Guard cell hydrogen peroxide and nitric oxide mediate elevated CO2-induced stomatal movement in tomato

Guard cell hydrogen peroxide and nitric oxide mediate elevated CO2-induced stomatal movement in tomato
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保卫细胞过氧化氢和一氧化氮介导二氧化碳诱导番茄气孔运动升高

DOI:
10.1111/nph.13621
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发表时间:
2015-10-01
期刊:
影响因子:
9.4
通讯作者:
Yu, Jingquan
Yu, Jingquan
中科院分区:
生物学1区
文献类型:
--
作者:
Shi, Kai;Li, Xin;Yu, Jingquan

文献摘要

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由于大气中二氧化碳的增加,气候变化影响了植物的光合作用和蒸腾作用。虽然气孔参与植物对CO2浓度升高的反应已经得到了很好的证实,但CO2浓度升高诱导气孔运动的潜在机制仍然很不清楚。生物化学方法和基因沉默来研究CO2浓度升高诱导番茄气孔运动的信号通路CO2浓度升高诱导的气孔关闭依赖于保卫细胞中呼吸爆发氧化酶1(RBOH 1)介导的过氧化氢(H2O2)和硝酸还原酶(NR)介导的一氧化氮(NO)的产生,而脱落酸(阿坝)不依赖于此。开放气孔1(open STOMATA 1,OST 1)基因的沉默可抑制CO2诱导的H2O2和NO的积累,抑制SLAC1基因的表达,抑制气孔开度的减小,而RBOH 1和NR基因的沉默对OST 1的表达没有影响。RBOH1依赖的H2O2和NR依赖的NO作用于OST 1的下游,调节SLAC1的表达和CO2诱导的气孔运动。这些信息对于加深对保卫细胞中CO2信号通路的理解至关重要。
Climate change as a consequence of increasing atmospheric CO2 influences plant photosynthesis and transpiration. Although the involvement of stomata in plant responses to elevated CO2 has been well established, the underlying mechanism of elevated CO2-induced stomatal movement remains largely unknown.We used diverse techniques, including laser scanning confocal microscopy, transmission electron microscopy, biochemical methodologies and gene silencing to investigate the signaling pathway for elevated CO2-induced stomatal movement in tomato (Solanum lycopersicum).Elevated CO2-induced stomatal closure was dependent on the production of RESPIRATORY BURST OXIDASE 1 (RBOH1)-mediated hydrogen peroxide (H2O2) and NITRATE REDUCTASE (NR)-mediated nitric oxide (NO) in guard cells in an abscisic acid (ABA)-independent manner. Silencing of OPEN STOMATA 1 (OST1) compromised the elevated CO2-induced accumulation of H2O2 and NO, upregulation of SLOW ANION CHANNEL ASSOCIATED 1 (SLAC1) gene expression and reduction of stomatal aperture, whereas silencing of RBOH1 or NR had no effects on the expression of OST1.Our results demonstrate that as critical signaling molecules, RBOH1-dependent H2O2 and NR-dependent NO act downstream of OST1 that regulate SLAC1 expression and elevated CO2-induced stomatal movement. This information is crucial to deepen the understanding of CO2 signaling pathway in guard cells.