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在缺少Dnmt3L的男性生殖细胞中发生精子性灾难和逆转移素的重新激活

Déborah Bourc'his¹, Timothy H Bestor

¹Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, 701 West 168th Street, New York, New York 10032, USA.

|August 20, 2004

概括

类似DNA甲基转移酶3 (Dnmt3L) 对于男性生殖细胞中逆转移体的新甲基化至关重要. 它的缺失导致逆转移子激活和介质性失效,突出显示Dnmt3L.

科学领域:

遗传学是一个遗传学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
发展生物学发展生物学

背景情况:

哺乳动物基因组利用细胞因子甲基化来静止转位子和调节基因表达.
指导特定序列DNA甲基化的机制在很大程度上仍未被描述.

研究的目的:

研究DNA甲基转移酶3样 (Dnmt3L) 在男性生殖细胞发育过程中的新甲基化中的作用.
了解Dnmt3L缺陷对逆转录素沉默和介质性进展的影响.

主要方法:

在围产期发育过程中对丸Dnmt3L表达的分析.
基因删除研究,以评估Dnmt3L损失对DNA甲基化模式的影响.
在突变的生殖细胞中评估逆转移素转录和介质性进展.

主要成果:

在retrotransposon de novo甲基化时,Dnmt3L在男性生殖线前体中短暂地表达.
缺少Dnmt3L阻止了LTR和非LTR逆转移体的新甲基化,导致它们的高水平转录.
丢失Dnmt3L导致精子细胞中介性失败,并改变分散重复的甲基化.

结论:

在早期的男性生殖细胞中,Dnmt3L在分散的逆转移体的新甲基化中发挥着关键作用.
通过Dnmt3L介导的甲基化似乎对于防止逆转移子激活和确保成功的半转化至关重要.
一个涉及Dnmt3L的premeiotic基因组扫描过程可能会针对出生周围的甲基化分散的重复.

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