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Plant Cell:拟南芥中CAMTA介导的SA免疫通路基因抑制的解除

已有 2160 次阅读 2017-10-9 08:44 |个人分类:每日摘要|系统分类:论文交流

CAMTA-Mediated Regulation of Salicylic Acid Immunity Pathway Genes in Arabidopsis Exposed to Low Temperature and Pathogen Infection


First author:Yong Sig Kim; Affiliations: Michigan State University (密歇根州立大学): East Lansing, USA

Corresponding author: Michael Thomashow


Arabidopsis thaliana Calmodulin-binding Transcription Activation (CAMTA; 钙调素结合转录激活) factors repress the expression of genes involved in salicylic acid (SA) biosynthesis and SA-mediated immunity in healthy plants grown at warm temperature (22°C). This repression is overcome in plants exposed to low temperature (4°C) for more than a week and in plants infected by biotrophic and hemibiotrophic pathogens (活体和半活体营养的病原菌). Here we present evidence that CAMTA3-mediated repression of SA pathway genes in non-stressed plants involves the action of an N-terminal repression module (NRM) that acts independently of calmodulin (CaM) binding to the IQ and CaM-binding (CaMB) domain, a finding that is contrary to current thinking that CAMTA3 repression activity requires binding of CaM to the CaMB domain. Induction (诱发) of SA-pathway genes in response to low temperature did not occur in plants expressing only the CAMTA3-NRM region of the protein. Mutational analysis provided evidence that the repression activity of the NRM was suppressed by action of the IQ and CaMB domains responding to signals generated in response to low temperature. Plants expressing the CAMTA3-NRM region were also impaired (有缺陷的) in defense against the bacterial hemibiotrophic pathogen Pseudomonas syringae (丁香假单胞菌) pv. tomato DC3000. Our results indicate that the regulation of CAMTA3 repression activity by low temperature and pathogen infection involves related mechanisms, but with distinct differences.


拟南芥钙调素结合转录激活因子CAMTA抑制22°C下健康生长的植株中水杨酸SA生物合成相关基因及SA介导的免疫。这个抑制会被低温处理(4°C)或者活体和半活体营养病原菌侵染所解除。本文研究显示CAMTA3介导的SA通路基因的抑制涉及到N端抑制单元NRM的表现,NRM起作用独立于钙调素CaM结合到IQ和CaM结合(CaMB)结构域。该发现与现有的推论认为CAMTA3抑制活性需要CaM结合到CaMB结构域上相违背。响应于低温处理的SA通路基因诱发在只表达CAMTA3-NRM区域的植株中并未检测到。突变分析显示NRM的抑制活性会被响应于低温处理产生的信号的IQ和CaMB结构域所抑制。表达CAMTA3-NRM区域的植株在对病毒性半活体病原菌丁香假单胞菌DC3000的抗性上有所缺陷。本文的研究结果表明低温处理和病原菌侵染调控的CAMTA3抑制活性涉及到一些分子机制,但两者有明显区分。


通讯:Michael Thomashow (https://prl.natsci.msu.edu/people/faculty/michael-thomashow/)


个人简介:1972年,加利福尼亚大学,细菌学学士;1972-1976年,加利福尼亚大学,微生物学USPHS博士前培训生;1976-1978年,加利福尼亚大学,微生物学助理研究员;1978年,加利福尼亚大学,微生物学博士;1978-1981年,华盛顿大学,微生物和免疫系Damon Runyon-Walter Winchell癌症基金研究员;1980年,华盛顿大学,微生物学博士后;1986年,华盛顿州立大学,微生物学副教授;1986-1991年,密歇根州立大学,植物、土壤和微生物系和微生物和分子遗传学系副教授;1991-至今,密歇根州立大学,植物、土壤和微生物系和微生物和分子遗传学系教授。


研究方向:植物对非生物胁迫的响应。


doi: https://doi.org/10.1105/tpc.16.00865


Journal: the Plant Cell
First Published data: October 5, 2017.

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