Thiol hypersensitivity in a mutant of Escherichia coli (IS16) was reve
rsed by complementation with a plasmid that carried the ubiX gene. The
mutant had low ubiquinone content. Complementation elevated the ubiqu
inone level and eliminated thiol hypersensitivity. Analysis of chromos
omal ubiX genes indicated that both parent and mutant strains were ubi
X mutants. The low ubiquinone content of IS16 was possibly caused by a
ubiD ubiX genotype. A ubiA mutant also exhibited thiol hypersensitivi
ty. Neither IS16 nor the ubiA mutant strain could produce alkaline pho
sphatase (in contrast to their parent strains) after 2 h of induction,
thus showing Dsb(-) phenotypes, The phenomena of thiol hypersensitivi
ty and low ubiquinone content may be linked by their connections to th
e periplasmic disulfide bond redox machinery.