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Purpose <p>This study investigates codon usage and amino acid usage bias in the genus<i> Acinetobacter</i> to uncover the evolutionary forces shaping these patterns and their implications for pathogenicity and biotechnology.</p> Methods <p>Codon usage patterns were examined in representative genomes of the genus <i>Acinetobacter</i> using standard codon bias indices, including GC content, relative synonymous codon usage (RSCU), effective number of codons (ENC), and codon adaptation index (CAI). Neutrality and parity plots were employed to evaluate the relative influence of mutational pressure and natural selection on codon preferences. Codon pair usage and amino acid composition were assessed to identify functional constraints, while phylogenetic relationships were inferred using gyrB gene sequences to explore evolutionary divergence in the genus <i>Acinetobacter</i>.</p> Results <p>A dynamic GC content range was observed, from 35.71% in <i>Acinetobacter equi</i> to 46.21% in <i>Acinetobacter indicus</i>, with the <i>Acinetobacter baumannii</i> complex. maintaining a balanced GC distribution (39%), suggesting genomic stability. AT-rich preferred codons indicated selective pressure favouring specific codons, while correlations with GC composition underscored the role of mutational bias. CAI values &gt;0.5 in highly expressed genes denote bias toward optimal codons. Codon pair usage revealed distinctive patterns, with notable similarities within the <i>Acinetobacter baumannii</i> complex, indicating functional congruence. The <i>gyrB</i> phylogeny clustered <i>Acinetobacter baumannii </i>complex despite evolutionary divergence.</p> Conclusion <p>Codon usage in the genus <i>Acinetobacter</i> reflects a complex interplay of mutational and selective forces, shaping genomic and functional diversity. Distinct disparities in codon usage between pathogenic and non-pathogenic species point to genomic signatures that may underpin virulence, warranting further investigation into their pathogenic potential.</p>

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Distinct codon usage signatures reflecting evolutionary and pathogenic adaptation in the Acinetobacter baumannii complex

  • 期刊论文

  • 发表日期：

    2025年9月10日

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  • Ujwal Dahal,
  • Anuj Sharma,
  • Karan Paul,
  • Anu Bansal,
  • Shelly Gupta

摘要

Purpose

This study investigates codon usage and amino acid usage bias in the genus Acinetobacter to uncover the evolutionary forces shaping these patterns and their implications for pathogenicity and biotechnology.

Methods

Codon usage patterns were examined in representative genomes of the genus Acinetobacter using standard codon bias indices, including GC content, relative synonymous codon usage (RSCU), effective number of codons (ENC), and codon adaptation index (CAI). Neutrality and parity plots were employed to evaluate the relative influence of mutational pressure and natural selection on codon preferences. Codon pair usage and amino acid composition were assessed to identify functional constraints, while phylogenetic relationships were inferred using gyrB gene sequences to explore evolutionary divergence in the genus Acinetobacter.

Results

A dynamic GC content range was observed, from 35.71% in Acinetobacter equi to 46.21% in Acinetobacter indicus, with the Acinetobacter baumannii complex. maintaining a balanced GC distribution (39%), suggesting genomic stability. AT-rich preferred codons indicated selective pressure favouring specific codons, while correlations with GC composition underscored the role of mutational bias. CAI values >0.5 in highly expressed genes denote bias toward optimal codons. Codon pair usage revealed distinctive patterns, with notable similarities within the Acinetobacter baumannii complex, indicating functional congruence. The gyrB phylogeny clustered Acinetobacter baumannii complex despite evolutionary divergence.

Conclusion

Codon usage in the genus Acinetobacter reflects a complex interplay of mutational and selective forces, shaping genomic and functional diversity. Distinct disparities in codon usage between pathogenic and non-pathogenic species point to genomic signatures that may underpin virulence, warranting further investigation into their pathogenic potential.