Jacob-Monod operon model

It was Jacob and Monod in 1961 who proposed the operon model for the regulation of transcription. The lac operon is a good example of how operons work (Fig. 1). The operon model proposes three elements ... 

The operon model was described in 1961 by F. Jacob and J. Monod to account for the molecular and genetic mechanisms involved in bacterial enzyme indue-... 

Figure 26.2 The operon model, as proposed in 1961 by Jacob and Monod. 

A number of publications have appeared on the dynamics of enzyme synthesis in a variety of situations. Most of the models are based on more or less sophisticated versions of the operon model of Jacob and Monod. The role of m-RNA and its stability were modeled by Terui (1972). Repressor and inducer control was treated by Knorre (1968), Imanaka et al. (1972 1973), van Dedem and Moo-Young (1973), and Suga et al. (1975). Allowance for dual control and catabolite repression was made by Toda (1976). [See also the kinetic treatment by Yagil and Yagil (1971), Imanaka and Aiba (1977), and Bajpai and Ghose (1978)]. A simple structured model was developed by Roels (1978) showing a combination of the features of the models published. More recently Toda (1981) reviewed the effects of induction and repression of enzymes in microbial cultures and their modeling. 

The operon model was developed by Jacob and Monod, and it has only been demonstrated in prokar-yotie systems. It is the basis for the explanation of Enzyme induction (see) and Enzyme repression (see). See also Attenuation. 

F. Jacob and J, Monod [9]. Operon model of control proposed. 

While a gene cluster might be an operon, it can be referred to as an operon in the strict sense of the Jacob-Monod model only if certain predictions of the model are met [1]. The evidence that the leu gene cluster is, in fact, an operon is as follows ... 

Other than the apparent arrangement of the genes in an operon, there is no evidence that any other features of the Jacob-Monod model are involved in expression of the leu genes. Although the cluster is repressed... 

More than 30 years ago Jacob and Monod introduced the Escherichia coli lac operon as a model for gene regulation. The lac repressor molecule functions as a switch, regulated by inducer molecules, which controls the synthesis of enzymes necessary for E. coli to use lactose as an energy source. In the absence of lactose the repressor binds tightly to the operator DNA preventing the synthesis of these enzymes. Conversely when lactose is present, the repressor dissociates from the operator, allowing transcription of the operon. 

Schematic model illustrating the operon hypothesis. This diagram is modified from the original proposed by Jacob and Monod, who thought i gene repressor was an RNA rather than a protein, (a) The i gene encodes a repressor that binds tightly to the operator o locus, thereby preventing transcription of the mRNA from the z, y, and a structural genes. (b) When inducer is present, it combines with repressor, changing its structure so it can no longer bind to the operator locus. Inducer also can remove repressor already complexed with the o locus.

The biosynthesis of a particular enzyme is itself an elaborate and complex process Involving several cellular components. The genetic information for any particular enzyme is carried in a stretch of DNA which is the structural gene for that protein. The pattern is transcribed in a strip of the messenger RNA that dictates the proper sequence of amino acids in the synthesis of the enzyme. Van Dedem and Moo-Young have made an interesting beginning into incorporation of the operon theory of Jacob and Monod into a kinetic model for enzyme syntheses [3]. Indeed even a relatively simple model leads to many unidentifiable kinetic constants. 

Study of the repression control of the histidine operon has suggested that it may be more complicated than the model proposed by Jacob and Monod. This possibility is predicated on failure to find a pure repressor gene. This failure has left open the possibility that control may be exerted by aminoacylated tRNA alone, possibly at the level of protein synthesis rather than mRNA synthesis. Alternatively, the repressor could be encoded by one of the regulatory genes discussed, but could also serve an additional function vital to the cell. The necessity of maintaining this second function would prevent the isolation of mutants which had totally lost repressor activity. In line with this latter possibility, the complex of histidyl-tRNA synthetase with aminoacylated tRNA may serve as the repressor. The mutual affinity of these two macromolecules and their concentrations within the cell are such that a large portion of the aminoacylated tRNA may be complexed to the synthetase [20,118a]. 

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