| View Larger Image | Spontaneous and cisplatin-induced recombination in Escherichia coli [An article from: DNA Repair] | Digitalby A. Nowosielska (Author), M.A. Calmann (Author), Z. Zdraveski (Author), Essigm (Author)
| List Price: | $8.95 | | | Available: | Available for download now |
| | Binding: | Digital | | Publisher: | Elsevier | | Publication Date: | July 02, 2004 |
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Product Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: To measure cisplatin (cis-diaminodichloroplatinum(II))-induced recombination, we have used a qualitative intrachromosomal assay utilizing duplicate inactive lac operons containing non-overlapping deletions and selection for Lac^+ recombinants. The two operons are separated by one Mb and conversion of one of them yields the Lac^+ phenotype. Lac^+ formation for both spontaneous and cisplatin-induced recombination requires the products of the recA, recBC, ruvA, ruvB, ruvC, priA and polA genes. Inactivation of the recF, recO, recR and recJ genes decreased cisplatin-induced, but not spontaneous, recombination. The dependence on PriA and RecBC suggests that recombination is induced following stalling or collapse of replication forks at DNA lesions to form double strand breaks. The lack of recombination induction by trans-DDP suggests that the recombinogenic lesions for cisplatin are purine-purine intrastrand crosslinks. |
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