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Volume 271, Number 22, Issue of May 31, 1996 pp. 12972-12976
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Strand Breaks Are Repaired Efficiently in Human Ribosomal Genes

(Received for publication, March 11, 1996, and in revised form, April 1, 1996)

From the Department of Biochemistry and Biophysics, Washington State University, Pullman, Washington 99164-4660

We examined repair of DNA strand breaks induced by the anti-cancer drug bleomycin in both Pol I and Pol II transcribed genes in permeabilized human fibroblasts. The majority of these breaks (>80%) are single strand breaks (SSBs) thought to be repaired by base excision repair enzymes. Repair was examined in each strand of a 7.2-kilobase fragment, completely within the Pol I transcribed region of ribosomal DNA (rDNA) and an 8.3-kilobase fragment completely within the Pol II transcribed region of the dihydrofolate reductase (DHFR) gene. Bleomycin dose-response studies revealed no bias for SSBs in either strand of the rDNA fragment. Furthermore, repair of SSBs is rapid (~80% resealed in 60 min) in both the transcribed and nontranscribed strands of rDNA. Rapid repair of SSBs is also observed in both strands of the DHFR gene (~60% resealed in 60 min). In contrast, little (or no) repair of UV photodimers occurs in either strand of human rDNA, regardless of whether cells are confluent or actively growing. Thus, DNA lesions in human ribosomal genes may be more accessible to base excision repair enzymes than those involved in nucleotide excision repair.

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