PMID:9789050
| Citation |
Fuchs, RP and Napolitano, RL (1998) Inactivation of DNA proofreading obviates the need for SOS induction in frameshift mutagenesis. Proc. Natl. Acad. Sci. U.S.A. 95:13114-9 |
|---|---|
| Abstract |
Translesion synthesis at replication-blocking lesions requires the induction of proteins that are controlled by the SOS system in Escherichia coli. Of the proteins identified so far, UmuD', UmuC, and RecA* were shown to facilitate replication across UV-light-induced lesions, yielding both error-free and mutagenic translesion-synthesis products. Similar to UV lesions, N-2-acetylaminofluorene (AAF), a chemical carcinogen that forms covalent adducts at the C8 position of guanine residues, is a strong replication-blocking lesion. Frameshift mutations are induced efficiently by AAF adducts when located within short repetitive sequences in a two-step mechanism; AAF adducts incorporate a cytosine across from the lesion and then form a primer-template misaligned intermediate that, upon elongation, yields frameshift mutations. Recently, we have shown that although elongation from the nonslipped intermediate depends on functional umuDC+ gene products, elongation from the slipped intermediate is umuDC+-independent but requires another, as yet biochemically uncharacterized, SOS function. We now show that in DNA Polymerase III-proofreading mutant strains (dnaQ49 and mutD5 strains), elongation from the slipped intermediate is highly efficient in the absence of SOS induction-in contrast to elongation from the nonslipped intermediate, which still requires UmuDC functions. |
| Links | |
| Keywords |
2-Acetylaminofluorene/pharmacology; Bacterial Proteins/metabolism; Base Sequence; Cytosine; DNA Replication; Escherichia coli/genetics; Escherichia coli/metabolism; Escherichia coli/radiation effects; Frameshift Mutation; Models, Genetic; Mutagenesis; Plasmids/drug effects; Plasmids/genetics; Plasmids/radiation effects; SOS Response (Genetics)/genetics; Templates, Genetic; Ultraviolet Rays |
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