Disease relevance of prfB

• The prfB gene encodes peptide-chain-release factor 2 of Escherichia coli, which catalyzes translation termination at UGA and UAA codons [1].
• Data are presented that suggest that supK, a mutation in Salmonella typhimurium that suppresses UGA termination, is the structural gene for Salmonella release factor 2 [1].
• Properties of peptide chain release factor 2 from Streptomyces coelicolor A3(2): conserved primary structure but no frameshift regulation [2].

High impact information on prfB

• Sequencing the prfB gene from E.coli B and MRE600 strains showed that residue 246 is coded as alanine, in contrast to K12 RF2 [3].
• Complementation, reversion, and gene fusion analyses led to the conclusion that supK is a S. typhimurium RF2 mutation and this opal RF2 mutation generates a UGA suppressor activity, presumably because of inefficient translation termination due to the reduced cellular level of RF2 [4].
• Thus, we refer to the two genes as the prfB-herC operon [1].
• The prfB gene is followed by an open reading frame encoding a 57,603-Da protein [1].
• The effect of introducing prfB mutations into mutant strains containing altered trp leader regions that influence basal level transcription readthrough was also determined [5].

Chemical compound and disease context of prfB

• Mutations in the prfB gene which encodes peptide-chain-release factor 2 of Escherichia coli were defined by DNA sequence analysis. prfB1 and prfB3 substitute lysine and asparagine for glutamate and aspartate at amino acid positions 89 and 143, respectively [6].
• Mutations in prfB, encoding release factor 2 (UGA- and UAA-specific), increase transcription termination at the trp operon attenuator in Escherichia coli strains grown in the presence of tryptophan [5].

Biological context of prfB

• The expression system was programmed with a plasmid containing a trpE-prfB fusion gene so that each of the products of the competing events could be measured [7].
• Termination at UGA competes with selenocysteine (Sec) incorporation at Sec-dedicated UGA codons, and RF2 thereby counteracts expression of selenoproteins. prfB is an essential gene in E. coli and can therefore not be removed in order to increase yield of recombinant selenoproteins [8].
• Comparison of the sequence of this region of the chromosome with DNA data bases identified the gene immediately downstream of recJ as prfB, which encodes translational release factor 2 and has been mapped near recJ at 62 min [9].

Other interactions of prfB

• The efficiency of natural frameshift was 18% as measured by using the monolysogenic lambda assay vector containing prfB-lacZ fusions, and increased up to 30% in the prfB mutants [6].

Analytical, diagnostic and therapeutic context of prfB

• Titration and Conditional Knockdown of the prfB Gene in Escherichia coli: Effects on Growth and Overproduction of the Recombinant Mammalian Selenoprotein Thioredoxin Reductase [8].

References