JOURNAL ARTICLE

The Arabidopsis mitochondria-localized pentatricopeptide repeat protein PGN functions in defense against necrotrophic fungi and abiotic stress tolerance

Kristin Laluk, Synan Abuqamar, Tesfaye Mengiste
Plant Physiology 2011, 156 (4): 2053-68
21653783
Pentatricopeptide repeat (PPR) proteins (PPRPs) are encoded by a large gene family in Arabidopsis (Arabidopsis thaliana), and their functions are largely unknown. The few studied PPRPs are implicated in different developmental processes through their function in RNA metabolism and posttranscriptional regulation in plant organelles. Here, we studied the functions of Arabidopsis PENTATRICOPEPTIDE REPEAT PROTEIN FOR GERMINATION ON NaCl (PGN) in plant defense and abiotic stress responses. Inactivation of PGN results in susceptibility to necrotrophic fungal pathogens as well as hypersensitivity to abscisic acid (ABA), glucose, and salinity. Interestingly, ectopic expression of PGN results in the same phenotypes as the pgn null allele, indicating that a tight regulation of the PGN transcript is required for normal function. Loss of PGN function dramatically enhanced reactive oxygen species accumulation in seedlings in response to salt stress. Inhibition of ABA synthesis and signaling partially alleviates the glucose sensitivity of pgn, suggesting that the mutant accumulates high endogenous ABA. Accordingly, induction of NCED3, encoding the rate-limiting enzyme in stress-induced ABA biosynthesis, is significantly higher in pgn, and the mutant has higher basal ABA levels, which may underlie its phenotypes. The pgn mutant has altered expression of other ABA-related genes as well as mitochondria-associated transcripts, most notably elevated levels of ABI4 and ALTERNATIVE OXIDASE1a, which are known for their roles in retrograde signaling induced by changes in or inhibition of mitochondrial function. These data, coupled with its mitochondrial localization, suggest that PGN functions in regulation of reactive oxygen species homeostasis in mitochondria during abiotic and biotic stress responses, likely through involvement in retrograde signaling.

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