Deletion of Escherichia Coli K30 Type I Capsule Assembly Gene wzc Confers Resistance to The Antibiotic Erythromycin in Solid Media

Escherichia coli K30 produce a Type I (Colanic Acid) capsule which protects the bacterium from environmental stresses, including host immune responses. It is unknown how the presence of Type I capsule affects antibiotic resistance in the bacterium. Previous studies have shown that the deletion of three key genes involved in Type I capsule production, wza, wzb, and wzc, confers increased resistance to erythromycin on solid media. It has been found that the single deletion of wza, but not wzb, is sufficient to confer this resistance phenotype. In this study, we investigated the effects of deleting the wzc gene on erythromycin sensitivity in E. coli K30. We tested erythromycin sensitivity in wild-type (WT) E. coli K30 strain E69 to knockout mutants lacking either the wza or wzc genes. On solid media, we observed that the deletion of wza and wzc confers increased resistance to erythromycin compared to WT cells. In contrast, assays completed in liquid media produced inconsistent and inconclusive results. Our results support the hypothesis that the Wza and Wzc proteins are involved in translocating macrolide ntibiotics, such as erythromycin, into the cell.