This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bhatia, P. K. Articles by Friedberg, E. C. Search for Related Content PubMed PubMed Citation Articles by Bhatia, P. K. Articles by Friedberg, E. C.

 Previous Article  |  Next Article 

J. Bacteriol., Oct 1996, 5977-5988, Vol 178, No. 20
Copyright © 1996, American Society for Microbiology

Molecular cloning and characterization of Saccharomyces cerevisiae RAD28, the yeast homolog of the human Cockayne syndrome A (CSA) gene

PK Bhatia, RA Verhage, J Brouwer and EC Friedberg
Laboratory of Molecular Pathology, Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75235, USA.

Cockayne syndrome patients exhibit severe developmental and neurological abnormalities. Cells derived from these patients are sensitive to killing by UV radiation and do not support the rapid repair of the transcribed strand of transcriptionally active genes observed in cells from normal individuals. We report the cloning of the Saccharomyces cerevisiae homolog of the Cockayne syndrome A (CSA) gene, which we designate as RAD28. A rad28 null mutant does not manifest increased sensitivity to killing by UV or gamma radiation or to methyl methanesulfonate. Additionally, the rate of repair of the transcribed and nontranscribed strands of the yeast RPB2 gene in the rad28 mutant is identical to that observed in wild-type cells following exposure to UV light. As previously shown for rad7 rad26 and rad16 rad26 double mutants, the rad28 null mutant shows slightly enhanced sensitivity to UV light in the presence of mutations in the RAD7 or RAD16 gene. Both rad28 and rad26 null mutants are hypermutable following exposure to UV light.

This article has been cited by other articles:

• Zhou, Y., Kou, H., Wang, Z. (2007). Tfb5 interacts with Tfb2 and facilitates nucleotide excision repair in yeast. Nucleic Acids Res 35: 861-871 [Abstract] [Full Text]  
• Li, S., Chen, X., Ruggiero, C., Ding, B., Smerdon, M. J. (2006). Modulation of Rad26- and Rpb9-mediated DNA Repair by Different Promoter Elements. J. Biol. Chem. 281: 36643-36651 [Abstract] [Full Text]  
• Wu, H. I., Brown, J. A., Dorie, M. J., Lazzeroni, L., Brown, J. M. (2004). Genome-Wide Identification of Genes Conferring Resistance to the Anticancer Agents Cisplatin, Oxaliplatin, and Mitomycin C. Cancer Res. 64: 3940-3948 [Abstract] [Full Text]  
• Gonzalez-Barrera, S., Prado, F., Verhage, R., Brouwer, J., Aguilera, A. (2002). Defective nucleotide excision repair in yeast hpr1 and tho2 mutants. Nucleic Acids Res 30: 2193-2201 [Abstract] [Full Text]  
• Morey, N. J., Greene, C. N., Jinks-Robertson, S. (2000). Genetic Analysis of Transcription-Associated Mutation in Saccharomyces cerevisiae. Genetics 154: 109-120 [Abstract] [Full Text]  
• Yasuhira, S., Morimyo, M., Yasui, A. (1999). Transcription Dependence and the Roles of Two Excision Repair Pathways for UV Damage in Fission Yeast Schizosaccharomyces pombe. J. Biol. Chem. 274: 26822-26827 [Abstract] [Full Text]  
• You, Z., Feaver, W. J., Friedberg, E. C. (1998). Yeast RNA Polymerase II Transcription In Vitro Is Inhibited in the Presence of Nucleotide Excision Repair: Complementation of Inhibition by Holo-TFIIH and Requirement for RAD26. Mol. Cell. Biol. 18: 2668-2676 [Abstract] [Full Text]  
• Tijsterman, M., Verhage, R. A., van de Putte, P., Jong, J. G. T.-d., Brouwer, J. (1997). Transitions in the coupling of transcription and nucleotide excision repair within RNA polymerase II-transcribed genes of Saccharomyces cerevisiae. Proc. Natl. Acad. Sci. USA 94: 8027-8032 [Abstract] [Full Text]  
• Nouspikel, T., Lalle, P., Leadon, S. A., Cooper, P. K., Clarkson, S. G. (1997). A common mutational pattern in Cockayne syndrome patients from xeroderma pigmentosum group G: Implications for a second XPG function. Proc. Natl. Acad. Sci. USA 94: 3116-3121 [Abstract] [Full Text]