A paper appearing in the PNAS Early Edition from Uppsala University's Karolina Edlund et al. examines the accuracy of reported mutations in an analysis of the TP53 mutation database. Taking a data-driven approach to assess several independent quality criteria, Edlund and colleagues generated a quality score for each report contributing to the database. They then validated that curation approach by "sequencing the entire TP53 gene from various types of cancer." Overall, 9.7 percent of the studies collected "should be excluded when analyzing TP53 mutations," the authors write.
Elsewhere, Harvard Medical School's Shiro Iuchi and Howard Green show in human embryonic stem cell-derived Nod keratinocytes that not only do "differently spliced transcripts from a gene result in totally opposite outcomes, [they] also present critical evidence of the complicated activities of KDM2A," the high expression of which has shown to improve poor proliferation of those cells.
A team led by investigators at Japan's National Institute of Agrobiological Sciences use positional cloning on chromosome 15 and Bombyx mori as a model to identify a candidate gene for a recessive form of resistance to Cry1Ab toxin in silkworm. "Sequences of 10 susceptible and seven resistant silkworm strains revealed a common tyrosine insertion in an outer loop of the predicted transmembrane structure of resistant alleles," the authors report in PNAS. The researchers then "confirmed the role of this ATP-binding cassette transporter gene in Bt resistance by converting a resistant silkworm strain into a susceptible one by using germline transformation," they add.