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Eukaryotic Cell, April 2005, p. 673-684, Vol. 4, No. 4
1535-9778/05/$08.00+0     doi:10.1128/EC.4.4.673-684.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Contribution of CAF-I to Anaphase-Promoting-Complex-Mediated Mitotic Chromatin Assembly in Saccharomyces cerevisiae

Troy A. A. Harkness,1* Terra G. Arnason,2 Charmaine Legrand,1 Marnie G. Pisclevich,1 Gerald F. Davies,1 and Emma L. Turner1

Department of Anatomy and Cell Biology,1 Department of Medicine, Royal University Hospital, University of Saskatchewan, Saskatoon, Saskatchewan, Canada2

Received 22 June 2004/ Accepted 21 January 2005

The anaphase-promoting complex (APC) is required for mitotic progression and genomic stability. Recently, we demonstrated that the APC is also required for mitotic chromatin assembly and longevity. Here, we investigated the role the APC plays in chromatin assembly. We show that apc5CA mutations genetically interact with the CAF-I genes as well as ASF1, HIR1, and HIR2. When present in multiple copies, the individual CAF-I genes, CAC1, CAC2, and MSI1, suppress apc5CA phenotypes in a CAF-1- and Asf1p-independent manner. CAF-I and the APC functionally overlap, as cac1{Delta} cac2{Delta} msi1{Delta} (caf1{Delta}) cells expressing apc5CA exhibit a phenotype more severe than that of apc5CA or caf1{Delta}. The Ts– phenotypes observed in apc5CA and apc5CA caf mutants may be rooted in compromised histone metabolism, as coexpression of histones H3 and H4 suppressed the Ts– defects. Synthetic genetic interactions were also observed in apc5CA asf1{Delta} cells. Furthermore, increased expression of genes encoding Asf1p, Hir1p, and Hir2p suppressed the apc5CA Ts– defect in a CAF-I-dependent manner. Together, these results suggest the existence of a complex molecular mechanism controlling APC-dependent chromatin assembly. Our data suggest the APC functions with the individual CAF-I subunits, Asf1p, and the Hir1p and Hir2p proteins. However, Asf1p and an intact CAF-I complex are dispensable for CAF-I subunit suppression, whereas CAF-I is necessary for ASF1, HIR1, and HIR2 suppression of apc5CA phenotypes. We discuss the implications of our observations.

* Corresponding author. Mailing address: Department of Anatomy and Cell Biology, College of Medicine, University of Saskatchewan, B313 Health Sciences Building, 107 Wiggins Road, Saskatoon, Saskatchewan S7N 5E5, Canada. Phone: (306) 966-1995. Fax: (306) 966-4298. E-mail: troy.harkness{at}usask.ca.

Eukaryotic Cell, April 2005, p. 673-684, Vol. 4, No. 4
1535-9778/05/$08.00+0     doi:10.1128/EC.4.4.673-684.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Kats, E. S., Albuquerque, C. P., Zhou, H., Kolodner, R. D. (2006). Checkpoint functions are required for normal S-phase progression in Saccharomyces cerevisiae RCAF- and CAF-I-defective mutants. Proc. Natl. Acad. Sci. USA 103: 3710-3715 [Abstract] [Full Text]  


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