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. 2011 Nov 26;287(4):2749–2758. doi: 10.1074/jbc.M111.315739

FIGURE 4.

FIGURE 4.

Development and chemotaxis of GbpC mutants. A, GbpC-GFP and GbpCΔGRAM-GFP were expressed in gbpC-null cells and starved on non-nutrient agar plates. Pictures of streaming cells were taken after 6 h of starvation. B, 7-h starved cells were monitored in a small population assay and scored for their ability to chemotax toward drops with 10−6 m cAMP. Experiments were performed in the presence of 50 μm LY (PI3K inhibitor) and p-bromophenylacyl bromide (PLA2 inhibitor), which causes chemotaxis to be critically dependent on the cGMP-pathway. The GbpC mutants were expressed in gbpC-null cells and compared with the chemotaxis data of AX3 and gbpC-null cells. The data presented are mean ± S.E. of at least three independent measurements on different days. *, p < 0.001 versus gbpC-null and not significantly different from AX3 at p > 0.05; **, p < 0.001 versus AX3 and not significantly different from gbpC-null; ***, significantly less than AX3 at p < 0.01 and significantly above gbpC-null at p < 0.01.