Why Vibrio cholerae Swims in Curves

Review written by: Megan Mauriello

Swimming motility of Vibrio cholerae is considered to be a virulence factor because it helps cells enter the mucus layer of the small intestine. crvA and crvB genes directly determine V. cholerae cell curvature, and deletion of both genes cause a straight rod phenotype. It has previously been demonstrated that loss of cell curvature decreases infectivity, but the mechanism through which this occurs is unknown.

The authors studied navigation of wild-type (WT) curved cells versus straight cell mutants (ΔcrvAB), including swimming (random movement) and chemotaxis (biased movement in chemical gradients). Single-cell behaviors were 3D tracked in a defined linear chemical gradient in liquid media, viscous media, or hydrogels. Both cell types displayed a run-reverse-flick motility in which turning angles are accomplished by a reversal and flick or a reversal and reversal. Additionally, both cell types occasionally decelerated during runs, and turning frequencies and turning angle distributions were similar.

Figure. Population-scale chemotactic performances in buffer and mucus-mimicking media. a Schematic of the multiscale chemotaxis assay (see also Grognot et al.10,11). Bacteria are 3D tracked in the middle of a microfluidic channel (blue box) where a linear serine gradient is established by diffusion between two reservoirs with equal bacterial concentrations, but with or without 200 μM L-serine. The chemotactic drift of the population is its net speed up the 200 μM/mm serine gradient, computed as the average of all signed instantaneous velocity components along the gradient direction. b Comparison of chemotactic drift velocity of curved wt against non-curved ΔcrvAB mutant in buffer (black, n = 10), viscous polymer PVP K90 (purple, approx. 38 centipoises, n = 5), or soft agar hydrogels (green, n = 7, 0.19–0.21% (w/v)). Each point is an independent biological replicate, representing a pair of drift measurements for both phenotypes, acquired on the same day in the same media. One independent biological replicate (one point) gathers per phenotype at least 2000 bacterial trajectories in buffer (typically 3000–6000), 900 in agar (typically 2000–4000), 500 in PVP (typ. 800–1200). Error bars reflect 95% confidence intervals estimated by a jackknife resampling procedure consisting of dividing the data into subsets of 200 trajectories and computing the SEM drift obtained for different subsets. The dotted red reference line marks identical performance of both phenotypes. c Normalized chemotactic drift velocity of ΔcrvAB relative to wt from the same biological replicate, in buffer (grey, n = 10), PVP K90 (purple, n = 5), or agar hydrogels (green, n = 7). Indicated p-values are from a two-sided paired t-test with unknown variance (p = 0.70, 0.0079, and 0.29 in buffer, hydrogels, and PVP, respectively). Error bars reflect 95% confidence intervals across ratios computed within each independent experiment. Datasets used in panels b and c are detailed in Table 1.

In liquid medium and viscous medium, there was no significant difference in chemotactic drift between WT and mutant cells. In hydrogels, WT cells showed an 86% increase in chemotactic drift compared to straight ones. Instantaneous swimming speeds were not significantly different between strains, but straight mutants experienced stalls more frequently. Cell curvature did not affect stall durations or turning rates. Chemotactic drift was positive on average during swimming, and negative on average during stalls; because curved cells stalled less, their greater chemotactic efficiency can be explained by greater time spent in the swimming phase.

Molecular dynamics simulations over a range of hydrogel stiffness agreed with experimental results. Simulations also identified an optimal cell curvature for movement through hydrogels, and this is close to the median curvature of WT cells. In the simulations, screw-like motions often prevented curved cells from stalling after deceleration by changing their trajectories, suggesting this may be how the real cells reduce their stall frequency.

The effect of V. cholerae cell curvature had not previously been studied in hydrogel or viscous environments. These findings more concretely demonstrate cell shape’s role as a virulence factor and highlight the importance of experimental systems mimicking real-world environments. These results are important to understanding how V. cholerae crosses the mucus barrier of the small intestine, but potentially are also important for understanding V. cholerae escape from biofilms.

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Malik M, Chen Z, Pyo AGT, Gitai Z, Wingreen NS, Grognot M. Cell-body curvature reduces stall frequency to enhance Vibrio cholerae swimming and chemotaxis through hydrogels. Commun Biol. 2026 Sep 8;9(1):1180. doi: 10.1038/s42003-026-10883-9. PMID: 42711462; PMCID: PMC13554207.