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SigE: A master regulator of Mycobacterium tuberculosis
Riccardo Manganelli1, Laura Cioetto-Mazzabò1, Greta Segafreddo1
1Department of Molecular Medicine, University of Padova, Padova, Italy.
Frontiers in Microbiology
|March 24, 2023
Summary
The Extracellular function (ECF) sigma factor SigE in Mycobacterium tuberculosis is crucial for virulence and stress response. Its complex regulation contributes to bacterial persistence and drug resistance.
Area of Science:
- Microbiology
- Molecular Biology
- Bacterial Pathogenesis
Background:
- The Extracellular function (ECF) sigma factor SigE is a key regulator in *Mycobacterium tuberculosis*.
- SigE plays a vital role in virulence, blocking phagosome maturation, and responding to environmental stresses like oxidative and acidic conditions.
- Its expression and activity are tightly controlled by multiple regulatory layers, including other sigma factors, a two-component system, and post-translational modifications.
Purpose of the Study:
- To elucidate the intricate regulatory network governing SigE activity in *Mycobacterium tuberculosis*.
- To understand SigE's role in bacterial adaptation to environmental challenges and its contribution to virulence.
- To explore the link between SigE regulation and the development of drug-tolerant persister cells.
Main Methods:
- Analysis of SigE's regulatory network, involving interactions with sigma factors (SigA, SigH), the MprAB two-component system, and the anti-sigma factor RseA.
- Investigation of post-translational regulation of SigE, including its response to redox potential and PknB-mediated phosphorylation.
- Examination of SigE's direct targets, such as SigB, ClgR, and MprAB, and genes involved in surface remodeling.
- Study of SigE's interaction with PhoP under acidic pH conditions.
Main Results:
- SigE is regulated by multiple sigma factors and the MprAB system, and post-translationally by RseA and PknB.
- SigE controls genes essential for surface integrity and other regulatory pathways.
- SigE interacts with PhoP to activate specific genes under acidic stress.
- The complex regulatory network suggests a bistable switch mechanism driving bacterial population heterogeneity.
Conclusions:
- SigE's multifaceted regulation is critical for *Mycobacterium tuberculosis* survival and pathogenesis.
- The regulatory network's complexity supports the development of heterogeneous bacterial populations, including persister cells.
- SigE's role in persistence highlights its potential as a therapeutic target for eradicating persistent infections.
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