Genome sequence of Chlamydophila caviae (Chlamydia psittaci GPIC): examining the role of niche-specific genes in the evolution of the Chlamydiaceae

Abstract

The genome of Chlamydophila caviae (formerly Chlamydia psittaci, GPIC isolate) (1 173 390 nt with a plasmid of 7966 nt) was determined, representing the fourth species with a complete genome sequence from the Chlamydiaceae family of obligate intracellular bacterial pathogens. Of 1009 annotated genes, 798 were conserved in all three other completed Chlamydiaceae genomes. The C.caviae genome contains 68 genes that lack orthologs in any other completed chlamydial genomes, including tryptophan and thiamine biosynthesis determinants and a ribose-phosphate pyrophosphokinase, the product of the prsA gene. Notable amongst these was a novel member of the virulence-associated invasin/intimin family (IIF) of Gram-negative bacteria. Intriguingly, two authentic frameshift mutations in the ORF indicate that this gene is not functional. Many of the unique genes are found in the replication termination region (RTR or plasticity zone), an area of frequent symmetrical inversion events around the replication terminus shown to be a hotspot for genome variation in previous genome sequencing studies. In C.caviae, the RTR includes several loci of particular interest including a large toxin gene and evidence of ancestral insertion(s) of a bacteriophage. This toxin gene, not present in Chlamydia pneumoniae, is a member of the YopT effector family of type III-secreted cysteine proteases. One gene cluster (guaBA-add) in the RTR is much more similar to orthologs in Chlamydia muridarum than those in the phylogenetically closest species C.pneumoniae, suggesting the possibility of horizontal transfer of genes between the rodent-associated Chlamydiae. With most genes observed in the other chlamydial genomes represented, C.caviae provides a good model for the Chlamydiaceae and a point of comparison against the human atherosclerosis-associated C.pneumoniae. This crucial addition to the set of completed Chlamydiaceae genome sequences is enabling dissection of the roles played by niche-specific genes in these important bacterial pathogens.

Chlamydia-Infected Cells Continue To Undergo Mitosis and Resist Induction of Apoptosis

“…It is possible that either chlamydia-derived toxins or toxic materials released by chlamydia-infected cells play some role in promoting apoptosis. Several chlamydial toxin homologue genes (including chlamydia muridarum and GPIC) encode a homologue of the complete clostridium large toxin (39,40,46). It has been demonstrated that the chlamydial toxin homologue genes are expressed late in the growth cycle, and chlamydia muridarum is more toxic to cultured cells than other C. trachomatis strains, which contain truncated toxin genes or no toxin genes at all (5).…”

A plasmid-cured Chlamydia muridarum strain displays altered plaque morphology and reduced infectivity in cell culture

“…We have observed that a variety of environmental factors can suppress the accumulation of glycogen within inclusions, including ampicillin treatment and substrate limitation (unpublished). Furthermore, it should be noted that neither Chlamydophila psittaci nor Chlamydophila pneumoniae accumulate glycogen within their inclusions, although the majority of C. psittaci and some C. pneumoniae strains carry the plasmid (Lusher et al, 1989;Thomas et al, 1997;McClenaghan et al, 1988) and the glycogen metabolic genes have been retained on the chromosome (Read et al, 2000(Read et al, , 2003Kalman et al, 1999). It would be highly desirable to reintroduce the cryptic plasmid into C. muridarum and demonstrate restoration of both intra-inclusion glycogen accumulation and plaquing efficiency.…”

Effect of host fatty acid-binding protein and fatty acid uptake on growth of Chlamydia trachomatis L2

“…Chlamydia pneumoniae is a major cause of various respiratory illnesses, and respiratory infection with C. pneumoniae is also linked to cardiovascular pathologies such as atherosclerosis (Campbell & Kuo, 2002. There are other chlamydial species that can cause various animal diseases (Azuma et al, 2006;Everett & Hatch, 1995;Read et al, 2003). Regardless of the diverse host tropism and disease phenotypes, all members of the genus Chlamydia have evolved a common biphasic intracellular life cycle (Hackstadt et al, 1997).…”