Normal IncA expression and fusogenicity of inclusions in Chlamydia trachomatis isolates with the incA I47T mutation

Y Pannekoek1, A van der Ende, P P Eijk

  • 1Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. y.pannekoek@amc.uva.nl

Insights

The incA I47T mutation in Chlamydia trachomatis does not cause a nonfusogenic phenotype. Sequencing of 25 isolates revealed the mutation is not linked to inclusion membrane fusion.

Area of Science:

  • Microbiology
  • Bacterial genetics
  • Cell biology

Background:

  • Chlamydia trachomatis forms a single large inclusion in host cells.
  • The incA gene product is involved in inclusion membrane fusion.
  • A specific mutation, I47T, in incA has been investigated for its role in this process.

Purpose of the Study:

  • To determine if the incA I47T mutation in Chlamydia trachomatis correlates with a nonfusogenic phenotype.
  • To analyze the genetic diversity of the incA gene in C. trachomatis isolates.

Main Methods:

  • Sequencing of the incA gene from 25 Chlamydia trachomatis isolates.
  • Analysis of sequence variations, including the I47T mutation.
  • Assessment of IncA expression and inclusion phenotype in infected cells.

Main Results:

  • Four distinct sequence types of the incA gene were identified.
  • The I47T mutation was present in 7 out of 25 (28%) isolates.
  • All investigated isolates, regardless of sequence type or I47T mutation status, exhibited IncA expression within a single, large inclusion, indicating a fusogenic phenotype.

Conclusions:

  • The incA I47T mutation is not associated with the nonfusogenic phenotype in Chlamydia trachomatis.
  • The genetic variation within the incA gene, including the I47T mutation, does not appear to disrupt the fusogenic properties of the inclusion membrane.