of the cell’s physical structure. It is composed of different protein complexes which form spontaneously through assembly of globular proteins (such as actin). The are several ways in which the process can be guided but strikingly it’s largely stochastic – i.e. mostly unguided, and it still succeeds in building a stable skeleton, simply by virtue of molecular properties encoded in the proteins.

I think this is a common theme of cell organisation: the elementary building blocks are encoded by the DNA, and their abundance is tightly regulated. Everything else, i.e. higher-level organisation – follows from that: abundance and localisation of the right proteins.

  As for differentation into different types of cells, and organization into tissue and organs: the information and control systems for that are currently unknown.

In fact, much is known here, and it goes back to regulation on the level of DNA: we know that genes are differentially expressed depending on the cell type and stage of development (and the stage in the cell cycle). This regulation is highly complex and decoding it is a slow process. Nevertheless, the factors involved here are decoded one by one. This is the domain of developmental biology.


Can anyone identify this spider for me, please? I live in Northern Indiana and I’ve seen 3 of these spiders in my house before, all different ones. When I first saw it, it scared me since it’s a pretty big spider in my opinion from what I usually have seen around here. This spider was bigger than a quarter all together. I know it’s not the best picture, but this is it on the wall a while ago. Also was a very fast spider so I couldn’t capture it too well. Are they harmless? I woke up with a bite today and then I remembered this!

The spider on your ceiling looks like a sac spider, more a Cheiracanthiid (like a yellow sac spider) than a clubionid (a leafcurling sac spider).
But the colour contrast of the dark red thorax to yellow abdomen suggests it may be broad-faced sac spider, which a is actually classified closer to a wolf spider than to the above two sac spiders. It is considered non-aggressive and non-harmful to humans.
It is hard to tell from the photo whether the cephalothorax is actually red or just dark. So you are probably the best judge from here.
Compare what you saw to:

trachelas tranquillus (broad-faced sac spiders) https://bugguide.net/node/view/26291/bgimage?from=72
cheiracanthium (yellow sac spider) https://bugguide.net/node/view/3383/bgimage?from=0


Determining the osmolarity and tonicity of a cell Consider a cell with urea concentration inside being 2mmol/L and outside being 2.5mmol/L. The cell itself is permeable to both urea and water. Ignoring the effect of other osmolytes,

A) Urea flows in, water flows out

B) Urea flows in, water flows in

C) Urea flows out, water flows out

D) Urea flows out, water flows in

I'm confused because I thought water would simply flow out of the cell to equate the concentrations inside and outside such that there is no net flow in urea.

The efflux of water isn't instantaneous. Since urea is free to move across the membrane, it will (and with a net movement from higher to lower concentration).


Gene vs Protein homology I am trying to find homologs for some proteins and I am wondering if it is better to find it by comparing the proteins or the coding genes or either is fine.

In most* scenarios you will probably want to look at a comparison of proteins following some additional matching that considers more than a single gene/protein. Luckily, this is a very common problem and one can often look up homologs through existing reference databases such as https://www.ncbi.nlm.nih.gov/homologene

Further, if genes are not present, their documentation will provide a good overview on ways to find homologs in other organisms.

*in some very special scenarios, gene sequences might be more suitable. For instance if one wanted to study similarity of non-coding regions of a gene. However these exceptions would seem beyond the general character of the question.


Does making yogurt from non-pasteurized milk work against possible disease bacteria? In the past, when there was no pasteurization, could making yogurt from milk lower the chance of getting infected by bovine tuberculosis (or other diseases from infected milk)?

For example, would yogurt cultures reduce the amount of "bad" bacteria or create a less hospitable environment for them?

In short, 'No.'

Yogurt, in and of itself, is the product of milk with specific strains of bacteria that are not particularly unique. Yogurt is just as hospitable to harmful bacteria as beneficial bacteria.

The two mechanisms which spring to my mind that would prevent infection by harmful bacteria in yogurt would be the following:

*The already dominant beneficial bacteria outcompete for the harmful bacteria, effectively limiting the capacity for harmful bacterial growth.

*The already present beneficial bacteria create extracellular products which damage harmful bacteria.

The second, if it happens at all, doesn't happen on a scale that I'm aware of. The first could happen, but I highly doubt it. It seems, to me, that it would be more likely to happen in cheese when most of the easy resources have been consumed, which in yogurt they haven't.

Yogurt, and all products stemming from milk, are inherently safer not because of any bacteria that take up residence, but because the mammary glands inside the animal producing the milk are effective filters for a variety of infections. Milk is a product that is constructed in the mammary glands, and the cells are selective about the output. Keep in mind, however, that it is by no means sterile. There are dozens of virii and diseases which can be imparted by breastmilk, and nursing women must adhere to guidelines concerning exposure to medications and diet. It's also possible for DDT and other compounds to become concentrated in breastmilk, resulting in harm to the child.

http://www.breastfeedingbasics.org/cgi-bin/deliver.cgi/content/Drugs/pre_pass.html

So, yes, while milk in and of itself is safer than other options, it is not risk free. A virus could easily infect the mammal or herd producing the milk for sale to humans, and only exhibit dangerous symptoms after the milk had been sold. This is why it's illegal to sell unpasteurized milk for human consumption in most U.S. states.


What is Mendelian Randomization, and how is it used to infer causality in epidemiology? Studies of human traits and diseases are inherently confined to observational studies, known as epidemiological studies. This can make it very hard to determine what actually causes a particular disease or trait, and what is just a by-product or biomarker of the disease.

Mendelian randomization is a statistical technique used by genetic epidemiologists to determine causal effects, for instance whether a biomarker actually influences disease risk, or whether it is just a statistical association.

From basics, how can genetics be used to determine causal associations between traits (such as blood markers) and increased risk of disease, and on what assumptions is this based?

Epidemiological studies analyze human observational cohort data to try to statistically link disease risk and biomarkers. For instance, it is know a well know fact that smoking increases the risk of lung cancer, yet before the 1950s it was widely considered otherwise until observational evidence proved irrefutable (Levin, 1950).

Confounding

However, inferring causality using observational data can be tricky. For instance, there is a very strong statistical association between ice-cream sales and risk of drowning in the UK. In this example it is quite clear that the association is confounded - that is, there is a 'hidden' variable we have not accounted for that links the 2. It is easy to infer that ice-cream sales don't increase your risk of drowning, but the 2 are correlated because both ice-cream sales and risk of drowning increase at the same time of year; both are positively correlated with 'nice weather' traits.

In the above example it is easy to say that the relationship is confounded. However, in a hypothetical study on type-2 diabetes that finds higher blood hematocrit (% volume of blood made up of red blood cells) is associated with increased odds of being diabetic, it is less clear whether higher hematocrit increases susceptibility/risk of becoming diabetic, or whether diabetes increases hematocrit. Longitudinal studies that follow the same individuals for many years help determine which came first - this is based on the assumption that if raised hematocrit is associated with increased risk of diabetes 5 years later, it is more likely that hematocrit is causal, and you have a biomarker for diabetes risk (although you still cannot say it is causal, it may just be a proxy for another 'hidden' trait, or the effect may be mediated by another unmeasured marker).

Causality

Genome-wide association (GWA) studies have become increasingly popular since the completion of the human genome project, and there are currently (15th August 2012) 7039 genetic variants (SNPs, single-nucleotide polymorphisms) documented in the catalogue of published GWA studies (www.genome.gov/gwastudies). These SNPs have been robustly associated with traits such as 'risk of type-2 diabetes', or 'blood adiponectin levels', by large genetic epidemiological studies, usually with many thousands of participants sampled.

The key point about SNP associations is that the direction of effect is always known; a particular SNP may affect your adiponectin levels, but adiponectin does not affect the SNPs you inherit.

Mendelian Randomization

In an observational study that finds an association between (for example) circulating triglyceride levels and type-2 diabetes (using fasting glucose and insulin as 'proxies') it is not possible to determine the causal direction; do triglycerides increase risk of diabetes or vice versa? (This is an actual case study by De Silva, et al. 2011).

Using the assumption that the inheritance of SNPs is essentially random (i.e. not affected by the trait you are measuring - in this example triglycerides) it is possible to determine the causal effect of triglycerides on the risk of diabetes. Note: this is only possible for traits (such as serum triglyceride levels) that have SNPs identified by GWA studies.

First of all, you have already calculated the association between triglyceride levels (in this study a 1 standard-deviation (SD) increase in triglycerides was associated, with an Odds Ratio (OR) of 2.68, with type-2 diabetes in almost 10,000 human participants). Because it is a cross-sectional study, only an association is reported, with no causal implications... yet!

Enter the SNPs

Having identified the SNPs that increase triglyceride levels (at the time of the study, 10 were reported in the literature), each participants genotype for these SNPs needs to be measured or inferred (generally this is performed in large cohort studies, which are then used for many different individual projects).

A combined 'score' is then derived for each individual. This is conceptually very simple; if an individual has 4 of the 10 triglyceride raising alleles, they are given a score or 4, and so on. This is complicated by the fact that the SNPs have different effects on the triglycerides, so a 'weighted allele score' is derived instead (simply put, the coefficient of the SNP~triglyceride association is taken into account when adding risk allele scores). By using this kind of score, a 'per allele' estimation of the effects can be estimated;

The association between the triglyceride levels and the allele score is then determined (by linear regression analysis - adjusted for age and sex, as these are known to affect triglycerides). There are actually 2 ways of performing the next analysis, the first of which is conceptually simpler, but the second of which is more robust.

Method 1: the 'triangulation' approach

The two observed associations calculated so far (per-SD trig. levels are associated with diabetes, and the per-allele SNP score are associated with per-SD trig. levels) can then be used to calculate an expected association. This is simply derived by multiplying the 2 coefficients together. Below is the 'triangulation' representation of this;

This expected association between the triglyceride-raising SNPs and risk of diabetes is only true if raised triglycerides increase the risk of diabetes. The observed association between the SNP-score and diabetes can then be calculated. If the expected and observed estimates are similar, then triglycerides raise diabetes risk, and are a causal biomarker. If the observed association is null (or, at least, much smaller), then triglycerides are likely to be secondary.

Method 2: the instrumental variable analysis

This method is for the more hardy statisticians. Instrumental variables are derived variables, and represent an intermediate between a proposed 'cause' and the 'effect', or outcome (in this case the triglyceride raising alleles are proposed to 'cause' diabetes, and this is mediated by the triglyceride levels themselves).

Using a linear regression, the "fitted values" from a model with triglyceride levels as the outcome, and the weighted SNP score as the only independent variable, are extracted. These fitted values represent the variance in the triglycerides that is predicted by the SNP score. We are using the SNPs as the instrument here, as they directly influence the biomarker (exposure, i.e. triglycerides), and are not affected by either the exposure or the outcome (diabetes). The important assumption here is that the effect of the SNPs on the outcome is not confounded, and can only be mediated by the exposure - this is true for genotypes (Lawlor, et al. 2008).

By then determining the association between the derived variable and diabetes, you will know whether the proportion of the triglyceride variance predicted by the SNPs is associated with diabetes - if so, then triglycerides increase the risk of diabetes.

Results

The study performed both types of Mendelian Randomization analysis and found no evidence to suggest a causal association between triglycerides and diabetes phenotypes.

So Mendelian Randomization is a useful tool for inferring causality with biomarkers. It is not necessarily conclusive evidence, but it can help distinguish biomarkers of particular importance and interest (with regard to interventions) from those that are just markers of the disease.


The alignment of fingers in our hand I noticed that in my hand the index and middle finger are aligned in one direction and the next two fingers somewhat in the opposite direction. My question is, why are our fingers aligned in that way?
Moreover, is it of any evolutionary significance?

For clarity, I am posting a picture of my hand.

This is normal, and the effect is accentuated dramatically if you pretend to be holding an imaginary round object (somewhat smaller than a baseball, for instance.) The fingertips will all approximately point towards the very end of the thumb.

(See upper right image.) If the stone were smaller, the effect would be more visible.)

This orientation of the fingers makes the hand and fingers extremely versatile, being able to grasp and manipulate objects of a wide variety of shapes.

It also allows fine manipulation of thumb and fingers. Touching each fingertip to the tip of the thumb quickly shows the same effect - the fingertips approximately align with the thumb. If they didn't align this way, we would lose some of our very fine (as in requiring great precision, not as in quality) motor skills.

I'm not going to hypothesize on why the hand evolved the way it did; it's very efficient and that seems reason enough.


Why are cell lines frozen in vapor phase? For most of the cell lines I've come across, ATCC recommends storing them in the vapor phase of liquid nitrogen. I'm taking that to mean any place above the level of liquid in the nitrogen storage tank. What is the reason for this? Under what conditions/requirements would one store cells/tissue submerged in liquid?

The storage itself can be done both in the liquid and also in the vapor phase in the liquid nitrogen. Both have their advantages and disadvantages. In my experience there are two main reasons why storage in the vapor phase (although there may be temperature fluctuations when the nitrogen gets low) is recommended.

First, you avoid cross contaminations of your cells lines with mycoplasma (and possible other contaminants) which can get transferred into the liquid nitrogen phase and then into your other cultures. This is not a theoretical danger, but pretty real. See the papers in the reference below.

Then liquid nitrogen will enter your cryotubes (which is also the cause for contaminations). If you use tubes which are not explicitly made for this kind of storage (which is not a problem for the vapor phase storage) then the liquid nitrogen which made it into the tube will expand upon thawing and can cause your tube to explode. This can cause injuries. For more details see here and here.

References:

Risk of contamination of germplasm during cryopreservation and
cryobanking in IVF units.
Microbial contamination of embryos and semen during long term
banking in liquid nitrogen


DNA extraction methods for hair? TLDR: Can anyone state a extraction and isolation method(s) for genomic DNA for hair that will be used for PCR, in detail is preferable since I am a novice.

I tried googling for DNA extraction methods for hair(follicles and/or root) and found various sources, the one that had the most detail involved the use or organic compounds we do not have access to. Is their preferred method of extracting DNA from hair, given that the genomic DNA would be in low amounts, I figure that might have something to do with the extraction process.

I've been trying to figure out something that works for some time.  I have recently tried 3 cheap protocols using commonly available lab reagents.  I was using buccal samples (0.2 ml of spit).

1) Boil the sample in Tris EDTA Buffer
2) NaOH Extraction
3) Direct N Lyse

I compared them to a genomic DNA extraction kit (FAST DNA Prep - MP Biomedicals).

I have heard lots of people use NaOH extraction to get DNA from tissue and cell preps, but none of the first three worked for me after 2-3 tries.  One of the people in my lab said that I could replace the bead beater with vortexing with glass beads.

I tried vortexing with beads with all four methods, including the kit and only the kit worked.  I got a PCR result from control primers.

When you look at the costs of getting all the ingredients for the buffers kits are not so expensive - $1-$2 per sample.

A lot of these kits can handle solid animal tissues, though the one I have doesn't specifically cite hair.  I would try it out.

I guess the point of my post was that there are lots of simple sounding published methods, but they don't always produce results without a bunch of debugging.  I know alkaline lysis has worked for several people I know and is the basis of the kits.  Its pretty simple.

That's my experience anyway.


Is diabetes mellitus a sex-linked disease? There are two types of diabetes mellitus.

a. Type 1 diabetes mellitus
b. Type 2 diabetes melliuts

Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?

Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?

Neither are sex-linked. Type 1 can be directly inherited (in a non-Mendelian fashion), but Type 2 genetic factors mostly increase risks. "Recessive genetic traits" are traits that only express themselves when ONLY the recessive alleles are present in the organism (a dominant allele, if present, will 'overpower' recessive one).

Longer info:

Diabetes mellitus Type 1 (Juvenile Diabetes) is inherited, but it is autosomal with complex dominant/recessive rules:

  Type 1 diabetes is a polygenic disease, meaning many different genes contribute to its onset. Depending on locus or combination of loci, it can be dominant, recessive, or somewhere in between.

That results in some interesting, albeit complex, expressions:

  The risk of a child developing type 1 diabetes is about 10% if the father has it, about 10% if a sibling has it, about 4% if the mother has type 1 diabetes and was aged 25 or younger when the child was born, and about 1% if the mother was over 25 years old when the child was born.

Diabetes mellitus Type 2 does have genetic components, but the vast majority merely increase the risk of developing Type 2 Diabetes. Environmental factors play a large role in Type 2.

  Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60-80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.


Questions about insects eating flour and living in the cracks of a wooden cutting boards I have a large wooden cutting board which is used in my kitchen mainly for preparing egg pasta. The wood type is Populus (poplar or aspen or cottonwood).

The main ingredients used with the cutting board are: flour (mainly soft wheat flour), hens' eggs, white sugar, butter, and baking powder.

After the food preparation, the cutting board is cleaned by scraping away the ingredients remains.

The board has some cracks and some small unknown insects are living inside the cracks.

The board has also a lot of holes due to woodboring beetles but I think the woodworms operated long time ago and they no longer live in the cutting board.

The unknown insect has an approximate length of 1 mm (along the direction of their movements) and a width of 0.3 mm. The unknown insects do not have wings, they just walk. I am not able to see how many pairs of legs they have.

The color of the insect is pale brown.

The cutting board was free from these unknown insects some months ago but then they appeared.

My questions:

What insects are they?
Are these insects poisonous to humans?
How can I get rid of them?

Update

The unknown insects could be Acarus siro, I will try to get a picture of the insects.

Update 2

Here is a picture. The bottom part of the image is a one Euro coin, the top part of the image is a caliper (each bright area is one mm tick).

Some more pictures:

This is a species of psocid (of the family Psocoptera, AKA booklice).

Species are best differentiated by their abdominal structure and antennae. Without a better (more magnified) image and info about the OP's location, identification to species is not possible. Though its small size will definitely narrow the options.
If I had to guess based on the limited detail (and my limited knowledge), I'd say it's a species in the genus Liposcelis or related genera.  See Oklahoma State's ENTOPLP ID key for examples and info. I've included 2 random images of Liposcelis species for reference: the (TOP) is Liposcelis brunnea and (BOTTOM) is Liposcelis corrodens.
You can find info about prevention and removal from Oklahoma state, King's College London or the Orkin man.
UPDATE: Though I, myself, cannot identify this psocid to species, according to this KCL article, Liposcelis bostrychophila is the most likely candidate. [See here for ID notes].

From the KCL article:

Liposcelis bostrychophila is the principal psocid pest species in the UK and in Europe. This single species, which is mainly an inhabitant of households, is responsible for virtually all of the psocid related complaints in the UK (Turner & Ali 1996)...Recent estimates are that 30% of households contain this species.
Several other small (about 1mm long), flattened, wingless liposcelid species (eg. Liposcelis corrodens, L. pearmani and L. brunnea) can become quite common in industrial sites, particularly in the summer months but are uncommon in domestic premises.


What's the mixture of plasma and haemoglobin called I know of oxyhaemoglobin but the mixture of plasma and haemoglobin in the blood gives what?

You and Dr. James must be friends ;)

There is no specific name for the mixture of plasma and haemoglobin, however, when hemoglobin is found in the plasma (i.e. not in blood cells) it is usually referred to as "free hemoglobin." This is a term you are most likely to encounter when dealing with plasma/ serum hemoglobin testing.

Additionally, when haemoglobin is broken down, it forms bilirubin, which contributes to the color of plasma (there is no specific name for the mixture of bilirubin and plasma either, except perhaps "plasma bilirubin").


How to identify the age of a "living" person? An Indian old man claims he is [180 years old] now.

We are not able to tell he is 180 or 181 probably. But can we tell he is 90, 120, 100 or 150?

Different people may age differently.
A 60-year old person may appear to be 80, while somebody else could appear younger than their mathematical age. Some other people may have progeria.

What is the most accurate way to identify a living person's age nowadays?
Are there reliable parameters to measure?

C-14 needs a long time base line. Hence, it is suitable for the bone of dead people.

What kind of method can guarantee it can distinguish a 30y and a 80y old person?  What's the error bar of that method?

The most accurate method known so far may be Horvath's methylation dating algorithm, which uses 353 CpG sites (Genome Biology research article, Nature news article).

From the Nature article, this method was validated with at least one population.

  [After the publication in Genome Biology] Marco Boks at the University Medical Centre Utrecht in the Netherlands applied [the algorithm] to blood samples collected from 96 Dutch veterans of the war in Afghanistan aged between 18 and 53. The correlation between predicted and actual ages was 99.7%, with a median error measured in months.

However, I did not read the original research article and it seems that the dating method works poorly on cancer patients.


Why do an eagle’s feet look ridged? Why are the knuckles of an eagles toes "ridged"?

(I found these pictures to explain.  One was from PBS and the other is one I found on Pinterest):

I circled the parts of the toes/feet I meant in red (from PBS):

The bubbly structures on the dorsal sides of the digits are scutes. Birds retained them from their dinosaurian ancestors. Here is a picture of similar structures on an alligator foot:


How do biological communities at deep-ocean hydrothermal vents migrate between vents? Much interest in the astrobiology community has been generated by the discovery of biological communities populating deep-ocean hydrothermal vents (i.e. "black smokers"). (1) These ecosystems rely on chemoautotrophic bacteria/archaea extremophiles as primary producers living at 40-80 C temperatures.

However, the lifetimes of these black smokers have been estimated to be of order 25 years. How  are these biological communities able to migrate to newer, active vent systems in conditions of extreme cold and high pressure?

(1) Lonsdale, P., 1977, Deep Sea Research, 24, 9

I did some research on the topic and came accross this paper by Johnson et al. I am not a zoologist, so everything I write here is taken from the references paper.

The authors used genetics to estimate gene flow between different populations of limpets Lepetodrilus fucensis which is considered to be an endemic hydrothermal vent animal. They used a mathematical demographic model "isolation with migration" to estimate the migration of the animals across different biotopes.

The vents are distributed along the ridge segments and can be seen as small islands isolated by tens of kms from each other along the same ridge segment and thousands of kilometers between distinct ridges.

The results suggest that there is certain migration between the adjacent vent locations, that means that the flora of one vent can indeed survive the distance towards the next most proximal vent.

So, from now on is my pure speculation. Since the distance between single vents along the same ridge segment seems not be to so high we can suggest that these organisms are capable to resist the pressure and temperature on the ocean bottom while travelling from one vent to another...


What is the philosophical definition of life? How does philosophy define life? And how does it overlap and contrast with the concepts and nuances of other sciences such as biology, chemistry, physics and mathematics?

They ask different questions. Philosophy may ask what is life, is there a purpose behind it, etc. Biology asks how does it work, chemistry what are the chemical reactions that drive it, physics maybe how does physics allow for life and how life utilizes and impacts physics, and mathematics how can life and its components be described mathematically.

It is good to remember that all scientific disciplines branched off from philosophy (and religious philosophy) and that they are interconnected.

This is the answer to the part of your question that includes biology. If you want to discuss the meaning of life philosophically, you are welcome to come to do it on the philosophy page!


Number of genes required to sustain life Are there estimates of the minimum number of genes required to sustain life?

In what I mean by life here, I don't include viruses.

Depends on what kind of life you want!  The Database of Essential Genes lists genes essential for life for a number of species, although I would be wary of some of the numbers; bacterial results are probably more reliable but it lists 118 for humans and 2114 for mice.  There are a bunch of different numbers for different E. coli strains, with larger numbers being published earlier, go figure.

It of course varies by species.  In mid-August of this year, scientists reported the smallest genome yet: 112kb with only 137 protein-coding genes (predicted).  Crazy!  That doesn't mean it's the smallest number of genes though, just what we've found.  Some folks in 2006 predicted the smallest would be 113kb and 151 genes - pretty close close to the above, all in all.

For something a little more familiar and studied, though, Craig Venter has made synthetic biology his goal.  Part of trying to create life is knowing what the bare minimum is.  Working with Mycoplasma genitalium, he and his crew knocked out each gene and found that 381 were indeed essential.


How are lipid-coated mRNA-based vaccines transported into cells for expression? In CNN's video Scientist says Coronavirus vaccine could be ready by 2021 after about 00:25 'Robin Shattock, the Head of Mucosal Infection and Immunity at Imperial College London' says:

We were able to access the sequence that was published by Chinese scientists and made globally available, which was a tremendous thing to do. And we went from that sequence to identifying part of the sequence that encodes for the surface proteins of the virus. And we’re using that sequence to manufacture our vaccine.
We’re using a particular approach where we make a synthetic vaccine based on RNA, so essentially it’s essentially genetic code, we package that in essentially a lipid droplet, and use that to inject in a muscle; it expresses that protein, and the body recognizes that as foreign and it makes protective antibodies.

I'm assuming that the RNA mentioned is mRNA, and so once it reaches the cytoplasm of the vaccine recipients muscle cells it will be expressed and somehow returned to the cells' membrane where it will be recognized as foreign by passing lymphocytes.
Questions:

Is this basically correct as far as it goes?
If so, what causes the lipid droplet to fuse with muscle (or other) cells in the first place?

I can't give an authoritative answer on this because my PhD work was based on mRNA delivery using peptides instead of lipids, but many of the concepts are the same. I also don't have time to provide proper citations, but this is probably too much for a comment.

Anyway, mRNA is a very fragile molecule, it can be broken down extremely quickly in the blood by serum nucleases. Therefore we must protect the mRNA by mixing it with some other chemical, in this case a mixture of positively charged lipids. The positively charged lipids are attracted to the negatively charged phosphate backbone of the mRNA, and form a nanoparticle trapping the mRNA inside and hiding it from the nucleases. The lipids are often, but not always, PEGylated, which means that a molecule of polyethylene glycol (PEG) is attached to the lipid. The PEG groups form a layer on the outer surface of the nanoparticle that helps prevent protein binding.

These mRNA lipid nanoparticles are then injected into a patient. This will probably be an intramuscular injection so that the particles are most likely to be taken up by muscle cells. The exact mechanism explaining why lipid nanoparticles are attracted to cells isn't entirely clear, but it's likely a combination of electrostatic attraction between the positively charged nanoparticle and the negatively charged cell membrane and proteins that bind to the nanoparticle and are then recognized by receptors on the cell surface.

After the particle is taken up by a cell it is usually trapped inside a membrane-bound structure called an endosome. As the endosome matures it is acidified, and as the pH drops from about 7 to about 5.5 the nanoparticle is disrupted. The lipids that made up the nanoparticle can merge with the lipids that make up the endosomal membrane, disrupting that membrane and breaking open the endosome, allowing the mRNA to escape into the cytoplasm.

Once in the cytoplasm the mRNA will find a ribosome and produce protein. Just like you said, the protein in this case will be membrane bound and expressed on the outer surface of the cells for eventual immune recognition.


Heterochromatin production limitations Currently playing with some ideas for a project and needed some guidance. I am wondering, both in Drosophila melanogaster and in general, is the amount of heterochromatin a cell/nucleus can produce limited/consistent or variable?

Does one cell in a D. melanogaster produce a similar amount of heterochromatin as another cell in the same fly or another fly (assuming same conditions - environment etc.) or is the heterochromatin production quite variable? How is heterochromatin production regulated?

Heterochromatin profile is of course different in different cells but I am not sure if absolute heterochromatin content will vary greatly. This DNAse hypersensitivity region data is for human cells but same principles apply to all organisms. If I have to take a guess then I would say that quiescent cells are likely to have more heterochromatin. Heterochromatin production is regulated by different epigenetic mechanisms but I cannot comment (I feel it is unlikely) if there is a mechanism to control absolute heterochromatin content.


Why do we have more male infants born? For every 104 male babies, we have 100 female babies and there are statistics which are more reliable. (Those tell us that we have 997 female infants born per 1000 male infants born.) What is the reason for that? Why do we have more male babies than female babies?

Note: This is based on literature searches I've done a while ago out of general curiosity. I'm in no way an expert on human reproduction.

First, I'm not sure if you are asking about evolutionary reasons or the  developmental causes for for a difference in sex ratio. Here, I will focus on the developmental causes.

There is much evidence for a male bias in human sex ratio at birth (secondary sex ratio), and the ratio have been shown to change over time, e.g. as in 20th centrury Europe after WWI and WWII (see data in Gellatly, 2009),in relation to environmental or parental factors (see e.g. Jacobsen et al, 1999), or between ethnic groups.

A bias in sex ratio can be due to (at least) three different mechanisms (Irving et al (1999)):

deviations in X/Y-ratio of sperm
selection of sperm within the female reproductive tract
biases in implantation success and/or survival for embryos of different sex

I guess that success of fertilization/zygote formation could maybe be considered a separate step (between 2-3). From what I've seen, there is little evidence for explanation one, see tests in e.g. Irving et al (1999) and Graffelman et al (1999). Graffelman et al (1999) also tests for an effect of male age, but do not find support for this idea.

A problem is that it is extremely difficult to study these factors under natural conditions (practically and ethically). Interestingely, there is also evidence for an excess loss of male fetuses in recognized pregnancies (Ingmarsson, 2003, Boklage, 2005), and this would indicate that the sex ratio close to conception is even more skewed towards males than the sex ratio at birth. This is even more curious with the background of an unbiased sex ratio in sperm (explanation 1 above). However, it is very problematic to study what happens in the first part of pregnancies, since a number of weeks have usually passed before the pregnancy is even recognized. I haven't found any papers reporting the human primary sex ratio (sex ratio at conception), which could be affected by factor 1 & 2 above.

Even so, the most likely explanation seems to be a strong bias during embryogenesis, as mentioned in Boklage (2005):

  The usual excess of males is present through pregnancy beyond clinical recognition, but not present at fertilization. The difference, therefore, must arise between fertilization and clinical recognition, through a preferential loss of females during embryogenesis.

The same paper also points out that fewer than 25% of natural human fertilizations go full term (probably even less), and 2/3 of these fail before the pregnancies have been clinically recognized. By back-calculating from the secondary sex ratio and the excess of failed male pregnancies, the sex ratio close to conception has been estimated to 125-135 male:100 female (Pergament et al, 2002))

The exact causes for such a bias during is not entirely known from what I've seen. However, Boklage (2005) mentions a couple of different explanations. For instance, among mammals in general, the earliest stages of embryogenesis proceeds more rapidly in male embryos:

  Since some of the products of these earliest stages are signals from one part of the embryo to another, or from the embryo to the maternal physiology, signals which are required for continuation and maintenance of the pregnancy, the establishment of viable, clinically recognizable pregnancy is correspondingly more efficient in general for male embryos (Krackow, 1995; Kochhar et al., 2003).

The same issue is also mentioned in Ingvarsson (2003):

  Studies in recent years indicate that sex differentiation begins at conception. The SRY gene on the Y-chromosome is already transcribed at the 2-cell stage and triggers growth acceleration in the XY embryos. This accelerated growth is believed to be important for the male embryo as it allows complete testicular differentiation before the levels of oestrogenic hormones become too high as pregnancy progresses.

Boklage (2005) also mentions genomic imprinting and chromosome X–Y segregation as possible explanations for a bias (see references in paper for more).

So, in summary; there is evidence for an male bias in secondary sex ratio (sex ratio at birth), even though there is usually a excess of failed male fetuses in recognized pregnancies, which means that the male bias must be even higher very early in pregnancies. There is some evidence that this might be due to a higher success of embryogenesis of male fetuses, but the evidence isn't strong and the issue is difficult to study.

  The evidence provided by these results is indirect. That is unlikely to change. Ethical, technical and financial considerations argue against the destruction for karyotyping of statistically sufficient numbers of products of natural human fertilizations. Granted, any bias of the sort we seek to discover and understand might, after all, operate differently, or not at all, in sham fertilizations of hamster oocytes, versus oocytes from artificially induced human ovulations, versus naturally fertilized human oocytes. The best evidence we have, or are likely to have in the foreseeable future, indicates that the consistent excess of males observed in human births does not originate in a consistent bias in spermatogenesis or in fertilization.
  (Boklage, 2005)

Finally, it should also be mentioned that the bias in sex ratio at birth can be partially due to sex-selective abortion and infanticide, but to what extent is not entirely known (see Wikipedia: Sex-selective abortion).

You might also find this related question on the heritability of sex ratio interesting: The gender of offspring of Twins?.


Why does ATP contain ribose rather than deoxyribose? I read in a textbook that ATP is made from ribose and not deoxyribose. Originally, I thought that the pentose sugar didn’t have functional importance.

Is there a functional reason why the ATP used in metabolism has to be made from ribose?

Short answer:

The pentose ring does not participate chemically in the energy transfer reactions involving hydrolysis of ATP to ADP.

Enzymes that catalyse these reactions would tend to be specific for ATP (rather than dATP) because they bind the whole molecule and this would most likely include the 2'-OH of the ribose ring. dATP would therefore bind less well or not at all. (There may also be an advantage for evolving such specifity so that dATP could not compete for the active sites.)

The reason that evolution produced ATP as the energy transfer molecule rather than dATP is purely a matter for speculation. One might argue that it is an extra energy expense to reduce the ribose ring, although I prefer a more mundane answer. That is that if one assume RNA genomes (and enzymes) predated DNA genomes evolutionarily, then molecules involved in energy metabolism that contain ribose — not just ATP, but NAD and coenzyme A — arose at that time. When the genomes switched to DNA there was no selective advantage in changing ATP (and NAD) as well, and such an advantage would have been required as the enzyme systems that used these small molecules would by then have been already established.


Risks of latent viruses that reside in ancient genomes under research? Some interesting research in reactivating mammoth genetic material (https://www.nature.com/articles/s41598-019-40546-1) made me wonder what risks are inherent (or are not inherent) in reviving older genomes that may have integrated latent viral code?

Are there potential biohazards in this line of research, where dormant viruses that have otherwise gone extinct (along with the extinct host) and which now may have the potential to be reactivated? Not just in terms of zoonoses that infect across species, but also viruses that infect modern animals that are more closely related or have relatively common ancestry (e.g., from mammoth to elephant).

Could a disease be brought back via this kind of research? Or are the conditions for waking latent viruses from starting material of this kind just not possible to recreate in a lab setting?

Edit: To clarify what I mean by potential biohazard in relation to this question: Experimental conditions result in a latent virus going into lytic phase. The virus is a communicable pathogen; it spreads outside the laboratory environment; it causes sickness or death to living organisms to the extent that it creates a public health, ecological, or other crisis of significance. For background, please also see: Cambridge, The Free Dictionary, and Wikipedia.

First, I don't understand why you are more worried about viruses of extinct species, instead of ancient viruses of species that haven't gone extinct. Clearly the infectious potential of the latter is greater for the current species. I haven't heard a peep in published literature about the dangers of resurrecting mammoth viruses, but surely recreating (in 2005) the 1918 influenza
did stir some fairly substantial safety debates.

In general, working with ancient DNA (aDNA) does require some safety precautions, but mainly because of the risk of contaminating the aDNA (with modern DNA)-.

Furthermore, I'm not aware of any research having resurrected an ancient virus from an extinct species aDNA (your specific scenario), but one ~5-million y.o. retrovirus (dubbed Phoenix) was assembled from current human DNA (in 2006); the authors were a little worried as to its infectious potential, so they engineered it so it couldn't replicate more than once.

More commonly, the genome of less ancient virus strains is being fairly routinely reassembled from e.g. from mummies, skeletons, or even packrat middens in order to study the evolution of common viral diseases. Most of this goes on without any safety controversies, as far as I can tell. Less commonly, ancient viruses of various species are found fairly intact in permafrost which does also stir some safety discussions (regarding the handling of permafrost).

So is your scenario possible in theory? Yes. Are experts worried about it? Not that I've heard...


Physical activity in fasted state: Glucose for brain vs muscles Let's consider this scenario:
You do sports in the morning in a fasted state (i.e. without consuming any calories after waking). Your brain of course needs glucose and your liver probably still has some of it in stock. So it keeps releasing it. Is there a mechanism to prevent the working muscles from consuming the glucose (so that the brain can be supplied longer)? If yes, how does it work?

(Please answer not too technically, so that people outside this area can also understand it.)

In general it is the reciprical action of the hormones of the fed and fasted state — insulin and glucagon — that are responsible for this, together with the differences in hormone-sensitivity of the glucose transporters in muscle and brain. See the accepted answer to this question: During starvation, does the human body do anything to prioritize which organs receive nutrients?.


Nonpancreatic digestion of tryglicerides In an answer about coconut oil I can read

  the digestion of coconut oil does not involve in the Pancreatic digestive enzyme system

In both primary and secondary school I have learned that fat needs to be processed by pancreatic lipase as tryglicerides can not be absorbed.

Are medium-chain tryglicerides an exception (they can be absorbed), are there other (nonpancreatic) lipases in human digestion system, or is the linked answer wrong?

There are two possibilities concerning the further metabolism of MCTs: the glycerides are absorbed and immediately transported through the portal vein to the liver whereupon they are oxidised to release energy.
Alternatively, dependent on the size of the MCT, ranging from hexanoic acid tails to dodecanoic acid tails, it may undergo the standard catalysis by pancreative lipase to form monoglycerides, diglycerides and free fatty acids.

More information regarding the physiological effects of middle-chain fatty acids may be available from: https://academic.oup.com/jn/article/132/3/329/4687297


Why do three nucleotides code for one amino acid? Why not 5 nucleotides? We all know why there are 3-base codons, and why there aren't any 2-base codons. But why is there not a 4-base a 5-base codon?

The more bases there are per codon the more information you can code for. There are only 22 different amino acids, in consequence we need minimum 3 bases per codon.

1 base-codon --> 4^1 = 4 possible codes which are:

A / T / C / G

2 base-codon --> 4^2 = 16 possible codes which are:

AA / AT / AC / AG / TT / TA / TC / TG / CC / CA / CG / CT / GG / GC / GT / GA

3 base-codon --> 4^3 = 64 possible codes which are:

AAA / AAT / AAC / AAG / ACA / ACT / ACG / ACC / AGA / AGT / etc...

4 base-codon --> 4^4 = 256 possible codes which are:

AAAA / AAAT / AAAC / AAAG / AATA / AATC / AATG / etc..

5 base codon --> 4^5 = 1024 possible codes

If we had only 2 bases per codon we couldn't code for all of the possible different amino-acids.

On the other hand there are several costs associated with carrying lots of DNA. It takes space, it takes energy and matter to get copied, it takes time to copy it (generation time might be limited by copying time), … I have just asked this question hoping to make things clear about the possible costs. If there is a cost associated with having a 4-base codon system compare to a 3-base codon system but there is no associated benefit. Such trait (that has a cost with no benefit) are not expected to evolve (counter-selected).

You'll notice that there are 64-22=42 extra possibilities. In consequence the genetic code is redundant. Meaning that several codon codes for the exact same amino-acid. And interestingly, it is often a the last of the three bases of the codon the does no yield to any change in the coding sequence as you can see here.

This post about the evolution of genetic code might interest you.


Does the growth in size of hippocampus of London taxi drivers affect their net number of brain cells? In the paper, London Taxi Drivers and Bus Drivers: A Structural MRI
and Neuropsychological Analysis in the Journal Hippocampus, the authors state that changes in the hippocampus of taxi drivers in London results from their specific occupation. The authors stated this was more pronounced than in bus-drivers.

What accounts for grey matter change? Do their brains have more brain cells than other people? Or the increased in size of the posterior hippocampus means some other region of their brain must have less brain cells to have enough to grow their hippocampus?

The study you linked was very interesting, and there is a reason that the authors of this paper and many others like it refer to grey matter density or grey matter volume.

From another study on grey matter (density), Neurolinguistics: structural plasticity in the bilingual brain,

  Whether grey-matter reorganization in this region is related to changes in neuropil, neuronal size, dendritic or axonal arborization will be revealed by methods other than whole-brain magnetic resonance imaging.

Meaning, there's really no way to know without autopsy and histological studies whether this means more neurons, increase in neuron size, more dendrites, more connections between neurons, etc. So, the answer to your question is, no one knows exactly.

Histopathological studies are usually done on diseased patients (e.g. Alzheimer's), not healthy taxi drivers.

However, one mouse study of loss of hippocampal grey matter did correllate MRI studies and histopathological studies, with the result that

  no changes in the number or volumes of the somas of neurons, astrocytes or oligodendrocytes were detected. A loss of synaptic spine density of up to 60 % occurred on different-order dendrites in the ACC and hippocampus...

Loss is not the same as gain, however, so the definitive cause cannot be ascertained yet.

Stress-Induced Grey Matter Loss Determined by MRI Is Primarily Due to Loss of Dendrites and Their Synapses


Stop codons and exons? If we had a hypotheical gene called gene exampleGene and this gene had 5 exons, labeled A, B, C, D, and E in that order on the chromosome, could it be the case that the stop codon for this gene be on exon D and the exon E still being a exon that would be transcribed in? I can not see this to be true, since If I  remember correctly, transcription stops BEFORE the stop codon, and when stopped, the pre-mRNA is then further processed, but everything after that stop would not be a part of the exampleGene ?

My lazy diagram of how I think of the supposed exampleGene to be:

---A-----B---C---------D(stop codon)-------E---

After transcription via RNA polymerase:

A-----B---C---------D

Take a look at this schematic of a mature mRNA.

[source]

The coding region (ie the part that is translated) is between the start and stop codons, but the 5' and 3' untranslated regions (UTRs) are also transcribed by RNA polymerase; these are part of the first and last exons, respectively. The transcription start site is labelled right in front of the 5' UTR. For the purpose of this answer, transcription termination can be said to occur at the poly(A) signal (the poly(A) tail is added post-transcriptionally, as is the 5' cap).

To be clear, the point I'm hopefully making is that transcription does not involve codons. RNA polymerase does not stop at the stop codon nor does it start at the start codon. In fact, it doesn't even "know" what codons are.


Why would I see no bands in DNA gel electrophoresis of red blood cells? For forensic inspection, you only obtained red blood cells from an individual and amplified for the D1S80 locus in chromosome 1. Twenty nine different alleles of D1S80 have been identified, and 435 allelic combinations are theoretically possible. Approximately 86% of the population is heterozygous at this locus. You set up a PCR reaction for this locus and ran a DNA gel electrophoresis. What would your expected results be based on the described protocol?

A) You would most likely see no bands

B) You would see more than two bands

C) You would see two bands for the heterozygous while one band for the homozygous

D) You would see two bands for the homozygous while two bands for the heterozygous

I thought the answer was C given that heterozygous people would have two bands, one for each allele, and homozygous people would have one band for their one allele. The answer points to choice A for some reason...

It is a trick question. Red Blood Cells (RBC) are anucleated in mammals. You are not going to be able to extract anything about chromosome 1 from RBC.

By the way, if you want to know how they got from 29 alleles to 435 possible combinations (in a diploid), you just have to do 29 + 28 + 27 + ... + 1 = 435.


What percent of the population has some form of synesthesia? Data I am trying to get my hands on:

What types of synesthesia (e.g. Grapheme-color synesthesia,  Chromesthesia, etc.) are most common across the population?
What percent of population has that type of synesthesia?

It would also be great if there's geographical (genealogical) data on what types of synesthesia are more common to what areas.

What percent of the population has what type of synesthesia?

The phenomenon

Synesthesia is a neurological phenomenon in which a stimulus in one sensory or cognitive pathway triggers an experience in another.  Some hallmarks:1

It tends to be developmental, arising early in childhood.
It is involuntary.
It is stable over time (i.e. the same stimulus leads to the same sensory experience).

Epidemiology

The best paper I found on the issue is by Simner et al, 2006.2 The authors first review prior literature on the topic and then describe their own methodology and study addressing the question of prevalence. Regarding prior research:

  Estimates of the prevalence of synesthesia have diverged widely....estimates range from 1 in 4.....to 1 in 25000 - 100 000.

Not so helpful.

They point out some problems with prior studies: one group of surveys relied on self-referral and made the (conservative) assumption that all non-responders to an invitation to participate were non-synesthetes. Another set of studies avoided this problem by questioning every member of a participant pool but established the prevalence only “subjectively” (their wording, although I note that this is an inherently subjective phenomenon!).

Simner's own group used a validated survey questionnaire about specific synesthetic experiences (the specificity and prior validation of this overcoming the  "subjective" aspect in their view). They found an overall prevalence of 4.4% for any type of synesthesia. Importantly, the male: female ratio was not significantly different from 1 in this group, in contrast to many prior studies which have found a marked female predominance, ranging from 2:1 to 5:1 (references in Simner's paper for those interested).

Modalities of experience

To address your question about the types of sensory experience involved, I turn to a more recent review article1 that compiled results from multiple studies. In this report, grapheme-color type synesthesia was most common (86%). These participants see a number or letter and experience a particular color in association. This was followed by followed by time-space type (62%), a group who associates units of time with a particular space relative to their body.  The third most common was music-color type (41%), which is fairly straightforward. The majority experienced more than one type (clearly, given the percentages).

Here is a graph showing the percentage of the cohort who reported particular synesthetic experiences, grouped according to the category of inducer:

Note that the most common type mentioned above, grapheme-color, includes all three of the first categories - "digits," "letters," and  "words" on this graph. Although only the inducers are listed here, the most common associated perceptions were indeed color (97%), followed by spatial configurations (62%). In most cases the color was static (73%) but in some people it moved in a specific direction (16%).

Niccolai V1, Jennes J, Stoerig P, Van Leeuwen TM. Modality and variability of synesthetic experience. Am J Psychol. 2012 Spring;125(1):81-94.
Simner J1, Mulvenna C, Sagiv N, Tsakanikos E, Witherby SA, Fraser C, Scott K, Ward J. Synaesthesia: the prevalence of atypical cross-modal experiences. Perception. 2006;35(8):1024-33.


Can you identify this phyllanthus tree? I have this tiny tree in my garden in Cancun, Q.Roo Mexico.

(More photos available here.)

The little tree started to grow in a planter. I did not pay any attention to it until it grew to 10 cm. It does grow like any bigger tree, starting with one curving branch with regular leaves. I buy unsterilized soil from locals and always get something growing without planting.
It is a phyllanthus plant, but that is all we know so far.
By now I have 20 little ones and one big one, which is a year and a half old.

It certainly is not a phyllanthus Niuri which is an incredible medicinal plant, but with way less "tree attitude" than this one.

This lovely bonsai tree could be unknown to the world, hidden in the deep vegetation of the Yucatan peninsula, one of the world's regions with the highest tree variety.

Can you identify this tree for me?

Phyllanthus caroliniensis

Phyllanthus caroliniensis, the Carolina leaf-flower, is a flowering plant native to the Americas, from the southeastern United States1 all the way to Argentina.2 The flowers are small and located where the leaf meets the stem.2

Kingdom: Plantae
Subkingdom: Tracheobionta
Superdivision: Spermatophyta
Division: Magnoliophyta
Class: Magnoliopsida – Dicotyledons
Subclass: Rosidae
Order: Euphorbiales
Family: Euphorbiaceae – Spurge family
Genus: Phyllanthus L. – leafflower

Sources:

http://plants.usda.gov/core/profile?symbol=PHCA9
https://en.wikipedia.org/wiki/Phyllanthus_caroliniensis
http://www.easttennesseewildflowers.com/gallery/index.php/Summer-Roadsides-White/Seedleaf50001
http://sura.ots.ac.cr/florula4/find_sp3.php?key_species_code=LS001041&key_kingdom=&key_phylum=&key_class=&key_order=&key_family=&key_genus=&specie_name=caroliniensis


Evolution of dominance of alleles Can someone tell me where can I find detailed text about mechanisms of evolution of dominance? Or, if it is possible, I would be grateful if someone will tell me about them here.

Welcome to Biology.SE!
I am not aware of any book that talks extensively about the evolution of dominance. It is a very interesting field of research. You can probably search for papers on the subject that will go much further than my below answer. For example, you may want to read Mayo and  Burger (1996), Bourguet (1999) and Billiard and Castric (2011) I hope that my answer below can provide the ground for more searching by presenting the two main (and of historical importance) hypotheses.

There are several hypotheses about the evolution of dominance. It is important first of all, to note that empirical observations show that beneficial alleles tend to be more dominant than detrimental alleles. There are a number of hypotheses and I won't be able to make a complete review. Among the two main hypotheses to explain the evolution of dominance, one has been formulated by Ronald Fisher and one by Sewall Wright (and J.B.S Haldane).
Fisher's hypothesis
According to Fisher's hypothesis, between two equally beneficial alleles, if one is more dominant than the other than it's heterozygote carrier will have higher fitness. In consequence, beneficial alleles evolve to become more dominant while detrimental alleles evolve to be recessive (so that they can hide from selection in heterozygotes). The main criticism to this model is that selection for dominance is possible only when the locus is polymorphic. This means that the strength of selection for dominance is of the level of the mutation rate, seemingly way too weak to explain the observed pattern of dominance.
Wright's hypothesis
According to Wright's hypothesis, beneficial alleles are more dominant because of the kinetic of biochemical reactions. The rate of a biochemical reaction is a function of the concentration in the substrates of interest. The function is called "Michaelis-Menten function" after the name of the authors. The Michaelis-Menten function looks like this:

Think about a knock-out mutation. Such mutation will decrease by half the concentration of protein the gene in question produce in heterozygotes. Imagine, the concentration of proteins in the wildtype homozygote was 3 (see above graph). The rate of reaction of this homozygote is therefore about 3. The heterozygote would have a concentration of 1.5 and the rate of the reaction is therefore about 2.5-2.75. Assuming that the rate of this biochemical reaction is directly related to fitness, then a the locus of interest, benefical alleles are necessarily dominant and detrimental alleles are necessarily recessive. Selection for dominance is not involved in Wirght's model.
In addition to that, if you have a series of biochemical reactions, you will likely have one reaction that is causing a bottleneck. One reaction that is the limiting factor of the speed of some biochemical pathway. Let's call this reaction process A. If a mutation occurs on a gene coding for any other reaction process B that is not the limiting factor (process A), then this mutation will have no effect on fitness as long as it is not important enough to make process B slower than process A. This may lead to pattern of dominance. I am not quite sure by how much of this has been formulated by Wright and Haldane though.
Is Fisher's or Wright's hypothesis correct?
To my understanding, current state of the art is to consider Wright's model to be correct and Fisher's model to be wrong. In reality, the truth probably lies somewhere in between these two extremes. There exists more detailed (and more mechanistic) models of the evolution of dominance that and the above dichotomy might not be very representative of the current debate on the subject. For example, I (vaguely) remember that during my undergrad, Sylvain Billiard gave a talk at my university in which he reported that some alleles actually have some domain that are directly responsible for decreasing the expression of the other allele on the sister chromosome suggesting that Fisher's hypothesis might sometime be quite a good explanation as well.

This answer was recycled from what I wrote here. But it is a much better fit to your question than to where it was originally posted.


What is the difference between drought resistant non-succulent plants and plants that cannot be allowed to dry out? What features make one plant able to withstand dry spells better than another with relatively similar structure? For instance, one of my Rudbeckias is wilting from drought at the moment, and an Oenothera next to it is not yet showing signs of dryness.

Or like jewelweed (Impatiens capensis), which wilts even while the soil is damp, in full sun, and ragweed (Ambrosia artemisiifolia), which will grow in very dry locations without being phased.

Is it caused by a faster transpiration rate in some plants than in others?

The difference may be related to how the plants fix carbon. While all plants convert CO₂ and H₂O to glucose and oxygen, there are at least three pathways that are used to do it. The C3 pathway is older and less efficient than the CAM and C4 pathways. Many drought tolerant plants use the CAM or C4 pathways because less water is needed. The C4 pathway is better than C3 in drier climates, hotter climates, and when CO₂ or nitrogen are limited. The hard part about this answer is that I'm not a botanist. Wikipedia lists some plants that use C4, CAM, and C3, but there is no comprehensive list, so I can't match up all the plants you mentioned in your question. In general, a higher percentage of monocots, especially grasses, use C4, but a wider diversity of dicots use C4. But you still can't draw conclusions about families of plants, because while corn and sorghum use C4, rice and barley use C3. Ragweed, a plant you say grows well in dry conditions, is a member of Asteraceae, which includes many plants that use C4. However, rudbeckias are also members of Asteraceae, but don't do as well in dry conditions. The C4 pathway has appeared and disappeared in several different plants, making any general claim hard to make. Here are some links that might help:

http://www.en.wikipedia.org/wiki/C4_carbon_fixation
http://www.en.wikipedia.org/wiki/C3_carbon_fixation
http://www.en.wikipedia.org/wiki/Crassulacean_acid_metabolism
http://www.brown.edu/Research/Edwards_Lab/reprints/sage_etal_2011jexb.pdf

If you know more about plants than me, that last link might be helpful, it's about the evolution of C4 pathway in plants and includes lists, but uses the formal species names I just don't recognize.


Does consuming sodium benzoate (preservative E211) cause problems during pregnancy? There seems to be strong evidence to support the claim that sodium benzoate (E211) causes hyperactivity in young children, e.g. Bateman et al. (2004) and McCann et al. (2007).  This leads me to consider whether or not E211 is harmful during pregnancy.

A study by Mowafy et al. (2001) found a slight decrease in survival rates for pups of pregnant rats given sodium benzoate; they also found a more significant drop in mean weight of their pups.

Question: Could the consumption of sodium benzoate by the mother be harmful during human pregnancy? How would this be the case?

References:

Bateman, B., Warner, J.O., Hutchinson, E., Dean, T., Rowlandson, P., Gant, C., Grundy, J., Fitzgerald, C. & Stevenson, J. (2004) The effects of a double blind, placebo controlled, artificial food colourings and benzoate preservative challenge on hyperactivity in a general population sample of preschool children. Archives of Disease in Childhood. [Online] 89 (6), 506 –511.
McCann, D., Barrett, A., Cooper, A., Crumpler, D., Dalen, L., Grimshaw, K., Kitchin, E., Lok, K., Porteous, L., Prince, E., Sonuga-Barke, E., Warner, J.O. & Stevenson, J. (2007) Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial. The Lancet. [Online] 370 (9598), 1560–1567.
Mowafy, A.R., Darwish, A.M., El-Kholy, S.A. & Abdel-Mohsen, S.H. (2001) Effect of food preservatives on mother rats and survival of their offspring. The Journal of the Egyptian Public Health Association. 76 (3-4), 281–295.

There is some evidence to support the idea that sodium benzoate may be detrimental to the development of the foetus:

TERATOGENIC EFFECTS: Classified POSSIBLE for human.
DEVELOPMENTAL TOXICITY: Classified Reproductive system/toxin/female, Reproductive system/ toxin/male [SUSPECTED].

MSDS for Sodium Benzoate
This has been shown experimentally in rats by Minor & Becker in 1971.  They introduced high doses of up to 1000 mgkg-1 intraperitoneally and recorded reduction in foetal weight and "gross anomalies".  Whilst I struggled to find a copy of their original paper, it is referenced in the Catalog of Teratogenic Agents1 (Thomas H. Shepard).
There is some evidence to refute this, however.  The Acceptable Daily Intake limits on sodium benzoate is a maximum of 5mgkg-1, at this dose there is no noticeable effect of exposure. (2,3)  The latter paper by EC food safety standards goes further:

There appear to be sufficient studies to conclude absence of teratogenic potential, with an overall NOAEL* for developmental toxicity of 500 mg/kg bw/day, based on effects on fetal weight.

*(No observed adverse effect level)
So the consensus from the food safety bodies suggests that E211 should not pose harm to an unborn child in the quantities allowed to be present as an additive.

1 Emire, Ronald J. "306: Benzoate, Sodium." Catalog of Teratogenic Agents. By Thomas H. Shepherd. JHU, 2004. 44-45. Google Books. Google. Web. 10 Feb. 2012.
2 Nair, B. "Final Report on the Safety Assessment of Benzyl Alcohol, Benzoic Acid, and Sodium Benzoate." International Journal of Toxicology 20.3 (2001). International Journal of Toxicology. Web. 10 Feb. 2012.
3 Scientific Committee on Food. Opinion of the Scientific Committee on Food on Benzoic acid and its salts. Rep. 24 Sept. 2002. EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL. 10 Feb. 2012


Sextuplet corn (Zea mays with branched ear) In 2019 I planted some sweet corn next to some Hopi blue flint type corn. Of course my mistake was apparent once I started to see the ears. The closer the two types were to each other, the more they were mixed. So this year, not realizing what might happen, I planted the solid blue seeds that I had saved. I don't know much about corn, clearly, and assumed that if I planted blue seeds, I'd get all blue corn. Not the case. Most was all kinds of different colors, shapes, including some kernels that were clearly sweet corn, with most being a field corn, some with a dent, most without. Then some plants had some nice large ears of large blue kernels.
Okay, so that is just the backstory in case it will help. I ended up with this one 'cob' that is actually 6 small cobs all on one stem. Very bizarre, and I can find nothing like this online. I am curious if anyone can tell me how this happened, and perhaps if planting those same seeds would result in more of this. I took a video to get the best look of this oddity. https://youtu.be/xIAYaRwgQ-k

This looks a lot like a ramosa mutant (for example see the ears in panels A,G,H - taken from Figure 2 from Gallavotti et. al. 20101).

Ramosa mutations affect the branching pattern of the inflorescence (i.e. the ear and tassel in maize - aka. corn in the US) and are typically highly variable.  These are thought to be partial reversions to the phenotype of teosinte, which is the putative ancestor of maize2,3.
The unusual ear you collected may have resulted from a spontaneous mutation (possibly transposon driven), but also could be due to infection by a fungus (these sometimes secrete hormones that create developmental effects), or even insect damage to the developing ear.
If this phenotype was due to a heritable mutation you may notice an effect on the tassel (more densely branched), but IIRC this can be quite subtle. The best evidence for this being genetic would be seeing this phenotype recurring in subsequent generations. If possible plant kernels from the strange ear in an isolated area. It is also possible to do controlled crossing in maize — if you go this route I would suggest that you try to self pollinate (i.e. take pollen from each plant's tassel and put it on that same plant's ear).
You also might find this short video to be of interest.
If you get plants with similar phenotypes in this or a subsequent generation I can put you in touch with someone working on ramosa genes who might be interested in having some of the seed if you're willing to share ...
References:
1: Gallavotti, A., Long, J. A., Stanfield, S., Yang, X., Jackson, D., Vollbrecht, E., & Schmidt, R. J. (2010). The control of axillary meristem fate in the maize ramosa pathway. Development, 137(17), 2849-2856.
2: Iltis, H. H. (1983). From teosinte to maize: the catastrophic sexual transmutation. Science, 222(4626), 886-894.
3: Bennetzen, J., Buckler, E., Chandler, V., Doebley, J., Dorweiler, J., Gaut, B., ... & Walbot, V. (2001). Genetic evidence and the origin of maize. Latin American Antiquity, 84-86.


Can proteins move outside cells? I am trying to learn about basic cell biology, and have what is probably an extremely simple question.

So this is how I understand it so far:
Proteins are made from amino acids. This process is called protein biosynthesis, which is carried out by the ribosomes. So proteins are made by the ribosomes in every single cell.

So are the proteins made by the ribosomes to stay in the cell? Or can a protein move to other cells, and if so, what's the reason behind it?

Yes. All proteins actually begin to get synthesized on cytoplasmic ribosomes but if they are going to be used for extracellular purposes, they are tagged and whole ribosome is taken to ER where protein synthesis is completed. The proteins are exocytosed with help of Golgi body, the post office tagging and packaging organelle (the Golgi body packages these proteins into the vesicles that fuse with the plasma membrane).

Examples of this process are: the pancreas secreting insulin for blood sugar control, digestive enzymes for digestion, the immune system telling the body there's a bacterium we must fight it and calls more immune cells (cytokines). Most proteins of course stay in the cell, and are necessary to make the cell or carry out metabolism or DNA transcription.


DAT1 dopamine and cocaine binding I've searched the internet for several minutes and I've looked at DAT but I'm having trouble finding the DAT binding location. Where (and to which aa) does dopamine and cocaine bind to hDAT1?

The following paper answers your question in detail:

  http://www.ncbi.nlm.nih.gov/pubmed/18568020

It seems like the following aa are responsible for the binding, but please refer to the paper for more details:

  Val152,Tyr156,Asn157,Ser422,(Asp79)


What determines the pathway of a neurological signal? My question is about the neurological signals. In our body when a signal, for example a hearing signal from hair cells, is built, it goes through a lot of neurons and it passes a lot of synapses. I am wondering how it doesn't lose it's correct path and chooses the right way to auditory cortex? I mean what are the features of a neurological signal that shows it the correct way?

In other words, how can a neurological signal be created and sent through a chain of neurons to the brain, how can it 'know' when entering a synapse contacting multiple neurons which is the correct one for going through it?

Short answer
Neuronal signals neither choose where to go, nor do they carry routing flags of some sort to guide them. Instead, neuronal signals are guided by the hard wiring of the nervous system.

Background
Neuronal signals (action potentials) basically follow a one-way path. When they encounter a cross roads, action potentials are simply propagated to all of those alternatives. External effects of neurons, hormones or drugs may alter these signals, for example by inhibiting action potential formation or propagation.

To take the example of the auditory system (Fig. 1):

Fig. 1. Auditory system. Source: New York University.

One can readily see that the signal from the hair cells are routed into the auditory nerve to the cochlear nucleus, from there to the colliculi in the brain stem and further up to the auditory cortex via the medial geniculate. Basically this is a one-way, straightforward route.

There is complexity in the system, however. For example, the fibers of the auditory nerve bifurcate on entering the cochlear nucleus and make synapses on a number of morphologically different types of neuron. Each of the latter sends its axon out of the cochlear nucleus with a distinctive projection pattern that gives rise to further divergence. Specifically, some cochlear nucleus neurons project directly to the inferior colliculus, whereas others project to various divisions of the superior olivary complex and nuclei of the lateral lemniscus, which in turn project to the inferior colliculus (Irvine, 1992).

But even in this complexity the divergence is basically generated by simple bifurcations. An action potential reaching such a junction by default simply gives rise to two parallel signals; there is no choice involved. Regulation is due to other neurons targeting these pathways.

Reference
- Irvine, The Mammalian Auditory Pathway: Neurophysiology Springer Handbook of Auditory Research (1992).


Telomerase in tetrahymena In this amazing video, at 26:03 we see this image

We now know that the telomerase contains a sequence complementary to the telomere sequence and so is able to do what it is capable of doing in this image.

My questions : What if we make a piece of dna with  five GGGGG at the 3' end ? Will the telomerase not work, as the RNA in telomerase has the sequence AACCCC and so won't be able to form complementary strand ? If so, has such a mutation been detected in any organism ie it's telomerase is unable to work just because it has a random insertion(maybe during replication) of one of the nucleotides in the telomere at the 3' end ?

This is speculation, as I haven't done or read of the required experiment. However, I imagine that this would not be a problem.

You're right that the RNA template (TERC) would not hybridize with a poly-G sequence, and so the telomerase would not be able to add more telomere repeats. You can imagine that the poly-G sequence is a cap, preventing telomerase activity.

However, without the telomere repeats other proteins are likely to recognize the chromosome end as a DNA break. Exonucleases would likely chew at the end of the chromosome until they got to the actual telomere sequence, which is bound by protective proteins (namely Shelterin). With the poly-G region degraded, the end of the chromosome would now have the true telomere repeats, and telomerase would be able to add even more repeats.

Even if the poly-G region was bound by protective proteins, the telomeres naturally shorten with each replication cycle, due to the nature of 5' to 3' DNA replication. Therefore, the poly-G region would eventually be removed revealing the true telomere repeats and allowing telomerase to extend the chromosome once again.

In a worst case scenario, rather than degrade the poly-G region the cell undergoes recombination between poly-G regions on multiple chromosomes, leading to either massive chromosomes or circular chromosomes. However, I'm sure these cells would die with some kind of massive mitotic failure.


Identify these hinged barbed bones My daughter Stella and I found these bones on the shore of Port Phillip Bay, Victoria, Australia.

The smaller, barbed bone is attached by a hinged joint that allows it to move through just over 90 degrees. The photos show it at its two extreme positions.

The photos include an Australian 20 cent coin for scale (29mm diameter).

Can anyone identify what kind of bones these are, and which species they come from?

I think it is part of a Australian trigger fish skull. check the pictures below, unfortunately someone sawed off most of the spine on the skull photo, but you can see the base of it, it is probably not the exact same species, but it is certainly part of a triggerfish skull. There are a half dozen species in Australia.

Cool find.


What's the maximum and minimum temperature a human can survive? This is a question that has been in my mind since I was a kid. I'm not a doctor, nor even a biology student, just a curious person. What is the minimum and maximum temperature a human body can stand without dying or suffering severe consequences (eg. a burn or a freeze)? While at this subject, how much more global warming will the human body be able to take? Seeing as temperatures keep on rising, I'm just wondering how much longer until the temperature starts having drastic effects.

In my country the temperature is about 35-40-45 degrees Celsius in mid-summer (I live in Romania, eastern Europe, and the climate is supposedly ideal here) which is very unhealthy. Does the human body suffer more and more as the temperatures change?

Hypothermia (when the body is too cold) is said to occur when the core body temperature of an individual has dropped below 35° celsius.  Normal core body temperature is 37°C. (1) Hypothermia is then further subdivided into levels of seriousness (2) (although all can be damaging to health if left for an extended period of time)

Mild 35–32 °C: shivering, vasoconstriction, liver failure (which would eventually be fatal) or hypo/hyper-glycemia (problems maintaining healthy blood sugar levels, both of which could eventually be fatal).
Moderate 32–28 °C: pronounced shivering, sufficient vasoconstriction to induce shock, cyanosis in extremities & lips (i.e. they turn blue), muscle mis-coordination becomes more apparent.
Severe 28–20 °C: this is where your body would start to rapidly give up.  Heart rate, respiratory rate and blood pressure fall to dangerous levels (HR of 30bpm would not be uncommon - normally around 70-100).  Multiple organs fail and clinical death (where the heart stops beating and breathing ceases) soon occurs.

However, as with most things in human biology, there is a wide scope for variation between individuals. The Swedish media reports the case of a seven year old girl recovering from hypothermia of 13°C (3) (though children are often more resilient than adults).

Hyperthermia (when the body is too hot - known in its acute form as heatstroke) and is medically defined as a core body temperature from 37.5–38.3 °C (4).  A body temperature of above 40°C is likely to be fatal due to the damage done to enzymes in critical biochemical pathways (e.g. respiratory enzymes).

As you mentioned burns, I will go into these too. Burns are a result of contact with a hot object or through infra-red (heat) radiation. Contact with hot liquid is referred to as a scald rather than a burn. Tests on animals showed that burns from hot objects start to take effect when the object is at least 50°C and the heat applied for over a minute. (5)

Freeze-burn/frostbite, which is harder to heal than heat burns(6) occurs when vaso-constriction progresses to the degree where blood flow to affected areas is virtually nil.  The tissue affected will eventually literally freeze, causing cell destruction. (7)  Similarly to hypothermia, frostbite is divided into four degrees (that can be viewed on Wikipedia).

As to the matter of global warming cooking us to death, I would imagine that it would be more indirect changes that got us first.  If the average temperature had risen  to the necessary 40°C to cause heat-stroke, sea levels would have risen hugely due to the melting of the polar ice caps.  Crops and other food sources would likely be affected too, therefore I don't think that global warming is overly likely to directly kill humans.


How do carbon 13:12 ratios confirm the biological origin of oldest microfossils? I was reading this article about how Schopf and Valley’s findings in 2017 confirmed that the 3.5 billion–year-old microfossils found in the Apex chert of Western Australia are indeed remnants of living organisms, as opposed to abiotic geological structures. The most detailed part of the article’s explanation is:

Using SIMS, Valley’s team was able to tease apart the carbon-12 from the carbon-13 within each fossil and measure the ratio of the two compared to a known carbon isotope standard and a fossil-less section of the rock in which they were found.
“The differences in carbon isotope ratios correlate with their shapes,” Valley says. “If they’re not biological there is no reason for such a correlation. Their C-13-to-C-12 ratios are characteristic of biology and metabolic function.”

Can someone explain this in more detail? In particular, why should this ratio be different in biological carbon samples, compared to abiotic carbon samples?

Via: https://en.wikipedia.org/wiki/Carbon-13#Uses_in_science

  Due to differential uptake in plants as well as marine carbonates of 13C, it is possible to use these isotopic signatures in earth science. Biological processes preferentially take up the lower mass isotope through kinetic fractionation.

Via: https://en.wikipedia.org/wiki/Kinetic_fractionation

  All organisms preferentially use lighter isotopic species, because "energy costs" are lower, resulting in a significant fractionation between the substrate (heavier) and the biologically mediated product (lighter). As an example, photosynthesis preferentially takes up the light isotope of carbon 12C during assimilation of an atmospheric CO2 molecule. This kinetic isotope fractionation explains why plant material (and thus fossil fuels, which are derived from plants) is typically depleted in 13C by 25 per mil (2.5 per cent) relative to most inorganic carbon on Earth.


Are there examples of encryption in nature? There are examples of mathematics in nature such as Fibonacci number, fractals, etc.  Are there examples of encrypted information?

What I am looking for is a pattern that seems random on the surface, but once you put it through a "decryption" process, it is actually something else.  Not patterns that seem random because they are complex.

One example that comes close is DNA.  But I see DNA as a form of encoding, not encryption.

One example is in the development of the immune system. V(D)J recombination, antibody production, and T-cell receptor production generates a specific "key" that, in most cases, can only be bypassed by that individual's molecular inventory.

In that sense, parasites, mutualists, and commensalists could be viewed as black, white, and grey hat hackers, respectively.

Another example is the organism-specific tRNA synthase inventory and the matching tRNAs.


Is this a deathstalker? I caught a scorpion in my house and wondering if it is a deathstalker? This was caught in Central Asia Northern Tajikistan.

No, it is not a "Deathstalker". The members of the Genus Leiurus are what are commonly referred to as the "Deathstalkers". I do not like using vernacular or common names as they can be too broad in iverlap for multiple species and so to avoid confusion and for clarity utilize Genus and where can be determined species and subspecies. The scorpion you found appears to be a member of the Genus Mesobuthus. While superficially similiar to Leiurus sp., the pedipalps in Mesobuthus are shorter and more bulbous...among several other features.
In 2018 there was a good paper on Mesobuthids in that region. A quick google scholar search should provide you sites for the paper to be viewed at.

Revision of the Mesobuthus caucasicus Complex from Central Asia, with Descriptions of Six New Species (Scorpiones: Buthidae)


Circulating Tumor Cell vs Circulating Tumor DNA I'm a little confused about the wording of these two phrases and under which context the epithelial-mesenchymal transition occurs.

For example:

Is it the circulating tumor cell that releases the ctDNA so that it undergoes EMT?

Or

ctDNA from the CTC somehow creating new instructions for the EMT phenomenon to occur?

I think there is something I am fundamentally confused about and or I am mixing several or different concepts and phenomenon together and would like to get some clarification on this.
Thanks.

EDIT: So this is my new hypothesis / thinking..

So when EMT occurs, CTCs are more likely to develop in the context of cancer, and so when CTCs circulates throughout the blood stream CTCs may be apoptosed of necrosed as a by-product thus leaving ctDNA in the bloodstream and or possibly through out the body.

Is that a correct explanation to my confusion?

I'm not sure the relationship you are trying to build between EMT and cancer cells.

Yes some "healthy" cells undergoing EMT could (due to specific underlying mutations) result in cancer cells but such a phenomenon is not a "hard and fast" rule.

The majority of ctDNA would likely be (as you suggest) from lysed cells, however, should mutations occur that allow for the aberrant export of DNA, then the latter could occur (I would assume this is rare but based on the currently available literature this possibility cannot be discounted).

Thus your "new hypothesis" seems to be the most likely.


Where do lost membrane proteins go after exocytosis? Exocytotic vesicles take away membrane proteins and glycocalyx on the cell's plasma membrane surface. When those vesicles are released into the interstitial fluid and wherever else, where do they go?

Do they stick to the vesicle everywhere? Or do they get removed from the vesicle? If the vesicle fuses into another cell, do those proteins and carbohydrate attachments stick to the new cell?

In the process of exocytosis materials which are about to be released are transported in small vesicles to the plasma membrane. The plasma membrane fuses with these vesicles and this sets the substances free on the outside of the cell. See the figure (from here):

The other possibility for transport vesicles is that they arrive at their target cell and either fuse with the membrane and release the transported substance into the cell or that they are taken up in another vesicle which is then targeted towards the endosome/lysosome. See the figure (from here):

It doesn't matter which way is chosen, the membrane of the vesicle is recycled either by integration into another membrane of by going through the lysosome.


Open Mass Spec Database Wondering if there is an open (freely available) database of Mass Spec Data, particularly for the Substances/Compounds listed in NCBI.

Specifically, I am not sure if NCBI includes the mass spectrometry data / datafiles in their FTP server related to any of their chemicals. So I am just wondering if there is an open database of mass spec datafiles out there somewhere.

The Human metabolome database (HMDB) contains many MS/MS and NMR spectra for human metabolites. You can acquire the spectra from the downloads section. The HMDB includes external identifiers for each compound. This includes the PubChem Compound IDs that are given on the NCBI database. There are 2 265 compounds with LC-MS/MS spectra in the HMDB.

The excellent MS-DIAL software package also comes with extensive positive and negative ion mode LC-MS/MS and GC-MS/MS spectral libraries in flat text format; that's also worth a look.

A lot of the raw spectral data is restricted due to multi party agreements (NIST, chemspider).


How and where do nerves share pathways to the brain? I am interested in understanding how pain receptors send signals to the somatosensory cortex (the part of the brain that registers various nerve signals such as pain, presure, temperatures, etc).

Specifically, I'm interested in whether or not two distinct nerves/receptors share, or don't share, "channels of communication" to the cortex.

For example, say I touch the very tip of my finger to a hot stove, and, say, only 10 "temperature-sensing nerves" are triggered to transmit pain signals to my brain:

Do each of these 10 nerves send 10 distinct signals to my brain, traveling down 10 completely 10 channels?; or
Do each of these 10 nerves send 10 distinct signals to, say, my spinal cord, where they are then combined into 1 large pain signal and forwarded on to the brain?; or
Something else entirely?

Here's an awful illustration of the question I'm asking:

In Scenario #1, both nerves send 2 distinct signals to the brain, and those signals are kept distinct/isolated throughout the course of their entire journey to the brain.

In Scenario #2, both nerves send 2 distinct signals to the spinal cord, but the spine then combines them and only forwards 1 signal on to the brain.

I''m sure in reality it's neither of these scenarios, and is something much more complex. But I'm curious and want to know!

The first layer of sensory integration from neural interconnection lies in the spinal dorsal horns (for somatosensory stimuli), and the spinal anterolateral system (for painful stimuli). It resembles option #2 much more than option #1.

Addenda: Since you are asking a lot about neuroanatomy and neurophysiology, I suggest those 2 beginner books:

Neuroanatomy Text and Atlas, John Martin
Neuroscience, Dale Purves


Is there an evolutionary purpose to armpit perspiration? Given that most Americans seem to do fine using anti-perspirant, it got me wondering: is there an evolutionary purpose to underarm perspiration?  I can't imagine it acts to attract the opposite sex.

Or is it just likely an unfortunate side effect of whole-body evaporative cooling via sweat?

There may be an evolutionary purpose to underarm perspiration, as alluded to in the "hidden hint" link of @DevashishDas, and also hinted at by the answer by @Chris. The apocrine sweat glands of our armpits produce steroids. One group of steroids secreted by the axillary apocrine glands are sex pheromones.  Although we may not consciously notice the chemical odors of sex pheromones, they do likely affect our behaviors.

For example, Wedekind et al. showed that females showed distinct preferences for certain male odors. Women tended to prefer the odors of males that were genetically different at the major histocompatibility complex (MHC) loci, a group of genes associated with our immune response system. Greater genetic variation of MHC genes generally translates to greater ability to combat disease.  Females that select males that are genetically different at the MHC would produce offspring with greater genetic variability at the complex, and therefore more likely to have greater resistance to disease or ability to fight disease.

These results suggest that the pheromones secreted in underarm perspiration is a sexually selected trait in humans. If so, underarm perspiration would have an evolutionary (fitness) advantage.


Why are X-linked illnesses less common in females if females have X-chromosome inactivation anyway? I have read this post but am still slightly confused about this. Do tissues in the human body not all develop from the same cell(s) in the embryo? If so, I do not see how the cell 'mosaic' would be grainy enough to mask the fact that half of the female's cells are not working properly. For example, all liver cells come from the same cell in the embryo which has an inactivated X. In that case, there is a 50% chance that the females liver is dysfunctional. So I would predict that some females would exhibit X-linked disorers even if they are heterozygous, but I haven't heard of this being the case...

Barr bodies (X-chromosome inactivation) don't form in the initial fertilized embryo — it's not that one X-chromosome is inactivated, and then that same inactivation is passed down to daughter cells. Rather, X-chromosome inactivation occurs on a cell-by-cell basis in differentiated cells.  Note how the accepted answer to the question you linked mentions that different cell lineages will have different X-chromosome inactivation patterns — in other words, inactivation occurs later in the differentiation and proliferation processes than I think you might be assuming.

To use your example: the liver cells do not all derive from a pluripotent (undifferentiated) cell with one inactivated X-chromosome, but instead derive from said pluripotent cell, and then undergo X-chromosome inactivation.

Although the jury is out, scientifically speaking, on the mechanisms of selection of the X-chromosome to be inactivated, it's been postulated that some sort of decision-making may occur on this cellular level, resulting in a higher likelihood of inactivating the damaged or deleterious chromosome, if one is present.

Regardless, as the accepted answer to the question you linked mentions, the 50% of functional cells that would result from chance or random X-chromosome inactivation tends to be sufficient for the body's needs.