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Ishak, Charles A.; Marshall, Aren E.; Passos, Daniel T.; White, Carlee R.; Kim, Seung J.; Cecchini, Matthew J.; Ferwati, Sara; MacDonald, William A.; Howlett, Christopher J.; Welch, Ian D.; Rubin, Seth M.; Mann, Mellissa R.W.; Dick, Frederick A.
Molecular cell, 12/2016, Letnik: 64, Številka: 6Journal Article
Repetitive genomic regions include tandem sequence repeats and interspersed repeats, such as endogenous retroviruses and LINE-1 elements. Repressive heterochromatin domains silence expression of these sequences through mechanisms that remain poorly understood. Here, we present evidence that the retinoblastoma protein (pRB) utilizes a cell-cycle-independent interaction with E2F1 to recruit enhancer of zeste homolog 2 (EZH2) to diverse repeat sequences. These include simple repeats, satellites, LINEs, and endogenous retroviruses as well as transposon fragments. We generated a mutant mouse strain carrying an F832A mutation in Rb1 that is defective for recruitment to repetitive sequences. Loss of pRB-EZH2 complexes from repeats disperses H3K27me3 from these genomic locations and permits repeat expression. Consistent with maintenance of H3K27me3 at the Hox clusters, these mice are developmentally normal. However, susceptibility to lymphoma suggests that pRB-EZH2 recruitment to repetitive elements may be cancer relevant. Display omitted •The retinoblastoma protein occupies repetitive sequences in somatic cells•RB-EZH2 is required for H3K27me3 deposition at repeats and repression•Loss of repeat repression by RB is associated with cancer susceptibility Ishak et al. discover that the retinoblastoma protein extensively occupies and represses expression of tandem and interspersed genomic repeats in somatic cells. RB-EZH2 recruitment to repeats establishes H3K27me3-dependent repression, and its loss permits lymphomagenesis in gene-targeted mice.
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in: SICRIS
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