In this week's Nature, a Max Planck Institute for Biology of Ageing-led team reports on the discovery that mutations in maternally transmitted mitochondrial DNA, or mtDNA, may aggravate aspects of normal human aging. The investigators created a series of mouse mutants to investigate the impact of inherited mtDNA mutations on aging, and they found that maternally transmitted mtDNA mutations can induce mild aging phenotypes in some wild-type mice. They suggest that this is because the inherited mutations provide a baseline mutation load upon which somatic mtDNA mutagenesis can act. Follow-up studies showed a combination of maternally transmitted and pre-existing mutations leading to brain malformations that were equally common in both sexes, but required large somatic mutations in mtDNA.
Meanwhile, in Nature Biotechnology, a group from the Chinese Academy of Sciences publish details of a method for generating conditional knockouts of Caenorhabditis elegans using plasmids expression transcription activator–like effector nucleases, or TALENs, in somatic cells. Using germline transformation with plasmids encoding TALENs under the control of an inducible or tissue-specific promoter, they saw "effective gene modifications and resulting phenotypes in specific developmental stages and tissues." Additionally, the method was used to bypass the embryonic requirement of cor-1, which encodes the homolog of human severe combined immunodeficiency protein coronin, and the researchers determined that it has an essential role in cell migration in larval Q-cell lineages.