The rimb1 (redox imbalanced 1) mutation was mapped to the RCD1 locus (radical-
induced cell death 1; At1g32230) demonstrating that a major factor involved in
redox-regulation genes for chloroplast antioxidant enzymes and protection
against photooxidative stress, RIMB1, is identical to the regulator of disease
response reactions and cell death, RCD1. Discovering this link let to our
investigation of its regulatory mechanism. We show in yeast that RCD1 can
physically interact with the transcription factor Rap2.4a which provides
redox-sensitivity to nuclear expression of genes for chloroplast antioxidant
enzymes. In the rimb1 (rcd1-6) mutant, a single nucleotide exchange results in
a truncated RCD1 protein lacking the transcription factor binding site.
Protein-protein interaction between full-length RCD1 and Rap2.4a is supported
by H2O2, but not sensitive to the antioxidants dithiotreitol and ascorbate. In
combination with transcript abundance analysis in Arabidopsis, it is concluded
that RCD1 stabilizes the Rap2.4-dependent redox-regulation of the genes
encoding chloroplast antioxidant enzymes in a widely redox-independent manner.
Over the years, rcd1-mutant alleles have been described to develop symptoms
like chlorosis, lesions along the leaf rims and in the mesophyll and
(secondary) induction of extra- and intra-plastidic antioxidant defense
mechanisms. All these rcd1 mutant characteristics were observed in rcd1-6 to
succeed low activation of the chloroplast antioxidant system and glutathione
biosynthesis. We conclude that RCD1 protects plant cells from running into
reactive oxygen species (ROS)-triggered programs, such as cell death and
activation of pathogen-responsive genes (PR genes) and extra-plastidic
antioxidant enzymes, by supporting the induction of the chloroplast
antioxidant system