Highlights from Nature (Jul 16th 09)

In the current edition of Nature:

-The Schistosoma japonicum genome reveals features of host–parasite interplay

-The genome of the blood fluke Schistosoma mansoni

-The active form of DNA polymerase V is UmuD′2C–RecA–ATP

-Contamination of the asteroid belt by primordial trans-Neptunian objects

-Manipulation of photons at the surface of three-dimensional photonic crystals

-Photoconductance and inverse photoconductance in films of functionalized metal nanoparticles

-Evidence for middle Eocene Arctic sea ice from diatoms and ice-rafted debris

-Migration of the subtropical front as a modulator of glacial climate

-Global patterns of speciation and diversity

-Evolution of a malaria resistance gene in wild primates

-Rapamycin fed late in life extends lifespan in genetically heterogeneous mice

-A conserved ubiquitination pathway determines longevity in response to diet restriction

-A reevaluation of X-irradiation-induced phocomelia and proximodistal limb patterning

-The AP-1 transcription factor Batf controls TH17 differentiation

-Cohesins form chromosomal cis-interactions at the developmentally regulated IFNG locus

I've briefly commented on the highlighted studies below the fold

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The study on Global patterns of speciation and diversity by de Aguiar et al employs a computational model to measure speciation.

We simulated the evolution of a population whose members, at the beginning, are uniformly distributed in space and have identical genomes. The population evolves under the combined influences of sexual reproduction, mutations and dispersal. During reproduction, potential mates are identified from among those in a spatial region around an individual (specified by a spatial mating distance, S) whose genomes are sufficiently similar to that of the individual (specified by a genetic mating distance, G). This is a minimal form of sexual selection, essential (necessary but not sufficient) for speciation, called assortative mating (postzygotic genetic incompatibilities may have a role but are not essential). A mate is chosen from this set at random. Reproduction with crossover and mutation occurs. An offspring is then dispersed within a region around the originating and expiring parent. Genetic variation grows over time, due to mutation and recombination. We identify a species as a group of organisms reproductively separated from all others by the genetic restriction on mating and connected among themselves by the same condition...

Here is a figure showing the speciation of a 2000-strong homogeneous population into several distinct 'species' (colours) without any geographical boundaries:



What is interesting about this result is that it correlates well with what is known to occur in nature, as explained here:

Examples of such patterns are the constant rate of speciation observed in the fossil record; the higher diversity of freshwater ray-finned fishes than of their marine counterparts; the species–area relationships of birds, flowering plants and tropical-forest trees; and the relative species abundance of birds and forest trees.

This is clearly just one step in the marathon that is understanding biodiversity, but it's informative, nicely presented and has lots of pretty colours!



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Next, the study by Schraml et al entitled The AP-1 transcription factor Batf controls TH17 differentiation investigates the role of Batf in TH17 cell maturation and hence how this transcription factor contributes to autoimmunity, my specific area of interest.

I've desribed the role of TH17 cells in autoimmunity in an earlier post. They are a subset of T helper cells, the others being TH1 and TH2 cells, which direct the immune response following pathogenic assault. However, overactivation or a lack of appropriate suppression of this response can result in autoimmunity as these cells will drive the response towards host cells in the absence of pathogens.

In this paper, the authors have generated Batf^-/- mice in order to study the effects of Batf on their experimental model, namely experimental autoimmune encephalomyelitis (EAE), an autoimmune disease in mice. They found that Batf^-/- mice produced less IL-17 than wildtype mice (figure below, b), suggesting that Batf is involved in TH17 cell development. The same mice showed normal IL2, IFN- and IL10 levels, indicative of normal TH1 cell function.

Interestingly, the Batf^-/- mice were resistent to EAE, as shown in the figure below (a, open triangles). This result adds further evidence to the role of TH17 cells in autoimmunity, and points to Batf as a critical transcription factor regulating its pathogenesis. To further prove this point, the authors gave the Batf^-/- mice functional naive T cells (CD4+) from wildtype mice and this resulted in the mice becoming susceptible once again to EAE (c, open triangles).



This adds to the TH17 story which is becoming a very hot area in immunology. If we can understand what is driving the differentiation of these cells, we will theoretically be able to suppress this to combat autoimmunity.