Nucleic Acids Research Advance Access originally published online on October 24, 2006
Nucleic Acids Research 2006 34(20):5880-5891; doi:10.1093/nar/gkl749
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Nucleic Acids Research, 2006, Vol. 34, No. 20 5880-5891
© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
The budding yeast protein Chl1p is required to preserve genome integrity upon DNA damage in S-phase
Department of Biochemistry, Bose Institute P1/12 CIT Scheme VII M, Kolkata 700 054, India
*To whom correspondence should be addressed. Tel: 91 33 23550256; Fax: 91 33 23343886; Email: pratima{at}bic.boseinst.ernet.in
Received June 25, 2006. Revised September 20, 2006. Accepted September 21, 2006.
The budding yeast protein, Chl1p, is required for sister-chromatid cohesion, transcriptional silencing, rDNA recombination and aging. In this work, we show that Chl1p is also required for viability when DNA replication is stressed, either due to mutations or if cells are treated with genotoxic agents like methylmethane sulfonate (MMS) and ultraviolet (UV) rays. The chl1 mutation caused synthetic growth defects with mutations in DNA replication genes. At semi-permissive temperatures, the double mutants grew poorly, were less viable and showed nuclear fragmentation. They were, however, not limited in their bulk DNA synthesis. When chl1 cells were treated with relatively low levels of MMS in S-phase, they lost viability. The S-phase DNA damage checkpoint pathway, however, remained active in these cells. Agarose gel electrophoresis of genomic DNA isolated from wild-type and chl1 cells, after recovery from MMS treatment, suggested that the wild-type was more proficient in the repair of DNA damage than the mutant. Our work suggests that Chl1p is required for genome integrity when cells suffer endogenously or exogenously induced DNA damage.
Present address: Sujata Hajra, Section of Molecular Genetics, Microbiology and Immunology, College of Natural Sciences, The University of Texas at Austin, Austin TX 78712, USA
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.