靶向降低DNA甲基化水平的5-氮杂胞苷促进medaka鱼Tol2转座元件的切除。

Atsuo Iida, Atsuko Shimada, Akihiro Shima, Naofumi Takamatsu, Hiroshi Hori, Kosei Takeuchi, Akihiko Koga
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引用次数: 22

摘要

medaka鱼类Oryzias latipes的Tol2元件是hAT (hobo/Activator/Tam3)转座元件家族的成员。有证据表明,过去在基因组和整个物种中都有快速扩增,但在当前的鱼类材料中没有观察到很高的自发转位率,这表明Tol2元件及其宿主物种已经获得了控制转位频率的相互作用机制。DNA甲基化是一个可能的促成因素,因为它与许多其他转座因子有关。因此,我们将胚胎浸泡在5-氮杂胞苷(一种导致DNA甲基化水平降低的试剂)中,并检测了反映体细胞切除频率的PCR产物的数量,获得了暴露促进Tol2切除的直接证据。因此,我们的研究结果表明,基因组DNA的甲基化是包括在Tol2元件转位控制的假定机制中的一个因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeted reduction of the DNA methylation level with 5-azacytidine promotes excision of the medaka fish Tol2 transposable element.

The Tol2 element of the medaka fish Oryzias latipes is a member of the hAT (hobo/Activator/Tam3) transposable element family. There is evidence for rapid expansion in the genome and throughout the species in the past but a high spontaneous transposition rate is not observed with current fish materials, suggesting that the Tol2 element and its host species have already acquired an interactive mechanism to control the transposition frequency. DNA methylation is a possible contributing factor, given its involvement with many other transposable elements. We therefore soaked embryos in 5-azacytidine, a reagent that causes reduction in the DNA methylation level, and examined amounts of PCR products reflecting the somatic excision frequency, obtaining direct evidence that exposure promotes Tol2 excision. Our results thus suggest that methylation of the genome DNA is a factor included in the putative mechanisms of control of transposition of the Tol2 element.

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