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Journal of Bacteriology, November 1999, p. 6756-6762, Vol. 181, No. 21
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Influence of S-Adenosylmethionine Pool
Size on Spontaneous Mutation, Dam Methylation, and Cell Growth of
Escherichia coli
Lauren M.
Posnick and
Leona D.
Samson*
Division of Toxicology, Department of Cancer
Cell Biology, Harvard School of Public Health, Boston,
Massachusetts 02115
Received 6 April 1999/Accepted 27 July 1999
Escherichia coli strains that are deficient in the Ada
and Ogt DNA repair methyltransferases display an elevated spontaneous G:C-to-A:T transition mutation rate, and this increase has been attributed to mutagenic O6-alkylguanine lesions
being formed via the alkylation of DNA by endogenous metabolites. Here
we test the frequently cited hypothesis that
S-adenosylmethionine (SAM) can act as a weak alkylating
agent in vivo and that it contributes to endogenous DNA alkylation. By
regulating the expression of the rat liver SAM synthetase and the
bacteriophage T3 SAM hydrolase proteins in E. coli, a
100-fold range of SAM levels could be achieved. However, neither
increasing nor decreasing SAM levels significantly affected spontaneous
mutation rates, leading us to conclude that SAM is not a major
contributor to the endogenous formation of
O6-methylguanine lesions in E. coli.
*
Corresponding author. Mailing address: Department of
Cancer Cell Biology, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115. Phone: (617) 432-1085. Fax: (617)
432-0400. E-mail: lsamson{at}sph.harvard.edu.
Journal of Bacteriology, November 1999, p. 6756-6762, Vol. 181, No. 21
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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