The Estuary Effect: Variations in Temperature and Salinity Alter msh Promoter Activity in Vibrio cholerae

Vibrio cholerae, a cholera-causing bacterium, thrives in warm aquatic environments. This pathogen's resilience is amplified through its capacity to colonize host reservoirs and build multicellular biofilms, leading to seasonal epidemics in tropical locales. The toxigenic strains of V. cholerae primarily employ type IVa mannose-sensitive hemagglutinin (MSHA) pili for colonization and biofilm development.

However, the effects of temperature and salinity on MSHA production specifically have remained unclear. Researchers employed transcriptional reporters and functional assays to investigate the impacts of temperature and salinity on msh promoter activity (msh-P1/msh-P2/msh-P3) and pilus biogenesis. Under normal lab conditions (30°C and 1% NaCl), only msh-P1 and msh-P2 were active and inversely correlated.

These promoters showed increased activity at higher temperatures (37°C) and lower salinity (0.25%/0.5% NaCl), but decreased activity at lower temperatures (20°C/25°C) and higher salinity (2%/3% NaCl). Changes in MSHA cell-surface levels did not immediately reflect these alterations in promoter activity. However, high salinity conditions led to reduced MSHA production.

When combined with high temperature (37°C) and high salinity (2%/3% NaCl), the salinity-mediated reduction of msh-P1/P2 activity was mitigated. Biofilm biomass increased notably at 25°C and 20°C, likely due to temperature-independent changes in MSHA levels and further temperature-regulated biofilm control mechanisms. Notably, msh-P1/P2 promoter activity and MSHA production varied considerably among toxigenic O1 and O139 serogroups, despite their identical genetic sequences.

These findings provide insight into how critical signals control MSHA pilus production, facilitating V. cholerae's persistence in aquatic habitats.