Heritable epigenetic mutation of a transposon-flanked Arabidopsis gene due to lack of the chromatin-remodeling factor DDM1
Heritable epigenetic mutation of a transposon-flanked Arabidopsis gene due to lack of the chromatin-remodeling factor DDM1
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DOI：
10.1038/sj.emboj.7601788
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发表时间：
2007-08-08
期刊：
影响因子：
11.4
通讯作者：
Kakutani, Tetsuji
中科院分区：
文献类型：
--
作者：
Saze, Hidetoshi;Kakutani, Tetsuji
表观遗传沉默转座子和重复序列在真核基因组中占有相当大的比例，但它们对细胞基因功能的影响在很大程度上仍未被探索。在拟南芥中，转座子被DNA甲基化沉默，这种甲基化通常被染色质重塑基因DDM1(DNA甲基化降低1)的突变所取消。Ddm1基因突变通过抑制转座子和重复序列，导致多种类型的发育异常。在这里，我们报告了一种治疗ddm1诱导的综合征的新机制，称为盆景(BNS)。通过遗传连锁分析和随后的转录分析，我们确定了BNS表型的相关基因。BNS的表型是由于一个假定的后期促进复合体(APC)13基因沉默所致。BNS基因沉默与DNA高甲基化有关，这与ddm1诱导的其他基因组区域的低甲基化形成鲜明对比。这种矛盾的BNS高甲基化是在ddm1突变体的自花授粉过程中被重复地诱导的，它是由BNS基因两侧的一个长的穿插的核元件(线)反转录转座子介导的。我们讨论了转座子介导的BNS基因座表观遗传变化的可能分子机制和进化意义。
Epigenetically silent transposons and repeats constitute a substantial proportion of eukaryotic genomes, but their impact on cellular gene function remains largely unexplored. In Arabidopsis, transposons are silenced by DNA methylation, and this methylation is often abolished by mutations in a chromatin-remodeling gene DDM1 (DECREASE IN DNA METHYLATION 1). The ddm1 mutation induces various types of developmental abnormalities through de-repression of transposons and repeats. Here, we report a novel mechanism for a ddm1-induced syndrome, called bonsai (bns). We identified the gene responsible for the bns phenotypes by genetic linkage analysis and subsequent transcriptional analysis. The bns phenotypes are due to silencing of a putative Anaphase-Promoting Complex (APC) 13 gene. The BNS gene silencing was associated with DNA hypermethylation, which is in contrast to the ddm1-induced hypomethylation in the other genomic regions. This paradoxical BNS hypermethylation was reproducibly induced during self-pollination of the ddm1 mutant, and it was mediated by a long interspersed nuclear element (LINE) retrotransposon flanking the BNS gene. We discuss possible molecular mechanisms and the evolutionary implications of transposon-mediated epigenetic changes in the BNS locus.