Abiotic stresses such as drought cause a reduction of plant growth and loss of crop yield. Stomatal aperture controls CO(2) uptake and water loss to the atmosphere, thus playing important roles in both the yield gain and drought tolerance of crops. Here, a rice homologue of SRO (similar to RCD one), termed OsSRO1c, was identified as a direct target gene of SNAC1 (stress-responsive NAC 1) involved in the regulation of stomatal aperture and oxidative response. SNAC1 could bind to the promoter of OsSRO1c and activate the expression of OsSRO1c. OsSRO1c was induced in guard cells by drought stress. The loss-of-function mutant of OsSRO1c showed increased stomatal aperture and sensitivity to drought, and faster water loss compared with the wild-type plant, whereas OsSRO1c overexpression led to decreased stomatal aperture and reduced water loss. Interestingly, OsSRO1c-overexpressing rice showed increased sensitivity to oxidative stress. Expression of DST, a reported zinc finger gene negatively regulating H(2)O(2)-induced stomatal closure, and the activity of H(2)O(2)-scavenging related enzymes were significantly suppressed, and H(2)O(2) in guard cells was accumulated in the overexpression lines. OsSRO1c interacted with various stress-related regulatory and functional proteins, and some of the OsSRO1c-interacting proteins are predicted to be involved in the control of stomatal aperture and oxidative stress tolerance. The results suggest that OsSRO1c has dual roles in drought and oxidative stress tolerance of rice by promoting stomatal closure and H(2)O(2) accumulation through a novel pathway involving regulators SNAC1 and DST.