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MacroH2A1 knockdown effects on the Peg3 imprinted domain

BACKGROUND: MacroH2A1 is a histone variant that is closely associated with the repressed regions of chromosomes. A recent study revealed that this histone variant is highly enriched in the inactive alleles of Imprinting Control Regions (ICRs). RESULTS: The current study investigates the potential ro...

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Autores principales: Choo, Jung Ha, Kim, Jeong Do, Kim, Joomyeong
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2241636/
https://www.ncbi.nlm.nih.gov/pubmed/18166131
http://dx.doi.org/10.1186/1471-2164-8-479
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author Choo, Jung Ha
Kim, Jeong Do
Kim, Joomyeong
author_facet Choo, Jung Ha
Kim, Jeong Do
Kim, Joomyeong
author_sort Choo, Jung Ha
collection PubMed
description BACKGROUND: MacroH2A1 is a histone variant that is closely associated with the repressed regions of chromosomes. A recent study revealed that this histone variant is highly enriched in the inactive alleles of Imprinting Control Regions (ICRs). RESULTS: The current study investigates the potential roles of macroH2A1 in genomic imprinting by lowering the cellular levels of the macroH2A1 protein. RNAi-based macroH2A1 knockdown experiments in Neuro2A cells changed the expression levels of a subset of genes, including Peg3 and Usp29 of the Peg3 domain. The expression of these genes was down-regulated, rather than up-regulated, in response to reduced protein levels of the potential repressor macroH2A1. This down-regulation was not accompanied with changes in the DNA methylation status of the Peg3 domain. CONCLUSION: MacroH2A1 may not function as a transcriptional repressor for this domain, but that macroH2A1 may participate in the heterochromatin formation with functions yet to be discovered.
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spelling pubmed-22416362008-02-13 MacroH2A1 knockdown effects on the Peg3 imprinted domain Choo, Jung Ha Kim, Jeong Do Kim, Joomyeong BMC Genomics Research Article BACKGROUND: MacroH2A1 is a histone variant that is closely associated with the repressed regions of chromosomes. A recent study revealed that this histone variant is highly enriched in the inactive alleles of Imprinting Control Regions (ICRs). RESULTS: The current study investigates the potential roles of macroH2A1 in genomic imprinting by lowering the cellular levels of the macroH2A1 protein. RNAi-based macroH2A1 knockdown experiments in Neuro2A cells changed the expression levels of a subset of genes, including Peg3 and Usp29 of the Peg3 domain. The expression of these genes was down-regulated, rather than up-regulated, in response to reduced protein levels of the potential repressor macroH2A1. This down-regulation was not accompanied with changes in the DNA methylation status of the Peg3 domain. CONCLUSION: MacroH2A1 may not function as a transcriptional repressor for this domain, but that macroH2A1 may participate in the heterochromatin formation with functions yet to be discovered. BioMed Central 2007-12-31 /pmc/articles/PMC2241636/ /pubmed/18166131 http://dx.doi.org/10.1186/1471-2164-8-479 Text en Copyright © 2007 Choo et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Choo, Jung Ha
Kim, Jeong Do
Kim, Joomyeong
MacroH2A1 knockdown effects on the Peg3 imprinted domain
title MacroH2A1 knockdown effects on the Peg3 imprinted domain
title_full MacroH2A1 knockdown effects on the Peg3 imprinted domain
title_fullStr MacroH2A1 knockdown effects on the Peg3 imprinted domain
title_full_unstemmed MacroH2A1 knockdown effects on the Peg3 imprinted domain
title_short MacroH2A1 knockdown effects on the Peg3 imprinted domain
title_sort macroh2a1 knockdown effects on the peg3 imprinted domain
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2241636/
https://www.ncbi.nlm.nih.gov/pubmed/18166131
http://dx.doi.org/10.1186/1471-2164-8-479
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