Rett syndrome mutations abolish the interaction of MeCP2 with the NCoR/SMRT co-repressor

In this study, the authors show that MeCP2 interacts with the NCoR/SMRT co-repressor complex and that a discrete cluster of Rett syndrome–causing mutations in the C-terminal domain of MeCP2 disrupts this interaction, impairing transcriptional repression. Knock-in mice expressing one of these MeCP2 m...

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Published inNature neuroscience Vol. 16; no. 7; pp. 898 - 902
Main Authors Lyst, Matthew J, Ekiert, Robert, Ebert, Daniel H, Merusi, Cara, Nowak, Jakub, Selfridge, Jim, Guy, Jacky, Kastan, Nathaniel R, Robinson, Nathaniel D, de Lima Alves, Flavia, Rappsilber, Juri, Greenberg, Michael E, Bird, Adrian
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.07.2013
Nature Publishing Group
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Abstract In this study, the authors show that MeCP2 interacts with the NCoR/SMRT co-repressor complex and that a discrete cluster of Rett syndrome–causing mutations in the C-terminal domain of MeCP2 disrupts this interaction, impairing transcriptional repression. Knock-in mice expressing one of these MeCP2 missense mutations exhibit severe motor phenotypes. Rett syndrome (RTT) is a severe neurological disorder that is caused by mutations in the MECP2 gene. Many missense mutations causing RTT are clustered in the DNA-binding domain of MeCP2, suggesting that association with chromatin is critical for its function. We identified a second mutational cluster in a previously uncharacterized region of MeCP2. We found that RTT mutations in this region abolished the interaction between MeCP2 and the NCoR/SMRT co-repressor complexes. Mice bearing a common missense RTT mutation in this domain exhibited severe RTT-like phenotypes. Our data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP2 'bridge' between the NCoR/SMRT co-repressors and chromatin.
AbstractList Rett syndrome (RTT) is a severe neurological disorder that is caused by mutations in the MECP2 gene. Many missense mutations causing RTT are clustered in the DNA-binding domain of MeCP2, suggesting that association with chromatin is critical for its function. We identified a second mutational cluster in a previously uncharacterized region of MeCP2. We found that RTT mutations in this region abolished the interaction between MeCP2 and the NCoR/SMRT co-repressor complexes. Mice bearing a common missense RTT mutation in this domain exhibited severe RTT-like phenotypes. Our data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP2 'bridge' between the NCoR/SMRT co-repressors and chromatin.
Rett syndrome (RTT) is a severe neurological disorder that is caused by mutations in the MECP2 gene. Many missense mutations causing RTT are clustered in the DNA-binding domain of MeCP2, suggesting that association with chromatin is critical for its function. We identified a second mutational cluster in a previously uncharacterized region of MeCP2. We found that RTT mutations in this region abolished the interaction between MeCP2 and the NCoR/SMRT co-repressor complexes. Mice bearing a common missense RTT mutation in this domain exhibited severe RTT-like phenotypes. Our data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP2 ‘bridge’ between the NCoR/SMRT co-repressors and chromatin.
In this study, the authors show that MeCP2 interacts with the NCoR/SMRT co-repressor complex and that a discrete cluster of Rett syndrome–causing mutations in the C-terminal domain of MeCP2 disrupts this interaction, impairing transcriptional repression. Knock-in mice expressing one of these MeCP2 missense mutations exhibit severe motor phenotypes. Rett syndrome (RTT) is a severe neurological disorder that is caused by mutations in the MECP2 gene. Many missense mutations causing RTT are clustered in the DNA-binding domain of MeCP2, suggesting that association with chromatin is critical for its function. We identified a second mutational cluster in a previously uncharacterized region of MeCP2. We found that RTT mutations in this region abolished the interaction between MeCP2 and the NCoR/SMRT co-repressor complexes. Mice bearing a common missense RTT mutation in this domain exhibited severe RTT-like phenotypes. Our data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP2 'bridge' between the NCoR/SMRT co-repressors and chromatin.
Audience Academic
Author Merusi, Cara
Selfridge, Jim
Rappsilber, Juri
Nowak, Jakub
Robinson, Nathaniel D
Lyst, Matthew J
de Lima Alves, Flavia
Ekiert, Robert
Bird, Adrian
Greenberg, Michael E
Ebert, Daniel H
Guy, Jacky
Kastan, Nathaniel R
AuthorAffiliation 2 Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, USA
1 The Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh, UK
AuthorAffiliation_xml – name: 2 Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, USA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/23770565$$D View this record in MEDLINE/PubMed
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AUTHOR CONTRIBUTIONS M.J.L. carried out protein purification for mass spectrometry, deletion analysis and mutation analysis. R.E. performed protein purification for mass spectrometry and repression assays. C.M. produced Mecp2R306C-EGFP knock-in ES cells, performed neuronal differentiation and immunofluorescence analysis. J.N. performed in vitro protein binding assays. J.G. and J.S. produced Mecp2-EGFP knock-in mice and Mecp2T158M-EGFP ES cells. F.d.L.A. and J.R. performed mass spectrometry analysis. D.H.E., N.R.K., N.D.R. and M.E.G. generated and phenotyped Mecp2R306C knock-in mice. M.J.L., R.E. and A.B. wrote the manuscript.
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Snippet In this study, the authors show that MeCP2 interacts with the NCoR/SMRT co-repressor complex and that a discrete cluster of Rett syndrome–causing mutations in...
Rett syndrome (RTT) is a severe neurological disorder that is caused by mutations in the MECP2 gene. Many missense mutations causing RTT are clustered in the...
Rett syndrome (RTT) is a severe neurological disorder that is caused by mutations in the MECP2 gene. Many missense mutations causing RTT are clustered in the...
SourceID pubmedcentral
proquest
gale
crossref
pubmed
springer
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 898
SubjectTerms 631/208/200
631/378/1689/1373
631/378/340
Amino acids
Animal Genetics and Genomics
Animals
Antibodies
Behavioral Sciences
Binding proteins
Biological Techniques
Biomedicine
Brain
Brain - metabolism
Brain - pathology
Cells, Cultured
Chromatin
Disease Models, Animal
DNA methylation
Exploratory Behavior - physiology
Genetic aspects
Green Fluorescent Proteins - genetics
Histone Deacetylases - genetics
Histone Deacetylases - metabolism
Immunoprecipitation
Methyl-CpG-Binding Protein 2 - genetics
Mice
Mice, Inbred C57BL
Mice, Transgenic
Models, Molecular
Mutation
Mutation - genetics
Neurobiology
Neurosciences
Nuclear Receptor Co-Repressor 1 - genetics
Nuclear Receptor Co-Repressor 1 - metabolism
Nuclear Receptor Co-Repressor 2 - genetics
Nuclear Receptor Co-Repressor 2 - metabolism
Peptides
Properties
Proteins
Repressor proteins
Rett syndrome
Rett Syndrome - genetics
Rett Syndrome - pathology
Rett Syndrome - physiopathology
Title Rett syndrome mutations abolish the interaction of MeCP2 with the NCoR/SMRT co-repressor
URI https://link.springer.com/article/10.1038/nn.3434
https://www.ncbi.nlm.nih.gov/pubmed/23770565
https://www.proquest.com/docview/1371388613
https://www.proquest.com/docview/1372079703
https://search.proquest.com/docview/1399918679
https://pubmed.ncbi.nlm.nih.gov/PMC3786392
Volume 16
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