The Arabidopsis Mitochondria-Localized Pentatricopeptide Repeat Protein PGN Functions in Defense against Necrotrophic Fungi and Abiotic Stress Tolerance      

Abstract

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.

The Roles of Mitochondrial Reactive Oxygen Species in Cellular Signaling and Stress Response in Plants

“…Evidence for an interplay between ABA and mitochondria via mtROS has been found in lines with different sensitivity to ABA (Laluk et al, 2011; Collectively, these reports show that the underlying causes of increased ABA sensitivity in a range of mutants are mitochondrial defects. In some of these mutants, increases in ROS were reported, while others report decrease, using a variety of different detection methods.…”

‘Omics’ and Plant Responses to Botrytis cinerea

“…Transcriptomics enables us to identify potential candidate genes functioning in plant defense, whereas mutant lines with knockout and/or overexpression traits allow us to elucidate their function in the defense response. Botrytis-induced kinase 1 ( BIK1 ), responsive to dehydration 20 ( RD20 ), pentatricopeptide repeat protein for germination on NaCl ( PGN ), and expansin-like A2 ( EXLA2 ) were identified as B. cinerea -responsive genes, and their mutants exhibited altered susceptibility to necrotrophic pathogens (Veronese et al, 2006; Laluk et al, 2011; AbuQamar et al, 2013; AbuQamar, 2014; Sham et al, 2015). Moreover, the Mediator 18 ( MED18 ), identified using RNAseq, was shown to modulate plant immunity and responses to hormones (Lai et al, 2014).…”

Selected reactive oxygen species and antioxidant enzymes in common bean after Pseudomonas syringae pv. phaseolicola and Botrytis cinerea infection

“…Generally it is accepted that the reactions of plants to necrotrophic pathogens are associated with jasmonic acid (JA) and/or ethylene (ET) signal transduction pathways, while biotrophic pathogens induce salicylic acid (SA) pathway (Glazebrook 2005). In addition, the recent studies have demonstrated that abscisic acid (ABA) is a regulator of plant defence against necrotrophs (Laluk et al 2011). Adie et al (2007) observed that ABA-impaired mutants simultaneously showed high susceptibility to Pythium irregulare and Alternaria brassicicola and increased resistance to Botrytis cinerea.…”