Physiological characterization and genetic modifiers of aberrant root thigmomorphogenesis in mutants of Arabidopsis thaliana MILDEW LOCUS O genes

Root architecture and growth patterns are plant features that are still poorly understood. When grown under in vitro conditions, seedlings with mutations in Arabidopsis thaliana genes MLO4 or MLO11 exhibit aberrant root growth patterns upon contact with hard surfaces, exemplified as tight root spirals. We used a set of physiological assays and genetic tools to characterize this thigmomorphogenic defect in detail. We observed that the mlo4/mlo11-associated root curling phenotype is not recapitulated in a set of mutants with altered root growth patterns or architecture. We further found that mlo4/mlo11-conditioned root curling is not dependent upon light and endogenous flavonoids, but is pH-sensitive and affected by exogenous calcium levels. Based upon the latter two characteristics, mlo4-associated root coiling appears to be mechanistically different from the natural strong root curvature of the Arabidopsis ecotype Landsberg erecta. Gravistimulation reversibly overrides the aberrant thigmomorphogenesis of mlo4 seedlings. Mutants with dominant negative defects in -tubulin modulate the extent and directionality of mlo4/mlo11-conditioned root coils, whereas mutants defective in polar auxin transport (axr4, aux1) or gravitropism (pgm1) completely suppress the mlo4 root curling phenotype. Our data implicate a joint contribution of calcium signalling, pH regulation, microtubular function, polar auxin transport and gravitropism in root thigmomorphogenesis. We examined the aberrant root thigmotropism phenotype of Arabidopsis thaliana mlo4 and mlo11 mutants, which is represented by tight root spirals, using a range of physiological assays and by genetic means. The characteristic root curls are not recapitulated in a set of tested mutants with abnormal root growth patterns. We found that the formation of the spirals is pH-dependent, affected by exogenous calcium levels, modulated by microtubule structure and suppressed by mutants with defective auxin transport and gravitropism.