retrotransposon-induced heterochromatin spreading in the mouse revealed by insertional polymorphismsretrotransposon-induced异染色质蔓延在鼠标显示插入多态性.pdfVIP

Retrotransposon-Induced Heterochromatin Spreading in the Mouse Revealed by Insertional Polymorphisms 1,2 2 3 1,2 1,2 Rita Rebollo , Mohammad M. Karimi , Misha Bilenky , Liane Gagnier , Katharine Miceli-Royer , Ying 1,2 2 4 2,3 3 2 Zhang , Preeti Goyal , Thomas M. Keane , Steven Jones , Martin Hirst , Matthew C. Lorincz *, Dixie L. Mager1,2* 1Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, Canada, 2 Department of Medical Genetics, University of British Columbia, Vancouver, Canada, 3 British Columbia Cancer Agency Genome Sciences Centre, Vancouver, Canada, 4 Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom Abstract The ‘‘arms race’’ relationship between transposable elements (TEs) and their host has promoted a series of epigenetic silencing mechanisms directed against TEs. Retrotransposons, a class of TEs, are often located in repressed regions and are thought to induce heterochromatin formation and spreading. However, direct evidence for TE–induced local heterochromatin in mammals is surprisingly scarce. To examine this phenomenon, we chose two mouse embryonic stem (ES) cell lines that possess insertionally polymorphic retrotransposons (IAP, ETn/MusD, and LINE elements) at specific loci in one cell line but not the other. Employing ChIP-seq data for these cell lines, we show that IAP elements robustly induce H3K9me3 and H4K20me3 marks in flanking genomic DNA. In contrast, such heterochromatin