| Abstract |
The tar and tap genes are located adjacent to one another in an operon of chemotaxis-related functions. They encode methyl-accepting chemotaxis proteins implicated in tactic responses to aspartate and maltose stimuli. The functional roles of these two gene products were investigated by isolating and characterizing nonpolar, single-gene deletion mutants at each locus. Deletions were obtained by selecting for loss or a defective Mu d1 prophage inserted in either the tar or tap gene. The extent of the tar deletions was determined by genetic mapping with Southern hybridization. Representative deletion mutants were surveyed for chemotactic responses on semisolid agar and by temporal stimulation in a tethered cell assay to assess flagellar rotational responses to chemoeffector compounds. The tar deletion strains exhibited complete loss of aspartate and maltose responses, whereas the tap deletion strains displayed a wild-type phenotype under all conditions tested. These findings indicate that the tap function is unable to promote chemotactic responses to aspartate and maltose, and its role in chemotaxis remains unclear.
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