Disease relevance of tet

• These results are consistent with the idea that the pBC16 tet gene is regulated by translation attenuation, a model originally proposed to explain the inducible regulation of the cat and erm genes in gram-positive bacteria [1].

High impact information on tet

• We provide evidence that translation of the tet leader peptide coding region blocks tet expression by preventing the formation of a secondary-structure complex that would, in the absence of leader translation, expose the tet ribosome binding site [1].
• As with inducible cat and erm genes, the pBC16 tet gene is preceded by a translated leader open reading frame consisting of a consensus ribosome binding site and an ATG initiation codon, followed by 19 sense codons and a stop codon [1].
• Tetracycline is proposed to induce tet by blocking or slowing leader translation [1].
• Expression of the tet resistance gene from plasmid pBC16 is induced by the antibiotic tetracycline, and induction is independent of the native promoter for the gene [1].
• The nucleotide sequence at the 5' end of the tet mRNA (the leader region) is predicted to assume a complex secondary structure that sequesters the ribosome binding site for the tet gene [1].

Biological context of tet

• In course of the incompatibility studies, the tet determinant was transposed from pLK1 into the chromosome, from the chromosome into the lac genes of an Flac plasmid, and from the Flac plasmid into another site on a second Flac plasmid [2].

References