Brian J. Haugen

TL;DR: This study represents the first assessment of any E. coli pathotype's transcriptome in vivo and provides specific insights into the mechanisms necessary for urinary tract pathogenesis.

TL;DR: Comparison of results with previous studies suggests that inversely coordinated expression of adhesin gene clusters does occur in vivo, and represents evidence for direct communication between genes relating to pathogenesis.

TL;DR: A role for d-serine catabolism and signaling in global virulence gene regulation of uropathogenic E. coli strain CFT073 results in a hypermotile strain with a hypercolonization phenotype in the bladder and kidneys of mice in a model of urinary tract infection (UTI).

TL;DR: In a direct competition model of urinary tract infection, the dsdA mutant was recovered 300‐times more frequently than the wild type in the bladders of mice 48 h after infection, suggesting that d‐serine catabolism provides a growth advantage in the urinary tract.

TL;DR: Haugen et al. as mentioned in this paper showed that deletion of the genes encoding l-serine deaminases SdaA and SdaB resulted in a mutant that accumulates higher intracellular levels of lserine than CFT073.