Disease relevance of aroG

• The nucleotide sequence of aroG, the gene for 3-deoxy-D-arabinoheptulosonate-7-phosphate synthetase (phe) in Escherichia coli K12 [1].

High impact information on aroG

• There is significant identity in the nucleotide sequences of aroG and aroH (the gene for 3-deoxy-D-arabinoheptulosonate-7-phosphate synthetase (trp), indicating that these two genes have evolved from a common ancestral gene [1].
• To validate our theoretical results, we performed site-directed mutagenesis to reduce the degree of DNA curvature in the regulatory sequences of the aroG, pyrC, and argCBH operons [2].
• In vitro chemical mutagenesis of the cloned aroG gene was used to identify residues and regions of the polypeptide essential for phenylalanine feedback inhibition [3].
• A mutation to site A of the ATP-binding site and other mutations in this region affect tyrosine-mediated repression but do not prevent activation or phenylalanine-mediated repression of aroG [4].
• Mutations in the aroG regulatory DNA were isolated by site-directed mutagenesis and cloned in a low-copy-number plasmid to generate aroG-lac fusions [5].

Chemical compound and disease context of aroG

• The promoter, operator, and 5' and 3' ends of the mRNA of the Escherichia coli gene aroG (encoding the phenylalanine-sensitive 3-deoxy-arabinoheptulosonate-7-phosphate synthase) were located [5].

Biological context of aroG

• The location of the aroG promoter was identified in both strands of the DNA by in vitro DNase I footprinting and methylation protection experiments with RNA polymerase [5].

Analytical, diagnostic and therapeutic context of aroG

• Here we describe the PCR amplification, cloning, and sequencing of aroG structural gene from M. tuberculosis H37Rv [6].

References