Epigenetic silencing of engineered L1 retrotransposition events in human embryonic carcinoma cells

Jose L. Garcia-Perez (), Maria Morell, Joshua O. Scheys, Deanna A. Kulpa, Santiago Morell, Christoph C. Carter, Gary D. Hammer, Kathleen L. Collins, K. Sue O’Shea, Pablo Menendez and John V. Moran ()
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Jose L. Garcia-Perez: 1241 East Catherine Street, University of Michigan Medical School
Maria Morell: Andalusian Stem Cell Bank, Consejeria de Salud Junta de Andalucia, Center for Biomedical Research, University of Granada
Joshua O. Scheys: Cellular and Molecular Biology Program, University of Michigan Medical School
Deanna A. Kulpa: University of Michigan Medical School
Santiago Morell: Andalusian Stem Cell Bank, Consejeria de Salud Junta de Andalucia, Center for Biomedical Research, University of Granada
Christoph C. Carter: Cellular and Molecular Biology Program, University of Michigan Medical School
Gary D. Hammer: University of Michigan Medical School
Kathleen L. Collins: Cellular and Molecular Biology Program, University of Michigan Medical School
K. Sue O’Shea: University of Michigan Medical School
Pablo Menendez: Andalusian Stem Cell Bank, Consejeria de Salud Junta de Andalucia, Center for Biomedical Research, University of Granada
John V. Moran: 1241 East Catherine Street, University of Michigan Medical School

Nature, 2010, vol. 466, issue 7307, 769-773

Abstract: Retrotransposons and genomic integrity 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.

Date: 2010
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DOI: 10.1038/nature09209

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