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The effect of penicillin on Chlamydia trachomatis DNA replication

The effect of penicillin on Chlamydia trachomatis DNA replication
The effect of penicillin on Chlamydia trachomatis DNA replication
Chlamydia trachomatis L2 was used to infect BGMK cells at an m.o.i. of 1.0, and the developmental cycle was followed by transmission electron microscopy and quantitative PCR (QPCR) for both chromosomal and plasmid DNA. Samples were taken at sequential 6 h time points. Subsequent analysis by QPCR showed that there was an initial slow replication period (0-18 h), followed by a rapid phase (18-36 h) coinciding with exponential division when the DNA doubling time was 4.6 h. Chromosomal DNA was amplified 100-200-fold corresponding to 7-8 generations for the complete developmental cycle. Penicillin (10 and 100 units ml(-1)) was added to cultures at 20 h post-infection (p.i.). This blocked binary fission and also prevented reticulate body (RB) to elementary body transition. However, exposure to penicillin did not prevent chromosomal or plasmid DNA replication. After a short lag period, following the addition of penicillin, chlamydial chromosomal DNA replication resumed at the same rate as in control C. trachomatis-infected cells. C. trachomatis-infected host cells exposed to penicillin did not lyse, but instead harboured large, aberrant RBs in massive inclusions that completely filled the cell cytoplasm. In these RBs, the DNA continued to replicate well beyond the end of the normal developmental cycle. At 60 h p.i. each aberrant RB contained a minimum of 16 chromosomal copies.
1350-0872
2573-2578
Lambden, Paul R.
4fcd536e-2d9a-4366-97c6-386e6b005698
Pickett, Mark A.
4b358cb6-2f2e-4691-a314-0e80df48eadb
Clarke, Ian N.
ff6c9324-3547-4039-bb2c-10c0b3327a8b
Lambden, Paul R.
4fcd536e-2d9a-4366-97c6-386e6b005698
Pickett, Mark A.
4b358cb6-2f2e-4691-a314-0e80df48eadb
Clarke, Ian N.
ff6c9324-3547-4039-bb2c-10c0b3327a8b

Lambden, Paul R., Pickett, Mark A. and Clarke, Ian N. (2006) The effect of penicillin on Chlamydia trachomatis DNA replication. Microbiology, 152 (9), 2573-2578. (doi:10.1099/mic.0.29032-0).

Record type: Article

Abstract

Chlamydia trachomatis L2 was used to infect BGMK cells at an m.o.i. of 1.0, and the developmental cycle was followed by transmission electron microscopy and quantitative PCR (QPCR) for both chromosomal and plasmid DNA. Samples were taken at sequential 6 h time points. Subsequent analysis by QPCR showed that there was an initial slow replication period (0-18 h), followed by a rapid phase (18-36 h) coinciding with exponential division when the DNA doubling time was 4.6 h. Chromosomal DNA was amplified 100-200-fold corresponding to 7-8 generations for the complete developmental cycle. Penicillin (10 and 100 units ml(-1)) was added to cultures at 20 h post-infection (p.i.). This blocked binary fission and also prevented reticulate body (RB) to elementary body transition. However, exposure to penicillin did not prevent chromosomal or plasmid DNA replication. After a short lag period, following the addition of penicillin, chlamydial chromosomal DNA replication resumed at the same rate as in control C. trachomatis-infected cells. C. trachomatis-infected host cells exposed to penicillin did not lyse, but instead harboured large, aberrant RBs in massive inclusions that completely filled the cell cytoplasm. In these RBs, the DNA continued to replicate well beyond the end of the normal developmental cycle. At 60 h p.i. each aberrant RB contained a minimum of 16 chromosomal copies.

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Published date: September 2006

Identifiers

Local EPrints ID: 59364
URI: http://eprints.soton.ac.uk/id/eprint/59364
ISSN: 1350-0872
PURE UUID: e1fdfd6f-164d-4ed0-885d-47d821b26a6d
ORCID for Ian N. Clarke: ORCID iD orcid.org/0000-0002-4938-1620

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Date deposited: 03 Sep 2008
Last modified: 16 Mar 2024 02:33

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Contributors

Author: Paul R. Lambden
Author: Mark A. Pickett
Author: Ian N. Clarke ORCID iD

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