Carbon catabolite repression (CCR) in Bacillus subtilis is mainly mediated via the central component CcpA. Nevertheless, it has been reported that some sugar metabolizing systems underlie additional CcpA-independent CCR mechanisms. Here, we present evidence supporting a potential function of glucose kinase (GlcK) in CCR, analyzing knockout mutants in CcpA and GlcK. On the one hand, GlcK inactivation has no effect on CCR by glucose or fructose of the xylose system. On the other hand, CCR of the trehalose system is affected but a remaining glucose CCR still persists. This remaining glucose repression can be explained by the appearance of unphosphorylated glucose obtained from cytoplasmic trehalose 6-phosphate hydrolysis, which is detectable in cell culture supernatant.
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Rosana-Ani et al. (1999) studied this question.
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