FIG. 3.

Abilities of wild-type and mutant GS proteins to inhibit TnrA DNA binding in the absence of the feedback inhibitor glutamine. A gel mobility shift assay was used to examine the binding of TnrA to amtB promoter DNA. TnrA (30 nM dimer) was present in the binding mixtures shown in all but the far-left lane. The abilities of high concentrations (100 μM subunit) of wild-type (WT), E65G, S66P, M68I, H195Y, and P318S GS proteins to inhibit TnrA binding were determined in the absence of feedback inhibitors. The percentage of bound amtB DNA indicated below each lane is the mean of four independent measurements. The sample standard deviation was less than 15% for all values.