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Markerless Gene Deletion by Floxed Cassette Allelic Exchange Mutagenesis in Chlamydia trachomatis
Published on: January 30, 2020
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Chlamydial Lytic Exit from Host Cells Is Plasmid Regulated
Chunfu Yang1, Tregei Starr2, Lihua Song3
1Laboratory of Clinical Infectious Diseases, NIAID, NIH, Bethesda, Maryland, USA.
Mbio
|November 12, 2015
Summary
Chlamydia trachomatis exit from host cells requires the plasmid-encoded Pgp4 protein, which regulates type III secretion. Plasmid-free bacteria and pgp4 mutants are trapped intracellularly, highlighting a key virulence mechanism.
Area of Science:
- Microbiology
- Cell Biology
- Pathogenesis
Background:
- Chlamydia trachomatis is a significant human pathogen requiring intracellular replication.
- The chlamydial inclusion, a host-derived vacuole, is stabilized by F-actin late in infection.
- Chlamydial exit from host cells is a critical virulence trait, but the underlying genetic mechanisms are poorly understood.
Purpose of the Study:
- To elucidate the genetic basis of Chlamydia trachomatis exit from host cells.
- To investigate the role of the chlamydial plasmid and its genes in host cell egress.
- To define the molecular mechanisms by which Chlamydia disrupts the host actin cytoskeleton for cell exit.
Main Methods:
- Utilized plasmid-free Chlamydia trachomatis strains and deletion mutants (Δpgp1-8) lacking specific plasmid genes.
- Investigated the role of Pgp4, a transcriptional regulator, in chlamydial exit.
- Examined the impact of type III secretion system (T3S) inhibitors and actin polymerization inhibitors (latrunculin B) on chlamydial egress.
- Assessed the association of F-actin with the chlamydial inclusion in different mutant strains.
Main Results:
- Plasmid-free Chlamydia trachomatis and Δpgp4 mutants are defective in disrupting the host actin cytoskeleton and fail to exit infected cells.
- Chlamydial exit is dependent on protein synthesis and is sensitive to inhibition of the type III secretion system.
- The inability of plasmid-free and Δpgp4 organisms to lyse infected cells was rescued by latrunculin B, indicating a role for actin dynamics.
- Pgp4 regulates the expression of a chromosomal type III secretion system effector required for chlamydial exit.
Conclusions:
- The chlamydial plasmid, specifically the Pgp4 protein, is essential for mediating chlamydial exit from host cells.
- Chlamydial exit is a Pgp4-regulated process involving the type III secretion system and manipulation of the host actin cytoskeleton.
- This study defines a novel genetic mechanism for bacterial cell egress, explaining the attenuation of plasmid-free Chlamydia and its immunogenicity.
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