Harald Klinger

TL;DR: Overexpression of YNO1 causes YCA1-dependent apoptosis, whereas deletion of the gene makes cells less sensitive to apoptotic stimuli, several independent lines of evidence point to regulation of the actin cytoskeleton by reactive oxygen species (ROS) produced by Yno1p.

TL;DR: It is shown that in S. cerevisiae induction of apoptosis by mild oxidative stress, replicative ageing or mutation of cdc48 leads to translocation of Mmi1p from the cytoplasm to the mitochondria, one of the few proteins establishing a functional link between microtubules and mitochondria which may be needed for correct localization of mitochondria during cell division.

TL;DR: In this paper, the authors present a new long-lived yeast deletion mutation,afo1 (for aging factor one), that confers a 60% increase in replicative lifespan.

TL;DR: The finding that aconitase of the mitochondrial matrix is readily inactivated by oxidative stress, but even in its inactive form is relatively long-lived and retains fluorescence in the Aco1p-eGFP form could indicate discrimination between active and no longer active mitochondria during the process.

TL;DR: A new long-lived yeast deletion mutation,afo1 (for aging factor one), that confers a 60% increase in replicative lifespan and establishes a new connection between mitochondria, metabolism and aging.