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独脚金内酯诱导的 SMXL7 和 SMXL8 降解有助于棉花中赤霉素和生长素介导的纤维细胞伸长。

Strigolactone-induced degradation of SMXL7 and SMXL8 contributes to gibberellin- and auxin-mediated fiber cell elongation in cotton.

机构信息

State Key Laboratory of Cotton Bio-breeding and Integrated Utilization, Institute of Cotton Research, Chinese Academy of Agricultural Sciences, Anyang 455000, China.

National Nanfan Research Institute (Sanya), Chinese Academy of Agricultural Sciences, Sanya, Hainan 572024, China.

出版信息

Plant Cell. 2024 Sep 3;36(9):3875-3893. doi: 10.1093/plcell/koae212.

Abstract

Cotton (Gossypium) fiber length, a key trait determining fiber yield and quality, is highly regulated by a class of recently identified phytohormones, strigolactones (SLs). However, the underlying molecular mechanisms of SL signaling involved in fiber cell development are largely unknown. Here, we show that the SL signaling repressors MORE AXILLARY GROWTH2-LIKE7 (GhSMXL7) and GhSMXL8 negatively regulate cotton fiber elongation. Specifically, GhSMXL7 and GhSMXL8 inhibit the polyubiquitination and degradation of the gibberellin (GA)-triggered DELLA protein (GhSLR1). Biochemical analysis revealed that GhSMXL7 and GhSMXL8 physically interact with GhSLR1, which interferes with the association of GhSLR1 with the E3 ligase GA INSENSITIVE2 (GhGID2), leading to the repression of GA signal transduction. GhSMXL7 also interacts with the transcription factor GhHOX3, preventing its binding to the promoters of essential fiber elongation regulatory genes. Moreover, both GhSMXL7 and GhSMXL8 directly bind to the promoter regions of the AUXIN RESPONSE FACTOR (ARF) genes GhARF18-10A, GhARF18-10D, and GhARF19-7D to suppress their expression. Cotton plants in which GhARF18-10A, GhARF18-10D, and GhARF19-7D transcript levels had been reduced by virus-induced gene silencing (VIGS) displayed reduced fiber length compared with control plants. Collectively, our findings reveal a mechanism illustrating how SL integrates GA and auxin signaling to coordinately regulate plant cell elongation at the single-cell level.

摘要

棉花(Gossypium)纤维长度是决定纤维产量和质量的关键特性,它受到一类最近发现的植物激素——独脚金内酯(SLs)的高度调控。然而,SL 信号参与纤维细胞发育的潜在分子机制在很大程度上尚不清楚。在这里,我们表明 SL 信号抑制剂 MORE AXILLARY GROWTH2-LIKE7(GhSMXL7)和 GhSMXL8 负调控棉花纤维伸长。具体而言,GhSMXL7 和 GhSMXL8 抑制赤霉素(GA)触发的 DELLA 蛋白(GhSLR1)的多泛素化和降解。生化分析显示,GhSMXL7 和 GhSMXL8 与 GhSLR1 物理相互作用,干扰 GhSLR1 与 E3 连接酶 GA INSENSITIVE2(GhGID2)的结合,从而抑制 GA 信号转导。GhSMXL7 还与转录因子 GhHOX3 相互作用,阻止其与必需纤维伸长调节基因的启动子结合。此外,GhSMXL7 和 GhSMXL8 均可直接结合 AUXIN RESPONSE FACTOR(ARF)基因 GhARF18-10A、GhARF18-10D 和 GhARF19-7D 的启动子区域,抑制其表达。通过病毒诱导的基因沉默(VIGS)降低 GhARF18-10A、GhARF18-10D 和 GhARF19-7D 转录本水平的棉花植株与对照植株相比,纤维长度变短。总之,我们的研究结果揭示了一种机制,说明 SL 如何整合 GA 和生长素信号,在单细胞水平上协调调控植物细胞伸长。

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