The mechanosensitive Ca2+ channel, OSCA1.1, modulates root hydrotropic bending in Arabidopsis thaliana

Roots exhibit positive hydrotropism in response to soil moisture gradients in arid conditions. However, the mechanisms that regulate hydrotropism are yet to be elucidated. Ca2+ is involved in this response, but the molecular factors that interact with Ca2+ are currently unknown. To understand the role of Ca2+ in hydrotropism, as well as to identify proteins that are involved in this process, we examined the physiology of Arabidopsis thaliana seedlings cultured in Ca2+-free medium. Treatment with cytosolic and apoplastic Ca2+ chelators triggered an increase in hydrotropic root bending, which became more pronounced during the latter stages of the hydrotropic response. Furthermore, we found that the phenotypes of mutants defective in OSCA1.1, a mecha-nosensitive Ca2+ channel, resembled those of wild-type seedlings treated with Ca2+ chelators. Although treatment with Ca2+ chelators also affected root gravitropism, no significant differences in root gravitropism were observed in osca1 mutants, suggesting that OSCA1.1 has a specific function in root hydrotropism. Moreover, transcript level of MIZ1 in OSCA1.1 knockout mutant was higher than that of wild type, specifically at latter stages of the hydrotropic response. Double mutants that carry miz1-1 or miz2 alleles in addition to the osca1 knockout allele lacked hydrotropic response, the phenotypes of which were resembled those of miz1-1 or miz2 single mutants. Our results suggest that OSCA1.1 functions within the same signaling pathway as MIZ1 and MIZ2, and that OSCA1.1-mediated Ca2+ influx across the plasma membrane is required to regulate hydrotropic root bending by regulating MIZ1 expression at the latter stages.