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This Week in Cell: Aug 14, 2013

A large research group led by researchers at the University of Washington brought together de novo mutation data for individuals with schizophrenia and gene expression information from normal fetal brain tissue to map the interactions between potential schizophrenia risk genes. The team tracked down some 50 genes that are not only prone to de novo alterations in schizophrenia, but which also fall in shared gene expression and protein networks in the prefrontal cortex region of the developing human brain. The set included genes implicated in processes such as neuron migration and synapse function, the study's authors note, hinting that "disruptions of fetal prefrontal cortical neurogenesis are critical to the pathophysiology of schizophrenia." GenomeWeb Daily News has more on the study, here.

By searching for regions of the genome that have been subject to artificial selection in dozens of lab rat strains, an Imperial College London-led group identified loci with apparent ties to some of the diseases that the animals have been bred to model. The researchers sequenced the genomes of 25 rat strains, including 11 strains designed to depict human conditions such as heart disease, high blood pressure, and metabolic problems. Using millions of SNPs found in the newly sequenced genomes and in the genomes of two rat strains that had been sequenced previously, they then looked at relationships between the lab rats and searched for evidence of selective sweeps and co-evolved genes coinciding with a given strain, trait, or condition.

A team from the UK, Canada, and Greece took a look at factors influencing changes to transcription factor binding patterns in six closely related rodent species. By doing chromatin immunoprecipitation sequencing experiments on liver samples from rat and from five mouse species, the researchers profiled binding patterns for three tissue-specific transcription factors with ties to gene expression in the liver. With these and other data, the group determined that collections of co-bound transcription factors typically alter their binding patterns in a coordinated manner, apparently contributing to rapid regulatory changes between related species.