Histidine regulation in Salmonella typhimurium: an activator attenuator model of gene regulation.
An activator-attenuator model of positive control, a s opposed to the classic repressor-operator model of negative control, is proposed for the major operon-specific mechanism governing expression of the histidine gene cluster of Salmonella typhimurium. Evidence for this mechanism is derived from experiments performed with a coupled in vitro transcription-translation system, as well as with a minimal in vitro transcription system [Kasai, T. (1974) Nature 249, 523--527]. The product (G enzyme, or N-1-[5'-phosphoribosyl]adenosine triphosphate:pyrophosphate phosphoribosyltransferase; EC 2.4.2.17) of the first structural gene (hisG) of the histidine operon is not involved in the positive control mechanism. However, a possible role for G enzyme as an accessory negative control element interacting at the attenuator can be accommodated in our model. The operon-specific mechanism works in conjunction with an independent mechanism involving guanosine 5'-diphosphate 3'-diphosphate (ppGpp) which appears to be a positive effector involved in regulating amino-acid-producing systems, in general [Stephens, J.C., Artz, S.W. & Ames, B.N. (1975) Proc. Nat. Acad. Sci. USA, in press].
D002474:Cell-Free System; D005809:Genes, Regulator; D006160:Guanosine Triphosphate / Q000031:analogs & derivatives / Q000378:metabolism; D006639:Histidine / Q000378:metabolism*; D008954:Models, Biological; D009876:Operon; D012486:Salmonella typhimurium / Q000378:metabolism*
D006639:Histidine; D006160:Guanosine Triphosphate