Studies on synonymous codon and amino acid usages in Aeromonas hydrophila phage Aeh1: architecture of protein-coding genes and therapeutic implications
Department of Biotechnology, Haldia Institute of Technology, Haldia, India
Received: November 1, 2005 Revised: February 28, 2006 Accepted: March 3, 2006
Background and purpose:
Codon and amino acid usage biases determined in numerous organisms have deciphered the architectures of their protein-coding genes to some extent. To understand the architecture of protein-coding genes of Aeromonas phages, codon and amino acid usage biases have been investigated in the protein-coding genes of the Aeromonas hydrophila phage Aeh1.
In order to study synonymous codon and amino acid usage biases in Aeh1, all of its protein-coding genes were downloaded and analyzed by standard software programs.
Phage Aeh1 harbors an AT-rich genome. The third position of its synonymous codons carries mostly A or T base and mutational pressure strongly influences the synonymous codon usage bias. Translational selection also influences the codon usage of Aeh1 as its putatively lowly- and highly-expressed genes are influenced by Aeh1-specific tRNAs and by the abundant cellular tRNAs, respectively. Further analysis of amino acid usage shows that amino acid residues are also not randomly utilized in Aeh1 proteins and factors such as hydropathy, aromaticity and cysteine content are mostly responsible for the variation of amino acid usage in Aeh1 proteins.
As Aeh1 does not carry any toxin/antibiotic resistant gene but carries moderately highly expressed genes and relatively few AhdI sites, this study proposes that Aeh1 may be utilized as a therapeutic agent for A. hydrophila infections. While codon usage bias in Aeh1 is dictated both by mutational pressure and translational selection, amino acid usage bias in Aeh1 is influenced by hydropathy, aromaticity and cysteine content. Phage Aeh1 may be utilized in phage therapy.
Aeromonas hydrophila; Amino acid metabolism; Bacteriophages; Codon; Gene expression regulation, bacterial
J Microbiol Immunol Infect 2007;40:24-33.