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• W2046415390 abstract "The ability of retrotransposons to mobilize and insert into genes presents a challenge to a cell needing to maintain its genomic integrity. Garcia-Perez et al. have studied retrotransposition in embryonic carcinoma-derived cells. On insertion into the DNA, the retrotransposon is quickly silenced by a chromatin-dependent mechanism. However, this process is specific for certain retrotransposons, implying that multiple silencing mechanisms may exist. Once cells differentiate, the ability to silence newly introduced retrotransposons is lost, but previously inactivated retrotransposons remain inactive. This suggests that either a crucial silencing factor is not expressed in differentiated cells, or that a repressor of silencing is activated in differentiated cells. The ability of retrotransposons to mobilize and insert into genes presents a challenge to a cell needing to maintain its genomic integrity. These authors have studied retrotransposition in embryonic carcinoma-derived cells. On insertion into DNA, the retrotransposon is quickly silenced, but the retrotransposon-specificity of this process implies that multiple silencing mechanisms may exist. Once cells differentiate, the ability to silence newly introduced retrotransposons is lost but previously inactivated retrotransposons remain inactive. Long interspersed element-1 (LINE-1 or L1) retrotransposition continues to affect human genome evolution1,2. L1s can retrotranspose in the germline, during early development and in select somatic cells3,4,5,6,7,8; however, the host response to L1 retrotransposition remains largely unexplored. Here we show that reporter genes introduced into the genome of various human embryonic carcinoma-derived cell lines (ECs) by L1 retrotransposition are rapidly and efficiently silenced either during or immediately after their integration. Treating ECs with histone deacetylase inhibitors rapidly reverses this silencing, and chromatin immunoprecipitation experiments revealed that reactivation of the reporter gene was correlated with changes in chromatin status at the L1 integration site. Under our assay conditions, rapid silencing was also observed when reporter genes were delivered into ECs by mouse L1s and a zebrafish LINE-2 element, but not when similar reporter genes were delivered into ECs by Moloney murine leukaemia virus or human immunodeficiency virus, suggesting that these integration events are silenced by distinct mechanisms. Finally, we demonstrate that subjecting ECs to culture conditions that promote differentiation attenuates the silencing of reporter genes delivered by L1 retrotransposition, but that differentiation, in itself, is not sufficient to reactivate previously silenced reporter genes. Thus, our data indicate that ECs differ from many differentiated cells in their ability to silence reporter genes delivered by L1 retrotransposition." @default.
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• W2046415390 date "2010-08-01" @default.
• W2046415390 modified "2023-10-16" @default.
• W2046415390 title "Epigenetic silencing of engineered L1 retrotransposition events in human embryonic carcinoma cells" @default.
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• W2046415390 doi "https://doi.org/10.1038/nature09209" @default.
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