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Background  Chlamydia have reduced genomes that reflect their obligately parasitic lifestyle. Despite their different tissue tropisms, chlamydial strains share a large number of common genes and have few recognized pseudogenes, indicating genomic stability. All of the  Chlamydiaceae  have homologs of the  aaxABC  gene cluster that encodes a functional arginine:agmatine exchange system in  Chlamydia  ( Chlamydophila ) pneumoniae . However,  Chlamydia trachomatis  serovar L2 strains have a nonsense mutation in their  aaxB  genes, and  C. trachomatis  serovar A and B strains have frameshift mutations in their  aaxC  homologs, suggesting that relaxed selection may have enabled the evolution of  aax  pseudogenes. Biochemical experiments were performed to determine whether the  aaxABC  genes from  C. trachomatis  strains were transcribed, and mutagenesis was used to identify nucleotide substitutions that prevent protein maturation and activity. Molecular evolution techniques were applied to determine the relaxation of selection and the scope of  aax  gene inactivation in the  Chlamydiales .    Results  The  aaxABC  genes were co-transcribed in  C. trachomatis  L2/434, during the mid-late stage of cellular infection. However, a stop codon in the  aaxB  gene from this strain prevented the heterologous production of an active pyruvoyl-dependent arginine decarboxylase. Replacing that ochre codon with its ancestral tryptophan codon rescued the activity of this self-cleaving enzyme. The  aaxB  gene from  C. trachomatis  D/UW-3 was heterologously expressed as a proenzyme that failed to cleave and form the catalytic pyruvoyl cofactor. This inactive protein could be rescued by replacing the arginine-115 codon with an ancestral glycine codon. The  aaxC  gene from the D/UW-3 strain encoded an active arginine:agmatine antiporter protein, while the L2/434 homolog was unexpectedly inactive. Yet the frequencies of nonsynonymous versus synonymous nucleotide substitutions show no signs of relaxed selection, consistent with the recent inactivation of these genes.    Conclusion  The ancestor of the  Chlamydiaceae  had a functional arginine:agmatine exchange system that is decaying through independent, parallel processes in the  C. trachomatis  lineage. Differences in arginine metabolism among  Chlamydiaceae  species may be partly associated with their tissue tropism, possibly due to the protection conferred by a functional arginine-agmatine exchange system against host nitric oxide production and innate immunity. The independent loss of AaxB activity in all sequenced  C. trachomatis  strains indicates continual gene inactivation and illustrates the difficulty of recognizing recent bacterial pseudogenes from sequence comparison, transcriptional profiling or the analysis of nucleotide substitution rates.

bmc evolutionary biology

Independent inactivation of arginine decarboxylase genes by nonsense and missense mutations led to pseudogene formation in Chlamydia trachomatisserovar L2 and D strains