干旱触发的 miR166 抑制促进大豆的耐旱性

Chen Zhao, Jingjing Ma, Chen Yan, Yu Jiang, Yaohua Zhang, Yudan Lu, Ye Zhang, Suxin Yang, Xianzhong Feng, Jun Yan
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引用次数: 0

摘要

干旱胁迫限制了全世界的农业生产力。鉴定和描述干旱胁迫耐受性网络的遗传元件可提高作物对干旱胁迫的耐受性。我们的研究表明,miR166与其靶基因ATHB14-LIKE组成的调控模块在大豆(Glycine max)的抗旱性调控中发挥作用。干旱胁迫抑制了 miR166 的积累,导致其靶基因上调。在稳定的转基因品系 GmSTTM166 中对 miR166 进行最佳敲除可获得耐旱性而不影响产量。ABA 信号通路基因的表达受到 miR166 介导的调控途径的调控,ATHB14-LIKE 直接激活了其中一些基因。ATHB14-LIKE 与 MIR166 基因之间存在反馈调控,ATHB14-LIKE 可抑制 MIR166 的表达。这些发现揭示了干旱触发调控 miR166 介导的调控途径可提高植物的抗旱性,为研究大豆干旱胁迫调控网络提供了新的视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Drought-triggered repression of miR166 promotes drought tolerance in soybean

Drought stress limits agricultural productivity worldwide. Identifying and characterizing genetic components of drought stress-tolerance networks may improve crop resistance to drought stress. We show that the regulatory module formed by miR166 and its target gene, ATHB14-LIKE, functions in the regulation of drought tolerance in soybean (Glycine max). Drought stress represses the accumulation of miR166, leading to upregulation of its target genes. Optimal knockdown of miR166 in the stable transgenic line GmSTTM166 conferred drought tolerance without affecting yield. Expression of ABA signaling pathway genes was regulated by the miR166-mediated regulatory pathway, and ATHB14-LIKE directly activates some of these genes. There is a feedback regulation between ATHB14-LIKE and MIR166 genes, and ATHB14-LIKE inhibits MIR166 expression. These findings reveal that drought-triggered regulation of the miR166-mediated regulatory pathway increases plants drought resistance, providing new insights into drought stress regulatory network in soybean.

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