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孔进, 谭艳平, 陈祖玉, 李绍清, 朱英国. 水稻红莲型不育系雄性配子发育过程中线粒体功能基因转录本的编辑位点研究[J]. 植物科学学报, 2006, 24(2): 95-99.
引用本文: 孔进, 谭艳平, 陈祖玉, 李绍清, 朱英国. 水稻红莲型不育系雄性配子发育过程中线粒体功能基因转录本的编辑位点研究[J]. 植物科学学报, 2006, 24(2): 95-99.
KONG Jin, TAN Yan-Ping, CHEN Zu-Yu, LI Shao-Qing, ZHU Ying-Guo. Study on the Editing Sites in Transcripts of Functional Genes of HL-cytoplasmic Male Sterility Rice Mitochondria during Microgametogenesis[J]. Plant Science Journal, 2006, 24(2): 95-99.
Citation: KONG Jin, TAN Yan-Ping, CHEN Zu-Yu, LI Shao-Qing, ZHU Ying-Guo. Study on the Editing Sites in Transcripts of Functional Genes of HL-cytoplasmic Male Sterility Rice Mitochondria during Microgametogenesis[J]. Plant Science Journal, 2006, 24(2): 95-99.

水稻红莲型不育系雄性配子发育过程中线粒体功能基因转录本的编辑位点研究

Study on the Editing Sites in Transcripts of Functional Genes of HL-cytoplasmic Male Sterility Rice Mitochondria during Microgametogenesis

  • 摘要: RNA编辑普遍存在于高等植物线粒体中,是线粒体产生功能蛋白所必不可少的过程。以红莲(HL)型水稻细胞质雄性不育系粤泰A、保持系粤泰B及杂种红莲优6四分体时期的花药、单核花粉和二核花粉为材料,研究了线粒体功能基因——atp6coxⅡ及嵌合基因aorfH79转录本的编辑位点。结果表明,atp6转录本的编辑能力明显受到恢复基因的影响。atp6转录本在不育系中不被编辑或部分编辑,而在引入了恢复基因的杂种一代中,其编辑能力均大幅提高。coxⅡ转录本在3个材料中编辑状态没有差别,而嵌合基因aorfH79在各个材料中均不被编辑。由此推测,红莲型水稻细胞质雄性不育与atp6转录本编辑能力的基本丧失紧密相关。

     

    Abstract: RNA editing exists extensively in the higher plant mitochondria,and is a required step for forming functional proteins.The editing of mitochondrial gene atp6,coxⅡ and orf H79 was studied with(using) the tetrad anthers,uninucleate and dinucleate pollens of gametophytice male sterility line YueTai A,maintainer line YueTai B,and the F1 hybrid HongLian You6 of HL-type cytoplasmic male sterility(CMS) rice.The results indicated the editing capability of atp6 gene was influenced markedly by nuclear restorer gene.The atp6 transcript was not edited or partially edited in male sterility line,but the higher editing capability was found in the F1 hybrid containing restorer gene.There was no difference in the editing level of coxⅡ gene among three lines,and the chimeric gene,orf H79 was not edited in all materials.So it is guessed that there is a close association between HL-CS and the loss of editing capability of atp6 gene.

     

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