In a paper published online in advance in Nature this week, a team led by investigators at the Osaka University Graduate School of Medicine in Japan show that mitochondrial DNA that escapes from autophagy "leads to TLR9-mediated inflammatory responses in cardiomyocytes, and is capable of inducing myocarditis and dilated cardiomyopathy."
Over in Nature Communications, an international team headed by researchers at Spain's Universidad Politécnica de Valencia shows that variation in inflorescence architecture in pea plants is controlled by Vegetative1, or VEG1, the mutation of which "replaces secondary inflorescences by vegetative branches." Further, the team says that the misexpression of VEG1 in meristem identity mutants "causes ectopic secondary inflorescence formation, suggesting a model for compound inflorescence development based on antagonistic interactions between VEG1 and genes conferring primary inflorescence and floral identity."
Finally, in Nature Methods this week, Dana-Farber Cancer Institute and Harvard School of Public Health's Shirley Liu and her colleagues present a "systematic evaluation of factors influencing ChIP-seq fidelity," which is based on their work using Drosophila melanogaster S2 cells to generate data for the site-specific transcription factor Suppressor of Hairy-wing and a histone modification, H3K36me3. "Paired-end sequencing revealed that single-end data underestimated ChIP-library complexity at high coverage," Liu et al. write, adding that "removal of reads originating at the same base reduced false-positives but had little effect on detection sensitivity."