Statistical analysis supports the size control mechanism of Chlamydia development.

Chlamydia is an intracellular bacterium that reproduces via an unusual developmental cycle that only occurs within a eukaryotic host cell. A replicating form of the bacterium (RB) repeatedly divides to produce about a thousand progeny, which convert in a delayed and asynchronous manner into the infe...

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Main Authors: Jinsu Kim, Christine Sütterlin, Ming Tan, German Enciso
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2025-07-01
Series:PLoS Computational Biology
Online Access:https://doi.org/10.1371/journal.pcbi.1013227
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author Jinsu Kim
Christine Sütterlin
Ming Tan
German Enciso
author_facet Jinsu Kim
Christine Sütterlin
Ming Tan
German Enciso
author_sort Jinsu Kim
collection DOAJ
description Chlamydia is an intracellular bacterium that reproduces via an unusual developmental cycle that only occurs within a eukaryotic host cell. A replicating form of the bacterium (RB) repeatedly divides to produce about a thousand progeny, which convert in a delayed and asynchronous manner into the infectious form (EB). The regulatory mechanisms that control this developmental switch are unknown, but they could potentially include extrinsic signals from the host cell or other chlamydiae, or an intrinsic signal such as chlamydial cell size. In this paper, we investigated the regulation of RB-to-EB conversion by developing and analyzing three mathematical models, each based on a different regulatory mechanism. To test these models, we derived statistical evidence from parameters, including number, size and location of RBs and EBs, obtained from experimental measurements and model fitting. All three models successfully reproduced the experimentally measured timing of RB-to-EB conversion and growth curves of the developmental forms in an infected cell. However, only the size control model, which postulates that RB size is an intrinsic signal that regulates the timing of RB-to-EB conversion, reproduced two additional statistical properties of the intracellular infection. These properties are a positive correlation between the number of RBs and EBs throughout the developmental cycle and the monotonic evolution of the coefficient of variation of EB number. This analysis thus provides support for the size control model.
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spelling doaj-art-a6a4bfd3a0cd4f5d90cba302a5a1c3552025-08-20T03:55:48ZengPublic Library of Science (PLoS)PLoS Computational Biology1553-734X1553-73582025-07-01217e101322710.1371/journal.pcbi.1013227Statistical analysis supports the size control mechanism of Chlamydia development.Jinsu KimChristine SütterlinMing TanGerman EncisoChlamydia is an intracellular bacterium that reproduces via an unusual developmental cycle that only occurs within a eukaryotic host cell. A replicating form of the bacterium (RB) repeatedly divides to produce about a thousand progeny, which convert in a delayed and asynchronous manner into the infectious form (EB). The regulatory mechanisms that control this developmental switch are unknown, but they could potentially include extrinsic signals from the host cell or other chlamydiae, or an intrinsic signal such as chlamydial cell size. In this paper, we investigated the regulation of RB-to-EB conversion by developing and analyzing three mathematical models, each based on a different regulatory mechanism. To test these models, we derived statistical evidence from parameters, including number, size and location of RBs and EBs, obtained from experimental measurements and model fitting. All three models successfully reproduced the experimentally measured timing of RB-to-EB conversion and growth curves of the developmental forms in an infected cell. However, only the size control model, which postulates that RB size is an intrinsic signal that regulates the timing of RB-to-EB conversion, reproduced two additional statistical properties of the intracellular infection. These properties are a positive correlation between the number of RBs and EBs throughout the developmental cycle and the monotonic evolution of the coefficient of variation of EB number. This analysis thus provides support for the size control model.https://doi.org/10.1371/journal.pcbi.1013227
spellingShingle Jinsu Kim
Christine Sütterlin
Ming Tan
German Enciso
Statistical analysis supports the size control mechanism of Chlamydia development.
PLoS Computational Biology
title Statistical analysis supports the size control mechanism of Chlamydia development.
title_full Statistical analysis supports the size control mechanism of Chlamydia development.
title_fullStr Statistical analysis supports the size control mechanism of Chlamydia development.
title_full_unstemmed Statistical analysis supports the size control mechanism of Chlamydia development.
title_short Statistical analysis supports the size control mechanism of Chlamydia development.
title_sort statistical analysis supports the size control mechanism of chlamydia development
url https://doi.org/10.1371/journal.pcbi.1013227
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AT christinesutterlin statisticalanalysissupportsthesizecontrolmechanismofchlamydiadevelopment
AT mingtan statisticalanalysissupportsthesizecontrolmechanismofchlamydiadevelopment
AT germanenciso statisticalanalysissupportsthesizecontrolmechanismofchlamydiadevelopment