SOME NOVEL TRANSCRIPTION ATTENUATION MECHANISMS USED BY BACTERIA

A variety of transcription attenuation mechanisms are used by bacteria to regulate gene and operon expression. This review summarizes previo us and current studies designed to elucidate the features of the speci fic attenuation mechanisms that regulate expression of the tryptophana se (tna) operon of Escherichia coli and the tryptophan (tip) operon of Bacillus subtilis. Initiation of transcription in the tna operon is r egulated by catabolite repression. Once initiated, transcription is re gulated by tryptophan-induced inhibition of Rho-mediated transcription termination in the leader region of the operon. An operon-encoded lea der peptide, TnaC, containing a crucial tryptophan residue, plays an e ssential role in induction. This peptide appears to act in cis on the ribosome translating tnaC to inhibit its release at the tnaC stop codo n. The stalled ribosome would block Rho's access to the tna transcript , thereby preventing termination. Transcription of the tip operon of B subtilis is regulated by an attenuation mechanism that responds to a tryptophan-activated eleven subunit RNA-binding regulatory protein, ca lled TRAP. Activated TRAP binds to repeated GAG sequences in the leade r segment of the tip operon transcript, disrupting an RNA antiterminat or and promoting formation of a terminator. Activated TRAP also regula tes translation of trpG in the folate operon by binding to repeat GAG sequences surrounding the trpG ribosome binding site. A temperature se nsitive tryptophanyl-tRNA synthetase (trpS) mutant was previously obse rved to overexpress the tip operon and trpG, when grown at elevated te mperatures in the presence of tryptophan. We have found that the trpS defect increases tip operon and trpG expression by interfering with TR AP's ability to act. We suggest that either accumulation of uncharged tRNA(Trp) or overproduction of a TRAP-binding transcript reduces the l evel of functional TRAP in the trpS mutant.