Regulation of Atg32 expression

Mitophagy, the selective degradation of damaged mitochondria by autophagy, is important for maintaining cellular homeostasis and its mechanism has been extensively studied in Saccharomyces cerevisiae. Here, autophagy-related protein 32 (ScAtg32) acts as a mitophagy receptor and, upon induction of mitophagy, is phosphorylated and interacts with the mitophagy adaptor ScAtg11, which then delivers the unwanted mitochondrion to the autophagosome. But because S. cerevisiae is a fermenting yeast and the volume of mitochondria depends on the metabolism of the organism, mitophagy might be regulated differently in most other non-fermenting organisms. Therefore, Tomotake Kanki and colleagues now (p. 3184) investigate the regulation of mitophagy in the almost non-fermenting yeast Pichia pastoris that has genetic similarities with S. cerevisiae. The authors first identify and characterise the Atg32 homologue in P. pastoris (PpAtg32), which – as they show here – is barely expressed before mitophagy but rapidly induced upon starvation-induced mitophagy. The authors then further examine the mechanism of PpAtg32 expression, and demonstrate its regulation through target of rapamycin (Tor) signalling and repression by the downstream PpSin3–PpRdp3 histone deacetylase complex. But, interestingly, Tor signalling does not regulate the phosphorylation of PpAtg32. The authors also show that ScAtg32 expression is regulated through a similar mechanism; taken together these data thus provide new important insights into the regulation of mitophagy.