H_2S位于SOS上游参与盐胁迫诱导的拟南芥气孔关闭  

H_2S Signals Salt-Induced Stomatal Closure in Arabidopsis thaliana by SOS Pathway

作　　者：车永梅[1] 邹雪[1] 王兰香[1] 张丹丹[1] 刘新[1] 

机构地区：[1]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

出　　处：《植物生理学报》2012年第11期1098-1104,共7页Plant Physiology Journal

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

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。Using Arabidopsis thaliana wild-type, salt overly sensitive （SOS） mutants Atsosl, 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 hydro- gen 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 in- creased dramaticly under salt stress. Salt stress could induce stomatal closure in A. thaliana wild-type and OEL- CDes and OED-CDes, but had no effect on Atl-cdes and Atd-cdes. The H2S scavenger hypotaurine （HT） inhibit- ed 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 Atsosl, Atsos2, Atsos3. Furthermore, salt-induced increase in H2S content and L-/D-CDes activity can be observed in wild type as well as Atsosl, Atsos2 and Atsos3. However, compared with wild-type, salt stress had no significant effect on gene expression ofAtSOS1, AtSOS2 and AtSOS2 in mu- tants neither Atl-cdes nor Atd-cdes. All these results indicated that H2S functions upstream of SOS in salt-in- duced stomatal closure in A. thaliana.

关 键 词：H2S SOS 盐胁迫 气孔关闭 

分 类 号：Q945.78[生物学—植物学]