Database Authors
Summary Chlamydia trachomatis is one of the most common sexually transmitted bacteria in the world and considered one of the most prevalent human pathogens responsible for genital tract pathologies, which often result in severe long-term reproductive complications including infertility, and for ocular pathologies, which can lead to blindness (trachoma). Chlamydia trachomatis is one of three major species of the only genus within their own taxonomic order, Chlamydiales. There are multiple serovars of C. trachomatis based on differences in the antigenic major outer membrane protein, MOMP, with serovars A - C being endemic to developing countries and the cause of trachoma, serovars D - K being sexually transmitted with mucosal membranes of urogenital tract being the primary site of infection, and serovars L1 - L3 being involved in lymphatic system infections. It should be noted, though, that serovars based on major outer membrane protein, MOMP variation are not associated with C. trachomatis biological variation or pathogenic potential; thus, other ways of defining C. trachomatis strains are being explored [Caldwell82, Byrne10, Elwell16, Witkin17].

This pathogenic bacterium is an obligate pathogen that has evolved mechanisms to avoid the immune system and persist within the epithelial cells of its only natural host: humans. All chlamydiae have small genomes, limited biosynthetic capability, and a unique, unsynchronized, developmental cycle that is tied to its intracellular survival. The cycle begins with small, metabolically reduced 'elementary bodies' (EB) with electron-dense, compacted DNA and rigid trilaminar cell walls that infect host cells through endocytosis. The EB within the chlamydial endocytic vesicle become non-infectious, larger, metabolically active 'reticulate bodies' (RB) with less condensed nucleoid structure and more flexible cell walls. These RB cells use nutrients and ATP from the host cytoplasm and divide by binary fission. The endocytic vesicles (also referred to as vacuoles) combine to form large inclusions within the cytoplasm of the host cells. The RBs reorganize their cellular structure and transition back into EB, which are released from the host cell ~48 - 72 hrs after infection, repeating the developmental cycle when another host cell is infected. It's been found that the immune response of epithelial host cells to Chlamydia infection is secretion of interferon-γ (IFN--γ), which leads to induction of indoleamine 2,3-dioxygenase (IDO) that degrades the essential amino acid tryptophan (Trp) causing Trp deprivation for C. trachomatis. This leads to development of a special chlamydial persistent form, the nonreplicating aberrant reticulate bodies (ARB), which are viable, but noncultivable [Omsland14, Elwell16, Ostergaard16, Witkin17].

Chlamydia trachomatis D/UW-3/CX presented here is the type strain of the serovar D group and was the first Chlamydia species to have its complete genome sequenced [Stephens98]. Its genome is small but within the range of other C. trachomatis genomes, being slightly greater than 1.04 kbp and containing a single 7,493 bp plasmid (which was not sequenced as part of the NCBI BioProject genome sequencing used for this PGDB). Comparative genomic analysis of 12 C. trachomatis strains revealed that a large proportion of their pan-genome consists of conserved core genes: 836 core genes out of 874-927 total genes found in each C. trachomatis genome [Joseph11]. Because of the obligate intracellular nature of chlamydiae, a number of genes related to biosynthesis capabilities are missing and a large portion of their genome is devoted to virulence factors, such as effectors that are secreted through specialized secretion systems [Stephens98, Byrne10, Elwell16, Witkin17].

This Pathway/Genome Database (PGDB) was generated on 15-Feb-2020 from the annotated genome of Chlamydia trachomatis D/UW-3/CX, as obtained from RefSeq (annotation date: 03-AUG-2016) and pathways were created computationally by the PathoLogic component of the Pathway Tools software (version 24.0) [Karp16, Karp11] using MetaCyc version 23.5 [Caspi20]. Many genes associated with virulence have also been manually curated and verified from publications.

Development of this PGDB was supported by BioCyc subscription revenues and by grant GM080746 from the National Institute of Health.

Genome
RepliconTotal GenesProtein GenesRNA GenesPseudogenesSize (bp)NCBI Link
NC_0001179358864541,042,519RefSeq:NC_000117
Ortholog data available?Yes
Database Contents
Genes935
Pathways87
Enzymatic Reactions554
Transport Reactions32
Polypeptides889
Protein Complexes32
Enzymes266
Transporters59
Compounds408
Transcription Units576
tRNAs37
Protein Features2,693
GO Terms11,232
Database Version29.0
Sequence SourceGCF_000008725.1
Synonyms Chlamydia trachomatis D/UW-3/CXGCF_000008725.1
Chlamydia trachomatis strain D/UW-3/CX
Chlamydia trachomatis D/UW-3/CX
Taxonomic Lineage cellular organisms
Bacteria <bacteria>
PVC group
Chlamydiota
Chlamydiia
Chlamydiales
Chlamydiaceae
Chlamydia/Chlamydophila group
Chlamydia
Chlamydia trachomatis
Chlamydia trachomatis D/UW-3/CX
Genetic Code Number 11 -- Bacterial, Archaeal and Plant Plastid (same as Standard, except for alternate initiation codons)
NCBI BioProjectPRJNA57637
NCBI-Taxonomy272561
Biotic Relationshipparasite
Pathogenicityhuman
HostHomo sapiens
NCBI Genome Typereference
Copyright 2020, SRI International. All Rights Reserved


References

Byrne10: Byrne GI (2010). "Chlamydia trachomatis strains and virulence: rethinking links to infection prevalence and disease severity." J Infect Dis 201 Suppl 2;S126-33. PMID: 20470049

Caldwell82: Caldwell HD, Schachter J (1982). "Antigenic analysis of the major outer membrane protein of Chlamydia spp." Infect Immun 35(3);1024-31. PMID: 7068209

Caspi20: Caspi R, Billington R, Keseler IM, Kothari A, Krummenacker M, Midford PE, Ong WK, Paley S, Subhraveti P, Karp PD (2020). "The MetaCyc database of metabolic pathways and enzymes - a 2019 update." Nucleic Acids Res 48(D1);D445-D453. PMID: 31586394

Elwell16: Elwell C, Mirrashidi K, Engel J (2016). "Chlamydia cell biology and pathogenesis." Nat Rev Microbiol 14(6);385-400. PMID: 27108705

Joseph11: Joseph SJ, Didelot X, Gandhi K, Dean D, Read TD (2011). "Interplay of recombination and selection in the genomes of Chlamydia trachomatis." Biol Direct 6;28. PMID: 21615910

Karp11: Karp PD, Latendresse M, Caspi R (2011). "The pathway tools pathway prediction algorithm." Stand Genomic Sci 5(3);424-9. PMID: 22675592

Karp16: Karp PD, Latendresse M, Paley SM, Krummenacker M, Ong QD, Billington R, Kothari A, Weaver D, Lee T, Subhraveti P, Spaulding A, Fulcher C, Keseler IM, Caspi R (2016). "Pathway Tools version 19.0 update: software for pathway/genome informatics and systems biology." Brief Bioinform 17(5);877-90. PMID: 26454094

Omsland14: Omsland A, Sixt BS, Horn M, Hackstadt T (2014). "Chlamydial metabolism revisited: interspecies metabolic variability and developmental stage-specific physiologic activities." FEMS Microbiol Rev 38(4);779-801. PMID: 24484402

Ostergaard16: Ostergaard O, Follmann F, Olsen AW, Heegaard NH, Andersen P, Rosenkrands I (2016). "Quantitative Protein Profiling of Chlamydia trachomatis Growth Forms Reveals Defense Strategies Against Tryptophan Starvation." Mol Cell Proteomics 15(12);3540-3550. PMID: 27784728

Stephens98: Stephens RS, Kalman S, Lammel C, Fan J, Marathe R, Aravind L, Mitchell W, Olinger L, Tatusov RL, Zhao Q, Koonin EV, Davis RW (1998). "Genome sequence of an obligate intracellular pathogen of humans: Chlamydia trachomatis." Science 282(5389);754-9. PMID: 9784136

Witkin17: Witkin SS, Minis E, Athanasiou A, Leizer J, Linhares IM (2017). "Chlamydia trachomatis: the Persistent Pathogen." Clin Vaccine Immunol 24(10). PMID: 28835360


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