Cytosolic alkalisation and nitric oxide production in UVB-induced stomatal closure in Arabidopsis thaliana
Xiao-Min Ge A , Yan Zhu A and Jun-Min He A BA School of Life Sciences, Shaanxi Normal University, Xi’an 710062, People’s Republic of China.
B Corresponding author. Email: hejm@snnu.edu.cn
Functional Plant Biology 41(8) 803-811 https://doi.org/10.1071/FP13222
Submitted: 29 July 2013 Accepted: 27 March 2014 Published: 28 April 2014
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 0.5 W m–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 60 min 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 60 min of UVB radiation, but prevented the UVB-induced cytosolic alkalisation after 60 min 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.
Additional keywords: cytosolic pH, nitric oxide, UVB irradiation.
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