A 2-deoxy--glucose-resistant mutant of a pLZ15-cured derivative of ATCC 393 was isolated on agar medium containing 10 mM 2-deoxy--glucose and 5 g lactose 1 The mutant was impaired in the main glucose transport mechanism, a PTS-type system. Additionally a proton-motive-force-dependent glucose permease was detected. The growth response and the sugar consumption rates of the wild-type and the PTS-deficient mutant suggested that the mutated element of the complex IIABC was, in the wild-type, responsible for a strong repression by glucose and mannose of the lactose and ribose assimilation genes, while assimilation of galactose was only weakly repressed. It is postulated that they are regulated by a different mechanism of catabolite repression.


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