《植物生理学报》 2012, 48(11): 1098-1104

H₂S位于SOS上游参与盐胁迫诱导的拟南芥气孔关闭

车永梅, 邹雪, 王兰香, 张丹丹, 刘新*

青岛农业大学生命科学学院, 山东省高校植物生物技术重点实验室, 山东青岛266109

通信作者：刘新；E-mail: liuxin6080@yahoo.com.cn；Tel: 0532-88030224

摘　要：

以拟南芥野生型、SOS突变体(Atsos1、Atsos2和Atsos3)、H2S合成相关酶L-/D-半胱氨酸脱巯基酶(L-/D-CDes)基因缺 失突变体(Atl-cdes和Atd-cdes)和过表达株系(OEL-CDes和OED-CDes)为材料研究了H2S和SOS信号转导途径在盐胁迫诱导 拟南芥气孔关闭中的作用及其相互关系。结果表明, 盐胁迫能够引起拟南芥叶片H2S含量、L-/D-CDes活性及其基因表达 量显著升高, 诱导野生型拟南芥和OEL-CDes和OED-CDes叶片气孔关闭, 但对Atl-cdes和Atd-cdes气孔开度无显著影响; 而 H2S清除剂次牛磺酸(hypotaurine, HT)可减弱盐胁迫诱导的拟南芥气孔关闭的作用, 表明H2S参与盐胁迫诱导的拟南芥气孔 关闭过程。外源H2S诱导野生型拟南芥气孔关闭, 但对SOS突变体气孔开度无显著影响; 同时盐胁迫下Atsos1、Atsos2和At- sos3亦表现出H2S含量及L-/D-CDes活性显著升高, 且与野生型相比, 盐胁迫对Atl-cdes和Atd-cdes叶片AtSOS基因表达量无显 著影响。表明盐胁迫诱导气孔关闭过程中H2S位于SOS上游。

关键词：H2S; SOS; 盐胁迫; 气孔关闭

收稿：2012-08-01   修定：2012-10-26

资助：国家自然科学基金(30970228和31170237)、山东省自然科 学基金(ZR2010CM024)和植物生理学与生物化学国家重 点实验室开放课题(SKLPPBKF11001)。

H₂S Signals Salt-Induced Stomatal Closure in Arabidopsis thaliana by SOS Pathway

CHE Yong-Mei, ZOU Xue, WANG Lan-Xiang, ZHANG Dan-Dan, LIU Xin*

Key Lab of Plant Biotechnology in Universities of Shandong Province, College of Life Sciences, Qingdao Agricultural University, Qingdao, Shandong 266109, China

Corresponding author: LIU Xin; E-mail: liuxin6080@yahoo.com.cn; Tel: 0532-88030224

Abstract:

Using Arabidopsis thaliana wild-type, salt overly sensitive (SOS) mutants Atsos1, Atsos2, Atsos3, L-/D-cysteine desulfhydrase (L-/D-CDes, enzymes participate in H₂S production) deficient mutants Atl-cdes and Atd-cdes as well as overexpression plants OEL-CDes and OED-CDes as materials, the participation of hydrogen sulfide (H₂S) and SOS signal pathway in salt-induced stomatal closure were studied. The results showed that H₂S content, AtL-CDes and AtD-CDes transcription as well as L-/D-CDes activity in A. thaliana leaves increased dramaticly under salt stress. Salt stress could induce stomatal closure in A. thaliana wild-type and OELCDes and OED-CDes, but had no effect on Atl-cdes and Atd-cdes. The H₂S scavenger hypotaurine (HT) inhibited the inducing effects of salt on stomatal closure in A. thaliana wild-type, it can be deduced that H₂S participated in salt-induced stomatal closure in A. thaliana. Exogenous H₂S induced stomatal closure in wild type. However, it had no effects on Atsos1, Atsos2, Atsos3. Furthermore, salt-induced increase in H₂S content and L-/D-CDes activity can be observed in wild type as well as Atsos1, Atsos2 and Atsos3. However, compared with wild-type, salt stress had no significant effect on gene expression of AtSOS1, AtSOS2 and AtSOS2 in mutants neither Atl-cdes nor Atd-cdes. All these results indicated that H₂S functions upstream of SOS in salt-induced stomatal closure in A. thaliana.

Key words: H₂S; SOS; salt stress; stomatal closure