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Chromatin signatures and retrotransposon profiling in mouse embryos reveal regulation of LINE-1 by RNA
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Chromatin signatures and retrotransposon profiling in mouse embryos reveal regulation of LINE-1 by RNA
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Chromatin signatures and retrotransposon profiling in mouse embryos reveal regulation of LINE-1 by RNA
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Journal Article
Chromatin signatures and retrotransposon profiling in mouse embryos reveal regulation of LINE-1 by RNA
2013
Overview
Repetitive elements in differentiated cells are usually silenced. Genome-wide analyses in early mouse development show that repetitive-element expression decreases during development accompanied by the loss of active chromatin marks. LINE-1 and IAP retrotransposons become reactivated after fertilization, and LINE-1 transcription is regulated by short LINE-1 RNAs, which suggests that repetitive elements may be regulated through RNA during the earliest developmental stages.
How a more plastic chromatin state is maintained and reversed during development is unknown. Heterochromatin-mediated silencing of repetitive elements occurs in differentiated cells. Here, we used repetitive elements, including retrotransposons, as model loci to address how and when heterochromatin forms during development. RNA sequencing throughout early mouse embryogenesis revealed that repetitive-element expression is dynamic and stage specific, with most repetitive elements becoming repressed before implantation. We show that LINE-1 and IAP retrotransposons become reactivated from both parental genomes after fertilization. Chromatin immunoprecipitation for H3K4me3 and H3K9me3 in 2- and 8-cell embryos indicates that their developmental silencing follows loss of activating marks rather than acquisition of conventional heterochromatic marks. Furthermore, short LINE-1 RNAs regulate LINE-1 transcription
in vivo
. Our data indicate that reprogramming after mammalian fertilization comprises a robust transcriptional activation of retrotransposons and that repetitive elements are initially regulated through RNA.
Publisher
Nature Publishing Group US,Nature Publishing Group
