根瘤菌分泌的结瘤因子是豆科植物与根瘤菌共生固氮过程中最重要的信号分子，在时间、空间上协同调控着根瘤菌的侵染与根瘤器官的形成。结瘤因子受体与结瘤因子结合后，受体蛋白如何完成其信号输出，进而形成有效根瘤，相关分子机理有待更多实验说明。为了回答上述的基本科学问题，我们进行了一系列的研究。在其中一项研究中，我们获得一个根瘤菌侵染缺陷的百脉根突变体itd4。ITD4编码一LRR-RLK类受体蛋白，其基因表达受结瘤因子诱导，并在瘤原基形成的部位特异表达；另外，ITD4蛋白分别与结瘤因子受体NFR1和NFR5相互作用。这些研究结果表明ITD4可能是通过与结瘤因子受体相互作用，调控受体的信号输出或是受体活性，从而调控根瘤菌的侵染。本项目拟在已有的研究基础上，详细的研究 ITD4与结瘤因子受体相互作用的分子机制和生物学意义，以及ITD4的生物学功能，从而揭示结瘤因子调控根瘤菌侵染和根瘤器官发育的分子机制。

Nodulation (Nod) factor secreted by rhizobia is the most important molecular signaling component during legume and rhizobia symbiotic nitrogen fixation. Nod factor coordinated mediates rhizobia infection process and the initiation of nodule primordia in temporal and spatial. But the molecular mechanisms remain unclear of how the Nod factor signals be output by the Nod factor receptors, then form an effective nodule after Nod factor receptors bind to Nod factor. To further investigate the underlying mechanisms of these scientific questions,we performed a series of studies. In one of our researches, we got an infection thread-deficient mutant itd4 from Lotus japonicas. ITD4 encoding a LRR type of receptor-like kinase, and it was induced by Nod factor and expressed at the site of nodule primordial formation. Moreover, ITD4 can interact with Nod factor receptors NFR1 and NFR5 respectively. All these results indicated that ITD4 regulates rhizobium infection through interacting with Nod factor receptors, then mediate NF receptors signals output or receptors activities. This project will focus on the molecular mechanisms and biological events of how Nod factor receptors interact with ITD4 and what is the biological function of ITD4. These results will unravel the underlying mechanisms of how the Nod factor coordinately mediates nodule organogenesis with rhizobia infection.