The Arabidopsis Rho of Plants GTPase AtROP6 Functions in Developmental and Pathogen Response Pathways1[C][W][OA]

A molecular switch integrates development and pathogen response signaling in plants. How plants coordinate developmental processes and environmental stress responses is a pressing question. Here, we show that Arabidopsis ( Arabidopsis thaliana ) Rho of Plants6 (AtROP6) integrates developmental and pathogen response signaling. AtROP6 expression is induced by auxin and detected in the root meristem, lateral root initials, and leaf hydathodes. Plants expressing a dominant negative AtROP6 (rop6 DN ) under the regulation of its endogenous promoter are small and have multiple inflorescence stems, twisted leaves, deformed leaf epidermis pavement cells, and differentially organized cytoskeleton. Microarray analyses of rop6 DN plants revealed that major changes in gene expression are associated with constitutive salicylic acid ( SA )-mediated defense responses. In agreement, their free and total SA levels resembled those of wild-type plants inoculated with a virulent powdery mildew pathogen. The constitutive SA -associated response in rop6 DN was suppressed in mutant backgrounds defective in SA signaling ( nonexpresser of PR genes1 [ npr1 ]) or biosynthesis ( salicylic acid induction deficient2 [ sid2 ]). However, the rop6 DN npr1 and rop6 DN sid2 double mutants retained the aberrant developmental phenotypes, indicating that the constitutive SA response can be uncoupled from ROP function(s) in development. rop6 DN plants exhibited enhanced preinvasive defense responses to a host-adapted virulent powdery mildew fungus but were impaired in preinvasive defenses upon inoculation with a nonadapted powdery mildew. The host-adapted powdery mildew had a reduced reproductive fitness on rop6 DN plants, which was retained in mutant backgrounds defective in SA biosynthesis or signaling. Our findings indicate that both the morphological aberrations and altered sensitivity to powdery mildews of rop6 DN plants result from perturbations that are independent from the SA -associated response. These perturbations uncouple SA -dependent defense signaling from disease resistance execution.