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This Week in Nature: Dec 10, 2015

In this week's Nature Genetics, a team led by Whitehead Institute researchers report the results of a genome-wide analysis linking short tandem repeats (STRs) to gene expression variation in humans. In the study, the investigators examined genomic data from 311 Europeans whose lymphoblastoid cell line expression profiles had been analyzed as part of the gEUVADIS project and whose whole genomes had been sequenced by the 1000 Genomes Project. They found more than 2,000 STRs were associated with expression changes, and estimated that these STRs contribute between 10 percent and 15 percent of the cis heritability mediated by all common variants and are enriched in various clinical conditions. GenomeWeb has more on this study here.

And in Nature Communications, a group of researchers from Germany and the US presents the results of a study suggesting that a single genetic mutation is behind the early onset of cold-aggravated peripheral pain in humans. In the study, the researchers performed whole-exome sequencing on two members of a family with three generations of members who suffered from this pain condition. In doing so, they identified one mutation that causes changes to a sodium ion channel, which in turn, changes the excitability of sensory neurons. Normally, the activity of these neurons is reduced at low temperatures, but the mutation causes the neurons to remain highly active in cold conditions.

And in Nature Chemical Biology, a Massachusetts Institute of Technology-led team reports two new strategies for controlling genetically modified bacteria. The first, called Deadman, involves modifying a bacterial strain so that it requires an external chemical to prevent a continuously expressed toxin from killing it. The other, called Passcode, uses hybrid transcription factors in which one section of the transcription factor protein responds to a chemical signal and another controls a specific segment of DNA, allowing researchers to change up the chemical signals to control the cell.