In a paper published online in advance in PNAS this week, investigators at the University of Geneva and elsewhere show that "loss of DNA methylation affects the recombination landscape in Arabidopsis." More specifically, the researchers report that while analyzing meiotic recombination in mutant plants with hypomethylated DNA, they "observed unexpected and counterintuitive effects of DNA methylation losses on CO [cross-over] distribution," and further evidence suggesting to them that loss of DNA meythlation leads to a global redistribution of crossovers along chromosomes. Analyzing crossover distribution in wild-type Arabidopsis lines "with randomly scattered and well-mapped hypomethylated chromosomal segments," among other experiments, led the researchers to say that DNA methylation "may influence the evolution of plant genomes through the control of meiotic recombination," they write.
Elsewhere in this week's Early Edition, a team led by researchers at the University of Chicago shows that PIM1 is the most frequently recurring cooperating gene in BCL6 transgenic mice. Working under the hypothesis that "mutated genes are likely to play an important cooperative role in BCL6-associated lymphoma development," the team took its study to human cells, analyzing 20 randomly selected BCL6-positive human B- and T-cell lymphomas. Because of their experimental results, the authors write in PNAS that "PIM1 kinase inhibition may be a promising therapy for BCL6/PIM1-positive human lymphomas."
Using a modified mutation accumulation approach, the University of Toronto's Nathaniel Sharp and Aneil Agrawal set out to "test whether genetic quality, the presence or absence of deleterious alleles, affects the mutation rate in Drosophila melanogaster." In a PNAS article published online in advance this week, Sharp and Agrawal say that "genotypes constructed to carry deleterious treatment alleles on one chromosome during mutation accumulation experience an elevated mutation rate on a different chromosome," adding that this elevation is "correlated with the effect of the treatment alleles on phenotypic condition." Overall, the Toronto researchers say that "mutation rates are sensitive to genetic stress, such that individuals with low-quality genotypes will produce offspring of even lower genetic quality, in a mutational positive feedback loop."