MPK3/6-MYBx-FIT模块调控拟南芥缺铁响应的分子机制

通过酵母双杂筛选，鉴定了一个与FIT（植物缺铁(Fe)响应的关键转录因子）互作的转录因子MYBx，并发现MYBx基因可能通过抑制FIT与bHLH Ib转录因子（如bHLH039）异源二聚体的形成来负调节拟南芥缺Fe响应；此外，还鉴定出丝裂原活化蛋白激酶MPK3/6与MYBx互作，且其参与缺Fe响应的调节，可能对MYBx蛋白磷酸化而改变MYBx生化功能。据此推测：在植物响应缺Fe过程中，MPK3/6蛋白激酶被激活并对转录因子MYBx进行磷酸化，从而解除MYBx对FIT与bHLH039互作形成的异源二聚体的抑制作用，进而增加IRT1和FRO2基因表达，促进Fe的吸收和耐受。本项目拟围绕上述工作假说开展相关研究，阐明一个新的植物响应缺Fe胁迫的分子模块：MPK3/6-MYBx-FIT。该研究不仅有助于揭示植物响应缺Fe胁迫的新机制，而且为作物矿质营养的遗传改良提供新的基因资源。

By screening yeast two hybrid library, we identified a transcription factor MYBx interacting with FIT, a key transcription factor involved in the response of plants to iron （Fe） deficiency. It was found that MYBx gene may negatively regulate Fe deficiency response in Arabidopsis by inhibiting the formation of heterodimers between FIT and bHLHIb transcription factors (such as bHLH039). In addition, it was also identified that mitogen activated protein kinases MPK3/6 interacted with MYBx, and were involved in the regulation of Fe deficiency response, which may phosphorylate MYBx protein to change its function. Thus we suspected that, in response of plants to Fe deficiency, MPK3/6 protein kinases were activated, which phosphorylated the transcription factor MYBx to change its biochemical function, thereby relieving the inhibitory effect of MYBx on heterodimer formed by interaction between FIT and bHLH039, thus increasing the expression of IRT1 and FRO2 genes and promoting Fe uptake and tolerance. In this project, a novel molecular module, MPK3/6-MYBx-FIT module, was proposed for plant to respond to Fe deficiency stress. This study not only helps to reveal the novel mechanism of plant response to Fe deficiency stress, but also provides new gene resources for the genetic improvement of crop mineral nutrition.