Abstract
BackgroundAutophagy is an evolutionarily conserved system for the degradation of intracellular components in eukaryotic organisms. Autophagy plays essential roles in preventing premature senescence and extending the longevity of vascular plants. However, the mechanisms and physiological roles of autophagy in preventing senescence in basal land plants are still obscure.ResultsHere, we investigated the functional roles of the autophagy-related gene PpATG3 from Physcomitrella patens and demonstrated that its deletion prevents autophagy. In addition, Ppatg3 mutant showed premature gametophore senescence and reduced protonema formation compared to wild-type (WT) plants under normal growth conditions. The abundance of nitrogen (N) but not carbon (C) differed significantly between Ppatg3 mutant and WT plants, as did relative fatty acid levels. In vivo protein localization indicated that PpATG3 localizes to the cytoplasm, and in vitro Y2H assays confirmed that PpATG3 interacts with PpATG7 and PpATG12. Plastoglobuli (PGs) accumulated in Ppatg3, indicating that the process that degrades damaged chloroplasts in senescent gametophore cells was impaired in this mutant. RNA-Seq uncovered a detailed, comprehensive set of regulatory pathways that were affected by the autophagy mutation.ConclusionsThe autophagy-related gene PpATG3 is essential for autophagosome formation in P. patens. Our findings provide evidence that autophagy functions in N utilization, fatty acid metabolism and damaged chloroplast degradation under non-stress conditions. We identified differentially expressed genes in Ppatg3 involved in numerous biosynthetic and metabolic pathways, such as chlorophyll biosynthesis, lipid metabolism, reactive oxygen species removal and the recycling of unnecessary proteins that might have led to the premature senescence of this mutant due to defective autophagy. Our study provides new insights into the role of autophagy in preventing senescence to increase longevity in basal land plants.
Highlights
Autophagy is an evolutionarily conserved system for the degradation of intracellular components in eukaryotic organisms
Our findings provide evidence that autophagy functions in N utilization, fatty acid metabolism and damaged chloroplast degradation under non-stress conditions
We identified differentially expressed genes in Ppatg3 involved in numerous biosynthetic and metabolic pathways, such as chlorophyll biosynthesis, lipid metabolism, reactive oxygen species removal and the recycling of unnecessary proteins that might have led to the premature senescence of this mutant due to defective autophagy
Summary
Autophagy is an evolutionarily conserved system for the degradation of intracellular components in eukaryotic organisms. Autophagy is an evolutionarily conserved, ubiquitous process in eukaryotic cells that degrades damaged or toxic intracellular components for recycling to maintain essential cellular functions and life activities [1,2,3]. At least 30 ATG proteins had been identified in yeast (Saccharomyces cerevisiae), which can be divided into several functional classes: a) the ATG1ATG13 kinase complex; b) ATG9 and ATG9-associated proteins; c) the phosphatidylinositol 3-kinase complex; and d) two ubiquitin-like conjugation systems mediated by ATG8 or ATG12 [8]. Most of these proteins have homologs in plants. Autophagosome formation is defective in ATG3 mutant in yeast [22] and Toxoplasma [23], and autophagic activity was enhanced by overexpressing ATG3 in tobacco [24]
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