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U.S. Department of Energy
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Molecular mechanisms of mutagenesis and carcinogenesis. Final report, November 1, 1978-October 31, 1979

Technical Report ·
DOI:https://doi.org/10.2172/5372652· OSTI ID:5372652
The recA gene product mediates induction of a battery of cellular functions in E. coli collectively known as the SOS inducible functions. These include prophage induction, induction of filamentous cell growth, induction of DNA repair systems and induction of the recA gene itself. Prophage induction has been demonstrated to result from cleavage of the phage repressor protein by a specific protease function of the recA protein. Such cleavage destroys repressor function in lysogenic cells and allows the prophage to enter the vegetative growth cycle. Normally, the protease function of recA protein only becomes active in the cell in response to signals produced by agents (carcinogens) or treatments that specifically damage DNA or interfere with DNA replication. In the tif-1 mutant of recA, however, the protease can be made to be active simply by raising the temperature of the culture from 30/sup 0/ to 40/sup 0/ C; lambda prophage is induced and the cell produces a normal burst of phage. Indeed, all known SOS functions are also induced under these conditions. Thus, it has been proposed that all SOS functions are similarly regulated by repressors that are sensitive to the recA portease function. We have sought to further characterize the recA-/mediated cleavage reaction and its requirements for lambda repressor in vitro and to extend our biochemical studies to a cellular SOS repressor, the lexA gene product which is proposed to negatively regulate several SOS inducible functions, including the recA gene, a gene controlling cell separation and lexA gene itself.
Research Organization:
Harvard Univ., Cambridge, MA (USA)
DOE Contract Number:
AS02-77EV04366
OSTI ID:
5372652
Report Number(s):
COO-4366-2
Country of Publication:
United States
Language:
English