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Updated: Jan 27, 2026

Spatiotemporal Control of Protein Activity through Optogenetic Allosteric Regulation
Published on: October 4, 2024
Spatiotemporal control of FlgZ activity impacts Pseudomonas aeruginosa flagellar motility
Sarina Bense1, Sebastian Bruchmann1, Anika Steffen2
1Department of Molecular Bacteriology, Helmholtz Center for Infection Research, Inhoffenstr. 7, Braunschweig, 38124, Germany.
Abstract:
The c-di-GMP-binding effector protein FlgZ has been demonstrated to control motility in the opportunistic pathogen Pseudomonas aeruginosa and it was suggested that c-di-GMP-bound FlgZ impedes motility via its interaction with the MotCD stator. To further understand how motility is downregulated in P. aeruginosa and to elucidate the general control mechanisms operating during bacterial growth, we examined the spatiotemporal activity of FlgZ. We re-annotated the P. aeruginosaflgZ open reading frame and demonstrated that FlgZ-mediated downregulation of motility is fine-tuned via three independent mechanisms. First, we found that flgZ gene is transcribed independently from flgMN in stationary growth phase to increase FlgZ protein levels in the cell. Second, FlgZ localizes to the cell pole upon c-di-GMP binding and third, we describe that FimV, a cell pole anchor protein, is involved in increasing the polar localized c-di-GMP bound FlgZ to inhibit both, swimming and swarming motility. Our results shed light on the complex dynamics and spatiotemporal control of c-di-GMP-dependent bacterial motility phenotypes and on how the polar anchor protein FimV, the motor brake FlgZ and the stator proteins function to repress flagella-driven swimming and swarming motility.
Insights
The Pseudomonas aeruginosa FlgZ protein fine-tunes bacterial motility through three mechanisms. FlgZ levels increase during stationary phase, it localizes to the cell pole, and FimV enhances its inhibitory effect on motility.
Area of Science:
- Microbiology
- Bacterial Physiology
- Molecular Biology
Background:
- The opportunistic pathogen Pseudomonas aeruginosa relies on motility for infection.
- The cyclic diguanylate (c-di-GMP) signaling molecule regulates various bacterial behaviors, including motility.
- FlgZ is a known effector protein that binds c-di-GMP and influences motility in P. aeruginosa.
Purpose of the Study:
- To investigate the spatiotemporal activity of FlgZ in P. aeruginosa.
- To elucidate the mechanisms by which FlgZ downregulates bacterial motility.
- To understand the role of FimV in FlgZ-mediated motility control.
Main Methods:
- Re-annotation of the P. aeruginosa flgZ open reading frame.
- Analysis of flgZ gene transcription during different growth phases.
- Microscopy to determine FlgZ localization upon c-di-GMP binding.
- Investigation of FimV's role in FlgZ function.
Main Results:
- FlgZ-mediated motility downregulation is controlled by three independent mechanisms.
- The flgZ gene is transcribed independently during stationary phase, increasing FlgZ protein levels.
- FlgZ localizes to the cell pole after binding c-di-GMP.
- FimV enhances the polar localization of c-di-GMP-bound FlgZ, inhibiting swimming and swarming motility.
Conclusions:
- FlgZ plays a crucial role in fine-tuning bacterial motility in P. aeruginosa.
- Motility regulation involves complex spatiotemporal control of c-di-GMP-dependent pathways.
- The interplay between FimV, FlgZ, and stator proteins represses flagellar-driven motility.
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