![AlkB dioxygenase in preventing MMS-induced mutagenesis in Escherichia coli: Effect of Pol V and AlkA proteins [An article from: DNA Repair]](https://www.ebooknetworking.net/books/B00/0RR/bigB000RR6KW8.jpg)
AlkB dioxygenase in preventing MMS-induced mutagenesis in Escherichia coli: Effect of Pol V and AlkA proteins [An article from: DNA Repair]
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PublisherElsevier
ISBN / ASINB000RR6KW8
ISBN-13978B000RR6KW4
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Description
This digital document is a journal article from DNA Repair, published by Elsevier in . 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:
The deleterious effect of defective alkB allele encoding 1meA/3meC dioxygenase on reactivation of MMS-treated phage DNA has been frequently studied. Here, it is shown that: (i) AlkB protects the cells not only against the genotoxic but also against the potent mutagenic activity of MMS; (ii) mutations arising in alkB-defected strains are umuDC-dependent, and deletion of umuDC dramatically reduce MMS-induced mutations resulting from the presence of 1meA/3meC in DNA; (iii) specificity of MMS-induced argE3->Arg^+ reversions in AB1157 alkB-defective cells are predominantly AT->TA transversions and GC->AT transitions; (iv) overproduction of AlkA and the resultant decrease in 3meA residues in DNA dramatically reduce MMS-induced mutations. This reduction is most probably a secondary effect of AlkA due to a decrease in 3meA residues in DNA and, in consequence, suppression of SOS induction and Pol V expression. Overproduction of UmuD'C proteins reverses this effect.
Description:
The deleterious effect of defective alkB allele encoding 1meA/3meC dioxygenase on reactivation of MMS-treated phage DNA has been frequently studied. Here, it is shown that: (i) AlkB protects the cells not only against the genotoxic but also against the potent mutagenic activity of MMS; (ii) mutations arising in alkB-defected strains are umuDC-dependent, and deletion of umuDC dramatically reduce MMS-induced mutations resulting from the presence of 1meA/3meC in DNA; (iii) specificity of MMS-induced argE3->Arg^+ reversions in AB1157 alkB-defective cells are predominantly AT->TA transversions and GC->AT transitions; (iv) overproduction of AlkA and the resultant decrease in 3meA residues in DNA dramatically reduce MMS-induced mutations. This reduction is most probably a secondary effect of AlkA due to a decrease in 3meA residues in DNA and, in consequence, suppression of SOS induction and Pol V expression. Overproduction of UmuD'C proteins reverses this effect.
