A novel role for RecA under non-stress: promotion of swarming motility in Escherichia coli K-12
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BioMed Central
Open Access
Research article
A novel role for RecA under non-stress: promotion of swarming motility in Escherichia coli K-12 José-María Gómez-Gómez*, Candela Manfredi, Juan-Carlos Alonso and Jesús Blázquez* Address: Departamento de Biotecnología Microbiana. Centro Nacional de Biotecnología, C/Darwin, 3, 28049-Madrid, Spain Email: José-María Gómez-Gómez* - [email protected]; Candela Manfredi - [email protected]; JuanCarlos Alonso - [email protected]; Jesús Blázquez* - [email protected] * Corresponding authors
Published: 28 March 2007 BMC Biology 2007, 5:14
doi:10.1186/1741-7007-5-14
Received: 23 October 2006 Accepted: 28 March 2007
This article is available from: http://www.biomedcentral.com/1741-7007/5/14 © 2007 Gómez-Gómez et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Bacterial motility is a crucial factor in the colonization of natural environments. Escherichia coli has two flagella-driven motility types: swimming and swarming. Swimming motility consists of individual cell movement in liquid medium or soft semisolid agar, whereas swarming is a coordinated cellular behaviour leading to a collective movement on semisolid surfaces. It is known that swimming motility can be influenced by several types of environmental stress. In nature, environmentally induced DNA damage (e.g. UV irradiation) is one of the most common types of stress. One of the key proteins involved in the response to DNA damage is RecA, a multifunctional protein required for maintaining genome integrity and the generation of genetic variation. Results: The ability of E. coli cells to develop swarming migration on semisolid surfaces was suppressed in the absence of RecA. However, swimming motility was not affected. The swarming defect of a ΔrecA strain was fully complemented by a plasmid-borne recA gene. Although the ΔrecA cells grown on semisolidsurfaces exhibited flagellar production, they also presented impaired individual movement as well as a fully inactive collective swarming migration. Both the comparative analysis of gene expression profiles in wild-type and ΔrecA cells grown on a semisolid surface and the motility of lexA1 [Ind-] mutant cells demonstrated that the RecA effect on swarming does not require induction of the SOS response. By using a RecA-GFP fusion protein we were able to segregate the effect of RecA on swarming from its other functions. This protein fusion failed to regulate the induction of the SOS response, the recombinational DNA repair of UV-treated cells and the genetic recombination, however, it was efficient in rescuing the swarming motility defect of the ΔrecA mutant. The RecA-GFP protein retains a residual ssDNA-dependent ATPase activity but does not perform DNA strand exchange. Conclusion: The experimental evi
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