Disease relevance of pheA

• pheAo mutants of Escherichia coli have a defective pheA attenuator [1].

High impact information on pheA

• Two classes of mutants affecting the regulation of pheA expression in Escherichia coli have been reported previously: trans-acting mutants involving the locus pheR, and cis-acting mutants involving the locus pheAo [1].
• Both pheAo351 and pheAo352 contained a G:C to A:T base pair transition, at different positions in the 3:4 stem of the pheA attenuator terminator [1].
• The phe operon consists of promoter, operator, leader region containing the phe attenuator and the pheA gene encoding chorismate mutase/prephenate dehydratase [2].
• In these clones, chromosomally located Tn4652 was transposed upstream from the coding sequencing of pheA (encoding phenol monooxygenase) [3].
• Lon-directed degradation of SulA was energy dependent, as was the increase in degradation of SulA in delta lon pAlp+ cells. alp maps close to pheA, at 57 min on the E. coli chromosome [4].

Chemical compound and disease context of pheA

• In Escherichia coli, the expression of the phenylalanine biosynthetic operon pheA is regulated by an attenuation mechanism [5].

Anatomical context of pheA

• To understand the factors that determine the basal level of pheA expression, we examined the role of ribosome release from the leader peptide stop codon UGA [5].

References