Intact piRNA pathway prevents L1 mobilization in male meiosis.

ABSTRACT: The PIWI-interacting RNA (piRNA) pathway is essential for retrotransposon silencing. In piRNA-deficient mice, L1-overexpressing male germ cells exhibit excessive DNA damage and meiotic defects. It remains unknown whether L1 expression simply highlights piRNA deficiency or actually drives the germ-cell demise. Specifically, the sheer abundance of genomic L1 copies prevents reliable quantification of new insertions. Here, we developed a codon-optimized L1 transgene that is controlled by an endogenous mouse L1 promoter. Importantly, DNA methylation dynamics of a single-copy transgene were indistinguishable from those of endogenous L1s. Analysis of Mov10l1^-/- testes established that de novo methylation of the L1 transgene required the intact piRNA pathway. Consistent with los

SUBMITTER: Newkirk SJ 

PROVIDER: S-EPMC5514719 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature