病原真菌对植物生长造成严重威胁，但目前真菌引发的植物免疫机制远不如细菌清楚，这极大制约了植物抗真菌基因资源的挖掘以及抗真菌新策略的开发。我们在前期研究中发现，拟南芥类受体胞质激酶PBL19能够正调控对灰霉菌和核盘菌的抗性。真菌几丁质能够诱导共受体CERK1磷酸化PBL19以及PBL19从细胞膜向细胞核的迁移。持续入核的PBL19会产生植株矮小和组成型免疫的表型。该表型依赖于PBL19自身启动子及激酶活性，并受到高温抑制。RNA-seq分析表明PBL19组成型入核会导致PBL19自身以及水杨酸（SA）相关基因的表达上调，这与该植株中SA的大量积累吻合。本项目拟在上述研究基础上，阐明PBL19介导几丁质信号转导及真菌抗性的分子机制。本研究首次发现几丁质受体下游具有可发生膜核迁移的信号转导蛋白，将为研究真菌引发的植物免疫信号转导提供新的范式，并将揭示几丁质诱导植物SA合成及真菌抗性的新机制。

Fungal pathogens pose a severe threat to plant growth. However, the plant immunity against fungal pathogens is much less understood compared to that against bacterial pathogens, which greatly limits the discovery of new fungi-resistant genes and the development of novel antifungal strategies. Our preliminary data indicate that the Arabidopsis PBL19, a receptor-like cytoplasmic kinase, can positively regulate plant immunity against fungal pathogens Botrytis cinerea and Sclerotinia sclerotiorum. Fungal elicitor chitin can trigger PBL19 phosphorylation by the co-receptor CERK1 and subsequent relocation to the nucleus from the plasma membrane. Constitutive nuclear localization of PBL19 will cause dwarfism and constitutive immunity in plants, which, however, also requires the kinase activity of PBL19 and the native promoter for PBL19 expression. In addition, the phenotypes of dwarfism and constitutive immunity can be suppressed by higher temperatures. RNA-seq analysis reveals that constitutive nuclear localization of PBL19 will lead to substantial upregulation of its own gene and SA-related genes, which is consistent with the finding that SA is overaccumulated in the plants. Based on these preliminary data, we propose to study the role and regulatory mechanism of PBL19 in chitin signaling and fungal resistance. The proposed work will identify the first membrane-nuclear trafficking component in chitin signaling and uncover new mechanism underlying chitin-induced SA biosynthesis and fungal resistance in plants.