Growth deficiency and enhanced basal immunity in Arabidopsis thaliana mutants of EDM2, EDM3 and IBM2 are genetically interlinked.

Abstract

Mutants of the Arabidopsis thaliana genes, EDM2 (Enhanced Downy Mildew 2), EDM3 (Enhanced Downy Mildew 3) and IBM2 (Increase in Bonsai Methylation 2) are known to show defects in a diverse set of defense and developmental processes. For example, they jointly exhibit enhanced levels of basal defense and stunted growth. Here we show that these two phenotypes are functionally connected by their dependency on the salicylic acid biosynthesis gene SID2 and the basal defense regulatory gene PAD4. Stunted growth of edm2, edm3 and ibm2 plants is a consequence of up-regulated basal defense. Constitutively enhanced activity of reactive oxygen species-generating peroxidases, we observed in these mutants, appears also to contribute to both, their enhanced basal defense and their growth retardation phenotypes. Furthermore, we found the histone H3 demethylase gene IBM1, a direct regulatory target of EDM2, EDM3 and IBM2, to be at least partially required for the basal defense and growth-related effects observed in these mutants. We recently reported that EDM2, EDM3 and IBM2 coordinate basal immunity with the timing of the floral transition by gradually reducing the extent of this defense mechanism prior to flowering. Together with these observations, data presented here show that at least some of the diverse phenotypic effects in edm2, edm3 and ibm2 mutants are genetically interlinked and functionally connected. Our new results show that repression of basal immunity by EDM2, EDM3 and IBM2 limits negative impact on growth and development.