# How chlamydia generates cytoskeletal scaffolds and their role during infection

> **NIH NIH R01** · THOMAS JEFFERSON UNIVERSITY · 2020 · $390,000

## Abstract

PROJECT SUMMARY
 The intracellular bacterium Chlamydia trachomatis is a major cause of sexually transmitted disease and
infectious blindness with over 150 million cases worldwide. Once inside the cell, Chlamydia replicates in a
parasitic compartment called an inclusion, which is encased in actin and microtubules scaffolds. Actin scaffolds
provide inclusion integrity, while microtubules (MT) control Golgi repositioning around the inclusion; both of
these events are necessary for Chlamydia survival. Despite the importance of cytoskeleton rearrangements for
Chlamydia's life cycle, a major gap exists regarding the molecular mechanism used by this bacterium to control
the cytoskeleton. Furthermore, Chlamydia redirects multiple host organelles to its inclusion during infection.
Remarkably, which cytoskeleton scaffold controls this repositioning remains to be identified. Of note, this is a
key question as organelle repositioning enhances lipid and nutrient transfer to the inclusion, which then
contribute to the growth of the inclusion membrane and the replication of the bacteria.
 Using recently established genetically-modified Chlamydia strains, we propose to study the role of novel
chlamydial proteins (also called effectors) in the formation of cytoskeleton scaffolds. These effectors have been
shown to interact with cytoskeleton proteins in transfected cells and are, therefore, ideal candidates to
manipulate cytoskeleton during infection. Specifically, we will test the hypotheses that 1) Chlamydia builds a
molecular platform composed of multiple bacterial and host proteins to coordinate actin and MT
rearrangements during infection, and 2) as cytoskeletal scaffolds are woven around the inclusion,
various organelles are then diverted towards the inclusion to promote Chlamydia's survival.
 Ultimately, this information will have a broad scientific impact as (i) It will establish the detailed mechanism
used by Chlamydia to repurpose two major cytoskeleton elements for its own benefit and will provide a better
understanding of disease progression; (ii) Cytoskeleton rearrangement plays a critical role in cancer
development. Since Chlamydia infection has been associated with an increased risk of cancer, understanding
how the cytoskeleton is reorganized during infection will shed light on this phenomenon; (iii) Understanding the
mechanism that controls cytoskeleton dynamics will provide critical insight into fundamental biological
pathways, and (iv) Finally, a detailed characterization of the proteins that control cytoskeletal dynamics during
Chlamydia infection will provide fundamental tools to screen for the presence of similar effectors in other major
human pathogens that also manipulate host cytoskeleton, in particular Salmonella, thus opening new avenues
of research in molecular pathogenesis.

## Key facts

- **NIH application ID:** 9852592
- **Project number:** 5R01AI144081-02
- **Recipient organization:** THOMAS JEFFERSON UNIVERSITY
- **Principal Investigator:** FABIENNE Michelle PAUMET
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $390,000
- **Award type:** 5
- **Project period:** 2019-01-22 → 2023-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9852592

## Citation

> US National Institutes of Health, RePORTER application 9852592, How chlamydia generates cytoskeletal scaffolds and their role during infection (5R01AI144081-02). Retrieved via AI Analytics 2026-06-11 from https://api.ai-analytics.org/grant/nih/9852592. Licensed CC0.

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