# Regulation of Pseudomonas aeruginosa Virulence Gene Expression by Temperature

> **NIH NIH R21** · EMORY UNIVERSITY · 2020 · $230,279

## Abstract

PROJECT SUMMARY.
Pathogenic microbes sense increased temperature as they transition from the external environment to the
human host. Pseudomonas aeruginosa is an important opportunistic pathogen responsible for community-
acquired and ventilator-associated pneumonia and infections after burns or corneal abrasion. In the hospital
setting, it mainly infects immunocompromised individuals and is the leading cause of chronic life-threatening
lung infections in people living with cystic fibrosis. P. aeruginosa is naturally antibiotic resistant and infections
are notoriously difficult to treat.
 Preventing the establishment of infection necessitates a better understanding of how microbes switch from
the external environment to the human host. P. aeruginosa can survive in a wide-range of environments and
temperatures, but must go through transcriptional shifts when transitioning between these environments; global
regulatory systems used during infection have been studied, but an emphasis has been on transcriptional
differences between acute and chronic infections, planktonic lifestyle to the biofilm mode of growth, and
regulatory pathways that respond to cell density (quorum-sensing) and nutrient availability. Modulation by
temperature, our focus, has been described for a number of bacterial pathogens, in addition to P. aeruginosa,
however the regulatory factors responsible have not been well studied. We propose to identify P. aeruginosa
regulators that modulate gene expression in response to variations in temperature.
 To address this, we will focus on one known virulence factor, PrpL, a lysyl-endopeptidase (also known as
protease IV, Piv, PIV, PA4175, or PA14_09900). In laboratory strains of P. aeruginosa, prpL is more highly
expressed at 22°C-28°C compared to 37°C. Preliminary Results we have generated indicate that the
temperature regulation of prpL is at the level of transcription initiation and furthermore that the known
regulators of prpL do not control the thermo-responsiveness of this gene. Here, we will identify the regulator
that controls prpL expression at different temperatures and determine whether this regulator controls the
expression of other genes. We will also address whether this temperature regulation of prpL is a conserved
trait in other strains from varied sources. We suggest that understanding the temperature regulation of
transcription of prpL will be informative not only for this important virulence factor, but may also potentially shed
light on a novel type of regulatory pathway for other thermo-regulated genes important in the establishment of
infection. These studies will lay the foundation for future R01 grant applications to further dissect the regulatory
mechanism underlying how bacteria respond to temperature, how this promotes survival in various
environments, and finally the role of this type of regulation in P. aeruginosa pathogenesis.

## Key facts

- **NIH application ID:** 9876950
- **Project number:** 5R21EY028320-02
- **Recipient organization:** EMORY UNIVERSITY
- **Principal Investigator:** Joanna B Goldberg
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $230,279
- **Award type:** 5
- **Project period:** 2019-03-01 → 2023-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9876950

## Citation

> US National Institutes of Health, RePORTER application 9876950, Regulation of Pseudomonas aeruginosa Virulence Gene Expression by Temperature (5R21EY028320-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9876950. Licensed CC0.

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