Transport of maltose in Lactobacillus casei BL23 is subject to regulation by inducer exclusion. The presence of glucose or other rapidly metabolized carbon sources blocks maltose transport by a control mechanism that depends on the phosphorylation of the HPr protein at serine residue 46. We have identified the L. casei gene cluster for maltose/maltodextrin utilization by sequence analysis and mutagenesis. It is composed of genes coding for a transcriptional regulator, oligosaccharide hydrolytic enzymes, an ABC transporter (MalEFGK2) and the enzymes for the metabolism of maltose or the degradation products of maltodextrins: maltose phosphorylase and beta-phospho-glucomutase. These genes are induced by maltose and repressed by the presence of glucose via the catabolite control protein A (CcpA). A mutant strain was constructed which expressed the hprKV267F allele and therefore formed large amounts of P-Ser-HPr even in the absence of a repressive carbon source. In this mutant, transport of maltose was severely impaired, whereas transport of sugars not subject to inducer exclusion was not changed. These results strengthen the idea that P-Ser-HPr controls inducer exclusion and make the maltose system of L. casei a suitable model for studying this process in Firmicutes.
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| rdf:type | |
| rdfs:comment |
Transport of maltose in Lactobacillus casei BL23 is subject to regulation by inducer exclusion. The presence of glucose or other rapidly metabolized carbon sources blocks maltose transport by a control mechanism that depends on the phosphorylation of the HPr protein at serine residue 46. We have identified the L. casei gene cluster for maltose/maltodextrin utilization by sequence analysis and mutagenesis. It is composed of genes coding for a transcriptional regulator, oligosaccharide hydrolytic enzymes, an ABC transporter (MalEFGK2) and the enzymes for the metabolism of maltose or the degradation products of maltodextrins: maltose phosphorylase and beta-phospho-glucomutase. These genes are induced by maltose and repressed by the presence of glucose via the catabolite control protein A (CcpA). A mutant strain was constructed which expressed the hprKV267F allele and therefore formed large amounts of P-Ser-HPr even in the absence of a repressive carbon source. In this mutant, transport of maltose was severely impaired, whereas transport of sugars not subject to inducer exclusion was not changed. These results strengthen the idea that P-Ser-HPr controls inducer exclusion and make the maltose system of L. casei a suitable model for studying this process in Firmicutes.
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| skos:exactMatch | |
| uniprot:name |
Res. Microbiol.
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| uniprot:author |
Deutscher J.,
Monedero V.,
Poncet S.,
Yebra M.J.
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| uniprot:date |
2008
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| uniprot:pages |
94-102
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| uniprot:title |
Maltose transport in Lactobacillus casei and its regulation by inducer exclusion.
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| uniprot:volume |
159
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| dc-term:identifier |
doi:10.1016/j.resmic.2007.10.002
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