L-arabinose operon

The L-arabinose operon of the model bacterium Escherichia coli has been a focus for research in molecular biology for over 40 years, and has been investigated extensively at the genetic, biochemical, physiological, and biophysical levels. It is controlled by a dual positive and negative system. There are 3 structural genes: araB, araA, and araD. They encode the metabolic enzymes for breaking down the monosaccharide sugar arabinose into D-xylulose-5-phosphate, which is then metabolised via the pentose phosphate pathway. The initiator region, containing an operator site as well as a promoter, is called araI (the last letter of araI is an uppercase letter "i"). Near this site lies the araC gene, which encodes an activator protein.[1] The AraC protein binds to initiator region araI.

Metabolism of arabinose in E. coli
Substrate Protein(s) Function Reversible Product
L-arabinose AraA isomerase yes L-ribulose
L-ribulose AraB ribulokinase no L-ribulose-phosphate
L-ribulose-phosphate AraD epimerase yes D-xylulose-phosphate

Activation

If arabinose is present, it builds a complex: AraC + arabinose
This complex is needed for RNA polymerase to bind to the promoter and transcribe the ara operon. Also for activation the binding of another structure to araI is needed: CAP + cyclic AMP
So the activation depends on the presence of arabinose and cAMP.

Repression

If arabinose is absent, the AraC protein assumes a different conformation. In this conformation the AraC protein binds to the araI DNA region as well as to the ara0 DNA region. This causes the DNA to form a loop, preventing transcription of the downstream ara operon elements.

Sequence of the Operon:

araC : araO : araI : araB : araA : araD

See also

Notes

  1. ^ Schleif, R. (2010). "AraC protein, regulation of the l-arabinose operon in Escherichia coli, and the light switch mechanism of AraC action". FEMS Microbiology Reviews: no. doi:10.1111/j.1574-6976.2010.00226.x.  edit

References

"Regulation of the L-arabinose operon of Escherichia coli". Trends in Genetics 16 (12): 559–565. December 2000. doi:10.1016/S0168-9525(00)02153-3. PMID 11102706.