dna sequencing - ChIP-seq vs ChIP-exo

ChIP-exo does seem to be the "ChIP-seq killer." I've seen Dr. Pugh present it a few times, and the audience is pretty much always impressed.

One thing I'd do if I were of the "experimental bent" would be to add random degenerate barcodes in the library prep to control for potential PCR artifacts. I imagine that since the "peaks" in ChIP-exo seem to be quite a bit narrower than ChIP-seq, I reckon it'd harder to use some coverage-in-local-neighborhood to remove such biases (assuming you wanted to do so).

To give you an idea of what I'm thinking of -- it would be somehow similar to what is depicted here.

dna sequencing - Mechanics of going from DNA sequence to metabolic network

The question is not too broad, just involves a fair bit of work to both do the research and compose a response. I'll do the latter, but in brief.

The strings of the four nucleotides encode genes. Sometimes these genes are broken into protein-coding portions (exons) and sometimes intervening, non-coding regions (introns). Bacteria, for example do not have introns within genes while most human genes do. The nucleotides in the protein-coding portion of the gene do just that - give instructions on how to synthesize the protein by directing which tRNAs the ribosome uses to translate the genetic code into a protein chain.

A useful phrase is protein sequence dictates protein structure and that structure dictates function. So, the proteins do things and many act as enzymes or modulators of enzyme activity. An enzyme catalyzes a biochemical reaction, lowering the activation energy to go from reactant(s) to product(s). One enzyme can be thought of as one unit within a metabolic network. A modulator might activate or deactivate an existing enzyme. A protein kinase is a good example of a modulator.

Next, string some of those enzymes together to build a pathway. A common example is glycolysis. Think of this as a chain where the output or product of enzyme A serves as input to enzyme B, whose product is the input to enzyme C, and so on. These pathways are two-way, but it is exceedingly difficult to travel from the final product all the way up such a pathway to the initial input within the confines of a biological system. Thus, the pathways in practical terms are thought of as one-way.

However, the pathways do not function in isolation. The final product may serve as input to one, two or more other pathways. Your pathway of choice may begin with the output of another process. Furthermore, pathways can branch: Glycolysis can proceed to glyceraldehyde 3-phosphate and pyruvate, or directly after glucose 6-phosphate formation can be shunted to the pentose phosphate pathway to yield reducing power and 5-carbon sugars (to be used in ATP, CoA, FAD, NAD+, DNA and RNA). Now, pathways leading to other pathways and branches and such make a network.

You and your colleagues might want to know if genes within a metabolic network are over- or under-represented in a test compared to control. Or, genes for a given network are not present in one species compared to several others. Or, one could estimate the flux through such a network given a set of measures.

Peruse examples at both KEGG and Reactome, expecially at KEGG where you can view pathways pertinent to your organism(s) of choice.

molecular biology - What are the different ways an exon gets spliced?

There are several ways splicing can occur, which depends on the RNA molecule to be spliced and the catalyst that performs the splicing:

1. mRNA splicing is carried out by spliceosome, which consists of small nuclear RNAs. There are sequences at the end of the introns and branch sties which indicate the splice sites. The so called lariat structure is formed when the 2'OH group of an adenosine residue in the branch site attacks the 5' splice site.




2. self-splicing of ribosomal RNA precursor - it is performed with the absence of spliceosome.




3. tRNA splicing - it requires three enzymes and ATP hydrolysis.

References:

Biochemistry, L. Stryer, 5th eddition

J. Abelson. tRNA Splicing

Can any protein be phosphorylated?

For one of the most comprehensive databases of protein post-translational modification (including phosphorylation, methylation, acetylation, ubiquitination, etc.), check out PhosphoSite. You can find links to sequences, diseases, motifs, publications, antibodies, mass spec experiments, structures, you name it.

ecology - How do biological communities at deep-ocean hydrothermal vents migrate between vents?

Following up on Alexander's response, I read a little more on the subject by looking at some of the references in the Johnson et al. paper.

This paper discusses an interesting case where researchers could study a hydrothermal vent ecology before and after a catastrophic eruption giving a "natural clearance" experiment. Since endemic organisms were eradicated, any pioneer species must come from other vent systems.

A number of species, in the form of larvae caught in larval traps, were observed to arrive at the vent. These species, including Cyathermia naticoides, Lepetodrilus spp and Gorgoleptis spiralis, arrived at a significantly different (P < 0.05, MANOVA and ANOVA) rate to the pre-eruption larval source population rate. Larvae of one gastropod species, Ctenopelta porifera, which had been seen only once pre-eruption, arrived in significant numbers post eruption. The source of these larvae may have been from a vent 300 km away.

These authors associate this change in the populations pre- and post-eruption with the specifics of the hydrodynamic transport processes operating in the region.

A more general sequence of vent re-population is given in this article.

However, the interesting thing for me was the significant, but changing fluxes of larval species at these deep-sea vents.

Weighing 2 vertical halves of the human body

Humans, like all vertebrates, belong in subregnum bilateria, a broad class of animals whose characteristic trait is having a bilaterally symmetric body plan at least in some of their life stages.

The common ancestor of all bilaterians was presumably something like a small marine worm. For a primitive animal living in water, an obvious advantage of bilateral symmetry is that it makes directed swimming easier. If the animal were completely asymmetric, it would have to continually exert active control over its heading to be able to swim straight. On the other hand, an even more symmetrical animal (such as one with 90° rotational symmetry) might have trouble controlling its vertical and lateral heading separately, which could be a problem in aquatic habitats where staying at a certain depth is often useful.

(Indeed, in many ways these reasons are the same as why pretty much all aircraft are bilaterally symmetric: in the absence of active steering, we want them to fly straight and level. That requires at least rough left–right symmetry and generally also some degree of top–down symmetry, although some breaking of the latter is usually needed both for landing and to account for the effects of gravity on flight dynamics. We could build completely asymmetric aircraft if we wanted, they just would be harder to fly.)

As for why this ancestral bilateral symmetry has survived so well throughout the course of evolution, that's presumably both because it's so deeply embedded in the genes that control our ontogeny, but also because the basic reasons why such symmetry is useful still remain, even though our size, shape, habitat and locomotion are very different from those of the first "urbilaterian". Even though we mostly move by walking instead of swimming, it's still useful for us to be able to walk straight without having to pay constant attention to it. Furthermore, once we've first learned to walk (or crawl) straight, it's useful that we can also learn to run, swim and jump (and ride a bike or drive a car) straight without having to always re-learn the exact amount of control needed to maintain a given heading with each of these modes of locomotion.

---

Ps. To answer your actual question, I'd guess, like Rory M, that the two halves of a human body probably won't weigh exactly the same, both due to the asymmetrical distribution of the internal organs and also due to uneven muscle development.

However, the difference is quite small compared to the total mass of the human body, so that the center of mass is presumably still quite close to the body's centerline. As I noted above, any significant deviation from that would cause issues with gait and balance. Although such issues can certainly be adapted to and overcome with active control — after all, even people who've lost a whole leg manage to get around one way or another — they're presumably still significant enough to be selected against over evolutionary timescales, which is why our body shape remains so nearly symmetrical.

human biology - Can a color-deficient person be made to visualize the missing colors?

It is a very interesting question and I did some efforts to investigate the literature on this topic, but yet I don't have a definitive answer for you. But let's start from the beginning.

First of all, the reason for color deficiency can be not only lack (rare) or impairment (more often) of certain types of color-perceiving cells (cones) in retina, but also brain injures: the central color blindness can develop after head trauma or as a result of some neurodegenerative deceases, like Parkinson's decease. In case of brain origin of the color blindness it is usually the complete color blindness (no color is percieved), whereas congenical primary color blindness (receptor-based) is usually just the unability to distinguish one or two colors, whereas the rest can be more or less separated.

I searched Pubmed for the literature on the topic and found a recent PNAS paper about the simulation of primary and secondary visual cortex on humans using intracranial electrodes. As they describe their results (bold font by me):

When percepts were elicited from late areas, subjects reported that
they were simple shapes and colors....

But the paper investigated only healthy humans, no color impaired subjects were used for the tests, so cannot conclude from here whether we can elicit the perception of the color the person is incapable to see with the eyes using these stimulations.

I took this paper as the starting point and did some reference research, looking for the paper referenced there and for newer publications referencing this one: PNAS is one of the top journals in this area with very high impact factor and if there were a publication about brain stimulation and color blindness I would have definitely identified it.

During my investigations I came accross a series of interesting articles devoted to "cortical visual neuroprosthesis for the blind" (read this paper^<1> from 2005 for review on this topic), but this is the treatment of conventional blindness, not the color blindness. There was no intersection in keywords or titles for color blindness and brain stimulation, both in the referenced articles and in the complete article database.

So, I would suggest that you address some talented experimentalist with your question and maybe one day, who knows, we will read your name under the Nature article dedicated to the novel way to cure color blindness.

---

^<1> -- unfortunately not available publicly for free, I am sorry.

human biology - Does cooking ginger reduce its anti-nausea effect?

There seems to be strong evidence to support the hypothesis that eating ginger helps reduce nausea e.g. during pregnancy (e.g. Vutyavanich et al.). It seems that gingerol is the active ingredient in preventing nausea (cf. Qian et al.). Wikipedia writes: "Cooking ginger transforms gingerol into zingerone...". Presumably, zingerone does not affect nausea.

Question: Does cooking ginger reduce its anti-nausea effect?

A Google search will reveal numerous suggestions for giving ginger tea to pregnant women to help with morning sickness. But boiling the ginger could conceivably defeat the purpose of taking the ginger in the first place (and any effects are primarily due to the placebo).

There's an article (Basirat et al.) which describes an experiment in which biscuits with ginger were given to patients (instead of ginger tablets), although their results alone have not convinced me one way or the other. The authors conclude that their results indicate an anti-nausea effect, but some of their tests do not match that conclusion (i.e. a placebo was comparably effective). Also, the group given the ginger biscuits started off with worse conditions on average.