Role and interrelationship of Gα protein, hydrogen peroxide and nitric oxide in UV-B-induced stomatal closure in Arabidopsis leaves
Xiange Ma, Ying Zhang, Junmin He*
School of Life Sciences, Shaanxi Normal University, Xi’an 710062, China
*Corresponding Author: Tel: (+8610) 029-85310266; Fax: (+8610) 029-85303736; E-mail: firstname.lastname@example.org
We found that 0.5 W m-2 UV-B triggered a significant increase in hydrogen peroxide (H2O2) or nitric oxide (NO) levels associated with stomatal closure in wild type, but these effects were abolished in the single and double mutants of AtrbohD and AtrbohF or in the Nia1 mutants respectively. Furthermore, we found that UV-B-mediated H2O2 and NO generation are regulated by GPA1, the Gα-subunit of heterotrimeric G proteins. UV-B-dependent H2O2 and NO accumulation were nullified in gpa1 knockout mutants but enhanced by overexpression of a constitutively active form of GPA1 (cGα). In addition, exogenously applied H2O2 or NO rescued the defect in UV-B-mediated stomatal closure in gpa1 mutants, whereas cGα AtrbohD/F and cGα nia1 constructs exhibited a similar response as AtrbohD/F and Nia1 did respectively. Finally, we demonstrated that Gα activation of NO production depends on H2O2. The mutants of AtrbohD and AtrbohF had impaired NO generation in response to UV-B, but UV-B-induced H2O2 accumulation was not impaired in Nia1. Moreover, exogenously applied NO rescued the defect in UV-B-mediated stomatal closure in the mutants of AtrbohD and AtrbohF. These findings establish a signaling pathway leading to UV-B-induced stomatal closure, which involves GPA1-dependent activation of H2O2 production and subsequent Nia1-dependent NO accumulation.
Key Words: Gα protein; hydrogen peroxide; nitric oxide; UV-B; stomatal movement; Arabidopsis thaliana