Reconstitution of Signaling in Bacterial Chemotaxis
Abstract
Strains missing several genes required for chemotaxis toward amino acids, peptides, and certain sugars were tethered and their rotational behavior was analyzed. Null strains (called gutted) were deleted for genes that code for the transducers Tsr, Tar, Tap, and Trg and for the cytoplasmic proteins CheA, CheW, CheR, CheB, CheY, and CheZ. Motor switch components were wild type, flaAII(cheC), or flaBll(cheV). Gutted cells with wild-type motors spun exclusively counterclockwise, while those with mutant motors changed their directions of rotation. CheY reduced the bias (the fraction of time that cells spun counterclockwise) in either case. CheZ offset the effect of CheY to an extent that varied with switch allele but did not change the bias when tested alone. Transducers also increased the bias in the presence of CheY but not when tested alone. However, cells containing transducers and CheY failed to respond to attractants or repellents normally detected in the periplasm. This sensitivity was restored by addition of CheA and CheW. Thus, CheY both enhances clockwise rotation and couples the transducers to the flagella. CheZ acts, at the level of the motor, as a CheY antagonist. CheA or CheW or both are required to complete the signal pathway. A model is presented that explains these results and is consistent with other data found in the literature.
Additional Information
© 1987 American Society for Microbiology. Received 10 November 1986; Accepted 22 January 1987. We thank F. W. Dahlquist, G. L. Hazelbauer, P. Matsumura, and J. S. Parkinson for gifts of bacterial strains, plasmids, and phage; we also thank D. F. Blair and K. Oosawa for their comments on the manuscript. This work was supported by the Public Health Service grant AI16478 from the National Institute of Allergy and Infectious Diseases. T.J.K received support from the National Institutes of Health through National Research Service Award training grant.Attached Files
Published - WOLjbact87.pdf
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Additional details
- PMCID
- PMC212038
- Eprint ID
- 32045
- Resolver ID
- CaltechAUTHORS:20120622-120016118
- AI-16478
- NIH
- NIH Predoctoral Fellowship
- Created
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2012-06-22Created from EPrint's datestamp field
- Updated
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2019-10-03Created from EPrint's last_modified field