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Articles by Bill Söderström
Bacterial strategies for surviving antibiotics during urinary tract infection: could uropathogenic Escherichia coli be persisters?
Abstract Treating bacterial infections, such as urinary tract infection (UTI), with antibiotics does not always resolve the infection and often results in subsequent re-infection. Treatment failure can be driven by bacterial mechanisms of resistance, tolerance or persistence, collectively known as the antibiotic non-response. Antibiotic resistance is well characterized across various bacterial species and implicated in poor clinical outcomes in various infection settings.
Genetic requirements for uropathogenic E. coli proliferation in the bladder cell infection cycle
Abstract Uropathogenic Escherichia coli (UPEC) requires an adaptable physiology to survive the wide range of environments experienced in the host, including gut and urinary tract surfaces. To identify UPEC genes required during intracellular infection, we developed a transposon-directed insertion-site sequencing (TraDIS) approach for cellular infection models and searched for genes in a library of ~20,000 E.
Bacterial filamentation during urinary tract infections
Fig 1. Simplified schematic of the UPEC morphology cycle during UTIs. (1) Rod-shaped bacteria adhere to BECs. (2) Invasion via endocytosis. (3) Rods undergo shape changes to a cocci-like form and densely cluster together in biofilm-like IBCs. In a second step, a subpopulation of the bacteria reinitiate growth, without dividing, to become filamentous. The exact molecular ques regulating this are unknown, but the cell division protein DamX is essential for filamentation [38].
Assembly dynamics of FtsZ and DamX during infection-related filamentation and division in uropathogenic E. coli - Nature Communications
Abstract During infection of bladder epithelial cells, uropathogenic Escherichia coli (UPEC) can stop dividing and grow into highly filamentous forms. Here, we find that some filaments of E. coli UTI89 released from infected cells grow very rapidly and by more than 100 μm before initiating division, whereas others do not survive, suggesting that infection-related filamentation (IRF) is a stress response that promotes bacterial dispersal.
Cell shape-independent FtsZ dynamics in synthetically remodeled bacterial cells
As a reference for unmodified division rings, we imaged Z-rings in E. coli cells expressing FtsZ-mNeonGreen as the only source of FtsZ22. Under our experimental conditions, this strain produced normal-looking, sharp Z-rings (Supplementary Figure 1) and grew and divided similarly to wild-type (WT) E. coli (MC4100) (Supplementary Figure 2a-e). We then trapped the cells in a vertical position in micron-sized holes that were produced in agarose pads using silica micron pillar arrays14 (Fig.
FtsZ does not initiate membrane constriction at the onset of division
Our initial goal was to determine if FtsZ was sufficient to generate a contractile force in vivo. Our working hypothesis was that, if FtsZ was sufficient we should see deformations of the inner membrane when only FtsZ and its membrane tethers FtsA23 and ZipA24 (aka the proto-ring) are present at midcell (but PG synthesizing enzymes are not). We cryogenically preserved Escherichia coli cells expressing a chromosomal copy of FtsZ-GFP by vitrification and imaged them by cryo-CLEM (Supplementary Fig.
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