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Loss-of-Function of a Ubiquitin-Related Modifier Promotes the Mobilization of the Active MITE mPing

Loss-of-Function of a Ubiquitin-Related Modifier Promotes the Mobilization of the Active MITE mPing

作     者:Takuji Tsukiyama Shota Teramoto KanakoYasuda Akira Horibata Nanako Mori Yutaka Okumoto Masayoshi Teraishi Hiroki Saito Akiko Onishi Kanako Tamura Takatoshi Tanisaka 

作者机构:Division of Agronomy and Horticulture Science Graduate School of Agriculture Kyoto University Kitashirakawa Sakyo Kyoto 606-8502 Japan Faculty of Biology-Oriented Science and Technology Kinki University Kinokawa Wakayama 649-6433 Japan 

出 版 物:《Molecular Plant》 (分子植物(英文版))

年 卷 期:2013年第6卷第3期

页      面:790-801页

核心收录:

学科分类:0710[理学-生物学] 071010[理学-生物化学与分子生物学] 07[理学] 09[农学] 0904[农学-植物保护] 0901[农学-作物学] 090402[农学-农业昆虫与害虫防治] 0902[农学-园艺学] 

基  金:TheMinistryofEducation Culture SportsandTechnologyofJapanintheformofGrants-in-AidforScientificResearch(21380004) 

主  题:Oryza sativa MITE mPing ubiquitin-related modifier methylation genome shock theory. 

摘      要:Miniature inverted-repeat transposable elements (MITEs) are widespread in both prokaryotic and eukaryotic genomes, where their copy numbers can attain several thousands. Little is known, however, about the genetic factor(s) affecting their transpositions. Here, we show that disruption of a gene encoding ubiquitin-like protein markedly enhances the transposition activity of a MITE roPing in intact rice plants without any exogenous stresses. We found that the transposition activity of roPing is far higher in the lines harboring a non-functional allele at the Rurml (Rice ubiquitin-related modifier-I) locus than in the wild-type line. Although the alteration of cytosine methylation pattern triggers the activation of transposable elements under exogenous stress conditions, the methylation degrees in the whole genome, the roPing-body region, and the roPing-flanking regions of the non-functional Rurml line were unchanged. This study provides experimental evidence for one of the models of genome shock theory that genetic accidents within cells enhance the transposition activities of transposable elements.

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