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This Week in PNAS: Jan 27, 2015

In a study appearing online this week in the Proceedings of the National Academy of Sciences, researchers from the University of Texas at Austin and the University of California, San Francisco, describe a role for viral microRNAs in inhibiting signaling by interferon, an antiviral cytokine in the human immune system. The team transfected human cell lines with a library of more than 70 miRNAs from viruses known to infect humans. The search led to miRNAs from several distantly related herpesviruses that were capable of dampening interferon activity, providing potential clues to understanding interferon therapy resistance that's been described in some Epstein-Barr virus-positive tumors.

A team from the US and the UK turned to transposon-mediated mutagenesis and sequencing to try to tease apart the mechanisms behind melanoma resistance to BRAF inhibition. The researchers used the Sleeping Beauty transposon to perform insertional mutagenesis on mice carrying a melanoma-related BRAF mutation. They then narrowed in on eight new and previously known resistance gene candidates based on transposon insertion sites they detected in mice that went on to relapse following initially successful treatment with a BRAF inhibitor. "Our work establishes Sleeping Beauty mutagenesis as a powerful tool for the identification of novel resistance genes and mechanisms in genetically modified mouse models," the study's authors write.

Finally, an international team led by investigators at Johns Hopkins University presents a biocontainment scheme for genetically engineered organisms that involves tweaks to their transcriptional regulation and recombination properties. For their proof-of-principle experiments, the researchers generated Saccharomyces cerevisiae yeast strains that contained histone genes under the control of an inducible promoter, creating transcriptional switches that could be chemically controlled. The strains also harbored site-specific recombinase enzymes that are lethal to the organism when induced as a second safeguard layer.