What are genome wide functional linkages? There are two types of interaction classifications used to describe Protein-protein interactions, namely physical and functional. Whilst physical interactions are obvious in nature and methodological determination, I was wondering what a functional interaction/linkage refers to, such as the one cited in the below paper, and is it purely inferred from genomic data?

"Visualization and interpretation of protein networks in Mycobacterium tuberculosis based on hierarchical clustering of genome-wide functional linkage maps."

Genome wide functional linkages refers to protein in a biochemical or signalling pathway. Inferences of functional interactions can be obtained from methods such as coexpression data from microarray analysis. Since experimental detection of genome-wide protein–protein interactions is costly and time-consuming a computational scope for essentially predictive genome-wide protein–protein interactions is created  [1], which is what the above paper is referring to. As obvious from the abstract of the paper, there are many ways of obtaining the linkages, which are often inferred by the Rosetta Stone, Phylogenetic Profile, Operon and Conserved Gene Neighbor computational methods [2].

Algorithms that identify genome-wide interactions between proteins mainly focus on coregulation of interacting proteins. These methods assume that the genes that are coregulated often occur close to each other on the genomes and show conserved gene order. Thus the genes, which are part of an operon, could be functionally linked.


Are gametes determined by the sex of an organism? In the Wikipedia article for biological sex, I read the following sentence.

  "The gametes produced by an organism are determined by its sex:..."

However, is it not through the gametes produced by an organism that "sex" is defined? Should this sentence be the other way around?

The gametes produced by an organism are determined by the organism's sex - Thus, that statement from Wikipedia appears correct to me. In the case of humans, males have two different sex chromosomes. Thus, males produce gametes with either a Y-chromosome or an X-chromosome (XY). Female humans also have two sex chromosomes, but they are two different X chromosomes (XX). Thus, when females produce gametes they have a single copy of one of the X chromosomes in each gamete. In most cases, a fertilized embryo results and is either XX or XY - in the case of males the embryo gets the Y from Dad and the other sex chromosome is one of the two X's from Mom. In the case of a female the embryo gets the X chromosome from Dad and one of the two X's from Mom.

Here is an image describing what I said above with a link to the page to read more:

Here is a link from a basic genetics course from Dr. Young in the UK that has a more in-depth explanation.

Here is a link to another article from Nature Education that help explain how this works in humans as well as some other organisms that are slightly different.


How are we able to find the specific sites at which DNA binding proteins bind? We know that some DNA binding proteins are site specific, that is they recognise and bind to a specific nucleotide sequence. My question is how can we precisely tell at which sites they bind? Is it the amino acid sequence of the protein? Or is it the repetitiveness factor in case they bind to multiple locations on the chromosome?

I will try to answer the question in the title: how can we know the sites where DNA binding proteins bind?
I'll explain two experimental methods to identify binding sites on DNA.

DNase footprinting
ChIP-seq (Chromatin Immuno-Precipitation with sequencing)

DNase footprinting
We can locate proteins bound to DNA by their ability to protect DNA from some degradation. DNase I cleaves DNA in an almost-random manner and is inhibited by proteins covering ('protecting') the DNA backbone.
In order to locate a site which is protected from DNase I cleavage, we need to take some genomic DNA and treat it. We need separate, short lengths of DNA to examine - we can obtain these from genomic DNA by PCR amplification of different stretches. We need to label these amplicons at one end only, beta radiation is a good choice of label.
Taking one labelled amplicon, exposing it to DNase I for a short time - not long enough for complete digestion - produces cleaved DNA of all possible lengths, which looks like a 'ladder' after separation by gel electrophoresis. Digestion time must be short, such that many DNA are only cleaved once, to have a complete ladder.
Repeating this digestion with your interesting protein present gives a ladder with a missing segment. This is because your protein protects a length of DNA from cleavage.

Important points: DNA is labelled at one end only. Hence we only see the label-end-piece of DNA after cleavage: if DNA is labelled 5' and cleaved in half, we only see 5' halves. Thanks to this, we can estimate the position of the binding site: if our DNA is 100bp and our ladder has lengths 0 to 70bp, a gap, then more from 85 to 100bp, then our binding site is somewhere inside 70-85bp from the labelled end. We can sequence the piece of DNA and read the sequence of nucleotides 70-85.
ChIP-seq
This is a more recently-developed method, which is more suited to studying where a protein binds all over the genome or all over a chromosome. It requires an antibody which specifically binds your interesting protein.
First, a 'snap-shot' of global protein-DNA binding is taken by irradiating cells with UV light, causing covalent cross-links between DNA and binding proteins. Chromatin (DNA with associated proteins) is isolated from cells and chopped up to smaller fragments; the cross-links preserve our 'snap-shot' of proteins and short lengths of their bound DNA.
This mixture is incubated with an antibody (immobilised on beads) which binds our protein of interest. We can separate the antibody-covered beads and hence our protein along with it.
Finally we can sequence the DNA fragments caught in this way. It's like "fishing for binding sequences". The end result is a distribution of where our protein was bound across the genome at the time of our snap-shot.

Ideally the DNA fragments should be long enough to place them uniquely in the genome. There are advanced PCR and sequencing methods which separate DNA fragments in to 'bubbles' in an emulsion containing one molecule of DNA each. In this way, we can sequence all the variants that are present and by counting the number of sequences ('reads') of each type, we have a measure of the abundance of each sequence. This abundance is interpreted as the occupancy of the protein at different binding sites.

Genome-wide studies of DNA binding have shown us that proteins are distributed around the genome. They have preferred binding sites but also have some affinity for similar sites, and spend some of their time bound to non-functional bits of the genome.
Especially in mammals, a 'true' binding site isn't only (and isn't always) determined by having the highest affinity sequence, but also by being clustered with binding sites for other co-factors. This is because, in mammals, proteins often bind DNA, not solo, but as parts of large complexes which can interact with nucleosomes and which allow regulation of transcription or whatever else.

My question is how can we precisely tell at which sites they bind? Is it the amino acid sequence of the protein? Or is it the repetitiveness factor in case they bind to multiple locations on the chromosome?

So, we can tell at which sequences (and where in the genome, even with what relative occupancy) proteins will bind to DNA by experiment. You could try to guess where they bind from their structure, but the way we precisely tell, is by experiment.
The amino acid sequence of a protein ultimately determines its folded structure, and there are many DNA-binding motifs or domains which appear in many different proteins. Some motifs bind the DNA backbone regardless of the sequence of bases, others bind specific sequences.
Let's take zinc fingers as an example. The best-known class of zinc fingers basically inserts an alpha-helix in to the major groove of the DNA double helix, where certain amino acids on the appropriate side of the alpha-helix make contacts with the nucleotide bases. These contacts can be hydrogen bonds, or van-der-Waals contact. (E.g. Histidine and serine tend to hydrogen bond guanine; phenylalanine 'ring-stacks' between As and Ts; and threonine contacts the methyl group of thymine.)

Zinc fingers are often found in arrays in proteins, as you might have been suggesting by "repetitiveness factor". Meaning, a single finger might recognise a specific 3 or 4bp sequence, which isn't very unique. A protein will usually have 3 or more fingers held with regular spacing, so that this string of motifs: ZFa-ZFa-ZFb might recognise the DNA sequence: GCTAxxxGCTAxxxCCAA which is a much more unique site (this is imaginary.)
So yes protein sequence and (thus) structure determines what sites a protein can bind (you can imagine a distribution of affinity for sequences, there will be a 'peak' sequence) - but again some proteins bind the DNA backbone non-specifically, and in mammals they often don't bind alone but within complexes.
People have studied protein-DNA binding by engineering their own arrays of zinc fingers or TALENs, and also by engineering their own DNA binding sites, through a process of 'artificial evolution': selecting the strongest binders, mutating them, and repeat. These kinds of studies might come up with a sort of optimal 'binding code'.


differentially expressed genes of the treated with estradiol samples I did differential analysis on samples treated (G1E-ER4) with estradiol (differentiation induced by estradiol) and control (G1E).
The genes that I gor as differentially expressed in G1E-ER4 showed following pathways.

I can explain the first five: estradiol causes stress and more hemoglobin is synthesized during cell differentiation, also tetrypyrrole is involved in hemoglobin synthesis. Cell death might also be caused by stress induced by estradiol.

However, I am not sure why I have cell division or starvation etc pathways.What is considered to be a starvation actually?

response to stress (GO:0006950)
heme metabolic process (GO:0042168)
tetrapyrrole metabolic process (GO:0033013)
regulation of apoptotic process (GO:0042981)
cell death (GO:0008219), death (GO:0016265),programmed cell death (GO:0012501)

mitotic cell cycle (GO:0000278), cell cycle (GO:0007049)
cell division (GO:0051301),nuclear division (GO:0000280)
cellular response to starvation (GO:0009267)
positive regulation of GTPase activity (GO:0043547)
regulation of localization (GO:0032879)

Pathway analysis can be a little tricky. Because pathway enrichment is estimated from the enrichment of genes (or miRNA or what have you) that participate in overlapping pathways, certain pathways often show up for reasons that may have little to do with your experiment. Cell cycle related pathways, in particular, come up a lot, since so many genes are "cell cycle-related". These papers both go over this phenomenon in more detail. The second one is behind a paywall...sorry for that. If you can't access it, but want to read it, I'm sure we can figure out a way to send a pdf.

I deal with this a lot in my own research. My usual strategy is to make pathway analysis only one part of the overall analysis. How that works exactly depends a lot on the nature of your project. For instance, pathway enrichment could just serve as a sanity check, to see that other results aren't widely off mark. Alternatively, you might want to put other results in the context of some pathway or the other & having pathway enrichment data would naturally be a part of this.

Regarding the question of what exactly starvation means in the context of your results, it's possible that, if this pathway doesn't make sense in the context of your experiment, then it shows up as enriched because more starvation-related genes came up as differentially expressed. The degree to which that means that your cells were undergoing starvation could be debatable. I would bet money that there's significant overlap between starvation-related gene sets and those related to "cellular stress" & "cell death". Cell death is one common response to serum starvation, for instance.

Hope that helps!


Are SNPs always in linkage disequilibrium with other SNPs Is it possible to have a SNP that is not found is be non-randomly associating with any other SNP?

There can be a number of reasons for Linkage Disequilibriunm (LD). Here is a non-exhaustive (non-referenced also) list.

Random LD happens
Epistasis
A recent selective sweep
Hybridization
Population structure
Genetic drift can also create negative LD (see Barton and Otto, 2005)

Of course, in all cases, reduced recombination rate will help to create an LD and to retain it for a longer period of time.


Does Amphibian embryo's blastocoel become a primitive yolk sac without yolk? The mammalian blastocoel becomes yolk sac without yolk according to my professor. I have not found any evidence that such a thing happens in amphibians like frog.

I need to be able to compare and contrast cleavage and formation of blastula in amphibians and in humans.
My thoughts raised another question.
My friend says that blastula exists only when blastocoel exists.

2. Is the thing without blastocoel but with yolk sac the blastula?

Amphibians are produced externally so they do not get proteins and ATP from the mother during their maturation and differentiation. This means that they must have some way to get those things to protect themselves and survive.

The way that they get these things is yolk. Amphibians start to have yolk-filled endoderm during blastulation, [page 9, Gilbert, Developmental Biology].

I am considering the frog here as an example of amphibian. To know that things need energy to survive and that they must get it somewhere, you can deduce this solution. So nutrition and external "hatching" or development outside of female is the key here.

The overall answer to the question:
The organism must have a yolk sac, since it has yolk.

The second question seems to be an idealized one.
Without blastocoele but with yolk-sac suggests me that the blastocoel has developed already to yolk-sac. If that is the case, then I would call the thing gastrula, since for instance some species' ectoderm develops into yolk-sac. I assume that the question refers with "yolk-sac" to complete yolk-sac, not to the developing one during gastrulation.

If it is about developing yolk-sac, I would say that the cell is still blastula but is developing to gastrula. The yolk sac is not ready until gastrulation is complete.


Are human chromosomes connected or separate molecules? Do the 46 human chromosomes form a single unbroken DNA helix?  Or is it rather that a human's genome consists of 46 disconnected helices?

If it is the former, does the common numbering scheme for the chromosomes have any correlation to their actual ordering in the one large strand?

If is the latter, is there a convention on how the chromosomes are ordered in genomic datasets?  Also, is there a clear understanding of how sister chromosomes "find" each other in Meiosis I?

Generally, during periods when Mitosis/Meiosis are not occurring,  what's a good physical picture for how the chromosomes are physically arranged (e.g. a bowl of 46 spaghetti noodles, or maybe the sister chromosomes always stay close together, etc)

thanks!

Each chromosome is a pair of distinct, separate DNA molecules.  A chromosome of an eukaryotic cell nucleus is a (long) helix of two linear molecules and so has two ends, which are called telomeres.  DNA naturally forms a double helix with its complementary DNA molecule, and the double helix can further curl in what are called supercoils.

In humans, the chromosomes occur in 23 pairs (totaling 46). Except for the sex chromosome pair, each member of the pair is identical in appearance in a karyotype (picture) and each such pair has a number assigned from 1 to 22; the numbering generally follows the size of the chromosome, with chromosome 1 being the longest.  In mammals, the sex chromosomes in a male are quite different in size and are labelled X and Y; a female has two identical X chromosomes.


Voltage sensitive dyes technique: What is the underlying measure? I just discovered voltage sensitive dyes technique: first of all what imaging techniques do we use? And I have seen that figures are labeled with ΔF/F0, what does it stands for?

Since these are fluorescent dyes, the most likely method of use is with some sort of fluorescent (likely confocal) microscope. The various types of dyes have different hydrophobic tails, so they target different types of membranes (plasma membrane, mitochondrial membranes, etc.). An excitatory light source (typically a laser, with a single wavelength) is applied to the sample, and the $F_0$ or baseline fluorescence intensity at time zero is measured. When an event happens, such as the contraction of a muscle, the $\Delta F$ or change in fluorescence intensity is measured. This difference is then divided by the baseline, and called the fractional fluorescence (${\Delta F}/{F_0}$). It is plotted like so:

Bu G et al. Biophys J. 2009 Mar 18;96(6):2532-46.


What is the science behind the inaccurate perception of colors? If I go into a green room (all walls are semitransparent and green) and spend some time - around 10+ min - in there, when I come out all my eyes see is white as pink. I see no (or very few other) colors due to this for a while - around 2 minutes. What is the science behind this? Why do eyes lose color perception in this case?

First recall that pink is white minus green, more or less.
Now, your perception can be explained by adaptation: Neurons try to control their gain (amplification factor) to have roughly the same range of output. So if there's a lot of stimuli they like, they will reduce their gain, and vice versa. It can be thought of as a form of fast time-scale homeostasis in this case.

While you were in the green room, your neurons that represent 'green' gets less sensitive to green stimuli due to strong green input (adaptation). Additionally, the 'non-green' representing neurons become more sensitive, since there's less visual stimuli that they like. When you suddenly come out of that room, now the green neurons do not respond as strongly as the non-green neurons in response to white, hence your perception of pink.


At which voltage will the conductance decrease due to the narrow pore in a voltage-gated potassium channel? If you have a voltage-gated potassium channel that do not inactivate, at which voltage would you see decrease in ion conductance related to the narrow path in the pore?

With that said I know that in a solutions with other ions there is a possibility that the high driving force eventually will lead to blockage of the pore by other ions. This is more of a theoretical question.

There is a point where diffusion into the pore can be a limiting factor in the channel's conductance. If the trans-membrane voltage and the recording solution viscosity are high enough, unitary ionic current departs the Ohms law; approaching a plateau. This asymptotic saturation amplitude represents the diffusion limited rate with which ions approach the channel entrance. The bigger the pore entrance, or the higher the ion concentration, or the larger the diffusion coefficient, the higher is the limiting asymptotic current. The pore entrance is measured as the capture radius.

The diffusion limited maximum unitary current (iDL) is directly proportional to the capture radius of the channel ($r_c$):

$$
iDL=2π z e_o r_c D C
$$

z is the valence of the ion, $e_o$ is the elementary charge, C is the bulk concentration of the ion, and D is its diffusion coefficient.

Here you can find a case in which single channel current is not linear with voltage and an example calculation of the capture radius of shaker $K^+$ channel.


The actual name of growth force I see how large trees and weeds that are capable of splitting concrete, and realized that I have no idea what this phenomenon is officially called. Google was no help, suggesting root pressure, but that's an interior force for water and sugar transport, not what I was looking for. Is there a name for the act of plants growing through things like concrete and rocks on their own, independent of weathering?

Turgor pressure is the force within the cell that pushes the plasma membrane against the cell wall.

It is also called hydrostatic pressure, the pressure measured by in fluid when at equilibrium.

It's term taught in biology class in school for plants that sag.

I saw a mushroom that had come through a new pavement once. it was cool.

pascal is the atmosphere at sea level:


Where do the electrons and protons formed from biological reactions go? In a reaction like disulphide bond formation protons and electrons are released. These particles are presumably damaging in high levels. What systems are in place to prevent a build up of electrons and protons?

I've reproduced the diagram that you linked to. It shows the oxidation of a pair of thiols to create a disulphide. What is missing from this scheme is the accompanying oxidising agent. So for example this could be carried out without catalysis in a reaction with molecular oxygen, in which case hydrogen peroxide would be formed. So the electrons and protons have ended up on the oxygen.

In a biological system this oxidation would usually be carried out by an enzyme, in which case the oxidising agent would probably be FAD (flavin adenine dinucleotide) or NAD+(nicotinamide adenine dinucleotide). These are by far the most commonly used redox cofactors. In a typical eukaryotic cell these would end up either (a) being reduced either by the mitochondrial electron transport chain (in which case the ultimate electron acceptor would again be oxygen); or (b) when they were used as a reducing agent in a metabolic reaction.


What is the ratio of breathing rate to heart rate? Breathing rate and heart rate are directly connected. This is because the heart is connected to the lungs via the pulmonary artery.

I first thought that breathing rate would be half of the heart rate since half of the heart cycle occurs in the lungs.

But I know that is not true with a normal 12 BPM(breaths per minute) breathing rate.

So what is the ratio of breathing rate to heart rate?

"This is because the heart is connected to the lungs via the pulmonary artery." It's not like heart rate or breathing rate are regulated by pulmonary arteries. The relation is more sophisticated than that. For example heart rate is controlled by nerves and hormones, and neither comes straight from the lung. But fast breathing leads to changes in blood oxygen and pH, which are picked up by sensors such as the carotid body, which informs the medulla, which then talks to the sinoatrial node. There is also more direct influence, because ample breathing increases pressure in the thorax.

But at each step, there are many other factors interfering, meaning the correlation between the two gets ever looser. There isn't really a "normal" ratio of heart rate to respiration rate. There is a healthy heart rate and a healthy respiratory rate, but they are both wide intervals (60-100 and 12-20, respectively). Dividing one by the other, you get a very wide interval, from 60 beats per minute / 20 breaths per minute = 3, to 100 beats per minute / 12 breaths per minute = 8.

Perhaps in practice the most common values for beats per breath are in a narrower interval. But "normal" values are defined in relationship to abnormal conditions, and there is no disease in which a change in this ratio is a cardinal feature. It makes little sense for clinicians to define a normal range for beats per breath, and therefore it makes little sense for epidemiologists to estimate most common values.


Human Immune Response to COVID-19 Virus I have tried to find an answer to this but have not found anything after multiple attempts.

The question on the table is if the human body is able to produce an immune response to the COVID-19 virus if one has been exposed? This would apply most specifically to persons that have been tested positive but have "survived" (i.e. not having succumbed to the serious lung complications that have caused deaths for some persons).

A follow on question that comes from this is if the human body is able to mount a suitable defense does the current practice of keeping people in quarantine for two weeks allow for this defense to reach full effectiveness?

We probably won't really know for certain until we have time to gather more data from survivors. However, infection with existing coronaviruses (including SARS-CoV, genetically very similar to the COVID-19 virus SARS-CoV-2; ref. https://www.nature.com/articles/s41564-020-0695-z) suggests that those who are infected and survive may develop temporary immunity (ref. https://www.statnews.com/2020/02/04/two-scenarios-if-new-coronavirus-isnt-contained/):

The toll of a seasonal-flu-like coronavirus also depends on immunity — which is also scientifically uncertain. Exposure to the four endemic coronaviruses produces immunity that lasts longer than that to influenza, Webby said, but not permanent immunity. Like respiratory syncytial virus, which can re-infect adults who had it in childhood, coronavirus immunity wanes.
“Everyone, by the time they reach adulthood, should have some immunity to some coronavirus,” said Tim Sheahan, a coronavirus researcher at University of North Carolina’s Gillings School of Global Public Health. But because it doesn’t last, older people can get reinfected. The elderly also have a higher death rate from coronaviruses such as SARS and MERS, a pattern 2019-nCoV is following.
“There is some evidence that people can be reinfected with the four coronaviruses and that there is no long-lasting immunity,” Dr. Susan Kline, an infectious disease specialist at of the University of Minnesota. “Like rhinoviruses [which cause the common cold], you could be infected multiple times over your life. You can mount an antibody response, but it wanes, so on subsequent exposure you don’t have protection.” Subsequent infections often produce milder illness, however.

It might also be possible that someone was infected with two different strains of SARS-CoV-2 and did not develop immunity from the first infection. But it could have also been a continuation of the first infection, or testing error. Without virus sequence data, it was not possible to determine what happened for certain (ref. https://www.wired.com/story/did-a-woman-get-coronavirus-twice-scientists-are-skeptical/):

What could be worse than getting the pneumonia-like illness now known as Covid-19? Getting it twice.
That’s what Japanese government officials say may have happened to a female tour bus guide in Osaka. The woman was first diagnosed with Covid-19 in late January, according to a statement released by Osaka’s prefectural government Wednesday. She was discharged shortly after, once her symptoms had improved. A subsequent test came back negative for the virus. Three weeks later she returned with a sore throat and chest pain and tested again. For a second time, she tested positive for Covid-19.
News reports detailing the case raised the possibility that people may not be developing immunity to the new coronavirus, even after they’ve recovered. But several infectious disease specialists say there’s not enough data to support that conclusion. Another possibility is that the virus subsided and flared up again. (Some viruses tend to do that.) Or the test was simply wrong.

If someone was infected twice, comparing the genomic sequences of the virus over time would have helped determine that with more certainty.


Why does the structure for cellular retinol binding protein show interactions with cadmium ions? A structure of cellular retinol binding protein (1CRB) contains two cadmium ions as ligands. Is Cd2+ a ligand of CRBP and, if so, is that interaction necessary for protein function or is the protein a transporter to remove cadmium? My other thought is that the interaction only appears as a result of the methods the scientists used to determine the structure of the protein.

As far as I am aware, there is no known requirement for Cd in mammalian systems, but it is extremely toxic (Waalkes & Goering).

It would seem that cadmium is required to get crystals of RBP, and its presence is an artifact of the crystallization process (ref):

  Pig holoRBP crystals were obtained at 277 K by the sitting-drop vapor- diffusion method, at a final protein concentration of approximately 8 mg ml ~ and in the presence of 8%(v/v) 2-methyl-2,4- pentanediol, 3mM cadmium acetate, 0.1 M Tris-acetate, pH = 6.8

The only mammalian Cd-binding protein I am aware of is metallothione (ref), which was originally isolated as a Cd-binding protein (ref), and allows safe transport of a highly toxic metal.

Carbonic anhydrase from the marine diatom Thalassiosira weissflogi can use Cd  as active-site metal (typically when Zn is low) and this may explain "the nutrient-like behaviour of cadmium in the ocean" [ref and ref]


How does it make sense to speak of heritability of qualitative traits? As far as I understand, heritability is defined as "proportion of variation of a phenotypical trait due to genetic variation between individuals in a population".

I see the concept is being applied on quantitative that can be measured with numbers, can be compared (i.e., $\mathrm{A}$ is taller than $\mathrm{B}$ by $x$ units of height) and varies continuously to form a distribution (e.g IQ forms a Gaussian distribution).

heritability in the narrow sense ($h^2$) has a mathematical definition. For a given quantitative trait $x$ of a population that forms a distribution with certain average and certain variance $V_P$ then $$h^2 = \dfrac{V_G}{V_P}$$ where $V_G$ is the variance in population due to variance in genetics and $V_P=V_G +V_E$ where $V_E$ is variance in population due to enviromental variation (I ignored other terms in the definition of $V_P$).

IQ has mean of 100 with $h^2=0.8$. So for a person whose IQ is 105 (5 points above average), genetic contribution contributed to this $0.8*5=4$ points difference and the remaining 1 point difference is environment.

I also see how the concept can be applied on qualitative traits (by this I mean traits that don't satisfy the properties of quantitative traits) even in the absence of well-defined notion of variance $V_P$ because the trait doesn't form a distribution. For example in a population of flowers that can only be red or blue.This red/blue trait does not have a well-defined $V_P$. We can still meaningfully say that this trait has $h^2=1$ since any variation in the color (red vs blue) is due to genetic variation. We can also speak meaningfully and say a certain qualitative trait has $h^2=0$ meaning any variation in the trait is due to different environments.

On the other hand, I think qualitative traits can have either $h^2=0$ or $1$ but no value in between, since $V_P$ is not well-defined (and hence $V_G$ and $V_E$ as well are not well-defined) for them.

Consider sexual orientation for example. Based on some twin studies it was estimated that homosexuality has $h^2=0.5$. But what does that mean really? how does homosexuality vary to form a variance? A person is either homosexual or not(heterosexual, bisexual or asexual).

My question is how to apply this $h^2=0.5$ value of homosexuality in the same way I applied it above on IQ?

More generally how to meaningfully be able to interpret heritiability of other qualitative traits (mental disorders for example like schizphrenia with $h^2=0.8$) that has has no well-defined $V_P$ and whose $h^2$ value is not $1$ or $0$ but rather lies between them?

The concept of heritability is a concept coming from quantitative genetics. It only applies to quantitative traits. This does not mean that the trait must be continuous. Discrete traits (such as the number of eyes for example) are quantitative traits.

For boolean traits, it is common to set one outcome to 0 and the other to 1. Which outcome is set to which value does not matter as it won't affect the variance. To take your example of homosexuality, one would classify all individuals as homosexual or heterosexual (with not in between or other variants) and set homosexual to 0 and heterosexual to 1 (or vice-versa) and compute the heritability from there.

As far as I know, for non-boolean nominal traits, the concept of heritability is undefined.


How many smaller muscles compose the interosseus muscle in the human hand? When looking at Wikipedia, I read that the interosseus muscle is actually composed of 3 muscles, but on the French Wikipedia, they talk about a 4th muscle.

So how many interosseus muscle components are there, 3 or 4?

The number of interosseous muscles is not constant, because of the evolutional process continuing in modern generations.

Some individuals have 4 interosseous muscles, other have three, however there are still debates about the subject:

+


Can all animals breathe manually? Originally I was pondering about why we have the ability to breathe manually. I couldn't think of any tangible advantage, given that the body can develop mechanisms to regulate the rate of breathing when needed.

An uncited source (on reddit) said "any animal that can vocalise 'can' breathe manually." Is that true?

Secondly, do non vocal animals, for eg., some arthropods, not have any conscious control over their rate of breathing?

Some mollusks have lungs and can use breath for nest building, defense and diving. They have 100 times less neurons than arthropods.

semi-aquatic insects can control air for going under-water, and some spiders, beetles and spittle-bugs can control bubbles. There are even shrimps that snap at water to produce bubbles.

Fish can hoover and squirt out targets using gulps, without even having lungs, build bubble nests and they also have a swim bladder that they can use to control buoyancy. Human lungs and fish swim-bladders are thought to have evolved from primitive fish that gulp air: https://mainichi.jp/english/articles/20160819/p2a/00m/0na/004000c

It illustrates early vertebrate control of breath-like mechanisms. It's sometimes their main mode of interacting with objects and prey.

Some reptiles hold their breath under water and use bubbles, i.e. iguanas, water anoles and crocodiles. Some reptiles can vocalize, i.e. gecko's : https://www.youtube.com/watch?v=0Q_1KW0Q-10
Scientists don't think that they have much conscious thought.

Amphibians can hold their breath for long periods to swim and use the throat to hoover prey, and most frogs can vocalize: https://youtu.be/y7F0ObBiHio

orang-utans can blow bubble gum, swimming birds and mammals can often do a lot of bubble stuff.

Perhaps the truth pivots on knowing what animal consciousness is, which is amply debated on the web.

Manual involves hands. Consciously and voluntarily involve thought, and those are the words used in biology.

Animal will and conscious reasoning is one of the most controversial topics in science, and scientists still argue both ways, because they CAN argue, and there is no agreed measure of consciousness.


What species of tree is this (found in Navarre, Spain, many tiny flowers)? It was planted within the urban area of Pamplona, Navarre, in Spain. It does not seem like it's native to the area, since no trees like it are found in nearby forests. Its size is of 7-9 meters, while its leaves were commonly 4-5 cm long. It was spring when these photos were taken. It had a great number of tiny, dark flowers. It also showed tumor-like growths where the trunk begins to branch.

[

I believe you are looking at Box Elder, Acer negundo.  It's a North American species but according to Wikipedia it is naturalized in Europe.  If you search online for images, you will see the leaves and flower structures in your own pictures.  Specimens I have seen in my area (Indiana, USA) are very similar to your pictures, even identical, and the trunk is gnarly, as you observed.


The significance of haplotype blocks I looked up haplotype blocks in Google Scholar, and the results returned seemed to show that almost all the relevant articles were published between 2001 and 2009, with almost nothing since 2010.
Why has interest in haplotype blocks apparently waned over the last decade? Has the concept been discredited?

Has interest in haplotype blocks waned over the decade?
No.
You can set a time range on Google Scholar, which the screenshot shows was not done. I did that and:

A search for ‘haplotype block’ from 2000 to 2009 gives 22,000 hits.

A search for ‘haplotype block’ from 2000 to 2009 gives 25,700 hits.

(The term haploblock is now often used as an abbreviation, but it turns out that haplotype block is still much more frequent.)
So I have to conclude there must have been something wrong with the approach adopted by the poster. It is worth mentioning, however, that a Google Books ngram analysis of haplotype block shows first usage in 2000, a peak at 2007 dropping to a approx. 30% of the maximum in 2019. This may just reflect an rush to publish books on a new topic that has subsided, although the rate of publication in journals has been more constant.
What are haplotype blocks, why are they interesting, and how do they differ from haplotypes?
This is illustrated by an interesting paper in a recent (2020) issue of Nature that comes from the work of a large consortium addressing the  question of the adaptation of sunflowers to different ecological niches. This involves the evolution of so-called ecotypes, differing in properties such as flowering time and ability to grow on sand dunes.
The problem is that these adaptations involve many different genes (and hence alleles) which means they involve different haplotypes, according to the definition in Wikipedia:

A haplotype (haploid genotype) is a group of alleles in an organism
that are inherited together from a single parent.

However these different sunflower ecotypes are not physically separated from others, so that one would expect hybridization between them to occur, resulting in the loss of the haplotype and the adaptation. As the paper points out, this problem is actually a reformulation of criticisms of Darwin’s theories by his contemporaries:
Romanes, G. J. “Physiological selection; an additional suggestion on the origin of species.” Zool. J. Linn. Soc. 19, 337–411 (1886).
(although I must admit not to have read the original.)
The fact that this does not happen is because the alleles constituting the haplotype exist in non-recombing blocks — haplotype blocks.

A haplotype block is a region of an organism’s genome in which there
is little evidence of a history of genetic recombination, and which
contain only a small number of distinct haplotypes.

What prevents the recombination of such blocks? It appears that the most come explanation is that rearrangement of the regions containing the haplotype blocks occurs, preventing recombination. One of the easiest rearrangement to understand is simple inversion, two large blocks of which were found on chromosome 5.
The studies in the paper started with two haplotype blocks which had been shown to be involved in the ecotypes shown, and which were found to contain genes previously implicated in these processes, such as FLOWERING LOCUS T and HEAT-INTOLERANT 1. By genome-wide association studies they identified a total of 37 haplotype blocks on the basis of linkage disequilibrium. A diagram of some of these blocks in different sunflower species may wet the reader’s appetite:

So, in answer to the poster’s specific query: The concept of haplotype blocks is very much alive!


Why does anxiety cause diarrhea or constipation? Anxiety sometimes cause diarrhea, sometimes constipation, and sometimes both. It's interesting because it seems their underlying neurophysiology is somehow different. What are underlying physiological processes that lead to these two symptoms in anxious people? Particularly in terms of the activity of sympathetic and parasympathetic nervous system?

Hraish is right about the relationship between emotions and gut-brain axis. Stress hormones released by the brain are responsible for the gut-brain reflexes. Anxiety is related to stress and stress hormones are released when anxiety is expressed by the individual.

Irritable bowel syndrome(IBS)  symptom-based diagnosis, which is having symptoms such as chronic abdominal pain, discomfort, bloating, alteration of bowel habits, diarrhea, constipation etc.

  Irritable bowel syndrome (IBS) is a functional digestive disorder characterized by abdominal pain, bloating and altered bowel habits without any organic cause.

  (Drossman 1999b; Mulak and Bonaz 2004).

  In addition, stress is able to increase visceral sensitivity either at the central and/or peripheral level. (Mulak and Bonaz 2004; Larauche, et al. 2011).

Stress is enabled through the  corticotrophin-releasing factor (CRF) system (CRF, urocortins and their receptors CRF1,2), is a key factor involved in the pathophysiology of IBS.

  Stress is able to modify visceral sensitivity as well as GI motility, permeability, intestinal microbiota, and immunity of the GI tract, all mechanisms that are involved in the pathophysiology of IBS. In addition, stress is able to modulate the hypothalamic pituitary adrenal (HPA) axis and the autonomic nervous system (ANS) which is the link between the gut and the CNS and an imbalance of the ANS is observed in IBS patients. The main brain areas involved in stress are the prefrontal cortex, the limbic system (e.g. the hippocampus and the amygdala) and the hypothalamus. Relations between the prefrontal cortex and the limbic system are important in the management of stress response.
  (Pellissier, et al. 2010a; Mazurak, et al. 2012)

  One of the most common gut related conditions seen
  by GPs and Gastroenterologists is Irritable Bowel Syndrome (IBS), previously known as
  colitis,mucous colitis, spastic colon, and spastic bowel disease.Around 10-20% of adolescents and adults have symptoms consistent with IBS (with females twice as likely as males to report IBS symptoms).
  IBS is associated with 12 months of abdominal pain or discomfort which is (1) relieved with
  defecation; and/or (2) associated with change in stool frequency and/
  or form (i.e., constipation and/or diarrhoea). IBS is also associated with other gut-related symptoms including: bloating,nausea,and excessive gas. Non-gut related symptoms include fatigue, headaches, sleep problems,and pain conditions, such as fibromyalgia.

  Individuals who experience IBS also identify that their gut problems increase doing times
  of stress.Itcan become a vicious cycle-IBS is exacerbated by stress and stress is inturn increased by symptoms of IBS.With anxiety comes increased muscle tension around the gut
  (affecting gutmotility) and activation of the flight fight response, reducing blood in the gut (this is what causes butterflies in the tummy!). These physical changes cause the
  gut-brain to send signals to the brain which in turn promote further stress and distress, most commonly in the form of anxiety.For individuals with IBS (or actually most gut conditions), the ongoing worry about their gut and unproductive patterns can be very
  debilitating. It can also be the starting point for their anxiety
  and/or depression.
  Reference

From the above definitions it is clear that anxiety and brain-gut relationships are valid and IBS is an important reason for gut related disorders when stress is been experienced by the person. Over 10-20 % of adults have symptoms related to IBS, which means a common type of disorder in the general public.

  References

  Stress Affects the Amygdala Activity

  Anxiety and the Brain-Gut-Axis


The 4-chambered heart Birds and humans have a four chambered heart. All animals having 4-chambered hearts are warm-blooded.
Why are crocodiles an exception? Why are they cold-blooded even though they have a 4-chambered heart?

The short answer is crocodiles may be secondarily cold blooded, but the long answer is warm blooded and cold blooded is not a binary condition but a spectrum.

It has to do with how much heat you generate with your own tissue as all organisms generate some heat and gain some from the environment when they can. on one end you have extreme ectotherms (some insects) at the other extreme endotherms (such as arctic mammals) and a huge range between them covering nearly every level of metabolic activty. The ancestors of crocodiles (Crocodylomorpha) were terriestial and highly active and was thus likely near the warm blooded end of the spectrum and thus with a four chambered heart. They actually look like what you would get if you tried to turn a crocodile into a wolf.  But it is believed that as the line that led to modern crocodiles adapted more for an aquatic environment they switched back to a more ancestral metabolism. Although  I should mention crocodiles and esspecally alligators are capable of producing considerable metabolic heat and activity even for prolonged period, more than other "reptiles", comparable to slowest metabolism mammals. they kep many anatomical adaptation to a higher metabolism as they also aid in diving and still benefit their higher metabolisms.


What is the genetic basis of blood type (ABO) system? What is the genetic basis of the A/B/B+/O/etc. blood type system? Are there definitive loci that correspond to each or can multiple different genotypes produce the same antigen profile? Also, is the blood type of a child necessarily one of the blood types of the parents, or can an A/B female cross to A/B male produce a child with blood type O?

I can answer only half your question.

It is not necessary that the child has to have the blood group of parents.
The inheritance is like this :
1.There are 3 alleles Ia , Ib and Io.

2.Ia and Ib are codominant i.e. they will both be expressed if present together.

3.Ia and Ib are dominant over Io. So, blood group O can only be expressed if the genotype is IoIo. IaIa or IaIo is blood group A and IbIb or IbIo is blood group B.

5.IaIb is blood group AB

So in the case of both the parents being AB blood group,the child can not have O group.S/he can have any other blood group.

The inheritance of negative and positive blood group follows simple mendelian inheritance.

Please feel free to correct me!


Are there any effects of elevated Cysteine levels on cognitive function? I'm looking at this diagram of homocysteine metabolism and see two distinct pathways that the amino acid may get metabolized to: with vitamin B12 it gets converted back into methionine, while with B6 it gets converted to cysteine.

I've followed the links for the products that Cysteine gets metabolized to and could not find any references to cognitive effects. Are there any cognitive effects of Cysteine or other amino acids that it gets metabolized to?

I'm interested in learning what are the possible effects of pharmacological (50mg - 100mg) doses of vitamin B6 on this metabolic cycle, while folate and B12 levels stay at the baseline levels. It seems to me that if vitamin B6 is more readily available, there will be a higher chance of homocysteine metabolized into Cysteine. Is this assumption correct? What are the implications to this metabolic cycle that may be caused  by elevated levels of vitamin B6, while keeping folate and B12 at baseline levels?

I'm particularly interested in the implications of this process on dreaming. There has been numerous reports among dreamers that 50-100mg of vitamin B6, taken in the 3rd-5th sleep cycle produces very intense and vivid dreams, sometimes featuring spontaneous awareness (lucid dreams), while B-complex vitamins (B6, B12, Folate, Niacin, etc) appear to produce the opposite effect - very vague dream recall.

I'm trying to understand if there is indeed a connection between the metabolic pathway that homocysteine may take and the vividness of dreams, capacity to recall them clearly and the phenomenon of being able to spontaneously realize the fact that the person is dreaming while still asleep.

Thank you for your input!

Diagram obtained from here

Your shown homocysteine pathway is way too simple. Especially the production of the neuromodulator H2S from excess sulfur amino acids is not shown. In the last years many more enzymes and reactions have been discovered. I have summarized human sulfur amino acid metabolism in reactome.org, so please use this link to discover all the details and new papers. I'll also append some of the relevant papers below.

Brosnan, JT, Brosnan, ME The sulfur-containing amino acids: an overview 2006 J Nutr PMID 16702333

Remethylation of homocysteine to methionine can also happen using betaine as a methyl donor. This reaction is also part of choline catabolism.

Li, F, Feng, Q, Lee, C, Wang, S, Pelleymounter, LL, Moon, I, Eckloff, BW, Wieben, ED, Schaid, DJ, Yee, V, Weinshilboum, RM Human betaine-homocysteine methyltransferase (BHMT) and BHMT2: common gene sequence variation and functional characterization 2008 Mol Genet Metab PMID 18457970

Bearden, SE, Beard RS, Jr, Pfau, JC Extracellular transsulfuration generates hydrogen sulfide from homocysteine and protects endothelium from redox stress 2010 Am J Physiol Heart Circ Physiol PMID 20817827

Dominy, JE, Stipanuk, MH New roles for cysteine and transsulfuration enzymes: production of H2S, a neuromodulator and smooth muscle relaxant 2004 Nutr Rev PMID 15497768

Stipanuk, MH, Ueki, I Dealing with methionine/homocysteine sulfur: cysteine metabolism to taurine and inorganic sulfur 2011 J Inherit Metab Dis PMID 20162368

Chiku, T, Padovani, D, Zhu, W, Singh, S, Vitvitsky, V, Banerjee, R H2S biogenesis by human cystathionine gamma-lyase leads to the novel sulfur metabolites lanthionine and homolanthionine and is responsive to the grade of hyperhomocysteinemia 2009 J Biol Chem PMID 19261609


"Higher plants" or "vascular plants"? What is the difference — if any — between "higher plants" and "vascular plants"?

On Wikipedia, "higher plants" redirects to "vascular plants", which seems like an indication that both terms are essentially the same.

Is one of the terms preferred over the other?

Is one of the terms preferred over the other?

Absolutely: "vascular plants" is the preferred one. "Higher plants" should be avoided. Here is a long explanation:

The Great Chain of Being

This term "higher plants", together with the term "higher animals", is just a remnant of a completely wrong concept that has (or shouldn't have) no place in the world after 1859: the Great Chain of Being, or scala naturae  in Latin.

This is the typical medieval representation of the scala naturae:

The Latin text on the ladder says: stone, fire, plant, beast, man, heaven, angel, god.

And here a more "modern" version of it (but equally wrong):

Unfortunately, this absurdity survived until the late twentieth century, and can be seen even today in some books/sites/lectures.

Linnaean Taxonomy

To understand the use of "higher plants" (and "higher animals") in biology, we have to go back a little in time.

When Linnaeus published his Systema Naturae, he divided the nature (Imperium Naturae) in 3 Kingdoms:

Regnum Animale: the animals;
Regnum Vegetabile: the plants;
Regnum Lapideum: the minerals (you read it right).

Note that, in this classification, "animals" correspond to what nowadays we call animals and protozoans, and "plants" correspond to what nowadays we call plants, algae, fungi and bacteria.

You have to keep in mind that this book was first published in 1735, well before the evolutionary biology being proposed in the XIX century and established in the XX century. Therefore, it is a book published when fixism was the current paradigm, full of mentions to the scala naturae.

So, the plants (as well as the animals) showed a continuum of species, going to the lower plants (the bacteria) to the higher plants (the flowering ones). It's worth mentioning again that, by that time, bacteria were plants: Phylum Schyzophyta, to be more precise.

Thus, we have "lower plants" and "higher plants", "lower animals" and "higher animals", as well as "lower minerals" and "higher minerals"!

Unfortunately, this terminology is so embedded in the biological sciences that even today, as I mentioned, we struggle to get rid of it.

Just drop "higher plants", whatever it means

As your Wikipedia link says, "higher plants" is a synonym of vascular plants. However, there are a lot of problems here:

First, this is a remnant of the scala naturae and, just because of that, should be avoided. Think of it as a meaningless term, just like "more evolved organism".

Second, there is no clear and indisputable definition of what is a "higher" plant. Some authors used to define the "higher plants" as the Angiosperms only, or the seed plants (Angiosperms + Gymnosperms), or the vascular plants (Angiosperms, Gymnosperms and Pteridophyta).

For instance, in lusophone biology books, it was very common a division in three groups:

lower plants: bacteria and algae;
intermediate plants: bryophytes and pteridophytes;
higher plants: gymnosperms and angiosperms.

In those books, "higher plants" doesn't mean vascular plants, but seed plants instead. One could argument that those books use an incorrect definition, but my point here is exactly that the definition of "higher plants" is imprecise and wrong by its very nature: there is no correct use.

In conclusion: the definition of "higher plant" is not precise, and because it's related to a completely wrong concept, its use should be avoided.


What evidence gives clues to the physiological basis for conversion disorder? Conversion disorder has a set of DSM diagnosis criteria, which, among other things, includes ruling out all neurological disease.

However, as the media has shown us (and one could argue a biased portrayal), many of these young people in Le Roy, NY who were diagnosed with conversion disorder have exhibited tics and starts that are highly reminiscent of Tourette's Syndrome, which is thought to have some basis in pathology of the basal ganglia (and perhaps the thalamus and frontal cortex).

Granted, the issue is being looked into as having an environmental cause, so I can understand how the diagnosis may be reshaped, but I'm more curious about the initial diagnosis of "mass hysteria".

If this syndrome causes real physical symptoms and yet is "psychogenic", through what physiological means is the disease acting?  Why would ruling out a neurological basis be a valid criterion?

It's usually important to rule out other medical conditions when considering many psychiatric diagnoses due to similarities in symptoms between them. There are many examples but I'm not sure if it's appropriate to note them here as a lot of symptoms have to be considered in a clinical context and might be mistaken as medical advice. It's also important to note that concurrent medical and psychiatric conditions frequently occur with individuals diagnosed with conversion disorder.(2).

Conversion disorder was previously combined with somatisation disorder and was known as hysteria.(2). Conversion disorder is a diagnosis of exclusion where the symptoms are not a result of:

neurological or other medical condition;
the effect of a substance; or
cultural behavior or experience.(1).

The key is that these are not intentionally or medically driven symptoms but rather physical manifestations of psychological needs ("unconscious manifestations of emotional conflict"(3)). Psychoanalytic theory suggests that "conversion disorder is caused by repression of unconscious intrapsychic conflict and conversion of anxiety into a physical symptom"(2).

In terms of physiological basis of conversion disorder, it's been suggested that an imbalance in metabolism between the dominant and non-dominant brain hemispheres; and impaired communication between the two may be an issue.(2). There are some other points you can also read at MedScape.

Ferri. Ferri's Clinical Advisor. 2012. Mosby.
Sadock. Kaplan & Sadock's Synopsis of Psychiatry. 10th ed. 2007. Wolters Kluwer.
Jacobson. Psychiatric Secrets. 2nd ed. 2001. Hanley and Belfus.


What percentage of Americans have Native Indian ancestry? What percentage of americans have native indian ancestry?

I tried to find the answer online and it's difficult to search for.

I found some averages from 23andme on sciencemag. It doesn't state the figures for all americans, although it says that 8 percent of white americans have some native american ancestry, afro-americans have on average 0.8%, and latino have 18% native american ancestry.


What triggers the switch between aerobic and anaerobic respiration? I understand that when there is a shortage of oxygen cells convert the pyruvic acid from glycolysis to lactic acid to regenerate NAD+. What I don’t understand is how they switch to anaerobic metabolism occurs. Is there a certain chemical message that triggers this?

The simplest method of control of metabolism is by substrate concentration. So if the concentration of NADH and pyruvate is low, lactate dehydrogenase cannot function. When they build up it can and will.

The situation is more complicated than this, because pyruvate will only build up if it is not converted to acetyl CoA by the pyruvate dehydrogenase complex (see Berg et al. section 17.1.1):

Although the overall reaction is oxidative, and ultimately requires NAD+, the latter is not directly involved in the initial irreversible reaction. It is presumably for this reason that the reaction is also controlled, either allosterically (in bacteria) or by phosphorylation (in mammals). In either case the regulators are the small molecules the concentration of which is altered by the lack of oxygen: NAD+/NADH and ATP/ADP. The figure below and its legend is also from Berg et al. (section 17.2.1) — available through NCBI Bookshelf.

[The complex is inhibited by its immediate products, NADH and acetyl CoA. The pyruvate dehydrogenase component is also regulated by covalent modification. A specific kinase phosphorylates and inactivates pyruvate dehydrogenase, and a phosphatase actives the dehydrogenase by removing the phosphoryl (group). The kinase and the phosphatase also are highly regulated enzymes.]

The actual situation is quite complex and this is something of a simplification.


Why are proteins in the insoluble form when they are in frozen water? Why would lowering the temperature of water change the intermolecular forces so much that proteins once soluble in water, become insoluble? I know freezing can create a crystal lattice, but I don't see how temperature would connect to the inter-molecular forces of water? If it even does?

EDIT:  So why would a temperature decrease change how a protein interacts with a POLAR solvent

If proteins change from being water soluble to water insoluble it means that their three-dimensional structure changed, because this determines how the protein interacts with the water. Most proteins have hydrophilic residues on the outside in their normal structure configuration, which makes the soluble. If this changes and some of the hydrophobic residues come to the protein surface the protein may not be soluble anymore.

The process of the structure changing (sometimes also called 'denaturing') can be caused by a lot of different factors - basically everything that is different from the inside of a cell (for humans: ~37°, salt concentrations, ...). If water freezes then the ice-crystal lattice can force the proteins out of their normal conformation/structure, after thawing the ice they may not get their structure back on their own (this depends on the protein).

To give an answer to your edit: the temperature does not affect the solubility directly, the effect is indirect through a change in structure


Core architecture of the body encoding First of all, I am not a biology guy; I am in Computer Science. But, I have a strong interest in all the mysteries of nature, from universe to human body. So, I want to ask a question related to genetics.
As I have read that all(both male's and female's) the biological traits of a person are passed genetically to the offspring(of course assuming the crossing). So if my mom's eye color is blue and my dad's eye color is also blue, I will get blue color too, but what about the core architecture of the body? I mean I have 2 legs at a certain location from my body(my waist but, not from my head!) and similarly other orientations. Why they are that certain way? If they somehow got changed, would the resultant body be stable?Is the answer different in case change is artificially engineered or natural?
Where is this core architectural information exactly stored(If the answer is DNA then how?) and in what form is it stored?How come that information is not changed in thousands of years or even millions of years? And is that information of such nature that it contains "exact" steps to develop a healthy say, brain structure(which is a really complex)?
My another question is: If there is a community of mutated people, will their offsprings be mutated always with 100% certainty?

I know these are a lot of questions but you can see that, they basically revolve around the information that I am curious about. Can someone address my curiosity?

Welcome to Biology.SE!

Your question is very broad. Also, your post has the default of containing severals questions in it. Make sure in the future to restrict your post to only question, it will be much more likely that you receive a good answer then. I hope that I can give some indications about how to get some more knowledge in this answer. In this answer, I do not consider all your questions one by one to answer them (or guide you to the answer) but I think that all your questions will get an answer as you learn more about the subjects I cite. Hope that answer will help you.

Very basics of molecular genetics

You should start to have a few ideas about genetics. Make sure you know what is a chromosome, a gene, an allele, a protein and a phenotype. Wikipedia will help you with that. Come back on Biology.SE if something seems unclear to you.

Basics of genetics and evolution

You are definitely interested in concept of segregation. This is a very fundamental concept in genetics. The basis of the laws governing segregation has been first discovered by Gregor Mendel and we still name these basics laws after Mendel. We talk about Mendelian segregation. You may want to google that.

Then you are interested in the concept of heritability. I have been talking about heritability in different posts. In the third sentence of my answer here, there is a short list of posts that define the concept of heritability.

Eye color you said?

You talked about the genetics of eye color inheritance. Here is a post that will interest you then.

The Genetics of Development

Your question is not only about genetics but is about the genetic of development. You may want to have a look to the basics of developmental biology. The most famous DNA sequence  involved in determining the body plan of many different living things are the so-called homeobox. There is plenty of interested things about this homeobox. This post may interest you btw.

Rough details about the evolution of development along the tree of life

  How come that information [architectural information] is not changed in thousands of years or even millions of years?

It really depends on what you call architectural information. But in any case it does evolve. If you think of things such as like size of an animal. Then it may evolve fairly quickly. You may thing of more important change, such as evolving a new pair of legs or evolving wings or a head, then it tends to take more time. Below are just a bunch of examples of how animals differ in terms of body plan along the tree of life.

You might be interested to study a bit the development or early animals. Some have a radial symmetry while other (like us) have bilateral symmetry (see wiki). Some animals have a head, some don't. Some animals have two dermes while others have three dermes. The Deuterostomata (vertebrates, tunicates, echinodermes, ...) have a development where the blastopore of the gastrula becomes the anus while in the protestomata (now thought to not be monophyletic and divided into ecdysozoa and lophotrocozoa (see here)) the blastopore becomes the mouth. Among the arthropoda (insects, spiders, millipedes, ...) the story is very interesting as well. Some have a highly segmented body with a pair of legs at each segment (millipedes) while other groups have fused those segments. Spiders have only two big body parts, while insects have three big body parts. In insects, the thorax (one of the 3 body parts with the head and the abdomen) contain three segments and each segment hold a pair of legs. The first flying insects also had three pairs of wings, now degenerated into two and even into one in Diptera.


What is the most genetically simple organism except viruses? What is the most genetically simple organism (except viruses) on this planet?

By simple I mean the least number of genes.

Mycoplasma genitalium was one of the first full bacterium genomes sequenced and since its a symbiotic organism that lives on the moist and warm genital skin surface it doesn't need as many genes as many bacteria.  It has a 582 kbp genome sequence with only 521 genes.

But that is so 1995.

The 159 kbp genome of Candidatus carsonella was published in 2006. It is thought to only contain 182 genes.  Its an endosymbiont of some sap eating insects.

But the current record holder, published this year, is Nasuia deltocephalinicola, discovered survey of insect endosymbionts, has only 112 kbp in its genome. Smaller than some viruses.  It's thought to contain 137 protein coding genes with 29 tRNA genes, so its not a lot smaller than Carsonella in terms of gene count.

There's no reason to expect that this is the minimal viable genome by any means.  I'm sure this response will need revision in a year or two.

M. genitalium has become the model system for minimal genome work.  Many of these other bacteria might be difficult to culture, molecular biology lab techniques might have to be developed, so hopping onto newly discovered bacteria isn't always the best idea from a standpoint of producing science.  It does suggest that M gentalium doesn't need all of its genes!  A possible cause for these extra genes might be a more complex immune response in human beings where its found.  It might also be because of the symbiotic requirements of insects is simpler.


Why are spiders afraid of flies caught in their web? I recently noticed a fly got caught in a spider web in my house. The fly was very energetic and, even though caught, continued to flap it's one wing (which I think might have been partially free) with hyper-speed.

Initially I thought it was just trying to get free from the web but then I noticed that when the tiny spider (it was smaller than the fly) approached it to, presumably, try to inject its venom the fly started to again energetically flap it's wing and it scared the spider off.

I was wondering - why did the spider got scared? I know animals do not perceive threats quite like us and even a big lioness might give way to a tiny mongoose if the mongoose threatens with a fight (I'm guessing both because unnecessary fighting expends precious energy and any wound can be bad with no hospitals around) but still as far as I know the fly can't harm the spider in any way even if it is free and much less when it is bound and while it would be smarter for the spider to just sit and patiently wait for the fly to drop out of exhaustion he is also risking it getting free, eventually.

So why are spiders scared of flies caught in their web?

from https://www.researchgate.net/figure/234696071_fig5_Figure-1-Differences-in-attack-strategies-upon-safe-and-dangerous-prey-in-orb-web

The linked article is pretty cool.  Bottom line: predators need to be careful.  If they get hurt they cant hunt and they starve.  Spiders have different strategies depending on perceived dangerousness of a prey item.  The linked article, for example, categorizes dipterans (flies) as nondangerous to spiders but orthopterans (crickets) as dangerous.  How are crickets dangerous?

For your spider I can think of 1 of 3 things.

1: Fly is dangerous to spider in a way not obvious to you.  Maybe it is poisonous, or can bite, or has sharp spines on the leg.

2:  Fly is perceived by spider as similar to dangerous prey.  I have watched spiders address wasps in their webs and the spiders are careful.   If there are flies that mimic the appearance of wasps / bees to get respect, why not one that behaves in the web like a wasp to get respect?  A cool idea and testable too.

3:  What you see is the danger.  A big fly thrashing around might be enough to damage the spider.  A spider not desperate for food might not want to risk getting hit.  Spiders are not that durable.  That makes sense to me.


Do vitamin enriched foods preserve their value when exposed to higher temperatures? At what temperatures do different kinds of vitamins are destroyed or lose their nutritional value?

Imagine you went to the store and bought vitamin enriched cacao powder. Then you made yourself a hot drink by pouring boiling water. How much in general(approximately) vitamins were destroyed by that heat.

"How to prepare/cook" usually doesn't have this kind of information. Thus any benefits of vitamins are lost(?).

Here's one estimation about how much vitamins or minerals can get lost due to various "food processing" (cooking, drying, freezing) methods:

According to NutritionData, cooking can result in a loss of vitamins:

Vitamin A: 25%
Vitamin C: 50 %
Vitamin B complex vitamins: 25-70%
Minerals: 25-70%; most important: potassium loss in cooking water. In this study with potatoes:

  Leaching alone did not significantly reduce levels of potassium or
  other minerals in tubers. Boiling tuber cubes and shredded tubers
  decreased potassium levels by 50% and 75%, respectively.

According to USDA retention factors, the following vitamins are most affected by food processing:

Vitamin C
Vitamin B1, B6, B12 and folate

Vitamin and mineral loss is related to both the temperature and time of cooking.

Mineral loss can be prevented by cooking in vapour (steaming) instead of cooking in water.

According to this source, the following can be loses after heat treatment at 70 °C and (90 °C):

Vitamin A: 10% (30-40%)
Vitamin D: 15% (35%)
Vitamin B1: 15% (50%)
Folic acid: 5-20% (45%)
Vitamin C: 40% (85%)


Is there an adhesive that could used for larval fish? I am currently working on an experimental design that requires a larval fish (~ 4mm long) to be affixed on a metal wire tip on its dorsal side. Now, I was thinking of a glue or adhesive to do the job, but it doesn't have to be strictly these, anything that sufficiently attaches the fish to the metal wire tip would do. The glue/adhesive would have to work well on wet surface and, ideally, something that is not toxic. Any advice or ideas are welcome.

You could try methyl cellulose, which my lab and others use. It's not exactly an adhesive, but it is quite viscous. It's common enough that it's in the Zebrafish Book: https://wiki.zfin.org/display/prot/Methyl+Cellulose+Mounting . Obviously, be sure whatever you do is approved by your animal care and use committee.


Geographic regions as subpopulations/demes I am developing a computational simulation for DNA barcoding. One of the parameters in my simulation is the number of subpopulation/demes, which I label as $K$. Most studies that use DNA barcodes tend to focus on a single geographic region.

My question is: is it valid to presume that a single geographic region is equivalent to a single subpopulation/deme?

For example, if the focus was on cichlids of Lake Malawi, would it be a safe assumption that Lake Malawi comprises a single subpopulation/deme?

Eventually, I would also like to incorporate migration rates into my simulation, but these are very difficult to estimate without accurate data on $F_{ST}$.

Any insight would be most helpful and is warmly welcomed.

It is impossible to answer your question in the general sense. Yes, detailed population structure may matter. It very much depends upon what your question is and what parameter space you are willing to answer but it is possible that assuming panmixis would be unrealistic.

Note that accurate data on $F_{ST}$ won't suffice to estimate migration rate $m$.

Note also that many simulation platform already exist and you might not have to reinvent the wheel (see Sequence evolution simulation tool).


Does the genetic sequence of SARS-CoV-2 end with 33 A's? Looking at the DNA (or RNA?) sequence of the Covid-19 virus here: https://www.ncbi.nlm.nih.gov/nuccore/MN908947.3

I notice it ends in 33 a's. Does the virus really look like that, or is it some artifact of the sequencing process, or some sort of padding to round out numbers?

Here's the last few lines:

29761 acagtgaaca atgctaggga gagctgccta tatggaagag ccctaatgtg taaaattaat
29821 tttagtagtg ctatccccat gtgattttaa tagcttctta ggagaatgac aaaaaaaaaa
29881 aaaaaaaaaa aaaaaaaaaa aaa

This is a poly(A) tail, which is a feature found in the majority of eukaryotic RNAs (especially mRNA) and is also not uncommon in RNA viruses (which essentially mimic endogenous mRNA for their own replication). As with mRNA, this poly(A) tail in coronaviruses is bound by poly(A) binding protein in the cytoplasm [1], which is involved in translation initiation. In coronaviruses, this poly(A) tail is also necessary for replication independent of its role in translation [2].

[1] Lin Y-J, Liao C-L, Lai MM. 1994. Identification of the cis-acting signal for minus-strand RNA synthesis of a murine coronavirus: implications for the role of minus-strand RNA in RNA replication and transcription. J Virol 68(12):8131-8140.

[2] Spagnolo JF, Hogue BG. 2000. Host protein interactions with the 3′ end of bovine coronavirus RNA and the requirement of the poly (A) tail for coronavirus defective genome replication. J Virol 74(11):5053-5065.


What are the total number of alleles for a single trait? Humans receive a copy of gene from both parents and each gene has an alternative form called allele. Does every person possess two genes and four alleles for a single trait?

To fully answer your question it would take an entire course of molecular genetics and quantitative genetics. I will be only very brief and will let you seek for more information on your own.

Basics of molecular genetics

You are confounding gene copy and allele. As we are diploid, we have two copies (I am ignoring here sexual chromosomes and mtDNA) of every locus. This is true for genes too. We have two copies of each genes. Now, we may or may not have the same allele at these two copies. If we have the same allele at both copes, we are homozygous, otherwise we are heterozygous at this locus.

You might want to have a look at the post Do men and women have the same number of genes?

Now, each chromosome is made of two sister chromatids (although this number varies depending upon the stage of life cycle). The sequences at the two sister chromatids are exactly the same, so you can't have different alleles at two sister chromatids.

You might want to have a look at the post What is the relationship between DNA molecules and the chromosomes?

Basics of quantitative genetics

Of course, a single phenotypic trait is not necessarily mapped out by a single locus. There are usually plenty of loci involved (see Quantitative Trait Loci, epistasis and eventually pleiotropy). There is also other source of phenotypic variance than genetic variance such as environmental variance for example.

You might want to have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?

  Ok ,but I can't get your point .As there are two copies of one gene each from father and mother and we have an allele for every gene copy so, combining these we got two genes and four alleles .?Can we?

We receive one copy of every locus (or gene as you seem to get stuck with this term) from each parent. If these two copies differ, then we have two different alleles (heterozygous), otherwise we have only one type of allele (homozygous). In some life stage of the cell cycle, each chromosome is made of two identical chromatids. When this is the case, there are 4 copies of the gene but never more than two different alleles.

You really seem to use the term "allele" when "gene copy" should be used. Think of an allele as a pokemon card. When you ask someone "do you have Pikachu?", you're not asking whether the person has the exact same card that the one that is in your deck of cards. Alleles are the same! So even if you have 2 copies of a given locus (that is two pokemon cards), you might or might not have two different alleles.

You also use the term "gene" where it would be more correct (or more general) to say "locus". You should check out the definition of locus.


Genetic Diversity and Adaptation I am somewhat new to evolutionary biology, having studied it on my free time as a computer science student.  There is one particular thing that has always bothered me for which I have not seen a good treatment, relating to adaptations to the environment with respect to genetic diversity.  If it is possible for a population to adapt to rapid environmental changes, and they don't have an adaptation for dealing with change directly (such as a complex brain), it seems to me that every generation must have present within them almost every possible environmental adaptation that the population is capable of expressing (including many irrelevant ones and a few relevant to the particular environmental challenge).  Otherwise, it may take too many generations to deal with a change, which may be disastrous for the population.

So my question would be: how does an evolutionary biologist explain the mechanics behind the ability for a population to adapt quickly?  Are most environmental changes slow or gradual enough that the population has a few generations to happen upon the mutations that will allow it to survive, and have generally been successful in this regard for 3.5 billion years?  Or, are a large majority of possible adaptations present in almost every generation, and just serve no purpose or advantage for most of the population if the provided "benefit" is unneeded (i.e., are effectively neutral)?  Or something in between?

Great question! A lot of things affect how quickly a population or species can adapt to a new environment, including population size, mutation rate, generation time, standing genetic diversity, and selective pressure.

The diversity of life encompasses practically all combinations of those variables. A bacterial population might very well contain enough diversity to allow a portion of the population to overcome a rapid change. In fact, applying antibiotics to a bacterial population and counting the survivors is a common measure of mutation rates.

On the other hand, organisms with small populations and long generation times will be much less likely to overcome a rapid environmental change. This is why there is so much concern over anthropogenic changes to the environment, including climate change.

It's hard to provide a definitive answer, since "rapid change" is a relative term, and the difficulty of adapting isn't known. Some striking adaptations can be caused by a single base pair mutation, such as in beetles and Monarch butterflies that are insensitive to toxic plant compounds.

It's important to point out that natural selection is based on relative fitness. Therefore, an adaptive mutation will spread because it's likely that carriers will be more fit than all of their neighbors. This does not necessarily mean that individuals without the mutation will die or fail to reproduce, only that those with the mutation will do it better.

Likewise, adaptation is not necessarily caused by the environment changing and wiping out all but a few lucky mutants like in the bacteria example. Instead, the environmental change might make things more difficult, but as long as the population can persist, then mutations will continue to enter the population which could confer a selective advantage against the change. So, no, a population does not (cannot) carry all possible adaptations. A population cannot adapt to an environment it hasn't encountered.

Finally, it's worth pointing out that a species can expand its range through migration. A new, unsuitable environment can act as a migration sink (that is, migrants make it there but fail to establish) for a nearby population. If this happens for long enough, some of the migrants may have a mutation allowing them to establish in the new environment.


Please identify organ This is the gut area of an Eastern Grey Kangaroo taken of a property in the Southern Highlands of NSW, Australia. The top red organ appears to be the spleen but what is the elongated tubular organ extending from the spleen? Is it a deformation or the result of disease?

As far as it can be deducted from the picture you ask about Appendix or just Coecum. This is a normal finding and not abnormal one. (You can see a terminal Ileum as well).
If other pictures were provided it could be possible to give more exact answer.


How do asexually reproductive organisms mutate? In accordance to my limited knowledge of biology, asexual organisms exactly copy their DNA as there is no "contaminant", which in sexual reproduction is the other organism's DNA.

It is not necessary that no mutation occurs in the system where no gene recombination or "contaminant" takes place. There are mutations (which are sudden abrupt inheritable changes)

There can be errors in genome which can cause mutations.

Take example of replication of DNA-:

There are many enzymes linked with it : DNA polymerases ( I, II,III) in prokaryotes where asexual reproduction occurs which add nucleotides to make replicas of DNA of parent ( you can check the complete process at wikipedia)

Come to the point : DNA polymerase III, after synthesising dna chains has ability of proof reading. It can correct the mismatches ( hope you know that adenine bonds with thymine and cytosine with guanine, they are nitrogen bases of dna)

DNA polymerase III can correct the mismatches but it is not error proof- it can't distinguish between thymine and uracil (another nitrogen base ; thymine is methylated uracil)

This is only one possible error, there can be many such hence asexual reproduction isn't error proof


Are Restriction Enzymes obsolete with CRISPR? Are Restriction Enzymes obsolete with CRISPR?

No.

While CRISPR allows you cut a piece of DNA anywhere, you need to order a guide RNA to target your desired cut site. All standard plasmids still carry traditional restriction sites, and it's often convenient to use these. Using CRISPR as a restriction enzyme is probably more expensive and more complicated than using traditional restriction digest. Additionally, there are limitations about PAM sites with CRISPR. And you can always PCR a plasmid using whatever primers you want to produce a blunt end product that is "cut" where ever you want, and I'd bet the DNA oligos needed for PCR are cheaper than the guide RNA you need for CRISPR.


What are these bumps on tomato stem? What are the bumps on this tomato stem? They are way off the ground so I doubt they are air roots.

What are they, what function do they have and why do they form?

Those bumps are aerial surface hairs, a type of trichome. They are epidermal outgrowths.
Therefore it's vines are of pubescent type.

In addition to facilitating better exchange of gases, it also facilitate the vining process, turning into roots wherever the plant is in contact with the ground and moisture, especially if the vine's connection to its original root has been damaged or severed.

Sources:

1:https://en.m.wikipedia.org/wiki/Trichome#/search

2:https://en.m.wikipedia.org/wiki/Tomato


How does the shoulder joint stay in place? I read that a human shoulder is a ball and socket joint, but when looking at a picture of a shoulder the socket part seemed way too small to hold the ball in place like a ball and socket joint. Usually the socket covers a little over half the ball and the shoulder socket covers almost none. How does the shoulder stay connected? Are the illustrations wrong?

Because it's

held together by muscles, tendons, and ligaments.

(image from Wikipedia.)
It's somewhat complicated how all these parts contribute to holding the joint in place because it depends on the position of the joint. E.g.

Shoulder muscle forces are usually powerful stabilizers of the glenohumeral joint, especially in mid-range positions when the passive stabilizers are lax. However, muscle forces can contribute to instability as well. Certain muscle forces decrease glenohumeral joint stability in end-range positions. We found this to be the case with both active and passive pectoralis major forces.

That study has some data based on computational models and actual tests on cadavers.


If I built a concrete pool, would it ever contain fish? Imagine that I built a concrete-walled pool the size of a football field and filled it with fresh water - obtained from another lake but free of bacteria, plantlife, eggs, etc.

Would it ever, over time, become a life-filled "lake" - with fish, amphibians, algae, plants and other water-dwellers?

If yes, how?

What would the chain of events look like?  I'm assume plant-life would get there first but how would it develop an established eco-system?

Please re-tag as appropriate as I am new to this SE site.

if the pool were just sitting out in open air, on earth and all that good stuff, it certainly would, given enough time.

This thought experiment is in the same vein that inspired Darwin when he reflected on his experiences on his visit to the Galapagos islands.

Think about it - the many islands which are formed by upheaval were lifeless when they first emerged from the ocean.  Over time, the winds or storms eventually populated them all - just about every island has animal life on it.  Not all animal types are found there that are best for the climate; its a matter of accident that some birds or lizards are found on the galapagos islands.  These accidental landings don't happen very often and sometimes a single animal will generate many species which will fill the role that other animals would normally fill on the mainland continents at the same latitude.

This is what happened on the islands- in different islands, Darwin found finches of sizes and shapes would be eating insects from bark or ant hills that might be done by an animal

Eventually, if you wait long enough a frog, then maybe a couple of fish will find their way into the pool from a nearby waterway (yeah that could take a long time I know).  If it takes too long then a new species will show up.  If you build walls around the pool it might not happen.  These accidents of animals showing up by accident can take millions of years.

This experience of Darwins' has inspired an entire field of biology - Island biogeography.  Each island is an experiment and ecological niches can be observed by taking a series of islands and seeing how different animals take up the various ecological roles on each.  A famous experiment EO Wilson and colleagues did was to fumigate some mangrove islands and watching them repopulate.


Which components grow in size but not in number and which grow in number but not in size? During growth of an individual animal some components of the body grow in size but not in number (type 1) while some others increase in number but not in size (type 2). Which of the following is correct?
(A) type 1: bones and muscle cells; type 2: hair follicles, red blood cells and epithelial cells.
(B) type 1: bones and red blood cells; type 2: hair follicles, muscle cells and epithelial cells.
(C) type 1: hair follicles and muscle cells; type 2: bones, red blood cells and epithelial cells.
(D) type 1: epithelial cells and bones; type 2: hair follicles, red blood cells and muscle cells.

I know muscle cells only grow in size. I am unsure about hair follicles, which is why I am confused between options A and C. I am also confused about bone growth. Does it ever increase in number? It would be nice if someone could clear that up.

We navigated through this question with Fenil in comments, I'll resume the answer here:

Osteocytes

We know from this page that "osteocytes have an average half life of 25 years, they do not divide" and that "when osteoblasts become trapped in the matrix that they secrete, they become osteocytes. Osteocytes are networked to each other via long cytoplasmic extensions that occupy tiny canals called canaliculi".

We can thus conclude that bone cells don't grow in numbers, but in size by their cytoplasmic extensions.

Hair follicles

Well, we draw the conclusion that hair follicles grow in number and not in size based on the following common sense observations:

We don't get to see tiny hair follicles in babies and giant ones in adults;
If they don't grow in size, either they grow in number or they become less and less dense as the skin surface grows with age. If the latter, we should see the same hair number in babies and in adults, whichever their height is, and this is obviously not the case.

So, they grow in number.

The answer is $A$.


Common english name for tissues which are separated from the blood by blood-tissue barriers Which general term is used to denote such organs/tissues as: brain, testis, thymus etc., which are separated from the blood by blood-tissue barriers?

I am not aware of any umbrella term: the barriers for each are not identical, the function and reasons for the barriers are not the same.

Often these organs are referred to as "immune privileged" because one of the important consequences of the separation is that immune responses in each of those organs are different than in the rest of the systemic circulation, even though this is of course not the only significance of blood-tissue barriers. The meaning of the term has also shifted a bit, though, and I still see different definitions in different places (for example, the Wikipedia definition is not the one I would use). As a consequence, it is easy to argue that some like the thymus should not be considered immune privileged, so my umbrella suggestion would be to just avoid umbrella terms.


Odds of finding superbug in soil? There are tons of soil, rock, etc. being dug up, dug into, and moved all around the world each day. Paleontologists likewise regularly excavate fossils and both buried and frozen specimens, and biologists take samples of permafrost, soil and underground bodies of water.

Given all of the upheaval of these ancient and underground substrates and specimens, I'm wondering what the odds are that we unearth a superbug?

by superbug, I mean an otherwise unknown microorganism that modern medicine does not have a way to kill.

I understand that this is likely too broad of a question to be answered here (but feel free to try!), so I will break this down into a more relevant set of questions to inform my research.

How many microbes (# of species and/or density) typically exist in a cubic meter of soil? (or some other volume)

This article seems to be a good start.

Do these microbe abundances and diversity change with depth?
What is the deepest place in the crust that has been found to harbor life?

This article from 2010 suggests almost 1400 meters. Have we found deeper?

What is the deepest place in the crust that has been found to harbor life?

The deepest living animal:

That award goes to the "Devil Worm" (Halicephalobus mephisto), a nematode that has been found living at 3.6 km below the surface!!

Halicephalobus mephisto is tiny (only 0.5mm long), and represents the deepest multicellular organism ever found.

The original paper can be found here: Borgonie et al. (2011)

I should note, that the paper found definitive Halicephalobus mephisto at 1.3km depth, but found rRNA gene sequence belonging to a specimen of Monhysteridae at the deep 3.6km depth.

Do these microbe abundances and diversity change with depth?

According to  Inagaki et al (2015), microbe density is very low at low depths:

  By counting the cells of these microbes, they also conclude that it is a small community, with just one cell in a cubic centimetre of sediment in some sections of the sediment


Is evolution a predictive theory? My feeling is that almost any observation can be explained by current evolutionary theory. Is there any example of someone developing a rigorous framework or mathematical model of how evolution works?

Evolutionary biology is a highly quantitative science and offers a fair amount of predictive power. However, at the same time, there are plenty of things that we are completely unable to predict.

What are we good at predicting?

There are plenty of things and it is impossible to list them all. Here are a few examples of things we can predict.

Number of pairwise differences (or other measures of molecular differentiation) do we expect between two lineages that recently split in a given number of years.
Number of pairwise differences between individuals coming from the same population.
Number of mutations of given fitness effects (whether beneficial or deleterious) do we expect to accumulate over a given period of time in a population. We can predict the age of a lineage.
Predictions about the evolution of multicellularity, sociality, etc. in lineages that are limit-cases (relating again to our ability at a short time only).
Speed of evolutionary change as measured in Haldanes or in Darwins (these are units) (from knowledge about the genetic variance).
Predictions about the heterozygosity of a population and the loss of heterozygosity through time.
predictions about the gene flow, migration rate or strength of selection.
Predictions of the consequences on fitness that a change in population size may cause.

Generally speaking, we have good predictive abilities at short time scale OR for neutral sequences OR for conserved sequences (strong purifying selection).

In short, we can predict a lot of things but by far not everything yet.

Main complications in doing predictions in evolutionary biology

I would suggest decomposing the reasons why predictions can be hard into the following categories. However, I might well forget something and one could argue that my semantic is less helpful some other semantic.

Environment

One issue related to making predictions at long time scale is that the environment changes through time in a way that we are not able to predict accurately enough yet.

Noise (incl. genetic drift)

I am not here talking about measurement error or sampling error (these are statistical concepts you may want to check if you don't know them), I am talking about the stochastic process that is inherent to biological systems such as the randomness of mutation processes and genetic drift.

Genotype-phenotype map

We have too little understanding of molecular genetics in order to be able to predict how different specific mutations would affect the phenotype. As a consequence, today we still have very little predictive power about the evolution of a phenotypic trait that is currently totally inexistent.

Complex systems

For example: demography affects evolution which affects the social environments, which affects demography which affects the pattern of species competitions which affects the evolution of another species which affects its demography which affects the evolution of a third species which affects the demography of our first species, etc... These kind of complex systems are often mathematically not tractable.

Parameters

We often don't know the exact parameters of the lineage we are interested in. There is a lot of measures to take to be able to make predictions and we often don't have the money (or the time) to make all these measurements (assuming we are able to accurately measure them). For this reason, we are often relatively good to make predictions for a few model organisms but pretty bad for the vast majority of species.

Applications of evolutionary biology

There are not a lot of applications of evolutionary biology for the moment but still, there are some proving its predictive power. These applications include

medicine and epidemiology (incl. evolution of resistance)
artificial selection and other techniques mainly to improve crops (e.g. nuts)
Various search algorithms such as the genetic algorithm

Note, my answer was partially recycled from this other answer of mine

Answering directly in your text

  It seems like almost any observation can be explained by current evolutionary theory

This is wrong. You should learn more about evolutionary biology (starting with Understanding Evolution by UC Berkeley for example) and you will understand why it is wrong. I can't make a whole introduction to evolutionary biology in a single post.

  Is there any example of someone developing a rigorous framework or model of how evolution works?

Yes, there are thousands of such models depending on the exact evolutionary process of interest. Just to give you a feeling of it, you could have a look at any book recommended on the post Book recommendation on population/evolutionary genetics?. If your knowledge in math is a little weak, then you might want to have a look at the introductory book A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day). While this book is quite introductory, I would still recommend starting with an even more introductory course as suggested above.

Standard mathematics methods used in evolutionary biology include branching processes, birth-death processes and other Markov Models, mathematical statistics and probability theory, diffusion equations, approximation theory, ...

On a side note, you would note that the development of statistics is very much related to evolutionary biology. This is true historically but is still true for the development of modern statistics. Just to cite one person, Ronald Fisher was an evolutionary geneticist (one of the fathers of the modern evolutionary synthesis) and he invented some of the most used statistical tests (t-test, anova-F-test, Fisher's tests).