Disease relevance of hipA

• The basis of joint tolerance to beta-lactam and fluoroquinolone antibiotics in Escherichia coli mediated by hipA was examined [1].

High impact information on hipA

• An antibiotic tolerance phenotype was produced by overexpression of hipA under conditions that did not affect the growth rate of the organism [1].
• Overexpressing hipA probably decreases the period in which bacteria are susceptible to the antibiotics by temporarily affecting some aspect of chromosome replication or cell division [1].
• We report here that the expression of wild-type hipA in excess of hipB inhibits protein, RNA, and DNA synthesis in vivo [2].
• Although disruption of hipA slightly increased expression from the hip-lac fusion, in vitro studies suggest that HipA does not bind to the hip regulatory region directly but indirectly via HipB [3].
• Moreover, hipA-containing plasmids cannot be replicated in strains defective in or lacking hipB [3].

Biological context of hipA

• The stop codon of a 264-bp open reading frame, hipB, and the start codon of a 1,320-bp open reading frame, hipA, share an adenine residue [4].

References