# NIH grant: Regulatory mechanisms for production of infectious Chlamydia (1R01AI202117-01) — retained record

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source: [us-gov-api](https://highsignal.app/data/us-gov-api) (us-gov-api:nih-reporter)  published 2026-08-07 00:00 ingested 2026-08-10 07:25

[original source ↗](https://reporter.nih.gov/project-details/1R01AI202117-01)

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NIH grant 1R01AI202117-01: Regulatory mechanisms for production of infectious Chlamydia
Institute: {'code': 'AI', 'abbreviation': 'NIAID', 'name': 'National Institute of Allergy and Infectious Diseases', 'admin_org_id': '12500003', 'admin_funding_url': ''}. PI: Ming  Tan. Award: $760663.
Start: 2026-08-07T00:00:00.
Project Summary/Abstract
 More than 1.6 million cases of Chlamydia trachomatis infections are reported to the
CDC each year, making it the most commonly reported infectious disease in the country.
This bacterial pathogen only reproduces inside a human or other eukaryotic host cell via
an unusual developmental cycle with two specialized chlamydial forms. The RB is the
intracellular, dividing form, but it cannot infect a new host cell and must instead convert
into a transmissible form called the EB. Production of EBs is critical for completing the
Chlamydia developmental cycle and for spreading the infection to another cell, but the
mechanisms that control it are not well understood. This project will study three
regulators that each control a specific mechanism of gene regulation that is important for
EB production. In Aim 1, we will study a Chlamydia-specific transcription factor Euo to
determine how it regulates late genes that are expressed at the late stage of the
developmental cycle to mediate RB-to-EB conversion. We will test a model in which Euo
binds and represses late genes until late times when there is loss of repression because
active Euo dimers are converted into inactive monomers. In Aim 2, we will study a
second form of late gene regulation by an alternative form of RNA polymerase that uses
its σ28 subunit to recognize specific late genes. We will test our model that an anti-sigma
factor RsbW binds and sequesters σ28 until late times when RsbW releases σ28 so that
σ28 RNA polymerase can form and transcribe its target late genes. In Aim 3, we will test
a novel model which proposes that a type 3 secretion (T3S) chaperone Scc2 has a
second function as a silencer of transcription in EBs. This model provides a mechanism
for activation of chlamydial transcription in a T3S-dependent manner when an EB binds
and enters a host cell. Each of these three regulators controls a specific temporal
mechanism for regulating chlamydial gene expression and EB production, and each aim
will investigate a novel molecular switch that controls the activity of the regulator. These
critical roles of Euo, RsbW and Scc2 in regulating production of infectious chlamydiae
make them attractive therapeutic targets for novel approaches to interrupt the
intracellular Chlamydia infection and prevent transmission.
```



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