Noncanonical ATG8-ABS3 interaction controls senescence in plants

摘要

Protein homeostasis is essential for cellular functions and longevity, and the loss of proteostasis is one of the hallmarks of senescence. Autophagy is an evolutionarily conserved cellular degradation pathway and is critical for the maintenance of proteostasis. Paradoxically, autophagy deficiency leads to accelerated protein loss by unknown mechanisms. We discover that ABS3 subfamily of multidrug and toxic compound extrusion (MATE) transporters promote senescence in natural and carbon-deprivation conditions in Arabidopsis thaliana. The senescence-promoting ABS3 pathway functions in parallel with the longevity-promoting autophagy to balance plant senescence and survival. Surprisingly, ABS3 subfamily MATE proteins interact with ATG8 at late endosome to promote senescence and protein degradation without the canonical cleavage and lipidation of ATG8. This non-autophagic ATG8-ABS3 interaction paradigm is likely conserved among dicots and monocots. Our findings uncover a previously unknown non-autophagic function of ATG8 and an unrecognized senescence regulatory pathway controlled by the ATG8-ABS3-mediated proteostasis.