2013年12月11日，国际著名刊物Nature以"ARTICLE"形式连续在线发表了我国科学家对独角金内酯(strigolactones)调控水稻分蘖分子机制研究方面取得的突破性进展。

分蘖，是决定水稻产量的重要农艺性状之一。它受到遗传因素的严格调控，其主要调控机制是通过植物激素信号通路协调分蘖芽的起始与伸长。长期的研究表明生长素和细胞分裂素是调控株型建成的主要激素。独角金内酯(strigolactones)是近年来发现的一种植物激素或其前体，能够抑制植物的分枝（蘖）和侧芽的生长，并与生长素和细胞分裂素一起调控植物的分枝（蘖）数量。但该激素如何调控水稻分蘖的分子机理仍不清楚。

在一篇在线发表的题为“DWARF 53 acts as a repressor of strigolactone signalling in rice"论文中，李家洋院士领导的课题组与中科院上海药物所徐华强课题组、中国水稻研究所（中国农科院）钱前课题组合作，在解析独角金内酯信号转导分子机理研究中取得了突破性进展。研究人员发现，D53基因编码一个double Clp-N motif-containing P-loop nucleoside triphosphate hydrolase, 负调控独角金内酯信号转导。分子遗传学和生化研究表明D53可能与转录抑制因子TPR形成复合物，协同抑制独角金内酯信号通路下游靶基因的表达，从而抑制该信号通路。独角金内酯诱导D53泛素化并通过蛋白酶体途径降解，且这一过程依赖于独角金内酯受体D14和泛素连接酶D3。D53蛋白的降解导致去抑制化，从而激活独角金内酯信号转导，精确地调控侧芽的伸长。在d53突变体中，D53基因的显性突变（dominant mutation）使其突变蛋白不能被降解，组成型抑制独角金内酯信号通路，从而导致d53矮化丛生的表型。独角金内酯信号转导的“去抑制化激活”机制与生长素、赤霉素、茉莉酸等重要激素的信号转导激活机制类似，表明这是植物在进化过程中选择的一种主要调控模式。

在另一篇在线发表的题为”D14-SCF^D3-dependent degradation of D53 regulates strigolactone signalling“论文中，南京农业大学和中国农业科学院作物科学研究所万建民教授科研团队及其合作者研究证实了D53蛋白能作为独脚金内酯信号途径的抑制子参与调控植物分蘖的生长发育。研究人员利用一个部分显性水稻矮化多分蘖突变体dwarf 53 (d53)，进行外源激素处理和内源激素测定表明，d53是一个独脚金内酯不敏感突变体。通过精细定位和图位克隆，获得了位于水稻第11号染色体短臂末端的D53基因，该基因编码一个新的在结构上与I类Clp ATPase类似的核蛋白。后续的功能分析发现，在独脚金内酯存在的条件下D53蛋白可与两个已知的独脚金内酯信号分子D14、D3互作，形成D53–D14–SCF^D3蛋白复合体，D53蛋白被泛素化，进而特异地被蛋白酶体系统降解，从而诱导下游目标基因的表达以及独脚金内酯信号的响应。这一结果为通过调控D53基因的表达量，影响独脚金内酯的信号转导，从而对水稻分蘖发挥调控作用提供了重要依据。 

Nature同时在NEWS & VIEWS专栏配发题为“Witchcraft and destruction”的专文评述，高度评价我国科学家在这项研究工作的理论意义和潜在应用价值。

论文摘要：DWARF 53 acts as a repressor of strigolactone signalling in rice

Strigolactones (SLs) are a group of newly identified plant hormones that control plant shoot branching. SL signalling requires the hormone-dependent interaction of DWARF 14 (D14), a probable candidate SL receptor, with DWARF 3 (D3), an F-box component of the Skp–Cullin–F-box (SCF) E3 ubiquitin ligase complex. Here we report the characterization of a dominant SL-insensitive rice (Oryza sativa) mutant dwarf 53 (d53) and the cloning of D53, which encodes a substrate of the SCFD3 ubiquitination complex and functions as a repressor of SL signalling. Treatments with GR24, a synthetic SL analogue, cause D53 degradation via the proteasome in a manner that requires D14 and the SCFD3 ubiquitin ligase, whereas the dominant form of D53 is resistant to SL-mediated degradation. Moreover, D53 can interact with transcriptional co-repressors known as TOPLESS-RELATED PROTEINS. Our results suggest a model of SL signalling that involves SL-dependent degradation of the D53 repressor mediated by the D14–D3 complex.

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论文摘要： D14-SCF^D3-dependent degradation of D53 regulates strigolactone signalling

Strigolactones (SLs), a newly discovered class of carotenoid-derived phytohormones, are essential for developmental processes that shape plant architecture and interactions with parasitic weeds and symbiotic arbuscular mycorrhizal fungi. Despite the rapid progress in elucidating the SL biosynthetic pathway, the perception and signalling mechanisms of SL remain poorly understood. Here we show that DWARF 53 (D53) acts as a repressor of SL signalling and that SLs induce its degradation. We find that the rice (Oryza sativa) d53 mutant, which produces an exaggerated number of tillers compared to wild-type plants, is caused by a gain-of-function mutation and is insensitive to exogenous SL treatment. The D53 gene product shares predicted features with the class I Clp ATPase proteins and can form a complex with the α/β hydrolase protein DWARF 14 (D14) and the F-box protein DWARF 3 (D3), two previously identified signalling components potentially responsible for SL perception. We demonstrate that, in a D14- and D3-dependent manner, SLs induce D53 degradation by the proteasome and abrogate its activity in promoting axillary bud outgrowth. Our combined genetic and biochemical data reveal that D53 acts as a repressor of the SL signalling pathway, whose hormone-induced degradation represents a key molecular link between SL perception and responses.

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