Disease relevance of aphA

• Indeed, the expression of a chromosomal tcpP-lacZ fusion was reduced in the delta aphA mutant and increased in both V. cholerae and Escherichia coli by introducing aphA expressed from an inducible promoter [1].
• We describe here a previously unidentified gene in Vibrio cholerae, aphA (activator of tcpP and tcpH expression), which is required for the transcription of the tcpPH operon [1].
• The aphA gene of Salmonella enterica sv [2].

High impact information on aphA

• Under conditions normally optimal for virulence gene expression, an in frame aphA deletion decreased the expression of a cholera toxin promoter fusion (ctx-lacZ) and prevented the production of the toxin co-regulated pilus (TCP) [1].
• Plasmids producing ToxT or TcpP/H, but not ToxR, restored ctx-lacZ expression and TCP production in the delta aphA strain, suggesting that the mutation interferes with toxT expression by influencing the transcription of tcpPH [1].
• (a) aphA was overexpressed in Escherichia coli with N-terminal His and S tags, and the protein was reconstituted by an optimized protocol with phycocyanobilin (PCB), to yield the photochromic chromoprotein, PCB-AphA, carrying the PCB chromophore [3].
• (d) Through deletion mutations of aphA, a short sequence IQPHGV [amino acids (aa) 26-31] was found essential for the lyase activity of AphA, indicating an interaction of the N terminus with the chromophore-binding domain around cysteine 259 [3].

References