独脚金内酯与油菜素甾醇协调控制水稻中胚轴伸长的细胞和分子机制研究

Mesocotyl elongation, an important crop architecture trait, is necessary for crop deep-seeding and direct-seeding cultivation, and is also the impetus for less cost cultivation modes. But the underlying mechanism is still uncovered. In our previous research, we found that brassinosteroid (BR) signaling is necessary and positive for rice mesocotyl elongation; We identified a key gene RME1 (Rice Mesocotyl Elongation 1), which plays a positive role in promoting mesocotyl elongation. In addition, RME1 can interact with GSK2 (a GSK3-like kinase, functions as a negative regulator in rice BR signaling) and D3 (a subunit of the Skp–Cullin–F-box (SCF) E3 ubiquitin ligase complex, acting as a positive regulator in rice strigolactone (SL) signaling), which indicates that RME1 might play a key role in SLs/BRs-regulated rice mesocotyl elongation in darkness. In this project, we'll reveal the cytology structures and the mechanism under BR-regulating rice mesocotyl elongation, and establish the regulatory networks under the mesocotyl elongation among the BR/GSK2, SL/D3, and RME1. In addition, we will make the genetic diversity and association analysis to identify the favorable alleles of the genes (GSK3, D3, and RME1) for rice mesocotyl genetic improvement using 533 rice mini-core accessions. The completion of this research will give us theoretical basis to make the ideal mesocotyl architecture for deep seeding and direct seeding.

禾本科作物中胚轴的伸长是重要农艺性状，与作物的深播和直播密切相关，是作物向高效节约型耕种模式转变的推动力，但其伸长的机制很不清楚。我们前期研究表明水稻油菜素甾醇(BRs)信号被抑制，中胚轴变短，反之，则伸长；而独脚金内酯(SLs)突变体的中胚轴显著伸长。我们还鉴定到调控水稻中胚轴伸长新基因RME1，分别与BR信号通路的负调节因子GSK2及SL信号通路的正调节因子D3互作，这些结果暗示RME1可能介导了BRs和SLs协同调控中胚轴伸长。因此，本项目将进一步研究BRs调控中胚轴伸长的细胞和分子基础；建立BRs和SLs通过RME1协同调控中胚轴伸长的细胞、遗传和分子机制。并对533份水稻微核心种质中胚轴伸长关联分析，鉴定并功能分析GSK2、D3和RME1的等位变异。本研究将揭示水稻中胚轴伸长的分子机制和调控网络，为促进作物的深播和直播的分子育种，推动高效、节能的耕种模式提供理论依据和基因资源。

胚轴的伸长是种子萌发后顶土出苗的动力，中胚轴的伸长是与禾本科作物出苗密切相关的重要株型性状。中胚轴的长度在野生稻和栽培稻中的多样性呈现明显差异，具有优良的中胚轴伸长能力的种质将能推动水稻从传统的移秧耕种方式向节约劳动力和水资源的直播耕种模式的转变。因此，揭示水稻中胚轴发育的驯化、遗传、细胞和生化机制是向高效节约型耕种模式转变的推动力。通过完成本项目，我们系统揭示了独脚金内酯和油菜素甾醇互作调控水稻中胚轴伸长的细胞、分子生化和驯化机制。我们通过水稻中胚轴长度的GWAS分析，证明油菜素甾醇（Brassinosteroids, BRs）信号通路的关键组分OsGSK2编码区的等位变异通过改变自身激酶活性决定了水稻中胚轴长度的自然变异和从野生稻到栽培稻的驯化；BRs促进水稻中胚轴伸长主要通过OsGSK2磷酸化调控一类植物特有的功能未知的细胞周期蛋白CYC U2 (RME1)的蛋白稳定性来促进细胞分裂；进一步研究发现独脚金内酯（Strigolactones，SLs）通过D3泛素化并促进降解被OsGSK2磷酸化的CYC U2来抑制中胚轴的伸长。该研究不仅揭示了BRs协同SLs共同调控水稻中胚轴的驯化和伸长的分子机制，也揭示了由OsGSK2介导的BR信号通路在水稻中的驯化机制。本研究发现的新细胞周期蛋白CYC U2受油菜素甾醇信号和独脚金内酯信号关键组分协同调控的遗传、生化和进化机制，回答了长期以来人们探究的油菜素甾醇和/或独脚金内酯如何调控中胚轴的细胞分裂从而调控中胚轴伸长的科学问题，具有重要的理论意义。为通过改良水稻中胚轴伸长从而促进水稻直播模式的发展提供了具有自主知识产权的新基因、独特的等位变异和新途径。