Control of the tRNA‐ tufB operon in Escherichia coli

Abstract

The expression of tufB , one of the two EF‐Tu‐encoding genes in Escherichia coli , is under autogenous control. Feedback inhibition of tufB expression by plasmid‐borne EF‐Tu has been used to answer the question of whether or not the integrity of the guanine‐nucleotide‐binding domain of EF‐Tu is required for the autoregulatory role of the factor protein. We show that a large deletion of tufB , causing the elimination of an 81‐amino‐acid segment from the plasmid‐borne EF‐Tu, does not abolish tufB repression. We conclude that the autoregulation of the cellular EF‐Tu level is not dependent on an intact guanine‐nucleotide‐binding domain and does not require binding of GTP to EF‐Tu. The repressor activity of the deletion derivative of EF‐Tu can be measured despite a rapid disappearance of the (altered) mutant protein from the soluble cytoplasmic fraction of the cell. Degradation and assembly in larger complexes are responsible for this disappearance.