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Published January 1, 1985 | public
Journal Article Open

Chemotactic signaling in filamentous cells of Escherichia coli


Video techniques were used to record chemotactic responses of filamentous cells of Escherichia coli stimulated iontophoretically with aspartate. Long, nonseptate cells were produced from polyhook strains either by introducing a cell division mutation or by growth in the presence of cephalexin. Markers indicating rotation of flagellar motors were attached with anti-hook antibodies. Aspartate was applied by iontophoretic ejection from a micropipette, and the effects on the direction of rotation of the markers were measured. Motors near the pipette responded, whereas those sufficiently far away did not, even when the pipette was near the cell surface. The response of a given motor decreased as the pipette was moved away, but it did so less steeply when the pipette remained near the cell surface than when it was moved out into the external medium. This shows that there is an internal signal, but its range is short, only a few micrometers. These experiments rule out signaling by changes in membrane potential, by simple release or binding of a small molecule, or by diffusion of the receptor-attractant complex. A likely candidate for the signal is a protein or ligand that is activated by the receptor and inactivated as it diffuses through the cytoplasm. The range of the signal was found to be substantially longer in a cheZ mutant, suggesting that the product of the cheZ gene contributes to this inactivation.

Additional Information

Copyright © 1985 by the American Society for Microbiology. Received 24 July 1984/Accepted 1 October 1984 J.E.S. and A.I. contributed equally to the work presented here. We thank J. S. Parkinson for gifts of strains and phage and for useful suggestions regarding strain constructions, M. Meister for suggesting the use of the electrical analog for steady-state diffusion, and S. M. Block for comments on the manuscript. This work was supported by Public Health Service grant A116478 from the National Institute of Allergy and Infectious Diseases. J.E.S. acknowledges support as a National Science Foundation predoctoral fellow during the early phase of this work.


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