Abstract:
: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 htl1Delta mutant displayed temperature-sensitive growth and a G(2)/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 htl1Delta growth arrest. Third, an htl1Delta 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 G(2)/M transition.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Romeo MJ,Angus-Hill ML,Sobering AK,Kamada Y,Cairns BR,Levin DEdoi
10.1128/mcb.22.23.8165-8174.2002subject
Has Abstractpub_date
2002-12-01 00:00:00pages
8165-74issue
23eissn
0270-7306issn
1098-5549journal_volume
22pub_type
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