Abstract
Autophagy is an evolutionarily conserved intracellular process for vacuolar degradation of cytoplasmic components. Thus far, it has been shown that autophagy defects in higher plants result in early senescence and excessive immunity-related programmed cell death (PCD) irrespective of nutrient conditions. However, the mechanisms by which cells die in the absence of autophagy have been unclear.
Recently, we found a conserved requirement for salicylic acid (SA) signaling for these phenomena in autophagy-defective mutants (atg mutants). The atg mutant phenotypes of accelerated PCD in senescence and immunity were SA signaling dependent but did not require intact jasmonic acid or ethylene signaling pathways. Application of an SA agonist restored the senescence/cell death phenotype in SA-deficient atg mutants but not in atg npr1 plants, suggesting that the cell death phenotypes in the atg mutants are dependent on the SA signal transducer NPR1. We also showed that autophagy was induced by the SA agonist. These findings imply that plant autophagy operates a novel negative feedback loop modulating SA signaling to negatively regulate senescence and immunity-related PCD.
