摘要
线粒体基因orf25异常可能导致烟草细胞质雄性不育(CMS)。为探讨orf25基因导致CMS的可能机理,本文采用生物信息学方法,分析烟草雄性不育系‘MS革新3号’及其保持系中的orf25基因在其编码蛋白各结构层次上存在的差异。结果显示,不育系中orf25基因因碱基改变提前出现终止子从而导致其编码蛋白缺失结构域,这极可能成为干扰线粒体F(0)F(1)-ATP合成酶功能的关键因素,从而成为导致烟草‘革新3号’CMS的根本原因之一。
It was reported that aberrant mitochondrial gene orf25 might cause tobacco cytoplasmic male sterility (CMS). To understand the mechanism of CMS, the differences of orf25 gene between CMS line ‘ Gexin 3 ’ and its maintainer line were analyzed by bioinformatics at different structure levels of coding protein. The results showed that the terminal codon appeared early because of the base change in the orf25 gene, which led to the lack of the structural domain in coding protein. It might be the key factor that disturbed the function of F(0)F(1)-ATP synthetase in mitochondrion, and become one of the fundamental causes which led to CMS of tobacco.
出处
《中国农学通报》
CSCD
北大核心
2011年第5期312-316,共5页
Chinese Agricultural Science Bulletin
基金
国家自然科学基金项目"新质源烟草胞质雄性不育相关基因的克隆"(No.30660099)
湖南农业大学大学生科技创新基金项目"烟草线粒体ORF25与CMS的关系"