Table 2. Inverse chemotaxis behavior of ncbA mutant and Nifedipine-treated wild-type.

Strain	Effector in capillary*	Positive chemotaxis†	Negative chemotaxis†
Wild-type-M	Aspartate	43.5 ± 2.8	—
SC34-M (ΔncbA)	Aspartate	—	26.2 ± 3.7
SC34-MR (ΔncbA, ncbA restored)	Aspartate	2.5 ± 0.4	—
Wild-type-M	Proline	83.0 ± 5.2	—
SC34-M	Proline	—	21.1 ± 4.1
Wild-type-M	Glucose	131.4 ± 4.3	—
SC34-M	Glucose	—	9.2 ± 1.1
Wild-type-M	pH 10.5	—	10.9 ± 0.6
SC34-M	pH 10.5	38.3 ± 3.5	—
Wild-type-M	pH 10.5 + 1 mM malate‡	27.3 ± 1.4	—
SC34-M	pH 10.5 + 1 mM malate‡	—	31.5 ± 3.6
Wild-type-M + 50 μM Nifedipine§	Aspartate	—	8.9 ± 1.3

^*Chemoeffectors were added at 1 mM and, except where noted, the buffer pH inside the capillary was 8.5. The buffer pH outside the capillary was always pH 8.5.

^†Positive chemotaxis is the number of cells (×10⁴) in the capillary tube with effector in excess of the cells found in the capillary tube without effector in the control experiment (pH 8.5 → pH 8.5, no effector present), whereas negative chemotaxis is the excess of cells (×10⁴) found in the capillary tube in the control without effector compared to the capillary tube with effector.

^‡An additional control was conducted with 1 mM malate in the capillary at pH 8.5; the accumulation was indistinguishable from the standard control with pH 8.5 in both compartments and no effector.

^§The control used for background correction was conducted in the presence of 50 μM Nifedipine.