Attenuation of the ilvB operon by amino acids reflecting substrates or products of the ilvB gene product.
AUTOR(ES)
Hauser, C A
RESUMO
Transcription termination at the ilvB attenuator of Escherichia coli K-12 has been quantitated by measuring the in vivo rate of synthesis and degradation of mRNA segments proximal and distal to the attenuator. This analysis demonstrates that a 4-fold deattenuation results in vivo when the growth of cells is limited by the availability of valine or leucine. The result suggests that attenuation is the major mechanism by which this operon is regulated by these end-product amino acids. On the basis of possible secondary structures of ilvB leader RNA, we predicted that attenuation of this operon should also be affected by growth of cells in limiting amounts of alanine or threonine. We report here that the ilvB operon is deattenuated when cells are starved for either of these amino acids. A rationale for the regulation of this operon by these four amino acids, which represent both the substrates and the products of the ilvB gene product, and by catabolite repression is presented.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=344613Documentos Relacionados
- Nucleotide sequence of the ilvB promoter-regulatory region: a biosynthetic operon controlled by attenuation and cyclic AMP.
- Starvation for ilvB operon leader amino acids other than leucine or valine does not increase acetohydroxy acid synthase activity in Escherichia coli.
- Regulation of expression of the ilvB operon in Salmonella typhimurium.
- Interaction of cyclic AMP receptor protein with the ilvB biosynthetic operon in E. coli.
- Valine-Resistant Escherichia coli K-12 Strains with Mutations in the ilvB Operon