Hyperinducibility as a result of mutation in structural genes and self-catabolite repression in the ara operon
- PMID: 4327512
- PMCID: PMC246883
- DOI: 10.1128/jb.107.1.34-52.1971
Hyperinducibility as a result of mutation in structural genes and self-catabolite repression in the ara operon
Abstract
Mutations in gene araB producing an l-arabinose-negative phenotype cause either an increase (hyperinducible), decrease (polar), or have no effect at all on the inducible rate of expression of the l-arabinose operon. Fourteen araB gene mutants exhibiting such effects were shown to be the result of: nonsense, frameshift, or missense mutations. All missense mutants were hyperinducible, exhibiting approximately a twofold increase in rate of l-arabinose isomerase production. All frameshift and most nonsense mutants exhibited polar effect. One nonsense mutant was hyperinducible. The cis-dominant polar effect of nonsense and frameshift mutants (as compared to induced wild type) were more pronounced in arabinose-utilizing merodiploids and in araBaraC(c) double mutants where inducible and constitutive enzyme levels are respectively determined. On the other hand, in arabinose-utilizing merodiploids, missense mutations no longer exhibited hyperinducibility but displayed a wild-type level of operon expression. Increases in the wild type-inducible rate of expression of the operon were found when growth rate was dependent on the concentration of l-arabinose. Cyclic 3',5'-adenosine monophosphate also stimulated expression of the operon with the wild type in a mineral l-arabinose medium. These observations are explained on the basis that the steady-state expression of the l-arabinose operon OIBAD is dependent on the concentration of (i) l-arabinose, the effector of this system, which stimulates the expression of the operon, and (ii) catabolite repressors, produced from l-arabinose, which dampen the expression of the operon. We have termed the latter phenomenon "self-catabolite" repression.
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