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International Conference on Mathematical Biology and

Annual Meeting of The Society for Mathematical Biology,

July 27-30, 2009

University of British Columbia, Vancouver

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Program

MSE4b
Matthew Cabeen
Yale University
Title Mechanical Control of Bacterial Cell Curvature
Abstract The cytoskeleton is a key regulator of cell morphogenesis in bacteria, as in eukaryotes. Eukaryotic intermediate filament proteins are notable for their ability to resist strain, or stretching forces. Crescentin, a bacterial intermediate filament-like protein, is required for the curved shape of Caulobacter crescentus and localizes along the inner cell curvature, but how crescentin governs cell curvature has been unclear. Here, we show that crescentin forms a single filamentous structure that collapses into a helical configuration when detached from the cell membrane by drug treatment, suggesting that the crescentin structure is normally maintained in a less favorable stretched configuration. As the peptidoglycan cell wall is the only bacterial structure with the requisite size and strength to maintain the crescentin structure in a stretched configuration, the crescentin structure must in turn apply a compressive force to the cell wall. We demonstrate that the presence of the crescentin structure along one side of the cell generates curvature by producing a gradient in cell wall elongation rate around the circumference of the sidewall, creating a longitudinal cell length differential. Consistent with a compressive force from the crescentin structure setting up an elongation rate gradient to produce cell curvature, physical force alone can produce curvature when straight, crescentin-null C. crescentus cells are grown in circular microchambers. We show that production of crescentin in the evolutionarily distant bacterium Escherichia coli causes this straight rod-shaped organism to adopt striking curved and helical morphology, arguing that crescentin does not require species-specific factors for its function in cell curvature. However, the function of the bacterial actin homolog MreB is important for crescentin function in C. crescentus, and crescentin is able to pull down MreB in both C. crescentus and E .coli. Our data argue for a model in which the crescentin structure, which is highly static and elongates from its ends only, is stretched as the cell elongates. The stretched crescentin structure applies a compressive force to the cell wall to which it is connected, locally lowering the strain borne by the cell wall and thereby reducing the kinetics of cell wall insertion to produce an elongation rate gradient and hence curved growth. Our study implies that bacteria may use the cytoskeleton for mechanical control of growth to alter morphology.
LocationWoodward 4