Titre
A switch in mitotic histone H4 lysine 20 methylation status is linked to M phase defects upon loss of HCF-1.
Type
article
Institution
Externe
Périodique
Auteur(s)
Julien, E.
Auteure/Auteur
Herr, W.
Auteure/Auteur
Liens vers les personnes
ISSN
1097-2765[print], 1097-2765[linking]
Statut éditorial
Publié
Date de publication
2004
Volume
14
Numéro
6
Première page
713
Dernière page/numéro d’article
725
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
Publication Status: ppublish
Publication Status: ppublish
Résumé
The abundant chromatin-associated human factor HCF-1 is a heterodimeric complex of HCF-1N and HCF-1C subunits that are essential for two stages of the cell cycle. The HCF-1N subunit promotes G1 phase progression, whereas the HCF-1C subunit ensures proper cytokinesis at completion of M phase. How the HCF-1C subunit functions is unknown. Here, we show that HCF-1C subunit depletion causes extensive mitotic defects, including a switch from monomethyl to dimethyl lysine 20 of histone H4 (H4-K20) and defective chromosome alignment and segregation. Consistent with these activities, the HCF-1C subunit can associate with chromatin independently of the HCF-1N subunit and regulates the expression of the H4-K20 methyltransferase PR-Set7. Indeed, upregulation of PR-Set7 expression upon loss of HCF-1 leads to improper mitotic H4-K20 methylation and cytokinesis defects. These results establish the HCF-1C subunit as an important M phase regulator and suggest that H4-K20 methylation status contributes to chromosome behavior during mitosis and proper cytokinesis.
Sujets
PID Serval
serval:BIB_FEB155C2ACE6
PMID
Open Access
Oui
Date de création
2008-01-24T14:36:38.210Z
Date de création dans IRIS
2025-05-21T05:39:56Z