CUL4-PRL1-MYB43调控拟南芥镉胁迫响应的分子机制

前期研究发现，转录因子MYB43可能通过抑制下游靶基因HMA2/3/4的转录来负调节拟南芥镉（Cd）胁迫耐受；此外，还鉴定出MYB43与CUL4-E3复合体识别因子PRL1及CUL4蛋白发生互作，且prl1和cul4功能缺失突变体对Cd胁迫敏感。由此推测：在植物响应Cd胁迫过程中，PRL1识别并通过CUL4-E3复合体促进MYB43蛋白的降解，从而解除MYB43对下游靶基因HMA2/3/4的转录抑制作用并增加其转录水平，进而HMA2和HMA4将植物根部Cd2+通过木质部转运到地上部，而HMA3则将根部和茎部细胞的细胞质中Cd2+转运到液泡中贮存，最终增加植物对Cd胁迫的耐受。本项目拟围绕上述假说展开系统研究，阐明一条植物响应Cd胁迫的信号转导的新通路：CUL4-PRL1-MYB43。该研究不仅有助于揭示植物抗重金属毒害的新机制，而且为植物修复基因工程提供新的基因资源。

It was previously found that the transcription factor MYB43 negatively modulates cadmium (Cd) tolerance in Arabidopsis by inhibiting transcription of HMA2/3/4 genes. In addition, MYB43 was also identified to interact with CUL4-E3 complex substrate receptor PRL1 and core subunit CUL4, and the prl1 and cul4 loss-of-function mutants were sensitive to Cd stress. It is speculated that, in response of plants to Cd stress, CUL4-E3 complex receptor PRL1 could recognize and CUL4-E3 complex promote the degradation of MYB43 protein, thereby abolishing the transcriptional inhibition of HMA2/3/4 genes by MYB43, and increasing their transcriptional levels. HMA2 and HMA4 transport Cd2+ from the roots of plants to the shoots through the xylem, while HMA3 transports Cd2+ in the cytoplasm of root and shoot cells, into the vacuoles to storage, thus improving the tolerance of plants to Cd stress. This project will focus on the above-mentioned hypothesis to reveal a novel signaling pathway for the response of plants to Cd stress: CUL4-PRL1-MYB43. This work not only revealed the novel mechanisms of plant responses to heavy metal stress, but also provided novel genes for phytoremediation genetic engineering.