Strigolactone Signaling in Arabidopsis Regulates Shoot Development by Targeting D53-Like SMXL Repressor Proteins for Ubiquitination and Degradation

Strigolactone Signaling in Arabidopsis Regulates Shoot Development by Targeting D53-Like SMXL Repressor Proteins for Ubiquitination and Degradation
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DOI:
10.1105/tpc.15.00605
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发表时间:
2015-11-01
期刊:
影响因子:
11.6
通讯作者:
Li, Jiayang
Li, Jiayang
中科院分区:
生物学1区
文献类型:
--
作者:
Wang, Lei;Wang, Bing;Li, Jiayang

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独脚金内酯(SL)是类胡萝卜素衍生的植物激素,其控制植物发育的许多方面,包括枝分枝、叶形状、茎次生加厚和侧根生长。在水稻(Oryza sativa)中,SL信号需要由包括D14和D3的复合物介导的DWARF 53(D53)的降解,但在拟南芥中,涉及D3直系同源物MORE AXILLARY GROWTH 2(MAX 2)的SL信号的组分和机制尚不清楚。在这里,我们表明,SL依赖的调节在拟南芥芽分支需要三个D53样蛋白,更多的轴突生长2-LIKE 6(SMXL 6),SMXL 7和SMXL 8。smxl 6 smxl 7 smxl 8三重突变体抑制max2和SL缺陷突变体max 3的高度分支表型。SMXL 6的突变体形式,这是抵抗SL诱导的泛素化和降解的过表达增强芽分支。SL类似物rac-GR 24的外源应用导致SMXL 6、7和8的泛素化和降解;这需要D14和MAX2。D53样SMXL与MAX 2和TPR 2形成复合物,并以GR 24应答方式与D14相互作用。此外,D53样SMXL表现出TPR 2依赖性转录抑制活性,并抑制BRANCHED 1的表达。我们的研究结果表明,在拟南芥中,D53样SMXLs与TPR 2一起抑制转录,从而允许侧芽生长,但SL诱导的D53样蛋白降解激活转录,抑制生长。
Strigolactones (SLs) are carotenoid-derived phytohormones that control many aspects of plant development, including shoot branching, leaf shape, stem secondary thickening, and lateral root growth. In rice (Oryza sativa), SL signaling requires the degradation of DWARF53 (D53), mediated by a complex including D14 and D3, but in Arabidopsis thaliana, the components and mechanism of SL signaling involving the D3 ortholog MORE AXILLARY GROWTH2 (MAX2) are unknown. Here, we show that SL-dependent regulation of shoot branching in Arabidopsis requires three D53-like proteins, SUPPRESSOR OF MORE AXILLARY GROWTH2-LIKE6 (SMXL6), SMXL7, and SMXL8. The smxl6 smxl7 smxl8 triple mutant suppresses the highly branched phenotypes of max2 and the SL-deficient mutant max3. Overexpression of a mutant form of SMXL6 that is resistant to SL-induced ubiquitination and degradation enhances shoot branching. Exogenous application of the SL analog rac-GR24 causes ubiquitination and degradation of SMXL6, 7, and 8; this requires D14 and MAX2. D53-like SMXLs form complexes with MAX2 and TOPLESS-RELATED PROTEIN2 (TPR2) and interact with D14 in a GR24-responsive manner. Furthermore, D53-like SMXLs exhibit TPR2-dependent transcriptional repression activity and repress the expression of BRANCHED1. Our findings reveal that in Arabidopsis, D53-like SMXLs act with TPR2 to repress transcription and so allow lateral bud outgrowth but that SL-induced degradation of D53-like proteins activates transcription to inhibit outgrowth.