Epigenetic regulation of the rice retrotransposon Tos17
Epigenetic regulation of the rice retrotransposon Tos17
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DOI：
10.1007/s00438-006-0141-9
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发表时间：
2006-10-01
影响因子：
3.1
通讯作者：
Hirochika, Hirohiko
中科院分区：
文献类型：
--
作者：
Cheng, Chaoyang;Daigen, Masaaki;Hirochika, Hirohiko
转座子是植物基因组的主要组成部分。它们的活动似乎受到基因沉默系统的表观遗传调控。在这里，我们报告了水稻品种中反转录转座子Tos17活性的表观遗传变异。在7号染色体(Tos17(chr.7))和10号染色体(Tos17(chr.10))上存在的两个Tos17拷贝中，Tos17(chr.7)在包括Moritawase在内的大多数品种的组织培养中都被强烈激活，尽管Moritawase和Nipponbarase的DNA序列相同。Tos17(chr.7)的活性与其甲基化状态有关，Moritawase中的Tos17(chr.7)高度甲基化，并被DNA甲基化抑制剂5-氮胞苷(5-azaC)激活。虽然Tos17的原始拷贝在所有品种中都有一定程度的甲基化，但愈伤组织中的转座拷贝大多没有甲基化。当愈伤组织再生植株时，随着植株的生长，Tos17基因的甲基化程度逐渐增加，在生殖周期结束后的下一代，DNA甲基化发生了显著的进展。随着DNA甲基化程度的增加，由自身和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。我们的结论是，Tos17 DNA甲基化控制Tos17的转座活性，并调节邻近基因的活性。基于对失活的Tos17(chr.10)的分析，我们提出了另一种机制，称为转录干扰，参与了Tos17活性的控制。
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 signifficant 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.