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Cellular responses to DNA damage.
For many years, the study of the regulation of the SOS network was complicated by both the complexities of the responses and the interrelationships of the key regulatory elements. However, recently the application of powerful genetic and molecular biological techniques has allowed us to gain a detai...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
1985
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1568711/ https://www.ncbi.nlm.nih.gov/pubmed/3910414 |
Sumario: | For many years, the study of the regulation of the SOS network was complicated by both the complexities of the responses and the interrelationships of the key regulatory elements. However, recently the application of powerful genetic and molecular biological techniques has allowed us to gain a detailed picture of the regulation of this complex network. The network is now known to consist of more than 17 genes, each of which is repressed by the LexA protein. Induction of the genes in the SOS network occurs when the RecA protein becomes activated in response to a signal generated by DNA damage. Two of the genes in this network, umuD and umuC, are absolutely required for mutagenesis by UV and various carcinogens. The umuD and umuC genes have molecular weights of 16,000 and 45,000 daltons, respectively, and are organized in an operon repressed by LexA. The mutagenesis-enhancing plasmid pKM101 carries two genes mucA and mucB, which are analogs of the umuD and umuC genes, respectively. |
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