J Bacteriol, July 1998, p. 3681-3685, Vol. 180, No. 14
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, California 92350
Received 15 December 1997/Accepted 9 May 1998
Thiol hypersensitivity in a mutant of Escherichia coli
(IS16) was reversed by complementation with a plasmid that carried the
ubiX gene. The mutant had low ubiquinone content.
Complementation elevated the ubiquinone level and eliminated thiol
hypersensitivity. Analysis of chromosomal ubiX genes
indicated that both parent and mutant strains were ubiX
mutants. The low ubiquinone content of IS16 was possibly caused by a
ubiD ubiX genotype. A ubiA mutant also
exhibited thiol hypersensitivity. Neither IS16 nor the ubiA mutant strain could produce alkaline phosphatase (in contrast to their
parent strains) after 2 h of induction, thus showing Dsb
phenotypes. The phenomena of thiol hypersensitivity
and low ubiquinone content may be linked by their connections to the
periplasmic disulfide bond redox machinery.
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