Comparative genomes of Chlamydia pneumoniae and C. trachomatis (original) (raw)

Nature Genetics volume 21, pages 385–389 (1999) Cite this article

Abstract

Chlamydia are obligate intracellular eubacteria that are phylogenetically separated from other bacterial divisions. C. trachomatis and C. pneumoniae are both pathogens of humans but differ in their tissue tropism and spectrum of diseases. C. pneumoniae is a newly recognized species of Chlamydia that is a natural pathogen of humans1, and causes pneumonia and bronchitis. In the United States, approximately 10% of pneumonia cases and 5% of bronchitis cases are attributed to C. pneumoniae infection2. Chronic disease may result following respiratory-acquired infection, such as reactive airway disease3, adult-onset asthma4 and potentially lung cancer5. In addition, C. pneumoniae infection has been associated with atherosclerosis6,7,8,9,10,11. C. trachomatis infection causes trachoma, an ocular infection that leads to blindness, and sexually transmitted diseases such as pelvic inflammatory disease, chronic pelvic pain, ectopic pregnancy and epididymitis12. Although relatively little is known about C. trachomatis biology13, even less is known concerning C. pneumoniae. Comparison of the C. pneumoniae genome with the C. trachomatis genome14 will provide an understanding of the common biological processes required for infection and survival in mammalian cells. Genomic differences are implicated in the unique properties that differentiate the two species in disease spectrum. Analysis of the 1,230,230-nt C. pneumoniae genome revealed 214 protein-coding sequences not found in C. trachomatis, most without homologues to other known sequences. Prominent comparative findings include expansion of a novel family of 21 sequence-variant outer-membrane proteins, conservation of a type-III secretion virulence system, three serine/threonine protein kinases and a pair of parologous phospholipase-D-like proteins, additional purine and biotin biosynthetic capability, a homologue for aromatic amino acid (tryptophan) hydroxylase and the loss of tryptophan biosynthesis genes.

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Acknowledgements

We thank C. Black for providing the C. pneumoniae strain and Incyte Pharmaceuticals, Inc. for financial support.

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Authors and Affiliations

  1. Stanford DNA Sequencing and Technology Center, Stanford University, Stanford, 94305, California, USA
    Sue Kalman, Rekha Marathe, Jun Fan, Richard W Hyman & Ronald W Davis
  2. Program in Infectious Diseases, University of California, Berkeley, 94720, California, USA
    Wayne Mitchell, Claudia Lammel, Lynn Olinger & Richard Stephens
  3. Francis I. Proctor Foundation, University of California, 94143, USA, San Francisco, California
    Wayne Mitchell, Lynn Olinger, Jane Grimwood & Richard Stephens

Authors

  1. Sue Kalman
  2. Wayne Mitchell
  3. Rekha Marathe
  4. Claudia Lammel
  5. Jun Fan
  6. Richard W Hyman
  7. Lynn Olinger
  8. Jane Grimwood
  9. Ronald W Davis
  10. Richard Stephens

Corresponding author

Correspondence toRichard Stephens.

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Kalman, S., Mitchell, W., Marathe, R. et al. Comparative genomes of Chlamydia pneumoniae and C. trachomatis .Nat Genet 21, 385–389 (1999). https://doi.org/10.1038/7716

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