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J. Biol. Chem., Vol. 276, Issue 21, 18597-18604, May 25, 2001
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From the Institute of Biosciences and Technology, Center
for Genome Research, Texas A & M University System Health Science
Center, Texas Medical Center, Houston, Texas 77030-3303 and
§ Genzyme Corporation, Framingham, Massachusetts 01701
The 2.5-kilobase pair
poly(purine·pyrimidine) (poly(R·Y)) tract present in intron 21 of
the polycystic kidney disease 1 (PKD1) gene has been
proposed to contribute to the high mutation frequency of the gene. To
evaluate this hypothesis, we investigated the growth rates of 11 Escherichia coli strains, with mutations in the nucleotide
excision repair, SOS, and topoisomerase I and/or gyrase genes,
harboring plasmids containing the full-length tract, six 5'-truncations
of the tract, and a control plasmid (pSPL3). The full-length
poly(R·Y) tract induced dramatic losses of cell viability during the
first few hours of growth and lengthened the doubling times of the
populations in strains with an inducible SOS response. The extent of
cell loss was correlated with the length of the poly(R·Y) tract and
the levels of negative supercoiling as modulated by the genotype of the
strains or drugs that specifically inhibited DNA gyrase or bound to DNA
directly, thereby affecting conformations at specific loci. We conclude
that the unusual DNA conformations formed by the PKD1
poly(R·Y) tract under the influence of negative supercoiling induced
the SOS response pathway, and they were recognized as lesions by the
nucleotide excision repair system and were cleaved, causing delays in
cell division and loss of the plasmid. These data support a role for
this sequence in the mutation of the PKD1 gene by
stimulating repair and/or recombination functions.
PKD1 Unusual DNA Conformations Are Recognized by
Nucleotide Excision Repair*
,
*
This work was supported by Polycystic Kidney Research
Foundation Grant 98004, National Institutes of Health Grants GM 52982 and NS 37554, and the Robert A. Welch Foundation.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Present address: Center for Microbiology and Virology, Polish
Academy of Sciences, 106 Lodowa St., 93-232 Lodz, Poland.
¶
To whom correspondence should be addressed: Institute of
Biosciences and Technology, Center for Genome Research, Texas A & M
University System Health Science Center, Texas Medical Center, 2121 Holcombe Blvd., Houston, TX 77030-3303. Tel.: 713-677-7651; Fax:
713-677-7689; E-mail: rwells@ibt.tamu.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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