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Submergence stress-induced hypocotyl elongation through ethylene signaling-mediated regulation of cortical microtubules in Arabidopsis.
Journal of Experimental Botany ( IF 5.6 ) Pub Date : 2020-01-23 , DOI: 10.1093/jxb/erz453
Xiaohong Wang 1 , Qianqian Ma 1 , Ran Wang 2 , Pan Wang 1 , Yimin Liu 1 , Tonglin Mao 1
Affiliation  

Plant growth is significantly altered in response to submergence stress. However, the molecular mechanisms used by seedlings in response to this stress, especially for hypocotyl growth, are largely unknown in terrestrial plants such as Arabidopsis thaliana. The microtubule cytoskeleton participates in plant cell growth, but it remains unclear whether submergence-mediated plant growth involves the microtubule cytoskeleton. We demonstrated that in Arabidopsis submergence induced underwater hypocotyl elongation through the activation of ethylene signaling, which modulated cortical microtubule reorganization. Submergence enhanced ethylene signaling, which then activated and stabilized its downstream transcription factor, phytochrome-interacting factor 3 (PIF3), to promote hypocotyl elongation. In particular, the regulation of microtubule organization was important for this physiological process. Microtubule-destabilizing protein 60 (MDP60), which was previously identified as a downstream effector of PIF3, played a positive role in submergence-induced hypocotyl elongation. Submergence induced MDP60 expression through ethylene signaling. The effects of submergence on hypocotyl elongation and cortical microtubule reorganization were suppressed in mdp60 mutants. These data suggest a potential mechanism by which submergence activates ethylene signaling to promote underwater hypocotyl elongation via alteration of the microtubule cytoskeleton in Arabidopsis.

中文翻译:

通过拟南芥中乙烯信号介导的皮层微管调节,淹水胁迫诱导的胚轴伸长。

响应于淹没胁迫,植物生长显着改变。但是,在陆地植物如拟南芥中,幼苗特别是对于下胚轴生长所使用的响应这一胁迫的分子机制在很大程度上是未知的。微管细胞骨架参与植物细胞的生长,但是尚不清楚淹没介导的植物生长是否涉及微管细胞骨架。我们证明,在拟南芥中,淹没通过乙烯信号传导的激活诱导了水下下胚轴的伸长,从而调节了皮层微管的重组。浸没增强了乙烯信号传导,然后激活并稳定了其下游转录因子,即植物色素相互作用因子3(PIF3),以促进下胚轴伸长。特别是,微管组织的调节对这一生理过程很重要。微管破坏蛋白60(MDP60),以前被确定为PIF3的下游效应子,在淹没诱导的下胚轴伸长中发挥了积极作用。淹没通过乙烯信号传导诱导了MDP60表达。在mdp60突变体中,浸没对下胚轴伸长和皮层微管重组的影响被抑制。这些数据表明了潜在的机制,浸没激活了乙烯信号传导,通过改变拟南芥中的微管细胞骨架来促进水下下胚轴伸长。在浸没诱导的下胚轴伸长中发挥了积极作用。淹没通过乙烯信号传导诱导了MDP60表达。在mdp60突变体中,浸没对下胚轴伸长和皮层微管重组的影响被抑制。这些数据表明了潜在的机制,通过其浸没激活乙烯信号传导,通过改变拟南芥中的微管细胞骨架来促进水下下胚轴伸长。在浸没诱导的下胚轴伸长中发挥了积极作用。淹没通过乙烯信号传导诱导了MDP60表达。在mdp60突变体中,浸没对下胚轴伸长和皮层微管重组的影响被抑制。这些数据表明了潜在的机制,通过其浸没激活乙烯信号传导,通过改变拟南芥中的微管细胞骨架来促进水下下胚轴伸长。
更新日期:2020-01-24
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