Abstract

Autophagy is a homeostatic degradation and recycling process that is also involved in defense against microbial pathogens and in certain forms of cellular suicide. Autophagy has been proposed to negatively regulate plant immunity-associated cell death related to the hypersensitive response (HR), as older autophagy-deficient mutants are unable to contain this type of cell death 5 to 10 d after infection. Such spreading cell death was found to require NPR1 (nonexpressor of PR genes 1), but surprisingly did not occur in younger atg mutants. In contrast, we find that npr1 mutants are not impaired in rapid programmed cell death activation upon pathogen recognition. Furthermore, our molecular evidence suggests that the NPR1-dependent spreading cell death in older atg mutants may originate from an inability to cope with excessive accumulation of ubiquitinated proteins and ER stress which derive from salicylic acid (SA)-dependent signaling (e. g., systemic acquired resistance). We also demonstrate that both senescence and immunity-related cell death seen in older atg mutants can be recapitulated in younger atg mutants primed with ER stress. We therefore propose that the reduction in SA signaling caused by npr1 loss-of-function is sufficient to alleviate the stress levels accumulated during aging in autophagy deficient cells which would otherwise become insurmountable and lead to uncontrolled cell death.

Keywords

age; atg; autophagy; cell death; ER stress; infection; npr1; senescence; ubiquitin

Published in

Autophagy
2014, Volume: 10, number: 9, pages: 1579-1587
Publisher: LANDES BIOSCIENCE

SLU Authors

• Hofius, Daniel

  • Department of Plant Biology, Swedish University of Agricultural Sciences
    

Associated SLU-program

SLU Plant Protection Network


UKÄ Subject classification

Developmental Biology
Plant Biotechnology
Cell Biology


Publication identifier

DOI: https://doi.org/10.4161/auto.29406

Permanent link to this page (URI)

https://res.slu.se/id/publ/66838