Al Mamun, Abu Amar M. et al. published their research in Mutation Research, Fundamental and Molecular Mechanisms of Mutagenesis in 2006 |CAS: 55662-66-3

The Article related to escherichia dna polymerase ii ethenocytosine lesion bypass mutagenesis, Biochemical Genetics: Genomic Processes and other aspects.Related Products of 55662-66-3

On January 29, 2006, Al Mamun, Abu Amar M.; Humayun, M. Zafri published an article.Related Products of 55662-66-3 The title of the article was Escherichia coli DNA polymerase II can efficiently bypass 3,N4-ethenocytosine lesions in vitro and in vivo. And the article contained the following:

Escherichia coli DNA polymerase II (pol-II) is a highly conserved protein that appears to have a role in replication restart, as well as in translesion synthesis across specific DNA adducts under some conditions. Here, we have investigated the effects of elevated expression of pol-II (without concomitant SOS induction) on translesion DNA synthesis and mutagenesis at 3,N 4-ethenocytosine (εC), a highly mutagenic DNA lesion induced by oxidative stress as well as by exposure to industrial chems. such as vinyl chloride. In normal cells, survival of transfected M13 single-stranded DNA bearing a single εC residue (εC-ssDNA) is about 20% of that of control DNA, with about 5% of the progeny phage bearing a mutation at the lesion site. Most mutations are C → A and C → T, with a slight predominance of transversions over transitions. In contrast, in cells expressing elevated levels of pol-II, survival of εC-ssDNA is close to 100%, with a concomitant mutation frequency of almost 99% suggesting highly efficient translesion DNA synthesis. Furthermore, an overwhelming majority of mutations at εC are C → T transitions. Purified pol-II efficiently catalyzes translesion synthesis at εC in vitro, accompanied by high levels of mutagenesis with the same specificity. These results suggest that the observed in vivo effects in pol-II over-expressing cells are due to pol-II-mediated DNA synthesis. Introduction of mutations in the carboxy terminus region (β interaction domain) of polB eliminates in vivo translesion synthesis at εC, suggesting that the ability of pol-II to compete with pol-III requires interaction with the β processivity subunit of pol-III. Thus, pol-II can compete with pol-III for translesion synthesis. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Related Products of 55662-66-3

The Article related to escherichia dna polymerase ii ethenocytosine lesion bypass mutagenesis, Biochemical Genetics: Genomic Processes and other aspects.Related Products of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem