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棉花Bax inhibitor-1影响内质网胁迫介导的细胞死亡的研究
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  • 英文篇名:Overexpression of Cotton Bax inhibitor-1 Affects Cell Death Mediated by Endoplasmic Reticulum Stress in Arabidopsis
  • 作者:张景霞 ; 霍雪寒 ; 王芙蓉 ; 张传云 ; 张军
  • 英文作者:Zhang Jingxia;Huo Xuehan;Wang Furong;Zhang Chuanyun;Zhang Jun;Shandong Cotton Research Center/Key Laboratory of Cotton Genetic Improvement and Cultivation Physiology in Huang-Huai-Hai Plain,Ministry of Agriculture;College of Life Sciences,Shandong Normal University;
  • 关键词:Bax ; inhibitor-1 ; 内质网胁迫 ; 细胞死亡 ; 棉花 ; 拟南芥 ; 衣霉素
  • 英文关键词:Bax inhibitor-1;;Endoplasmic reticulum stress;;Cell death;;Cotton;;Arabidopsis;;Tunicamycin
  • 中文刊名:AGRI
  • 英文刊名:Shandong Agricultural Sciences
  • 机构:山东棉花研究中心/农业部黄淮海棉花遗传改良与栽培生理重点实验室;山东师范大学生命科学学院;
  • 出版日期:2018-05-30
  • 出版单位:山东农业科学
  • 年:2018
  • 期:v.50;No.321
  • 基金:山东省农业科学院青年科研基金项目(2015YQN04);; 国家自然科学基金项目(31501351)
  • 语种:中文;
  • 页:AGRI201805001
  • 页数:6
  • CN:05
  • ISSN:37-1148/S
  • 分类号:6-11
摘要
Bax inhibitor-1(BI-1)是调控内质网胁迫(endoplasmic reticulum stress,ER stress)介导的细胞死亡的关键因子,在植物耐逆中具有重要作用。目前,棉花BI-1(GhBI-1)的耐逆功能及其调控细胞死亡的相关报道较少。在本研究中,采用ER stress专一性诱导毒素——衣霉素(tunicamycin,TM)对棉花幼苗进行胁迫处理,实时定量PCR结果表明,GhBI-1的TM诱导表达具有组织特异性,根GhBI-1对TM的响应更加强烈。通过TM抗性试验及细胞死亡的分析发现,GhBI-1的表达提高了拟南芥的TM抗性,减缓了ER stress介导的细胞死亡。此外,未折叠蛋白反应信号通路中的bZip60转录因子基因的表达受GhBI-1的调控。
        Bax inhibitor-1(BI-1) regulates cell death mediated by endoplasmic reticulum stress(ER stress),and plays important roles in plant stress tolerance. Up to now,the role of cotton BI-1(GhBI-1)involved in stress tolerance and cell death remain largely unknown. In the present study,we characterized the expression patterns of GhBI-1 under ER stress conditions induced by tunicamycin(TM). The results of real-time quantitative PCRs showed that the inducible expression pattern of GhBI-1 was tissue specific. The expression of GhBI-1 in roots is stronger compared with in leaves under ER stress conditions. The overexpression of GhBI-1 increased the TM resistance of transgenic Arabidopsis and delayed cell death mediated by ER stress. The analysis of the expression of b Zip60 involved in unfolded protein response showed that GhBI-1 activated the avtivity of b Zip60 and improved cell tolerance to ER stress.
引文
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