Genomic plasticity of pathogenic <i>Escherichia coli</i> mediates <scp>d</scp> -serine tolerance via multiple adaptive mechanisms
Nicky O’Boyle, James P. R. Connolly, Nicholas P. Tucker, Andrew J. Roe
Abstract
Significance Pathogens ensure infection of favored sites in the body by responding to chemical signals. One chemical abundant in urine, the amino acid d -Ser, is toxic to EHEC and reduces expression of the machinery used for host cell attachment, making the bladder an unfavorable environment. We observed that under d -Ser stress, EHEC acquires genetic changes that lead to blocking d -Ser uptake into the cell or activating a silent enzyme for degrading d -Ser. This prevents growth inhibition and, critically, inhibits the repression of attachment machinery normally caused by d -Ser. These findings highlight the importance of pathogen evolution in determining how host molecules regulate colonization. These interactions underpin a process known as niche restriction that is important for pathogen success within the host.