Chlamydia trachomatis-induced alterations in the host cell proteome are required for intracellular growth

Cell Host Microbe. 2014 Jan 15;15(1):113-24. doi: 10.1016/j.chom.2013.12.009.


Intracellular pathogens directly alter host cells in order to replicate and survive. While infection-induced changes in host transcription can be readily assessed, posttranscriptional alterations are more difficult to catalog. We applied the global protein stability (GPS) platform, which assesses protein stability based on relative changes in an adjoining fluorescent tag, to identify changes in the host proteome following infection with the obligate intracellular bacteria Chlamydia trachomatis. Our results indicate that C. trachomatis profoundly remodels the host proteome independently of changes in transcription. Additionally, C. trachomatis replication depends on a subset of altered proteins, such as Pin1 and Men1, that regulate the host transcription factor AP-1 controlling host inflammation, stress, and cell survival. Furthermore, AP-1-dependent transcription is activated during infection and required for efficient Chlamydia growth. In summary, this experimental approach revealed that C. trachomatis broadly alters host proteins and can be applied to examine host-pathogen interactions and develop host-based therapeutics.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Survival
  • Chlamydia Infections / genetics
  • Chlamydia Infections / metabolism
  • Chlamydia Infections / microbiology*
  • Chlamydia trachomatis / physiology*
  • DNA Replication
  • Female
  • Fluorescent Dyes
  • HeLa Cells
  • Host-Pathogen Interactions
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Microscopy, Fluorescence
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Peptidylprolyl Isomerase / genetics
  • Peptidylprolyl Isomerase / metabolism
  • Protein Processing, Post-Translational*
  • Proteome / genetics
  • Proteome / metabolism*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism
  • Signal Transduction
  • Transcription Factor AP-1 / genetics
  • Transcription Factor AP-1 / metabolism*
  • Transcription, Genetic


  • Fluorescent Dyes
  • MEN1 protein, human
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Proteome
  • Proto-Oncogene Proteins
  • Transcription Factor AP-1
  • PIN1 protein, human
  • Peptidylprolyl Isomerase
  • Pin1 protein, mouse