Epigenetic regulation of histone H3 serine 10 phosphorylation status by HCF-1 proteins in C. elegans and mammalian cells.

Détails

Ressource 1Télécharger: BIB_AEF37F36FA67.P001.pdf (691.87 [Ko])
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_AEF37F36FA67
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Epigenetic regulation of histone H3 serine 10 phosphorylation status by HCF-1 proteins in C. elegans and mammalian cells.
Périodique
PLoS ONE
Auteur⸱e⸱s
Lee S., Horn V., Julien E., Liu Y., Wysocka J., Bowerman B., Hengartner M.O., Herr W.
ISSN
1932-6203
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
2
Numéro
11
Pages
e1213
Langue
anglais
Résumé
BACKGROUND: The human herpes simplex virus (HSV) host cell factor HCF-1 is a transcriptional coregulator that associates with both histone methyl- and acetyltransferases, and a histone deacetylase and regulates cell proliferation and division. In HSV-infected cells, HCF-1 associates with the viral protein VP16 to promote formation of a multiprotein-DNA transcriptional activator complex. The ability of HCF proteins to stabilize this VP16-induced complex has been conserved in diverse animal species including Drosophila melanogaster and Caenorhabditis elegans suggesting that VP16 targets a conserved cellular function of HCF-1. METHODOLOGY/PRINCIPAL FINDINGS: To investigate the role of HCF proteins in animal development, we have characterized the effects of loss of the HCF-1 homolog in C. elegans, called Ce HCF-1. Two large hcf-1 deletion mutants (pk924 and ok559) are viable but display reduced fertility. Loss of Ce HCF-1 protein at reduced temperatures (e.g., 12 degrees C), however, leads to a high incidence of embryonic lethality and early embryonic mitotic and cytokinetic defects reminiscent of mammalian cell-division defects upon loss of HCF-1 function. Even when viable, however, at normal temperature, mutant embryos display reduced levels of phospho-histone H3 serine 10 (H3S10P), a modification implicated in both transcriptional and mitotic regulation. Mammalian cells with defective HCF-1 also display defects in mitotic H3S10P status. CONCLUSIONS/SIGNIFICANCE: These results suggest that HCF-1 proteins possess conserved roles in the regulation of cell division and mitotic histone phosphorylation.
Mots-clé
Animals, Base Sequence, Caenorhabditis elegans, Caenorhabditis elegans Proteins, DNA Primers, Epigenesis, Genetic, Histones, Host Cell Factor C1, Humans, Microscopy, Fluorescence, Mutation, Phosphorylation, Serine
Pubmed
Web of science
Open Access
Oui
Création de la notice
09/07/2008 11:47
Dernière modification de la notice
20/08/2019 16:18
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