Epigenetic control of CACTA transposon mobility in Arabidopsis thaliana

Epigenetic control of CACTA transposon mobility in Arabidopsis thaliana
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DOI:
10.1534/genetics.104.029637
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发表时间:
2004-10-01
期刊:
影响因子:
3.3
通讯作者:
Kakutani, T
Kakutani, T
中科院分区:
生物学2区
文献类型:
--
作者:
Kato, M;Takashima, K;Kakutani, T

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表观遗传突变(Epigenetic mutation)是一种非基于核苷酸序列改变的可遗传发育变异,在植物中广泛报道。然而,这种突变的发育和进化意义仍然是个谜。基于我们对拟南芥内源转座子CACTA的研究,我们提出表观遗传基因沉默的遗传可以作为一种跨代的基因组防御机制来对抗转座子的有害运动。我们以前报道过沉默CACTA1被DNA低甲基化突变ddm 1(DNA甲基化减少)动员。在这项研究中,我们报告说,CACTA激活的ddm 1突变仍然移动的存在的野生型DDM 1基因,这表明从头沉默是不是有效的防御基因组对CA CTA运动。这种防御依赖于转座子沉默在几代人中的维持。此外,我们发现,激活CACTA1元件转座整个基因组中的DDM1植物,如以前报道的dDM1背景。此外,CACTA1元件整合到DDM1衍生的和DDM1衍生的染色体区域在DDM1野生型植物,这表明这类转座子不表现出有针对性的整合到异染色质,尽管它的积累在近着丝粒区域在自然种群。自然选择作为转座子的积累和异染色质进化的机制的可能贡献进行了讨论。
Epigenetic mutation, heritable developmental variation not based on a change in nucleotide sequence, is widely reported in plants. However, the developmental and evolutionary significance of such mutations remains enigmatic. On the basis of our studies of the endogenous Arabidopsis transposon CACTA, we propose that the inheritance of epigenetic gene silencing over generations can function as a transgenerational genome defense mechanism against deleterious movement of transposons. We previously reported that silent CACTA1 is mobilized by the DNA hypomethylation mutation ddm1 (decrease in DNA methylation). In this study, we report that CACTA activated by the ddm1 mutation remains mobile in the presence of the wild-type DDM1 gene, suggesting that de novo silencing is not efficient for the defense of the genome against CA CTA movement. The defense depends on maintenance of transposon silencing over generations. In addition, we show that the activated CACTA1 element transposes throughout the genome in DDMI plants, as reported previously for ddm1 backgrounds. Furthermore, the CACTA1 element integrated into both the ddm1-derived and the DDM1-derived chromosomal regions in the DDMI wild-type plants, demonstrating that this class of transposons does not exhibit targeted integration into heterochromatin, despite its accumulation in the pericentromeric regions in natural populations. The possible contribution of natural selection as a mechanism for the accumulation of transposons and evolution of heterochromatin is discussed.