Cytosolic alkalisation and nitric oxide production in UVB-induced stomatal closure in Arabidopsis thaliana.

Abstract

The role and the interrelationship of cytosolic alkalisation and nitric oxide (NO) in UVB-induced stomatal closure were investigated in Arabidopsis thaliana (L.) Heynh. by stomatal bioassay and laser-scanning confocal microscopy. In response to 0.5Wm-2 UVB radiation, the rise of NO levels in guard cells occurred after cytosolic alkalisation but preceded stomatal closure. UVB-induced NO production and stomatal closure were both inhibited by NO scavengers, nitrate reductase (NR) inhibitors and a Nia2-5/Nia1-2 mutation, and also by butyrate. Methylamine induced NO generation and stomatal closure in the wild-type but not in the Nia2-5/Nia1-2 mutant or wild-type plants pretreated with NO scavengers or NR inhibitors while enhancing the cytosolic pH in guard cells under light. NO generation in wild-type guard cells was largely induced after 60min of UVB radiation. The defect in UVB-induced NO generation in Nia2-5/Nia1-2 guard cells did not affect the changes of guard cell pH before 60min of UVB radiation, but prevented the UVB-induced cytosolic alkalisation after 60min of radiation. Meanwhile, exogenous NO caused a marked rise of cytosolic pH in guard cells. Together, our results show that cytosolic alkalisation and NR-dependent NO production coordinately function in UVB signalling in A. thaliana guard cells.