A calmodulin‐like protein regulates plasmodesmal closure during bacterial immune responses
A calmodulin‐like protein regulates plasmodesmal closure during bacterial immune responses
复制标题
类钙调蛋白在细菌免疫反应过程中调节胞间连丝闭合
作者：
J. Louarn;F. Cornet;P. Kuempel
植物通过激活模式识别受体（PPRs）来感知微生物信号，从而触发一系列细胞防御。一种反应是胞间连丝的关闭，这减少了共塑连通性和宿主细胞之间直接分子交换的能力。胞浆间质通量受到多种环境因素的调节，但下游信号通路的定义不明确，尤其是钙调节胞浆间质关闭的方式。在这里，我们发现响应细菌鞭毛蛋白而不是真菌几丁质的胞间连丝的关闭是由胞间连丝定位的Ca2+结合蛋白Calmodulin - like 41 （CML41）介导的。CML41受flg22的转录上调，并促进flg22处理后间连丝处的胼胝质快速沉积。CML41独立于由flg22感知触发的其他防御反应并减少细菌感染。我们提出CML41在细菌病原体攻击期间能够实现Ca2+信号特异性，并且是针对丁香假单胞菌的完整防御反应所必需的。
Summary Plants sense microbial signatures via activation of pattern recognition receptors (PPRs), which trigger a range of cellular defences. One response is the closure of plasmodesmata, which reduces symplastic connectivity and the capacity for direct molecular exchange between host cells. Plasmodesmal flux is regulated by a variety of environmental cues but the downstream signalling pathways are poorly defined, especially the way in which calcium regulates plasmodesmal closure. Here, we identify that closure of plasmodesmata in response to bacterial flagellin, but not fungal chitin, is mediated by a plasmodesmal‐localized Ca2+‐binding protein Calmodulin‐like 41 (CML41). CML41 is transcriptionally upregulated by flg22 and facilitates rapid callose deposition at plasmodesmata following flg22 treatment. CML41 acts independently of other defence responses triggered by flg22 perception and reduces bacterial infection. We propose that CML41 enables Ca2+‐signalling specificity during bacterial pathogen attack and is required for a complete defence response against Pseudomonas syringae.
影响因子：
3.7
作者：
Fernandez-Calvino L;Faulkner C;Walshaw J;Saalbach G;Bayer E;Benitez-Alfonso Y;Maule A
通讯作者：
Maule A