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Eukaryotic Cell, December 2004, p. 1557-1566, Vol. 3, No. 6
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.6.1557-1566.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Increased Genome Instability and Telomere Length in the elg1-Deficient Saccharomyces cerevisiae Mutant Are Regulated by S-Phase Checkpoints

Soma Banerjee and Kyungjae Myung*

Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland

Received 9 July 2004/ Accepted 13 August 2004

Gross chromosomal rearrangements (GCRs) are frequently observed in cancer cells. Abnormalities in different DNA metabolism including DNA replication, cell cycle checkpoints, chromatin remodeling, telomere maintenance, and DNA recombination and repair cause GCRs in Saccharomyces cerevisiae. Recently, we used genome-wide screening to identify several genes the deletion of which increases GCRs in S. cerevisiae. Elg1, which was discovered during this screening, functions in DNA replication by participating in an alternative replication factor complex. Here we further characterize the GCR suppression mechanisms observed in the elg1{Delta} mutant strain in conjunction with the telomere maintenance role of Elg1. The elg1{Delta} mutation enhanced spontaneous DNA damage and resulted in GCR formation. However, DNA damage due to inactivation of Elg1 activates the intra-S checkpoints, which suppress further GCR formation. The intra-S checkpoints activated by the elg1{Delta} mutation also suppress GCR formation in strains defective in the DNA replication checkpoint. Lastly, the elg1{Delta} mutation increases telomere size independently of other previously known telomere maintenance proteins such as the telomerase inhibitor Pif1 or the telomere size regulator Rif1. The increase in telomere length caused by the elg1{Delta} mutation was suppressed by a defect in the DNA replication checkpoint, which suggests that DNA replication surveillance by Dpb11-Mec1/Tel1-Dun1 also has an important role in telomere length regulation.

* Corresponding author. Mailing address: Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Building 49, Room 4A22, Bethesda, MD 20892. Phone: (301) 451-8748. Fax: (301) 402-4929. E-mail: kmyung{at}nhgri.nih.gov.

Eukaryotic Cell, December 2004, p. 1557-1566, Vol. 3, No. 6
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.6.1557-1566.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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