Δημοσίευση

Mechanism of Polycomb recruitment to CpG islands revealed by inherited disease-associated mutation.

ΤίτλοςMechanism of Polycomb recruitment to CpG islands revealed by inherited disease-associated mutation.
Publication TypeJournal Article
Year of Publication2013
AuthorsCaputo, V. S., Costa J. R., Makarona K., Georgiou E., D Layton M., Roberts I., & Karadimitris A.
JournalHum Mol Genet
Volume22
Issue16
Pagination3187-94
Date Published2013 Aug 15
ISSN1460-2083
Λέξεις κλειδιάActivating Transcription Factors, B-Lymphocytes, Base Sequence, Cells, Cultured, CpG Islands, DNA Methylation, DNA-Binding Proteins, Gene Expression Regulation, Genes, Essential, Glycosylphosphatidylinositols, Hemoglobinuria, Paroxysmal, Histones, Humans, Mannosyltransferases, Molecular Sequence Data, Nucleosomes, Point Mutation, Polycomb-Group Proteins, Promoter Regions, Genetic, Protein Binding, Seizures
Abstract

How the transcription repressing complex Polycomb interacts with transcriptional regulators at housekeeping genes in somatic cells is not well understood. By exploiting a CpG island (CGI) point mutation causing a Mendelian disease, we show that DNA binding of activating transcription factor (TF) determines histone acetylation and nucleosomal depletion commensurate with Polycomb exclusion from the target promoter. Lack of TF binding leads to reversible transcriptional repression imposed by nucleosomal compaction and consolidated by Polycomb recruitment and establishment of bivalent chromatin status. Thus, within a functional hierarchy of transcriptional regulators, TF binding is the main determinant of Polycomb recruitment to the CGI of a housekeeping gene in somatic cells.

DOI10.1093/hmg/ddt171
Alternate JournalHum Mol Genet
PubMed ID23591993
Grant ListG0802401 / / Medical Research Council / United Kingdom

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