Abstract In plants, autophagy is a conserved recycling system essential for development and stress responses by targeting cellular components for massive degradation in the vacuole. Our previous work suggested that autophagy contributes to Arabidopsis ( Arabidopsis thaliana ) stress responses by modulating NADPH-oxidase-mediated reactive oxygen species (ROS) homeostasis; however, the molecular link between extracellular ROS and autophagy remains unknown. We performed a yeast two-hybrid screen to identify components involved in autophagy, using the central autophagy component ATG8e as a bait. We identified MEMBRANE ATTACK COMPLEX/PERFORIN-LIKE 2 (MACP2) as an interactor of ATG8e via its the ATG8-interacting motif and confirmed this interaction by co-immunoprecipitation and bimolecular fluorescence complementation assays. MACP2- overexpressing lines showed enhanced sensitivity to nutritional starvation, accelerated leaf senescence, and increased hydrogen peroxide (H 2 O 2 ) levels, resembling the phenotypes of atg mutants defective in autophagy. Conversely, macp2 knockouts exhibited diminished starvation-induced H 2 O 2 accumulation and attenuated autophagosome formation and fully suppressed the starvation-hypersensitive phenotypes of the atg5-1 mutant. In particular, MACP2 was degraded through the autophagy machinery during prolonged starvation, suggesting a feedback regulatory mechanism for maintaining MACP2 homeostasis. Our findings suggest that MACP2 acts as a key regulator in autophagy induction by controlling influx of extracellular H 2 O 2 in Arabidopsis.
Zhou et al. (Wed,) studied this question.
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