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MBC in Press, published online ahead of print November 12, 2008
Mol. Biol. Cell 10.1091/mbc.E08-01-0099

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Submitted on February 8, 2008
Revised on October 1, 2008
Accepted on November 4, 2008

Sub-telomeric ACS-containing Proto-silencers Act as Anti-silencers in Replication Factors Mutants in S. cerevisiae

Muhammad Attiq Rehman,* Dongliang Wang,* Genevieve Fourel,{dagger} Eric Gilson,{dagger} and Krassimir Yankulov*

*Department of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario N1G 2W1, Canada; {dagger}Laboratoire de Biologie Moléculaire de la Cellule de l’Ecole Normale Supérieure de Lyon, CNRS UMR5161, IFR 128, F-69364, Lyon, France

Monitoring Editor: Yixian Zheng

Subtelomeric genes are either fully active or completely repressed and can switch their state about once per twenty generations. This meta-stable Telomeric Position Effect (TPE) is mediated by strong repression signals emitted by the telomere and relayed/enhanced by weaker repressor elements called proto-silencers. In addition, subtelomeric regions contain sequences with chromatin partitioning and anti-silencing activities referred to as STARs (Sub-Telomeric Anti-silencing Regions). Using extensive mutational analysis of subtelomeric elements, we show that ACS (ARS Consensus Sequence)-containing proto-silencers convert to anti-silencers in several replication factor mutants. We point out the significance of the B1 auxiliary sequence next to ACS in mediating these effects. In contrast, an origin-derived ACS does not convert to anti-silencer in mutants and its B1 element has little bearing on silencing. These results are specific for the analyzed ACS and in addition to the effects of each mutation (relative to wild type) on global silencing. Another line of experiments shows that Mcm5p possesses anti-silencing activity and is recruited to telomeres in an ACS-dependent manner. Mcm5p persists at this location at the late stages of S-phase. We propose that telomeric ACS are not static proto-silencers, but conduct finely tuned silencing and anti-silencing activities mediated by ACS-bound factors.

Address correspondence to: Krassimir Yankulov (yankulov{at}uoguelph.ca)






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