# Polarized Chlamydial Cell Division in the Absence of FtsZ

> **NIH NIH R35** · UNIVERSITY OF NEBRASKA MEDICAL CENTER · 2021 · $320,528

## Abstract

Project Summary: Polarized Chlamydial Cell Division in the Absence of FtsZ
 Chlamydia is an obligate intracellular bacterial pathogen that causes a range of serious diseases in
humans. In developed countries, Chlamydia trachomatis is the primary cause of bacterial sexually
transmitted infections (STI) whereas Chlamydia pneumoniae causes community-acquired respiratory
infections. In developing countries, C. trachomatis is not only a significant cause of STI, it is also responsible
for the primary cause of infectious preventable blindness, trachoma. The major concern of chlamydial
infections is that they are often asymptomatic and undiagnosed, which can lead to chronic sequelae. These
include pelvic inflammatory disease, tubal factor infertility, and reactive arthritis for C. trachomatis and
possibly atherosclerosis and adult onset asthma for C. pneumoniae. Consequently, chlamydial diseases
remain a significant burden on health care systems around the world.
 In adapting to obligate intracellular growth, Chlamydia has significantly reduced its genome size and
eliminated genes from various pathways as it relies on the host cell for its metabolic needs. This is a
common trait amongst bacteria that evolve to obligate intracellular growth. However, Chlamydia has also
lost genes that are considered essential in other bacteria. This proposal outlines a series of studies to
investigate the essential process of chlamydial cell division. Chlamydia lacks the gene ftsZ, which encodes
the bacterial tubulin-like homolog that is critical for organizing the cell division machinery at the site of
division. Thus, how Chlamydia divides is an intriguing microbiological question. We have previously
proposed that Chlamydia has substituted the bacterial actin-like homolog MreB for the function of FtsZ. This
is unusual for many reasons, one of which is that MreB is important in imparting the rod shape to certain
types of bacteria such as E. coli. Chlamydia is a round, coccoid bacterium yet encodes multiple rod-shape
determining proteins. Recent evidence from our lab and others suggests that Chlamydia uses these proteins
for cell division. Yet, the assumption has been that Chlamydia still utilizes the classic binary fission
mechanism to separate daughter cells. Rather, new data from our labs have revealed that Chlamydia uses a
polarized budding mechanism similar to yeast to accomplish division. Budding is rare in bacteria, and we
intend to use Chlamydia as a model system to understand how budding occurs. We propose a series of
experiments to understand the role of bacterial cytoskeletal proteins in bacterial budding as well as how they
are regulated and with what other proteins they interact. Because budding is rare, any unique targets
represent ideal candidates for anti-chlamydial antibiotic development that would have limited effects on
normal flora.

## Key facts

- **NIH application ID:** 10249151
- **Project number:** 5R35GM124798-05
- **Recipient organization:** UNIVERSITY OF NEBRASKA MEDICAL CENTER
- **Principal Investigator:** Scot P Ouellette
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $320,528
- **Award type:** 5
- **Project period:** 2017-09-01 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10249151

## Citation

> US National Institutes of Health, RePORTER application 10249151, Polarized Chlamydial Cell Division in the Absence of FtsZ (5R35GM124798-05). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10249151. Licensed CC0.

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