Functional disruption of the pentatricopeptide protein SLG1 affects mitochondrial RNA editing, plant development, and responses to abiotic stresses in Arabidopsis.

Land plants contain a large family of genes that encode for pentatricopeptide (PPR) proteins. To date, few of these PPR proteins have been functionally characterized. In this study, we have analyzed an Arabidopsis mutant, slg1, which exhibits slow growth and delayed development. In addition, slg1 shows an enhanced response to ABA and increased tolerance to drought stress. The SLG1 gene encodes a PPR protein that is localized in mitochondria. In the slg1 mutant, RNA editing in a single site of the mitochondrial transcript nad3 is abolished. nad3 is a subunit of complex I of the electron transport chain in mitochondria. As a consequence, the NADH dehydrogenase activity of complex I in slg1 is strongly impaired and production of ATP is reduced. When responding to ABA treatment, slg1 accumulates more H(2) O(2) in its guard cells than the wild type. The slg1 mutant also has an increased expression of genes involved in the alternative respiratory pathway, which may compensate for the disrupted function of complex I and help scavenge the excess accumulation of H(2) O(2). Our functional characterization of the slg1 mutant revealed a putative link between mitochondrial RNA editing and plant responses to abiotic stress.