The Department of Health Sciences is pleased to announce an upcoming research seminar, and this event will be offered in-person as well as virtually via Zoom (virtual registration https://carleton-ca.zoom.us/meeting/register/tJcpde2vrzgoGdxYsjOE6PE1FLqBloEh-h6z).

Title: Bacterial division arrest as a mechanism for LL-37 resistance in uropathogenic E. coli

Abstract
Urinary tract infections (UTIs) are one of the most common bacterial infections, with up to 1 million infections occurring annually in Canada alone. The vast majority of simple UTIs are caused by uropathogenic E. coli (UPEC) and these bacteria have evolved a number of adaptations to induce infection and to resist innate host defenses. During UTI, UPEC undergo a series of morphological changes in which a proportion of intracellular bacteria stop dividing and form long filaments, presumably due to cell division arrest of this proportion of the intracellular bacterial population. The role of these filaments in the infection process is unclear. We show that the antimicrobial peptide, LL-37 preferentially targets actively dividing bacterial cells, and that this division-associated killing occurs at a late phase of bacterial divisome assembly and maturation. Bacterial division arrest, induced either through the PhoPQ-dependent induction of the moonlighting protein QueE, or through overexpression of other known cell-division inhibitors SulA or DamX, results in enhanced resistance to LL-37, suggesting that the cell-division arrest induced during intracellular growth allows UPEC filaments to resist the high concentrations of LL-37 present on the bladder epithelium to enhance recolonization of those surfaces following the resolution of filamentation.

Presenter
Dr. Joseph B. McPhee
Associate Professor, Department of Chemistry and Biology
Biomedical Sciences Undergraduate Program Director
Biology Academic Coordinator G. Raymond Chang School of Continuing Education