A Glycine soja methionine sulfoxide reductase B5a interacts with the Ca~(2+)/CAM-binding kinase GsCBRLK and activates ROS signaling under carbonate alkaline stress
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- 英文论文题名：A Glycine soja methionine sulfoxide reductase B5a interacts with the Ca~(2+)/CAM-binding kinase GsCBRLK and activates ROS signaling under carbonate alkaline stress
- 论文作者：Xiaoli Sun ; Mingzhe Sun ; Bowei Jia ; Yanming Zhu
- 英文论文作者：Xiaoli Sun ; Mingzhe Sun ; Bowei Jia ; Yanming Zhu ; Crop Stress Molecular Biology Laboratory ; Heilongjiang Bayi Agricultural University
- 年：2016
- 作者机构：Crop Stress Molecular Biology Laboratory,Heilongjiang Bayi Agricultural University;
- 英文论文关键词：carbonate alkaline stress ; methionine sulfoxide reductase ; Ca2+/CAM- binding kinase ; ROS signaling ; Glycine soja ; Arabidopsis
- 会议召开时间：2016-10-09
- 会议录名称：2016年全国植物生物学大会摘要集
- 语种：英文
- 分类号：Q945.78
- 学会代码：ZGZO
- 会议名称：2016年全国植物生物学大会
- 会议地点：中国湖北武汉
- 主办单位：中国遗传学会、中国细胞生物学学会、中国植物学会、中国植物生理与植物分子生物学学会、中国作物学会
- 学会名称：中国植物学会
- 页数：1
- 文件大小：841k
- 原文格式：D
- 会议级别：全国
摘要
Although researches have extensively illustrated the molecular basis of plant responses to salt and high p H stresses,the knowledge on carbonate alkaline stress is poor and the specific responsive mechanism remains elusive. We have previously characterized a Glycine soja Ca2+/CAM-dependent kinase GsCBRLK,which could increase salt tolerance. Here,we characterized a methionine sulfoxide reductase B protein GsMSRB5 a as a GsCBRLK interactor by using Y2 H and Bi Fc assays. Further analyses showed that the N-terminal variable domain of GsCBRLK contributed to GsMSRB5 a interaction. Y2 H assays also revealed the interaction specificity of GsCBRLK with wild soybean MSRB subfamily proteins,and determined that the Box I/Box II-containing regions within GsMSRBs were responsible for their interaction. Furthermore,we also illustrated that the N-terminal basic regions in GsMSRBs functioned as transit peptides,which targeted themselves into chloroplasts and thereby prevented their interaction with GsCBRLK. Nevertheless,deletion of these regions allowed them to localize on PM and interact with GsCBRLK. In addition,we also showed that GsMSRB5 a and GsCBRLK displayed overlapping tissue expression specificity and coincident expression patterns under carbonate alkaline stress. Phenotypic experiments demonstrated that GsMSRB5 a and GsCBRLK overexpression in Arabidopsis enhanced carbonate alkaline stress tolerance. Further investigations elucidated that GsMSRB5 a and GsCBRLK inhibited ROS accumulation by modifying expression of ROS signaling,biosynthesis and scavenging genes. Summarily,our results demonstrated that GsCBRLK and GsMSRB5 a interacted with each other,and activated ROS signaling under carbonate alkaline stress.
Although researches have extensively illustrated the molecular basis of plant responses to salt and high p H stresses,the knowledge on carbonate alkaline stress is poor and the specific responsive mechanism remains elusive. We have previously characterized a Glycine soja Ca2+/CAM-dependent kinase GsCBRLK,which could increase salt tolerance. Here,we characterized a methionine sulfoxide reductase B protein GsMSRB5 a as a GsCBRLK interactor by using Y2 H and Bi Fc assays. Further analyses showed that the N-terminal variable domain of GsCBRLK contributed to GsMSRB5 a interaction. Y2 H assays also revealed the interaction specificity of GsCBRLK with wild soybean MSRB subfamily proteins,and determined that the Box I/Box II-containing regions within GsMSRBs were responsible for their interaction. Furthermore,we also illustrated that the N-terminal basic regions in GsMSRBs functioned as transit peptides,which targeted themselves into chloroplasts and thereby prevented their interaction with GsCBRLK. Nevertheless,deletion of these regions allowed them to localize on PM and interact with GsCBRLK. In addition,we also showed that GsMSRB5 a and GsCBRLK displayed overlapping tissue expression specificity and coincident expression patterns under carbonate alkaline stress. Phenotypic experiments demonstrated that GsMSRB5 a and GsCBRLK overexpression in Arabidopsis enhanced carbonate alkaline stress tolerance. Further investigations elucidated that GsMSRB5 a and GsCBRLK inhibited ROS accumulation by modifying expression of ROS signaling,biosynthesis and scavenging genes. Summarily,our results demonstrated that GsCBRLK and GsMSRB5 a interacted with each other,and activated ROS signaling under carbonate alkaline stress.
Although researches have extensively illustrated the molecular basis of plant responses to salt and high p H stresses,the knowledge on carbonate alkaline stress is poor and the specific responsive mechanism remains elusive. We have previously characterized a Glycine soja Ca2+/CAM-dependent kinase GsCBRLK,which could increase salt tolerance. Here,we characterized a methionine sulfoxide reductase B protein GsMSRB5 a as a GsCBRLK interactor by using Y2 H and Bi Fc assays. Further analyses showed that the N-terminal variable domain of GsCBRLK contributed to GsMSRB5 a interaction. Y2 H assays also revealed the interaction specificity of GsCBRLK with wild soybean MSRB subfamily proteins,and determined that the Box I/Box II-containing regions within GsMSRBs were responsible for their interaction. Furthermore,we also illustrated that the N-terminal basic regions in GsMSRBs functioned as transit peptides,which targeted themselves into chloroplasts and thereby prevented their interaction with GsCBRLK. Nevertheless,deletion of these regions allowed them to localize on PM and interact with GsCBRLK. In addition,we also showed that GsMSRB5 a and GsCBRLK displayed overlapping tissue expression specificity and coincident expression patterns under carbonate alkaline stress. Phenotypic experiments demonstrated that GsMSRB5 a and GsCBRLK overexpression in Arabidopsis enhanced carbonate alkaline stress tolerance. Further investigations elucidated that GsMSRB5 a and GsCBRLK inhibited ROS accumulation by modifying expression of ROS signaling,biosynthesis and scavenging genes. Summarily,our results demonstrated that GsCBRLK and GsMSRB5 a interacted with each other,and activated ROS signaling under carbonate alkaline stress.
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