A dominant function of CCaMK in intracellular accommodation of bacterial and fungal endosymbionts.
A dominant function of CCaMK in intracellular accommodation of bacterial and fungal endosymbionts.
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DOI：
10.1111/j.1365-313x.2010.04228.x
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发表时间：
2010-07-01
期刊：
影响因子：
--
通讯作者：
Imaizumi-Anraku H
中科院分区：
文献类型：
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作者：
Hayashi T;Banba M;Shimoda Y;Kouchi H;Hayashi M;Imaizumi-Anraku H
在豆科植物中，钙/钙调蛋白依赖的蛋白激酶(CCaMK)是根瘤(RN)和丛枝菌根(AM)共生所必需的共生基因的组成部分，被认为是钙尖峰的解码者，钙尖峰是细胞对微生物信号最早的反应之一。CCaMK的功能获得突变已被证明可以在没有根瘤菌的情况下诱导自发结瘤，但CCaMK激活在细菌和/或真菌感染过程中的意义尚不完全清楚。在这里，我们证明了功能获得的CCaMKT265D抑制了共同共生基因的功能缺失突变，这不仅是根瘤器官发生所需的，也是成功感染根瘤菌和AM真菌所需的，证明了钙尖峰上游的共同共生基因只需要激活CCaMK。然而，在根瘤共生中，CCaMKT265D诱导了结瘤因子受体(NFR)突变体的根瘤器官发生，而不是根瘤侵染。我们提出了一个在寄主豆科植物中的共生信号模型，其中CCaMK在侵染线形成和根瘤器官发生的协调诱导中起着关键作用。
In legumes, Ca2+/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 Ca2+ 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 CCaMKT265D suppresses loss-of-function mutations of common symbiosis genes required for the generation of Ca2+ spiking, not only for nodule organogenesis but also for successful infection of rhizobia and AM fungi, demonstrating that the common symbiosis genes upstream of Ca2+ spiking are required solely to activate CCaMK. In RN symbiosis, however, CCaMKT265D 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.