Fig. 8: Proposed model for the adapter role of PsAF5 in ROS-induced mitophagy.
After sensing infection by pathogens, host-derived ROS can be produced in the apoplastic space of plant cells. Of those ROS, H2O2 can be transported into the cytoplasm of haustoria through aquaporins on the plasma cell membrane of the pathogen. H2O2 elevation can promote PsAF5 interaction with PsATG8 through the AIM1 motif. ROS stress can also lead to mitochondrial rupture and the exposure of the IMM mitophagy receptor PsPHB2 to the cytoplasm, increasing the chance of PsAF5 contacting and interacting with PsPHB2 through its ANK domain. This interaction aids the recruitment of lipidated PsATG8 (PsATG8-PE) and the phagophore to stressed mitochondria, thereby promoting mitophagy. The autophagosome that envelops the mitochondrial further fuses with vacuoles, helping decrease the pH that activates acidic hydrolytic enzymes for the degradation of the stressed mitochondria. The ΔPsAF5 mutant cannot efficiently remove damaged mitochondria through mitophagy in time, resulting in ROS accumulation and abnormal mycelial physiology. Ub indicates mitochondrial ubiquitination.
