Abstract
It is now well established that treatment, which blocks semi-conservative DNA synthesis, induces in bacteria a series of pleiotropic effects called SOS functions [1–3]. The bacterial RecA protein, in the presence of single-strand DNA, displays a protease activity, which will specifically cleave its own repressor — the LexA protein — and the repressor of λ phage leading to prophage induction in a lysogenic bacteria. The cleavage of the LexA protein turns on several other genes which belong to the SOS response such as recA, umuC, sfiA, uvrA, uvrB genes (see Fig. 1). Among these responses, the umuC gene product seems to be partly responsible for the error-prone repair pathway expressed in treated-bacteria. Since SOS functions in bacteria are strongly mutagenic and can lead to virus induction, it is of great interest to determine if such functions could also be induced in mammalian cells treated with carcinogens. The expression of some specific mutations and/or the induction of some integrated viral genomes could very well represent one of the first steps in the initiation of carcinogenesis. In order to approach this problem, we have studied the properties of the DNA replication process in SOS conditions (i.e., in cells treated with chemical or physical carcinogens) trying to answer two specific questions: 1) Does an error-prone replication pathway exist in mammalian cells? 2) Are any specific replication enzymes induced in carcinogen-treated mammalian cells?
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Sarasin, A., Mezzina, M. (1983). SOS Functions Induced in Carcinogen-Treated Mammalian Cells. In: Castellani, A. (eds) The Use of Human Cells for the Evaluation of Risk from Physical and Chemical Agents. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1117-2_23
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DOI: https://doi.org/10.1007/978-1-4757-1117-2_23
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