Many members of the phylum Bacteroidetes, such as Flavobacterium johnsoniae, can glide over a solid surface: an ability called gliding motility. It can be usually observed on agar plates as thin, flat, spreading colonies with irregular, feathery edges; this phenomenon is called colony spreading. Colony spreading of F. johnsoniae on 1.5% agar plates containing poor nutrients is dose-dependently inhibited by addition of D-glucose, as previously reported. Accordingly, here, we created mutants (by transposon mutagenesis) that partially suppressed glucose-mediated inhibition of colony spreading. Among the isolates, we found that one had a transposon insertion in Fjoh_4565, tentatively named mfsA, which encodes a major facilitator superfamily (MFS) transporter previously shown to be required for growth on glucose, N-acetyl-glucosamine, and chitin. We constructed an mfsA deletion mutant and found that the mutant showed no glucose-mediated acceleration of growth or glucose uptake. The mfsA gene complemented the phenotype of a glucose-negative Escherichia coli. These results suggest that the mfsA gene encodes the sole MFS transporter of glucose in F. johnsoniae and that glucose uptake is partially required for the glucose-mediated inhibition of F. johnsoniae colony spreading.
Keywords: colony spreading; gliding motility; glucose uptake; major facilitator superfamily transporter.
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