Open AccessInvolvement of the Checkpoint Protein Mec1p in Silencing of Gene Expression at Telomeres in Saccharomyces cerevisiae
Author(s) -
Rolf J. Craven,
Thomas D. Petes
Publication year - 2000
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.20.7.2378-2384.2000
Subject(s) - telomere , gene silencing , biology , gene , saccharomyces cerevisiae , mutation , genetics , microbiology and biotechnology , null allele , telomere binding protein , g2 m dna damage checkpoint , allele , cell cycle , cell cycle checkpoint , dna binding protein , transcription factor
Yeast strains with a mutation in theMEC1 gene are deficient in the cellular checkpoint response to DNA-damaging agents and have short telomeres (K. B. Ritchie, J. C. Mallory, and T. D. Petes, Mol. Cell. Biol. 19:6065–6075, 1999; T. A. Weinert, G. L. Kiser, and L. H. Hartwell, Genes Dev. 8:652–665, 1994). In wild-type yeast cells, genes inserted near the telomeres are transcriptionally silenced (D. E. Gottschling, O. M. Aparichio, B. L. Billington, and V. A. Zakian, Cell 63:751–762, 1990). We show thatmec1 strains have reduced ability to silence gene expression near the telomere. This deficiency was alleviated by thesml1 mutation. Overexpression of Mec1p also resulted in a silencing defect, although this overexpression did not affect the checkpoint function of Mec1p. Telomeric silencing was not affected by mutations in several other genes in the Mec1p checkpoint pathway (null mutations inRAD9 andCHK1 or in several hypomorphicrad53 alleles) but was reduced by a null mutation ofDUN1 . In addition, the loss of telomeric silencing inmec1 strains was not a consequence of the slightly shortened telomeres observed in these strains.