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Journal of Bacteriology, June 2000, p. 3361-3367, Vol. 182, No. 12
Department of Genetics, Sankt-Petersburg
State University, Saint Petersburg 199034, Russia,1 and Laboratory of Molecular
Genetics, National Institute of Environmental Health Sciences,
Research Triangle Park, North Carolina 277092
Received 3 February 2000/Accepted 31 March 2000
We have shown previously that Escherichia coli and
Salmonella enterica serovar Typhimurium strains carrying a
deletion of the uvrB-bio region are hypersensitive to the
mutagenic and toxic action of 6-hydroxylaminopurine (HAP) and
related base analogs. This sensitivity is not due to the
uvrB excision repair defect associated with this deletion
because a uvrB point mutation or a uvrA
deficiency does not cause hypersensitivity. In the present work, we
have investigated which gene(s) within the deleted region may be
responsible for this effect. Using independent approaches, we isolated
both a point mutation and a transposon insertion in the
moeA gene, which is located in the region covered by the
deletion, that conferred HAP sensitivity equal to that conferred by the uvrB-bio deletion. The moeAB operon provides
one of a large number of genes responsible for biosynthesis of the
molybdenum cofactor. Defects in other genes in the same pathway, such
as moa or mod, also lead to the same
HAP-hypersensitive phenotype. We propose that the molybdenum cofactor
is required as a cofactor for an as yet unidentified enzyme (or
enzymes) that acts to inactivate HAP and other related compounds.
0021-9193/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Hypersensitivity of Escherichia coli
(uvrB-bio) Mutants to 6-Hydroxylaminopurine and
Other Base Analogs Is Due to a Defect in Molybdenum Cofactor
Biosynthesis
*
Corresponding author. Mailing address: Laboratory of
Molecular Genetics, MD E3-01, National Institute of Environmental
Health Sciences, 111 TW Alexander Dr., Research Triangle Park, NC
27709. Phone: (919) 541-4250. Fax: (919) 541-7613. E-mail:
schaaper{at}niehs.nih.gov.
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