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Strigolactone-induced degradation of SUPPRESSOR OF MORE AXILLARY GROWTH2-LIKE7 (SMXL7) and SMXL8 contributes to gibberellin- and auxin-mediated fiber cell elongation in cotton
The Plant Cell ( IF 10.0 ) Pub Date : 2024-07-25 , DOI: 10.1093/plcell/koae212
Yaru Sun 1 , Zailong Tian 1, 2 , Dongyun Zuo 1 , Hailiang Cheng 1, 3 , Qiaolian Wang 1 , Youping Zhang 1 , Limin Lv 1 , Guoli Song 1, 2, 3
Affiliation  

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.

中文翻译:


独角金内酯诱导的 SUPPRESSOR OF MORE AXILLARY GROWTH2-LIKE7 (SMXL7) 和 SMXL8 降解有助于赤霉素和生长素介导的棉花纤维细胞伸长



棉花(Gossypium)纤维长度是决定纤维产量和质量的关键性状,受到最近发现的一类植物激素——独脚金内酯(SL)的高度调节。然而,参与纤维细胞发育的 SL 信号传导的潜在分子机制在很大程度上尚不清楚。在这里,我们发现 SL 信号抑制因子 MORE AXILLARY GROWTH2-LIKE7 (GhSMXL7) 和 GhSMXL8 负向调节棉纤维伸长。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。生化分析表明,GhSMXL7 和 GhSMXL8 与 GhSLR1 发生物理相互作用,干扰 GhSLR1 与 E3 连接酶 GA INSENSITIVE2 (GhGID2) 的结合,导致 GA 信号转导受到抑制。 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都直接结合生长素反应因子(ARF)基因GhARF18-10A、GhARF18-10D和GhARF19-7D的启动子区域以抑制其表达。与对照植物相比,病毒诱导的基因沉默(VIGS)降低了 GhARF18-10A、GhARF18-10D 和 GhARF19-7D 转录水平的棉花植物显示纤维长度减少。总的来说,我们的研究结果揭示了一种机制,说明 SL 如何整合 GA 和生长素信号传导,在单细胞水平上协调调节植物细胞伸长。
更新日期:2024-07-25
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