Operon polarity

Jordan, E., Saedler, H., and Starlinger, P. (1967). Strong polar mutations in the transferase gene of the galactose operon in E. coli. Molec. Gen. Genet. 100 296-306. 

The adherence mechanisms involved in Salmonella infection have been studied in great deal. Disease associated with S. enterica serovars is initiated by attachment to and invasion of hosf cells, followed by subse-quenf inflammation of the lamina propria and lymph nodes (Darwin and Miller, 1999). Several genetically defined fimbrial or piliar adhesins con-tribufe fo fhe initial attachment and the overall infection process of Salmonella. Some of fhese include t)q)e 1 fimbriae (Fim), plasmid-encoded (PE) fimbriae, long polar (LP) fimbriae, and thin aggregative fimbriae (curli). However, many ofher putative fimbrial operons have been identified within various S. enterica serovar genomes, but the expression of fhese proteins is currently undefined. 

Polar mutation. A mutation in one gene that reduces the expression of a gene or genes distal to the promoter in the same operon. 

T., and Reeve, J.N. (2008) Polarity in archaeal operon transcription in Jher-mococcus kodakaraensis. J. Bacterial., 190, 2244-2248. 

If his4 is an operon, then kis4A, B, and C regions must specify three polypeptides which aggregate to form the final multifunctional product. A difficulty with the operon model is the complete polarity of his4A nonsense mutants. Some complementation between his4A nonsense mutants and other his4 mutants should have been observed. Alterna-... 

Polarity is in the direction araB, ara A, araP. Nonsense mutations in gene araB lead to reduced levels of L-arabinose isomerase and L-ribulose 5-phosphate 4-epimerase [5,6]. Nonsense mutations in gene araA result in redueed levels of L-ribulose 5-phosphate 4-epimerase, but do not effect a reduction of kinase levels [40]. Thus the controlling elements for this operon must be the proximal end of the araB gene—that is, the end farthest from gene araA. 

Thus the direction of polarity in the operon and the observed differences between strains containing deletions of the type B.. Cleu and 5.. C on the one hand and Cleu on the other, with regard to sensitivity to activation by L-arabinose (C allele in the trans position), offer conclusive proof that the activator-sensitive controlling site aral) is located between genes araB and araC. 

Some polar mutations of the lac operon have been found to be suppressed by other genes which are known to act as amber, ochre, or UGA suppressors. When z nonsense mutants are suppressed, an amino acid is inserted at the point of the mutation and the mutated enzyme activity is restored. The inserted amino acid has been found to be related to the class of suppressor employed. Suppressor genes produce mutated species of tRNA s which recognize nonsense codons, and insert amino acids at that point. For example the tyrosine tRNA of suppressor III recognizes the nonsense triplet UAG and inserts tyrosine on the growing peptide chain, thereby competing with the chain release reaction. 

In Section III,B, the phenomenon of polarity was discussed in relation to its implications for a polycistronic mRNA for the histidine operon. For the deduction of the presence of a polycistronic mRNA, it was not necessary to know the specific mechanism by which polar mutations exerted their effect. However, a great deal of effort has been expended in trying to understand this mechanism, and these studies have produced a greater understanding of the translation process. 

In an attempt to study natural polarity, mutations in different parts of the histidine operon were isolated which cause polarity, but do not result in a histidine requirement [70]. The very existence of these modulation mutants shows that it is possible for the cell to optimize the gradient of production of the enzymes of an operon. The analysis of one of these mutants is discussed in the following section. 

Imamoto and Yanofsky [225,239] studied the production of tryptophan mRNA in strains with nonsense mutations. They found that the tryptophan mRNA of strong polarity mutant strains was deficient in regions corresponding to the genes of the operon on the operator-distal side of the mutated gene. In such strains the majority of tryptophan... 

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