On page 803, Gourlay et al. report the first evidence that the actin cytoskeleton can affect release of reactive oxygen species (ROS) by mitochondria, and thus life span in yeast.
Certain mutant Saccharomyces cerevisiae strains with alleles that reduce actin dynamics possess defective mitochondria. The team went on to show that such strains display increased levels of mitochondrially-derived ROS and die early compared with wild-type yeast.
In an exciting contrast, mutant yeast with increased actin dynamics had lower levels of ROS and substantially increased longevity. Actin dynamics was increased either via a mutant actin allele or deletion of the gene encoding the actin-stabilizing protein SCP1, which has homology to vertebrate SM22/transgelin protein. In the latter case, the yeast lived up to 40 generations longer.
The function of the actin–ROS connection is unknown. But actin, as a relatively abundant protein with an intrinsic ATPase activity, may be a convenient indicator of cellular excitement. Thus, cells that are metabolically active, producing a lot of ROS, and in need of a vigorous ROS-suppressing machinery may pick up on the dynamics of actin as a proxy for cellular metabolism and respond by dampening pathways that cause ROS release. Alternatively, actin may directly bind to and regulate the opening of mitochondrial channels involved in ROS release. ▪