Chlorophagy does not require PLANT U-BOX4-mediated ubiquitination.

Chloroplasts and mitochondria serve as intracellular energy production sites that are powered by the electron transport chain in their membranes. These organelles constantly accumulate damage, as their energetic reactions generate reactive oxygen species. To prevent the accumulation of damaged organelles and perturbation of cellular homeostasis, eukaryotic cells must remove damaged mitochondria and chloroplasts. Autophagy is the main route by which organelles are degraded. A type of mitochondrion-targeted autophagy known as mitophagy removes damaged mitochondria in mammalian cells; dysfunctional mitochondria that lose their membrane potential are marked by protein ubiquitination, becoming targets of selective mitophagy. Studies of the quality control system for chloroplasts in plants revealed the involvement of both autophagy and ubiquitination in the degradation of damaged chloroplasts. We recently assessed the relationship between chloroplast-associated ubiquitination mediated by PLANT U-BOX4 (PUB4) and chloroplast-targeted autophagy (chlorophagy) in the turnover of oxidatively damaged chloroplasts. Multiple assays using an Arabidopsis thaliana mutant revealed that PUB4-associated ubiquitination is dispensable for the induction of chlorophagy. Here, we describe the parallel functions of PUB4 and chlorophagy in chloroplast turnover and plant growth.