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Molecular and Cellular Biology, December 2002, p. 8165-8174, Vol. 22, No. 23
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.23.8165-8174.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

HTL1 Encodes a Novel Factor That Interacts with the RSC Chromatin Remodeling Complex in Saccharomyces cerevisiae

Martin J. Romeo,1 Melinda L. Angus-Hill,2 Andrew K. Sobering,1,{dagger} Yoshiaki Kamada,1,{ddagger} Bradley R. Cairns,2 and David E. Levin1*

Department of Biochemistry & Molecular Biology, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, Maryland 21205,1 Howard Hughes Medical Institute, Department of Oncological Sciences, University of Utah School of Medicine, Salt Lake City, Utah 841122

Received 20 June 2002/ Returned for modification 5 August 2002/ Accepted 26 August 2002

RSC is an essential chromatin remodeling complex in Saccharomyces cerevisiae that performs central roles in transcriptional regulation and cell cycle progression. Here we identify Htl1 as a novel factor that associates with the RSC complex both physically and functionally. We isolated HTL1 through a genetic screen for mutants that displayed additive growth defects with a conditional mutation in the protein kinase C gene (PKC1), which has been suggested through genetic connections to interact functionally with RSC. Several lines of evidence connect HTL1 to RSC function. First, an htl1{Delta} mutant displayed temperature-sensitive growth and a G2/M cell cycle arrest at restrictive temperatures, a phenotype similar to that of strains with conditional mutations in essential RSC components. Second, we isolated RSC3, which encodes a component of the RSC complex, as a dosage suppressor of the htl1{Delta} growth arrest. Third, an htl1{Delta} mutant displayed additive growth defects with conditional rsc3 alleles. Fourth, overexpression of HTL1 suppressed the growth defect of a strain with a conditional mutation in another RSC component, RSC8. Finally, we demonstrate that Htl1 is a nuclear protein that can associate in vivo with a fraction of the RSC complex. We propose that an RSC-Htl1 complex acts coordinately with protein kinase C to regulate the G2/M transition.

* Corresponding author. Mailing address: Department of Biochemistry & Molecular Biology, The Johns Hopkins University, Bloomberg School of Public Health, 615 N. Wolfe St., Baltimore, MD 21205. Phone: (410) 955-9825. Fax: (410) 955-2926. E-mail: dlevin1{at}jhem.jhmi.edu.

{dagger} Present address: Institut de Genetique et Microbiologie, Université Paris-Sud, 91405 Orsay Cedex, France.

{ddagger} Present address: Department of Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan.

Molecular and Cellular Biology, December 2002, p. 8165-8174, Vol. 22, No. 23
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.23.8165-8174.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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