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Molecular and Cellular Biology, July 2005, p. 5920-5932, Vol. 25, No. 14
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.14.5920-5932.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Sum1p, the Origin Recognition Complex, and the Spreading of a Promoter-Specific Repressor in Saccharomyces cerevisiae

Patrick J. Lynch,1 Hunter B. Fraser,2 Elena Sevastopoulos,2 Jasper Rine,2 and Laura N. Rusche1*

Department of Biochemistry and Institute for Genome Sciences and Policy, Duke University, Durham, North Carolina,1 Molecular and Cell Biology Department, University of California, Berkeley, Berkeley, California2

Received 3 March 2005/ Returned for modification 7 April 2005/ Accepted 20 April 2005

In Saccharomyces cerevisiae, Sum1p is a promoter-specific repressor. A single amino acid change generates the mutant Sum1-1p, which causes regional silencing at new loci where wild-type Sum1p does not act. Thus, Sum1-1p is a model for understanding how the spreading of repressive chromatin is regulated. When wild-type Sum1p was targeted to a locus where mutant Sum1-1p spreads, wild-type Sum1p did not spread as efficiently as mutant Sum1-1p did, despite being in the same genomic context. Thus, the SUM1-1 mutation altered the ability of the protein to spread. The spreading of Sum1-1p required both an enzymatically active deacetylase, Hst1p, and the N-terminal tail of histone H4, consistent with the spreading of Sum1-1p involving sequential modification of and binding to histone tails, as observed for other silencing proteins. Furthermore, deletion of the N-terminal tail of H4 caused Sum1-1p to return to loci where wild-type Sum1p acts, consistent with the SUM1-1 mutation increasing the affinity of the protein for H4 tails. These results imply that the spreading of repressive chromatin proteins is regulated by their affinities for histone tails. Finally, this study uncovered a functional connection between wild-type Sum1p and the origin recognition complex, and this relationship also contributes to mutant Sum1-1p localization.

* Corresponding author. Mailing address: Institute for Genome Sciences and Policy, 101 Science Drive, Box 3382, Durham, NC 27708. Phone: (919) 684-0354. Fax: (919) 668-0795. E-mail: lrusche{at}biochem.duke.edu.

Molecular and Cellular Biology, July 2005, p. 5920-5932, Vol. 25, No. 14
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.14.5920-5932.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Lynch, P. J., Rusche, L. N. (2009). A Silencer Promotes the Assembly of Silenced Chromatin Independently of Recruitment. Mol. Cell. Biol. 29: 43-56 [Abstract] [Full Text]  
  • Safi, A., Wallace, K. A., Rusche, L. N. (2008). Evolution of New Function through a Single Amino Acid Change in the Yeast Repressor Sum1p. Mol. Cell. Biol. 28: 2567-2578 [Abstract] [Full Text]  
  • Darst, R. P., Garcia, S. N., Koch, M. R., Pillus, L. (2008). Slx5 Promotes Transcriptional Silencing and Is Required for Robust Growth in the Absence of Sir2. Mol. Cell. Biol. 28: 1361-1372 [Abstract] [Full Text]  
  • Mead, J., McCord, R., Youngster, L., Sharma, M., Gartenberg, M. R., Vershon, A. K. (2007). Swapping the Gene-Specific and Regional Silencing Specificities of the Hst1 and Sir2 Histone Deacetylases. Mol. Cell. Biol. 27: 2466-2475 [Abstract] [Full Text]  
  • Valenzuela, L., Gangadharan, S., Kamakaka, R. T. (2006). Analyses of SUM1-1-Mediated Long-Range Repression. Genetics 172: 99-112 [Abstract] [Full Text]  


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