Spontaneous reversion of tsBN67 cell proliferation and cytokinesis defects in the absence of HCF-1 function.

Détails

ID Serval
serval:BIB_8A67137E7FD6
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Spontaneous reversion of tsBN67 cell proliferation and cytokinesis defects in the absence of HCF-1 function.
Périodique
Experimental Cell Research
Auteur(s)
Reilly P.T., Herr W.
ISSN
0014-4827[print], 0014-4827[linking]
Statut éditorial
Publié
Date de publication
2002
Volume
277
Numéro
1
Pages
119-130
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
Résumé
Mammalian HCF-1 is a highly conserved and abundant chromatin-bound protein that plays a role in both herpes simplex virus (HSV) immediate-early (IE) gene transcription and cell proliferation. Its role in cell proliferation has been evidenced through the analysis of a temperature-sensitive hamster cell line called tsBN67. When placed at nonpermissive temperature, tsBN67 cells undergo a stable and reversible proliferation arrest after a lag of 36-48 h. This phenotype results from a single point mutation in HCF-1, which disrupts HCF-1 association with both chromatin and the HSV IE transactivator VP16 at nonpermissive temperature. Here, we report the isolation and characterization of spontaneous tsBN67 growth-revertant cells that are able to proliferate at nonpermissive temperatures. These cells retain the tsBN67 HCF-1 point mutation and grow in the absence of HCF-1 chromatin association, demonstrating that complete restoration of tsBN67 HCF-1 functions is not essential for cell proliferation. Phenotypic analysis of both mutant and revertant tsBN67 cells shows that, in addition to a cell proliferation defect, these cells display a conspicuous multinucleated phenotype in a significant population of arrested cells. This defect in cytokinesis is also a result of loss of HCF-1 function, suggesting that HCF-1 plays a role in cell exit from mitosis. The revertant tsBN67 cells display a coincident restoration of cell proliferation and suppression of the cytokinetic defect, suggesting that HCF-1 plays a shared role in cell proliferation and cytokinesis.
Mots-clé
Animals, Biological Markers, Cell Division, Cell Line, Cricetinae, G2 Phase, Host Cell Factor C1, Mitosis, Phenotype, Point Mutation, Proteins/genetics, Proteins/physiology, Temperature, Transcription Factors
Pubmed
Web of science
Création de la notice
24/01/2008 16:36
Dernière modification de la notice
03/03/2018 19:09
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