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水稻反转录转座子Tos17的表观遗传调控

Epigenetic regulation of the rice retrotransposon Tos17.

作者信息

Cheng Chaoyang, Daigen Masaaki, Hirochika Hirohiko

机构信息

Molecular Genetics Department, National Institute of Agrobiological Sciences, Kannondai 2-1-2, Tsukuba, Ibaraki, 305-8602, Japan.

出版信息

Mol Genet Genomics. 2006 Oct;276(4):378-90. doi: 10.1007/s00438-006-0141-9. Epub 2006 Jul 5.

Abstract

Transposable elements are major components of plant genomes. Their activity seems to be epigenetically regulated by gene silencing systems. Here we report epigenetic variation in the retrotransposon Tos17 activity in rice varieties. Of the two copies of Tos17 present in chromosome 7 (Tos17 (chr.7)) and chromosome 10 (Tos17 (chr.10)), Tos17 (chr.7) is strongly activated by tissue culture in most varieties including Nipponbare except for Moritawase, despite the identity of the DNA sequences in Moritawase and Nipponbare. Tos17 (chr.7) activity correlated with its methylation status, and Tos17 (chr.7 )in Moritawase was heavily methylated and activated by treatment of 5-azacytidine (5-azaC), a DNA methylation inhibitor. Although the original copies of Tos17 are methylated to some extent in all varieties examined, the transposed copies in calli mostly are not methylated. When plants were regenerated from calli, the degree of methylation of the Tos17 DNA increased gradually with the growth of plants, and a significant progress of DNA methylation occurred in the next generation after a completed reproductive cycle. With increasing DNA methylation, the transcription of transposed and original Tos17 copies driven by its own as well as by a flanking gene promoter were suppressed. We conclude that Tos17 DNA methylation controls the transpositional activity of Tos17, and modulates the activity of neighboring genes. Based on the analysis of the inactive Tos17 (chr.10), we propose that another mechanism, called transcriptional interference, is involved in the control of Tos17 activity.

摘要

转座元件是植物基因组的主要组成部分。它们的活性似乎受到基因沉默系统的表观遗传调控。在此,我们报告了水稻品种中逆转座子Tos17活性的表观遗传变异。在第7号染色体(Tos17 (chr.7))和第10号染色体(Tos17 (chr.10))上存在的两个Tos17拷贝中,除了盛合早生外,在包括日本晴在内的大多数品种中,Tos17 (chr.7)在组织培养中被强烈激活,尽管盛合早生和日本晴的DNA序列相同。Tos17 (chr.7)的活性与其甲基化状态相关,盛合早生中的Tos17 (chr.7)高度甲基化,并通过DNA甲基化抑制剂5-氮杂胞苷(5-azaC)处理而被激活。尽管在所有检测的品种中,Tos17的原始拷贝都有一定程度的甲基化,但愈伤组织中转座的拷贝大多没有甲基化。当从愈伤组织再生植株时,Tos17 DNA的甲基化程度随着植株的生长而逐渐增加,并且在一个完整的生殖周期后的下一代中发生了显著的DNA甲基化进程。随着DNA甲基化的增加,由其自身以及侧翼基因启动子驱动的转座和原始Tos17拷贝的转录受到抑制。我们得出结论,Tos17 DNA甲基化控制Tos17的转座活性,并调节邻近基因的活性。基于对无活性的Tos17 (chr.10)的分析,我们提出另一种机制,称为转录干扰,参与了Tos17活性的控制。

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