Autophagy Promotes Cell Death Induced by Hydrogen Peroxide in Physcomitrium patens.

This article investigates how autophagy influences cell death in the moss Physcomitrium patens under oxidative stress induced by hydrogen peroxide (H₂O₂). It demonstrates that autophagy-defective mutants (atg3, atg5, and atg7) survive high concentrations of H₂O₂ that are lethal to wild-type (WT) plants, indicating that autophagy promotes H₂O₂-induced cell death. The study shows that autophagy activation after H₂O₂ treatment leads to increased amino acid production in vacuoles, which are catabolized via mitochondrial and chloroplast electron transport chains (ETCs), generating reactive oxygen species (ROS) and sustaining elevated intracellular H₂O₂ levels (termed H₂O₂ plateaus). These elevated H₂O₂ levels cause vacuole collapse and subsequent cell death in WT plants, while autophagy inhibition or substitution with endocytosed bovine serum albumin reduces H₂O₂ accumulation and cell death. The findings suggest a mechanism whereby autophagy-derived amino acids fuel ROS production through damaged ETCs, linking autophagy to oxidative stress–induced vacuolar cell death in P. patens.