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在适宜的水分、温度和光照条件下，诱导赤霉素(GA)生物合成并触发种子萌发。GA促进种子萌发的一个主要机制是促进DELLA蛋白RGL2的降解，该蛋白是拟南芥种子萌发的一个主要抑制因子。通过对cop1突变体和cop1- ox /cop1-4细胞系对GA和多效唑(PAC)响应的表型分析，发现cop1在种子萌发过程中发挥积极作用，并与GA信号转导有关。COP1 -4突变体种子表现出PAC过敏反应，但用COP1过表达构建物转化使其PAC不敏感，其表型与rgl2突变体(rgl2- sk54)种子相似。此外，COP1 -4 RGL2 - sk54双突变体表现出与RGL2 - sk54相似的pac不敏感萌发表型，表明COP1是RGL2的上游负调控因子。COP1直接与RGL2相互作用，在体内SPA1能增强这种相互作用。COP1直接泛素化RGL2促进其降解。此外，GA稳定COP1，导致RGL2失稳。通过揭示COP1- rgl2调控模块，我们揭示了COP1正向调控种子萌发并控制促发芽基因表达的新机制。 Figure 8. Model of the COP1-RGL2 regulatory module in seed germination. Under favorable moisture, temperature and light conditions, gibberellin (GA) biosynthesis is induced and triggers seed germination. A major mechanism by which GA promotes seed germination is by promoting the degradation of the DELLA protein RGL2, a major repressor of germination in Arabidopsis seeds. Analysis of seed germination phenotypes of constitutively photomorphogenic 1 (cop1) mutants and complemented COP1-OX/cop1-4 lines in response to GA and paclobutrazol (PAC) suggested a positive role for COP1 in seed germination and a relation with GA signaling. cop1-4 mutant seeds showed PAC hypersensitivity, but transformation with a COP1 overexpression construct rendered them PAC insensitive, with a phenotype similar to that of rgl2 mutant (rgl2-SK54) seeds. Furthermore, cop1-4 rgl2-SK54 double mutants showed a PAC-insensitive germination phenotype like that of rgl2-SK54, identifying COP1 as an upstream negative regulator of RGL2. COP1 interacts directly with RGL2 and in vivo this interaction is strongly enhanced by SPA1. COP1 directly ubiquitinates RGL2 to promote its degradation. Moreover, GA stabilizes COP1 with consequent RGL2 destabilization. By uncovering this COP1-RGL2 regulatory module, we reveal a novel mechanism whereby COP1 positively regulates seed germination and controls the expression of germination-promoting genes.  文章来源网络整理；如有侵权请及时联系PaperRSS小编删除，转载请注明来源。 温馨提示： 为方便PaperRSS粉丝们科研、就业等话题交流。我们根据10多个专业方向（植物、医学、药学、人工智能、化学、物理、财经管理、体育等），特建立了30个国内外博士交流群。群成员来源欧美、日韩、新加坡、清华北大、中科院等全球名校。 |
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