植物免疫受体感知病原信号分子并迅速激活自身免疫反应, 对植物抵御病原微生物入侵至关重要。但在未受到病原侵染时, 这些免疫受体的活性需受到严密控制, 以保证植物的正常生长。水稻(Oryza sativa)受体激酶OsCERK1是重要的免疫受体或共受体, 可感知病原真菌细胞壁组分几丁质。同时, OsCERK1还对感知丛枝菌根真菌的共生信号菌根因子不可或缺。最近的一项研究发现OsCERK1的一个精密调控机制, 既能在植株正常生长时有效抑制OsCERK1活性, 又能保证病原入侵时OsCERK1充分激活免疫反应。他们发现, 正常情况下, 水稻E3泛素连接酶OsCIE1通过泛素化修饰OsCERK1的激酶结构域, 抑制后者的激酶活性, 从而抑制免疫过度激活以保持稳态; 被几丁质激活后, OsCERK1又能通过特异磷酸化OsCIE1的关键位点, 阻断后者的E3连接酶活性, 进而解除OsCIE1对OsCERK1的抑制。该发现对利用免疫受体进行水稻抗病改良具有重要意义。

Plant immune receptors such as the rice OsCERK1 protein is crucial for sensing immunogenic signal from pathogenic microbes and activate defenses. The immune activity of these immune receptors, however, must be tightly controlled to ensure normal growth when the pathogen is not present. How plants properly manage the speed of immune activation and stringent control is important for the survival of plants in a complex environment. A recent research discovered an E3 ligase, OsCIE1, that acts as a molecular brake controlling OsCERK1 activation in the absence of the immunogenic signal chitin. OsCIE1 inhibits the kinase activity of OsCERK1 by ubiquitination, thereby negatively regulating immunity. Upon perception of chitin, OsCERK1 phosphorylates OsCIE1 to inhibit the E3 ligase activity, thereby releasing the brake and allowing robust activation of defenses.