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Molecular and Cellular Biology, January 2003, p. 382-388, Vol. 23, No. 1
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.1.382-388.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Stalling of Transcription at Abasic Sites Is Highly Mutagenic

Sung-Lim Yu, Sung-Keun Lee, Robert E. Johnson, Louise Prakash, and Satya Prakash*

Sealy Center for Molecular Science, University of Texas Medical Branch, Galveston, Texas 77555-1061

Received 20 August 2002/ Returned for modification 1 October 2002/ Accepted 8 October 2002

Abasic (AP) sites represent one of the most frequently formed lesions in DNA. Here, we examine the consequences of the stalling of RNA polymerase II at AP sites in DNA in Saccharomyces cerevisiae. A severe inhibition of transcription occurs in strains that are defective in the removal of AP sites and that also lack the RAD26 gene, a homolog of the human Cockayne syndrome group B (CSB) gene, and, importantly, a dramatic rise in mutagenesis is incurred in such strains. From the various observations presented here, we infer that the stalling of transcription at AP sites is highly mutagenic.

* Corresponding author. Mailing address: Sealy Center for Molecular Science, University of Texas Medical Branch, 6.104 Blocker Medical Research Building, 11th and Mechanic Streets, Galveston, TX 77555-1061. Phone: (409) 747-8602. Fax: (409) 747-8608. E-mail: s.prakash{at}utmb.edu.

Molecular and Cellular Biology, January 2003, p. 382-388, Vol. 23, No. 1
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.1.382-388.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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