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首页> 外文期刊>Journal of Experimental Botany >The SNAC1-targeted gene OsSRO1c modulates stomatal closure and oxidative stress tolerance by regulating hydrogen peroxide in rice.
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The SNAC1-targeted gene OsSRO1c modulates stomatal closure and oxidative stress tolerance by regulating hydrogen peroxide in rice.

机译：SNAC1靶向基因OsSRO1c通过调节水稻中的过氧化氢来调节气孔关闭和氧化胁迫耐受性。

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摘要

Abiotic stresses such as drought cause a reduction of plant growth and loss of crop yield. Stomatal aperture controls CO2 uptake and water loss to the atmosphere, thus playing important roles in both the yield gain and drought tolerance of crops. Here, a rice homologue of SRO (similar to RCD one), termed OsSRO1c, was identified as a direct target gene of SNAC1 (stress-responsive NAC 1) involved in the regulation of stomatal aperture and oxidative response. SNAC1 could bind to the promoter of OsSRO1c and activate the expression of OsSRO1c. OsSRO1c was induced in guard cells by drought stress. The loss-of-function mutant of OsSRO1c showed increased stomatal aperture and sensitivity to drought, and faster water loss compared with the wild-type plant, whereas OsSRO1c overexpression led to decreased stomatal aperture and reduced water loss. Interestingly, OsSRO1c-overexpressing rice showed increased sensitivity to oxidative stress. Expression of DST, a reported zinc finger gene negatively regulating H2O2-induced stomatal closure, and the activity of H2O2-scavenging related enzymes were significantly suppressed, and H2O2 in guard cells was accumulated in the overexpression lines. OsSRO1c interacted with various stress-related regulatory and functional proteins, and some of the OsSRO1c-interacting proteins are predicted to be involved in the control of stomatal aperture and oxidative stress tolerance. The results suggest that OsSRO1c has dual roles in drought and oxidative stress tolerance of rice by promoting stomatal closure and H2O2 accumulation through a novel pathway involving regulators SNAC1 and DST.
机译：非生物胁迫（例如干旱）导致植物生长减少和农作物减产。气孔孔径控制了CO 2 的吸收和向大气的水分流失，因此在作物的增产和耐旱性中都发挥着重要作用。在这里，被称为OsSRO1c的SRO的水稻同源物（类似于RCD 1）被鉴定为SNAC1（应激反应性NAC 1）的直接靶基因，参与了气孔孔径和氧化反应的调控。 SNAC1可以与OsSRO1c的启动子结合并激活OsSRO1c的表达。干旱胁迫在保卫细胞中诱导了OsSRO1c。与野生型植物相比，OsSRO1c的功能丧失突变体显示出气孔孔径和对干旱的敏感性增加，并且水分损失更快，而OsSRO1c的过表达导致气孔孔径降低和水分损失减少。有趣的是，过表达OsSRO1c的水稻对氧化应激的敏感性增强。 DST的表达，已报道的锌指基因负调控H 2 O 2 诱导的气孔关闭，以及H 2 O 2 清除相关酶被显着抑制，保卫细胞中的H 2 O 2 在过表达系中积累。 OsSRO1c与各种与压力有关的调节蛋白和功能蛋白相互作用，并且某些与OsSRO1c相互作用的蛋白预计与气孔孔径和氧化应激耐受性的控制有关。结果表明，OsSRO1c通过调控SNAC1和DST的新途径促进气孔关闭和H 2 O 2 积累，从而在水稻的干旱和氧化胁迫耐受中具有双重作用。

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