Control of replication initiation and heterochromatin formation in 
Saccharomyces cerevisiae by a regulator of meiotic gene expression

Irlbacher, Horst; Franke, Jacqueline; Manke, Thomas; Vingron, Martin; Ehrenhofer-Murray, Ann E.

doi:10.1101/gad.334805

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学術論文

Control of replication initiation and heterochromatin formation in Saccharomyces cerevisiae by a regulator of meiotic gene expression

MPS-Authors

Irlbacher, Horst
Max Planck Society;

Franke, Jacqueline
Max Planck Society;

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Manke, Thomas
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Vingron, Martin
Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Ehrenhofer-Murray, Ann E.
Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society;

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引用

Irlbacher, H., Franke, J., Manke, T., Vingron, M., & Ehrenhofer-Murray, A. E. (2005). Control of replication initiation and heterochromatin formation in Saccharomyces cerevisiae by a regulator of meiotic gene expression. Genes & Development, 19(15), 1811-1822. doi:10.1101/gad.334805.

引用: https://hdl.handle.net/11858/00-001M-0000-0010-85D8-3

要旨

Heterochromatinization at the silent mating-type loci HMR and HML in Saccharomyces cerevisiae is achieved by targeting the Sir complex to these regions via a set of anchor proteins that bind to the silencers. Here, we have identified a novel heterochromatin-targeting factor for HML, the protein Sum1, a repressor of meiotic genes during vegetative growth. Sum1 bound both in vitro and in vivo to HML via a functional element within the HML-E silencer, and sum1{Delta} caused HML derepression. Significantly, Sum1 was also required for origin activity of HML-E, demonstrating a role of Sum1 in replication initiation. In a genome-wide search for Sum1-regulated origins, we identified a set of autonomous replicative sequences (ARS elements) that bound both the origin recognition complex and Sum1. Full initiation activity of these origins required Sum1, and their origin activity was decreased upon removal of the Sum1-binding site. Thus, Sum1 constitutes a novel global regulator of replication initiation in yeast.