genetics - What is the functional and structural distinction between core (H2A, H2B, H3,H4) and linker(H1/H5) histones?

The core histones are H2A, H2B, H3, and H4, and the linker histones are H1 and H5. The structure of the nucleosome is well explained in wikipedia:

Two of each of the core histones assemble to form one octameric nucleosome core particle, and 147 base pairs of DNA wrap around this core particle 1.65 times in a left-handed super-helical turn. The linker histone H1 binds the nucleosome and the entry and exit sites of the DNA, thus locking the DNA into place and allowing the formation of higher order structure. The most basic such formation is the 10 nm fiber or beads on a string conformation. This involves the wrapping of DNA around nucleosomes with approximately 50 base pairs of DNA separating each pair of nucleosomes (also referred to as linker DNA). The assembled histones and DNA is called chromatin. Higher-order structures include the 30 nm fiber (forming an irregular zigzag) and 100 nm fiber, these being the structures found in normal cells. During mitosis and meiosis, the condensed chromosomes are assembled through interactions between nucleosomes and other regulatory proteins.

The core histones have a positive net charge, which facilitates the interaction with the negatively charged phosphate groups of DNA.

Apart from defining the nucleosome structure, the function of the core histones is regulatory: it can switch on/off gene expression by histone modifications like acetylation or methylation.

The gene expression is ON when there is:

• DNA demethylation

• histones acetylation
• H3K4 methylation
• H3K36 methylation

• H3K9 demethylation
• H3K27 demethylation

The gene expression is OFF when there is:

• DNA methylation
• histones deacetylation
• H3K4 demethylation
• H3K36 demethylation
• H3K9 methylation
• H3K27 methylation

// H3K4 demethylation is abbreviation for: Lysine 4 of H3 is demethylated.

Berger SL. 2002. Histone modifications in transcriptional regulation. Current Opinion in Genetics & Development 12: 142–148 is also a nice review.

the sun - What triggers solar flares?

Magnetic fields are generated by currents - i.e. by the motion of charged particles. As you say, the Sun is full of freely moving charged particles, and these generate currents which in turn generate magnetic fields. No metals required.

Most of the magnetic field generation is thought to occur at the interface between the radiative interior of the Sun and an outer convective envelope. This region, called the tachocline, is subject to large shearing motions which are able to take small magnetic fields and amplify them. The stronger magnetic fields are then buoyant, because magnetic fields in a plasma exert a pressure. They therefore emerge at the solar surface in the form of loops of magnetic field.

These loops are strongly coupled to the plasma in the Sun. As the plasma moves around turbulently, driven by convective motions and differential rotation on the Sun's surface, the footpoints of the loops are sheared and twisted. There comes a point where the loop will snap back into a configuration with lower magnetic potential energy through a process called reconnection. The reconnection process has a side effect of accelerating particles within the magnetic loops. These relativistic particles smash into the photosphere (actually, they are mainly stopped in the chromosphere which sits above the photosphere), where they release their energy, heating plasma to millions of degrees, which evaporates into the corona. This is a solar flare.

dna - How distantly related are eusocial insects? Aren't members of a species much more related than 1/4, 1/2, or 3/4?

In evolutionary genetic comparison, you are talking about members within species. They will share almost all genes, because if they didn't they would belong to a different species.

However, within species there exist different versions of the same genes, called 'alleles'. When we say that you are 0.5 related to each of your parents, we mean that statistically, 50% of your alleles should be those which your father has, and 50% of your alleles are those passed down from your mother.

Eusocial insects have different mechanisms. Bee males are produced without fertilisation, meaning that they only have one copy of each bee gene. When the male produces sperm, it only has this one set, so all sperms end up carrying the same set of alleles.

Females on the other hand have the normal double set, with two different versions of each gene. So if you look at one gene, half of the female's egg should have one version and the other half should have the other version. All females of one hive are produced by the same queen and the one male that she mated with. Remember, the male only has one set, so the versions coming from the male are the same in all female offspring.

This means a female's genes are made up of: 50% from the father (these are the same across all females) and 50% from the mother (where half the females have one version and half have the other version). Statistically, this means that looking at one gene, there is a 75% chance that two bees will have the same version of that gene.

observation - Around what apparent magnitude can the naked eye observe an object during full moon

It may shave off 1 or 2 magnitudes, but it depends on many factors: nature of the object (star, nebula, galaxy), altitude (higher altitude has less light scatter), transparency, etc. There's no One Single Answer To Rule Them All.

Light pollution from artificial sources has a greater impact in most cases.

On the genetics behind caste marriages

Is the son of a couple engaged in farming better suited to the same profession unless he receives a couple of recessive alleles from both parents?

Not everything is coded in the genome, environmental cues play a very important role in shaping who you are. Profession is just one of those things that is not encoded in genes.
Many people do not continue doing the job of their parents, but they do very well in life.
Also note that, aside from the fact that there is no "agriculture" gene, having a recessive allele does not mean you will miss a certain phenotype.
What is true is that someone who has higher education will probably be more keen to have their kids studying. On the contrary, the kids of someone who is a poor farmer and is barely able to provide for his family will probably not have the opportunity of going to school (let alone university) and therefore will continue to work the land. It has nothing to do with genetics.

Generally there is a lot of unscientific information floating around about these matters. One of the grapevines is that it is genetically better for one to marry outside their caste to create diversity(?). Is such a thing true?

Continuing to reproduce in the same group of people will limit diversity in the genome, and create an accumulation of mutations, which is generally a bad thing. That is why it is very common to have particular illnesses in closed communities.

For instance Amish people have an higher incidence of genetic disorders such as Ellis-van Creveld syndrome (a form of dwarfism)

From The Gene for the Ellis–van Creveld Syndrome Is Located on Chromosome 4p16 - Ruiz-Perez et al., Nat. Genetics 2000

Autosomal recessive transmission of the disorder is supported by
multiple affected siblings with unaffected parents in families with
known parental consanguinity. The largest known pedigree segregating
with EVC is that reported by McKusick and his colleagues in the Old
Order Amish (McKusick et al., 1964). The prevalence of living persons
affected with EVC among the Lancaster County Amish was estimated to be
2 in 1000, whereas the frequency of occurrence among live births was 5
in 1000. McKusick et al. estimated that the frequency of heterozygous
carriers in the Old Order Amish is as high as 13% (McKusick et al.,
1964). All cases of EVC in the Amish at that time were traced to a
common founding couple, Samuel King and his wife, who immigrated to
Pennsylvania in 1744.

This is a well known effect, called the founder effect.

As for India, a study on the genetic behind casts has been done a couple of years ago.

Reconstructing Indian Population History - Reich et al., Nature 2010

From the paper:

Haldane wrote 45 years ago that “if inter-caste marriages in India become common, various… recessive characters will become rarer”. However, it has not been generally appreciated that this applies to groups throughout India, and not only to groups in the south where consanguinity is common. We hypothesize that founder effects are responsible for an even higher burden of recessive diseases in India than consanguinity.
To test this hypothesis, we used our data to estimate the probability that two alleles from a group share a common ancestor more recently than that group’s divergence from other Indians, and compared this to the probability that an individual’s two alleles share an ancestor in the last few generations due to consanguinity. Nine of the 15 Indian groups for which we could make this assessment had a higher probability of recessive disease due to founder events than to consanguinity, including all the Indo-European speaking groups.
An additional reason why some diseases are expected to occur at elevated frequencies in India is shared descent from a common Indian ancestral population. An example is a 25 base pair deletion in MYBPC3 that increases heart failure risk by about 7-fold, and occurs at around 4% throughout India but is nearly absent elsewhere.

They conclude that:

We have documented a high level of population substructure in India, and have shown that the model of mixture between two ancestral populations ASI and ANI provides an excellent description of genetic variation in many Indian groups.
[...]
By showing that a large proportion of Indian groups descend from strong founder events, these results highlight the importance of identifying recessive diseases in these groups and mapping causal genes.

It is very important to understand that this results in no way show a genetic basis for the existence of casts, which remain purely social entities. They rather show that an environmental constraint can influence the distribution of genetic traits, due to a restriction in the possibility of mixing genes in the population.

star - Rate of Mass Loss from the Solar Wind

This is problem 1-4 from Principles of Stellar Evolution and Nucleosynthesis by Clayton:

Assuming at the Earth a characteristic velocity of 400km/s and density of 10amu/cm$^{3}$ for the solar wind, calculate the rate of mass loss for the sun.

There weren't any formulas about this in the section so I made a stab at it with dimensional analysis.

$$frac{dM}{dt} = frac{rho V}{Delta t} = rho v A$$
$$frac{dM}{dt} = left( frac{10 amu}{cm^{3}} right) left( frac{400km}{s} right) left( frac{4 pi (6.96e10 cm)^{2}}{1} right) left( frac{10^{5}cm}{km} right) left(frac{10^{-24} g}{1 amu} right) left( frac{M_{odot}}{2 times 10^{33} g} right) left( frac{3600s}{hr} right) left( frac{24 hr}{day}right)left(frac{365day}{yr}right)$$
$$frac{dM}{dt} = 3.84 times 10^{-19} M_{odot} / yr $$

However, the answer given in the book is $0.4 times 10^{-13} M_{odot} / yr$. So, I'm off by about five magnitudes. Can anyone point out where I went wrong and/or point me in the correct direction?

zoology - How does a jumping spider manage to "jump" on the ceiling?

I just witnessed a small jumping spider jump on some kind of louse or bed bug on the ceiling. How does it do that without falling? I have yet to find a high-speed-camera video of a jumping spider jumping on a ceiling.

My hypothesis is that the spider would spit silk and anchor it on the ceiling, then jump, and allow itself to be swung by the silk onto the prey. But I don't have a high speed camera to prove that.

EDIT:
I now have some evidence that supports my hypothesis: I just saw a jumping spider attempt to jump on a prey and failing to land properly. It didn't fall directly to the floor. Instead, it dangled from its own silk, at about 2 cm from the ceiling, then climbed right back up the thread of silk, onto the ceiling.