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RtNAC055通过与茉莉酸甲酯/过氧化氢信号相关的气孔关闭途径促进干旱耐受性。

RtNAC055 promotes drought tolerance via a stomatal closure pathway linked to methyl jasmonate/hydrogen peroxide signaling in .

作者信息

Ma Binjie, Zhang Jie, Guo Shuyu, Xie Xinlei, Yan Lang, Chen Huijing, Zhang Hongyi, Bu Xiangqi, Zheng Linlin, Wang Yingchun

机构信息

Key Laboratory of Herbage and Endemic Crop Biology, and College of Life Sciences, Inner Mongolia University, Hohhot 010070, China.

Institute of Crop Sciences (ICS), Chinese Academy of Agricultural Sciences (CAAS), Beijing 100081, China.

出版信息

Hortic Res. 2024 Jan 3;11(2):uhae001. doi: 10.1093/hr/uhae001. eCollection 2024 Feb.

Abstract

The stomata regulate CO uptake and efficient water usage, thereby promoting drought stress tolerance. NAC proteins (NAM, ATAF1/2, and CUC2) participate in plant reactions following drought stress, but the molecular mechanisms underlying NAC-mediated regulation of stomatal movement are unclear. In this study, a novel NAC gene from , , was found to enhance drought tolerance via a stomatal closure pathway. It was regulated by RtMYC2 and integrated with jasmonic acid signaling and was predominantly expressed in stomata and root. The suppression of could improve jasmonic acid and HO production and increase the drought tolerance of transgenic callus. Ectopic expression of in the mutant rescued its drought-sensitive phenotype by decreasing stomatal aperture. Under drought stress, overexpression of in poplar promoted ROS (HO) accumulation in stomata, which accelerated stomatal closure and maintained a high photosynthetic rate. Drought upregulated the expression of , , and ., as well as antioxidant enzyme activities in heterologous expression poplars. RtNAC055 promoted HO production in guard cells by directly binding to the promoter of , thus regulating stomatal closure. The stress-related genes . were directly regulated by RtNAC055. These results indicate that RtNAC055 regulates stomatal closure by maintaining the balance between the antioxidant system and HO level, reducing the transpiration rate and water loss, and improving photosynthetic efficiency and drought resistance.

摘要

气孔调节二氧化碳吸收和水分有效利用,从而提高对干旱胁迫的耐受性。NAC蛋白(NAM、ATAF1/2和CUC2)参与干旱胁迫后的植物反应,但NAC介导气孔运动调节的分子机制尚不清楚。在本研究中,发现一个来自[具体物种]的新NAC基因通过气孔关闭途径增强耐旱性。它受RtMYC2调控并与茉莉酸信号整合,主要在气孔和根中表达。抑制[该基因名称]可提高茉莉酸和过氧化氢产量,并增加转基因[植物名称]愈伤组织的耐旱性。在[突变体名称]突变体中异位表达[该基因名称]可通过减小气孔孔径挽救其干旱敏感表型。在干旱胁迫下,杨树中[该基因名称]的过表达促进气孔中活性氧(过氧化氢)积累,加速气孔关闭并维持高光合速率。干旱上调了异源表达杨树中[该基因名称]、[相关基因名称1]和[相关基因名称2]的表达以及抗氧化酶活性。RtNAC055通过直接结合[相关基因名称3]的启动子促进保卫细胞中过氧化氢的产生,从而调节气孔关闭。胁迫相关基因[相关基因名称4]受RtNAC055直接调控。这些结果表明,RtNAC055通过维持抗氧化系统和过氧化氢水平之间的平衡、降低蒸腾速率和水分流失以及提高光合效率和抗旱性来调节气孔关闭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3373/10901477/5523f94d516f/uhae001f1.jpg

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