Allelic inactivation of the pseudoautosomal gene SYBL1 is controlled by epigenetic mechanisms common to the X and Y chromosomes
Autor: | Maria Luigia De Bonis, Richard I. Gregory, Maria R. Matarazzo, Marcella Vacca, Grazia Mercadante, R. Scott Hansen, Robert Feil, Michele D'Urso, Maurizio D'Esposito |
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Přispěvatelé: | Institut de Génétique Moléculaire de Montpellier (IGMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM) |
Jazyk: | angličtina |
Rok vydání: | 2002 |
Předmět: |
Male
Herpesvirus 4 Human Alleles Cell Line Hybrid Cells Biology X-inactivation Histones R-SNARE Proteins 03 medical and health sciences Epigenetics of physical exercise Histone methylation Genetics Humans [SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology Gene Silencing Lymphocytes Epigenetics Transformed Chromatin/genetics Chromosomes Promoter Regions Genetic Molecular Biology RNA-Directed DNA Methylation Alleles Genetics (clinical) Cell Line Transformed 030304 developmental biology Epigenomics Chromosomes Human X 0303 health sciences Chromosomes Human Y Genetic Carrier Screening 030305 genetics & heredity Membrane Proteins General Medicine DNA Methylation Fibroblasts X/*genetics Chromosomes Molecular biology Chromatin Human Heterozygote Detection Histones/chemistry/metabolism Humans Hybrid Cells Lymphocytes/chemistry/metabolism/virology Male Membrane Proteins/biosynthesis/*genetics Promoter Regions Genetic/genetics R-SNARE Proteins Gene Expression Regulation Histone methyltransferase DNA methylation CpG Islands Female Y/*genetics CpG Islands/genetics DNA Methylation Female Fibroblasts/chemistry/metabolism/virology Gene Expression Regulation/genetics *Gene Silencing Herpesvirus 4 Human |
Zdroj: | Human Molecular Genetics Human Molecular Genetics, Oxford University Press (OUP), 2002, 11 (25), pp.3191--8. ⟨10.1093/hmg/11.25.3191⟩ Human molecular genetics 25 (2002): 3191–3198. doi:10.1093/hmg/11.25.3191 info:cnr-pdr/source/autori:Matarazzo MR, De Bonis ML, Gregory RI, Vacca M, Hansen RS, Mercadante G, D'Urso M, Feil R, D'Esposito M./titolo:Allelic inactivation of the pseudoautosomal gene SYBL1 is controlled by epigenetic mechanisms common to the X and Y chromosomes./doi:10.1093%2Fhmg%2F11.25.3191/rivista:Human molecular genetics (Print)/anno:2002/pagina_da:3191/pagina_a:3198/intervallo_pagine:3191–3198/volume:25 |
ISSN: | 0964-6906 1460-2083 |
DOI: | 10.1093/hmg/11.25.3191⟩ |
Popis: | On the human long-arm pseudoautosomal region (XqPAR), genes that are subject to inactivation are closely linked with those that escape. Genes subject to inactivation are not only silenced on the inactive X in females, but they are also inactivated on the Y chromosome in males. One of the genes subject to this unusual inactivation pattern is the synaptobrevin-like 1 gene (SYBL1). Previously we showed that its silencing on the inactive X and the Y allele involves DNA methylation. This study explores the molecular events associated with SYBL1 silencing and investigates their relationship. Promoter DNA methylation profiles were determined by bisulfite sequencing and immunoprecipitation experiments demonstrate that chromatin on the repressed Xi and the Y alleles has underacetylated histones H3 and H4 and H3-lysine 9 methylation. In addition, the inactive X and the Y allele were found to have a condensed chromatin conformation. In contrast, the expressed allele shows H3 and H4 acetylation, H3-lysine 4 methylation and a less compacted chromatin conformation. In ICF syndrome, a human disease affecting DNA methylation, SYBL1 escapes from silencing and this correlates with altered patterns of histone methylation and acetylation. Combined, our data suggest that specific combinations of histone methylation and acetylation are involved in the somatic maintenance of permissive and repressed chromatin states at SYBL1. Although it is unclear at present how this allele-specific silencing comes about, the data also indicate that the epigenetic features of the 'Y inactivation' of SYBL1 are mechanistically similar to those associated with X-chromosome inactivation. |
Databáze: | OpenAIRE |
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