PMID: 7528882Jan 1, 1995Paper

Correlation of doxorubicin footprints with deletion endpoints in lacO of E. coli

Mutation Research
W D SedwickM L Veigl

Abstract

This study explored the possibility that the sequence location of doxorubicin-induced deletion endpoints might relate to DNA structural alterations caused by doxorubicin binding to DNA. The 3'-OH endpoints of doxorubicin-induced deletions terminating in the 35-bp region of lacO appear to distribute differently from spontaneous deletion endpoints. Doxorubicin-induced deletions focus in the 26-bp palindrome which is separated by a 9-bp region with no reverse complementary, whereas spontaneous deletion 3'-OH endpoints are found distributed throughout the operator region. In order to explore the mechanism of deletion induction by doxorubicin, drug footprinting studies were carried out with DNA labeled at the 5' end of each of the complementary DNA strands encompassed by lacO. Doxorubicin protected the 9-bp region between the palindromic sequences from DNase I cutting and caused enhanced DNase I cleavage at symmetrical sites in the palindrome, which were inherently resistant to the nuclease in the absence of the drug. These symmetrical sites also define regions in which the occurrence of deletion endpoints is enhanced 6-fold in the presence of doxorubicin. This enhanced cutting and mutation occur in regions of the palindrome that ar...Continue Reading

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