National Institute of Agrobiological Sciences, Tsukuba, Ibaraki 305-8602, Japan.
Plant J. 2010 Jul 1;63(1):141-54. doi: 10.1111/j.1365-313X.2010.04228.x. Epub 2010 Apr 16.
In legumes, Ca(2+)/calmodulin-dependent protein kinase (CCaMK) is a component of the common symbiosis genes that are required for both root nodule (RN) and arbuscular mycorrhiza (AM) symbioses and is thought to be a decoder of Ca(2+) spiking, one of the earliest cellular responses to microbial signals. A gain-of-function mutation of CCaMK has been shown to induce spontaneous nodulation without rhizobia, but the significance of CCaMK activation in bacterial and/or fungal infection processes is not fully understood. Here we show that a gain-of-function CCaMK(T265D) suppresses loss-of-function mutations of common symbiosis genes required for the generation of Ca(2+) spiking, not only for nodule organogenesis but also for successful infection of rhizobia and AM fungi, demonstrating that the common symbiosis genes upstream of Ca(2+) spiking are required solely to activate CCaMK. In RN symbiosis, however, CCaMK(T265D) induced nodule organogenesis, but not rhizobial infection, on Nod factor receptor (NFRs) mutants. We propose a model of symbiotic signaling in host legume plants, in which CCaMK plays a key role in the coordinated induction of infection thread formation and nodule organogenesis.
在豆科植物中,Ca(2+)/钙调蛋白依赖性蛋白激酶(CCaMK)是共同共生基因的一个组成部分,对于根瘤(RN)和丛枝菌根(AM)共生都是必需的,并且被认为是 Ca(2+)爆发的解码器,这是对微生物信号的最早的细胞反应之一。已经表明,CCaMK 的功能获得性突变会诱导自发结瘤而无需根瘤菌,但 CCaMK 激活在细菌和/或真菌感染过程中的意义尚未完全理解。在这里,我们表明功能获得性 CCaMK(T265D) 抑制了 Ca(2+)爆发所需的共同共生基因的功能丧失突变,不仅对于结节器官发生,而且对于根瘤菌和 AM 真菌的成功感染都是必需的,表明 Ca(2+)爆发上游的共同共生基因仅用于激活 CCaMK。然而,在 RN 共生中,CCaMK(T265D) 在 Nod 因子受体(NFRs)突变体上诱导结节器官发生,但不诱导根瘤菌感染。我们提出了宿主豆科植物共生信号转导的模型,其中 CCaMK 在协调诱导感染线形成和结节器官发生中起关键作用。