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Chlamydia trachomatis co-opts GBF1 and CERT to acquire host sphingomyelin for distinct roles during intracellular

Cherilyn A Elwell1, Shaobo Jiang, Jung Hwa Kim

  • 1Department of Medicine, University of California, San Francisco, California, United States of America.

Plos Pathogens
|September 13, 2011
PubMed

Insights

Chlamydia trachomatis hijacks host sphingomyelin (SM) using both vesicular and non-vesicular pathways. One pathway aids inclusion growth, while another supports bacterial replication by creating a local SM factory.

Area of Science:

  • Microbiology
  • Cell Biology
  • Biochemistry

Background:

  • Chlamydia trachomatis is an obligate intracellular pathogen that replicates within a host-derived membrane-bound inclusion.
  • Sphingomyelin (SM) acquisition by the inclusion is crucial for Chlamydia replication and inclusion biogenesis.
  • Previous studies indicated SM acquisition via a Brefeldin A (BFA)-sensitive pathway, but this pathway is dispensable for replication, suggesting alternative mechanisms.

Purpose of the Study:

  • To investigate the roles of BFA-sensitive and BFA-insensitive lipid trafficking pathways in sphingomyelin (SM) acquisition by Chlamydia trachomatis.
  • To define how Chlamydia trachomatis utilizes SM obtained through different lipid acquisition pathways.

Main Methods:

  • Interrogation of specific components within BFA-sensitive and BFA-insensitive lipid trafficking pathways.
  • Analysis of the contribution of GBF1 (a BFA target) and CERT (a non-vesicular lipid transfer protein) in SM acquisition.
  • Investigation of the recruitment of CERT, VAP-A, and SM synthases (SMS1, SMS2) to the inclusion.

Main Results:

  • Chlamydia trachomatis utilizes both vesicular (GBF1-dependent) and non-vesicular (CERT-dependent) pathways for SM acquisition.
  • The Arf1/GBF1-dependent pathway is essential for inclusion membrane growth and stability but not bacterial replication.
  • The CERT-dependent pathway, involving ceramide transport and on-site SM synthesis, is critical for Chlamydia replication.

Conclusions:

  • Chlamydia trachomatis employs distinct lipid trafficking pathways to acquire SM for different essential functions.
  • The GBF1 pathway supports inclusion biogenesis, while the CERT pathway facilitates bacterial replication through localized SM synthesis.
  • This study reveals a novel mechanism of pathogen-host lipid manipulation, where Chlamydia redirects host SM biosynthesis to its replicative niche.

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