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Molecular and Cellular Biology, March 2006, p. 1955-1966, Vol. 26, No. 5
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.5.1955-1966.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Tolerance of Sir1p/Origin Recognition Complex-Dependent Silencing for Enhanced Origin Firing at HMRa

Kristopher H. McConnell, Philipp Müller, and Catherine A. Fox*

Department of Biomolecular Chemistry, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53706

Received 6 September 2005/ Returned for modification 24 October 2005/ Accepted 9 December 2005

The HMR-E silencer is a DNA element that directs the formation of silent chromatin at the HMRa locus in Saccharomyces cerevisiae. Sir1p is one of four Sir proteins required for silent chromatin formation at HMRa. Sir1p functions by binding the origin recognition complex (ORC), which binds to HMR-E, and recruiting the other Sir proteins (Sir2p to -4p). ORCs also bind to hundreds of nonsilencer positions distributed throughout the genome, marking them as replication origins, the sites for replication initiation. HMR-E also acts as a replication origin, but compared to many origins in the genome, it fires extremely inefficiently and late during S phase. One postulate to explain this observation is that ORC's role in origin firing is incompatible with its role in binding Sir1p and/or the formation of silent chromatin. Here we examined a mutant HMR-E silencer and fusions between robust replication origins and HMR-E for HMRa silencing, origin firing, and replication timing. Origin firing within HMRa and from the HMR-E silencer itself could be significantly enhanced, and the timing of HMRa replication during an otherwise normal S phase advanced, without a substantial reduction in SIR1-dependent silencing. However, although the robust origin/silencer fusions silenced HMRa quite well, they were measurably less effective than a comparable silencer containing HMR-E's native ORC binding site.

* Corresponding author. Mailing address: Department of Biomolecular Chemistry, University of Wisconsin School of Medicine and Public Health, 587 MSC, 1300 University Ave., Madison, WI 53706-1532. Phone: (608) 262-9370. Fax: (608) 262-5253. E-mail: cfox{at}wisc.edu.

Molecular and Cellular Biology, March 2006, p. 1955-1966, Vol. 26, No. 5
0022-538X/06/$08.00+0     doi:10.1128/MCB.26.5.1955-1966.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Casey, L., Patterson, E. E., Muller, U., Fox, C. A. (2008). Conversion of a Replication Origin to a Silencer through a Pathway Shared by a Forkhead Transcription Factor and an S Phase Cyclin. Mol. Biol. Cell 19: 608-622 [Abstract] [Full Text]  


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