<i>dsdA</i> Does Not Affect Colonization of the Murine Urinary Tract by <i>Escherichia coli</i> CFT073

<div><p>The urinary tract environment provides many conditions that deter colonization by microorganisms. D-serine is thought to be one of these stressors and is present at high concentrations in urine. D-serine interferes with L-serine and pantothenate metabolism and is bacteriostatic to many species. Uropathogenic <i>Escherichia coli</i> commonly possess the <i>dsdCXA</i> genetic locus, which allows them to use D-serine as a sole carbon, nitrogen, and energy source. It was previously reported that in the model UPEC strain CFT073, a <i>dsdA</i> mutant outcompetes wild type in the murine model of urinary tract infection. This “hypercolonization” was used to propose a model whereby UPEC strains sense D-serine in the urinary tract and subsequently up-regulate genes necessary for pathogenesis. Here, we show that inactivation of <i>dsdA</i> does not lead to hypercolonization. We suggest that this previously observed effect is due to an unrecognized secondary mutation in <i>rpoS</i> and that some D-serine specific effects described in other studies may be affected by the <i>rpoS</i> status of the strains used. Inactivation of <i>dsdA</i> in the original clinical isolate of CFT073 gives CFT073 Δ<i>dsdA</i> a growth defect in human urine and renders it unable to grow on minimal medium containing D-serine as the sole carbon source. However, CFT073 Δ<i>dsdA</i> is able to colonize the urinary tracts of CBA/J mice indistinguishably from wild type. These findings indicate that D-serine catabolism, though it may play role(s) during urinary tract infection, does not affect the ability of uropathogenic <i>E</i>. <i>coli</i> to colonize the murine urinary tract.</p>