NDLI: Epigenetic control of mammalian LINE-1 retrotransposon by retinoblastoma proteins.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Montoya-Durango, Diego E. Liu, Yongqing Teneng, Ivo Kalbfleisch, Ted Lacy, Mary E. Steffen, Marlene C. Ramos, Kenneth S.
Description	Country affiliation: United States Author Affiliation: Montoya-Durango DE ( Department of Biochemistry and Molecular Biology and Center for Genetics and Molecular Medicine, University of Louisville School of Medicine Health Sciences Center, Louisville, KY 40202, USA.)
Abstract	Long interspersed nuclear elements (LINEs or L1 elements) are targeted for epigenetic silencing during early embryonic development and remain inactive in most cells and tissues. Here we show that E2F-Rb family complexes participate in L1 elements epigenetic regulation via nucleosomal histone modifications and recruitment of histone deacetylases (HDACs) HDAC1 and HDAC2. Our experiments demonstrated that (i) Rb and E2F interact with human and mouse L1 elements, (ii) L1 elements are deficient in both heterochromatin-associated histone marks H3 tri methyl K9 and H4 tri methyl K20 in Rb family triple knock out (Rb, p107, and p130) fibroblasts (TKO), (iii) L1 promoter exhibits increased histone H3 acetylation in the absence of HDAC1 and HDAC2 recruitment, (iv) L1 expression in TKO fibroblasts is upregulated compared to wild type counterparts, (v) L1 expression increases in the presence of the HDAC inhibitor TSA. On the basis of these findings we propose a model in which L1 sequences throughout the genome serve as centers for heterochromatin formation in an Rb family-dependent manner. As such, Rb proteins and L1 elements may play key roles in heterochromatin formation beyond pericentromeric chromosomal regions. These findings describe a novel mechanism of L1 reactivation in mammalian cells mediated by failure of corepressor protein recruitment by Rb, loss of histone epigenetic marks, heterochromatin formation, and increased histone H3 acetylation.
File Format	HTM / HTML
ISSN	13835718
e-ISSN	18793592
DOI	10.1016/j.mrfmmm.2009.02.011
Journal	Mutation Research/Genetic Toxicology and Environmental Mutagenesis
Issue Number	1-2
Volume Number	665
Language	English
Publisher	Elsevier
Publisher Date	2009-06-01
Publisher Place	Netherlands
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Epigenesis, Genetic Multiprotein Complexes Retinoblastoma Protein Heterochromatin E2f Transcription Factors Histones Genetics Acetylation Retinoblastoma-like Protein P107 Cell Line Retinoblastoma-like Protein P130 Discipline Genetics Deficiency Cells, Cultured Discipline Biochemistry Histone Deacetylases Metabolism Mice, Knockout Chemistry Animals Long Interspersed Nucleotide Elements Mice Hela Cells
Content Type	Text
Resource Type	Article
Subject	Genetics Health, Toxicology and Mutagenesis

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E2F mediates cell cycle-dependent transcriptional repression in vivo by recruitment of an HDAC1/mSin3B corepressor complex.

Combinatorial roles for pRB, p107, and p130 in E2F-mediated cell cycle control.

The three members of the pocket proteins family share the ability to repress E2F activity through recruitment of a histone deacetylase.

Retinoblastoma/p107/p130 pocket proteins: protein dynamics and interactions with target gene promoters.

Retinoblastoma protein (pRb), but not p107 or p130, is required for maintenance of enterocyte quiescence and differentiation in small intestine.

Rb and p130 control cell cycle gene silencing to maintain the postmitotic phenotype in cardiac myocytes

Duplication and Maintenance of Heterochromatin Domains

Ablation of the retinoblastoma gene family deregulates G(1) control causing immortalization and increased cell turnover under growth-restricting conditions.

Structural mechanisms of DREAM complex assembly and regulation.

Epigenetic control of mammalian LINE-1 retrotransposon by retinoblastoma proteins.

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E2F mediates cell cycle-dependent transcriptional repression in vivo by recruitment of an HDAC1/mSin3B corepressor complex.

Combinatorial roles for pRB, p107, and p130 in E2F-mediated cell cycle control.

The three members of the pocket proteins family share the ability to repress E2F activity through recruitment of a histone deacetylase.

Retinoblastoma/p107/p130 pocket proteins: protein dynamics and interactions with target gene promoters.

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