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System for Efficacy and Cytotoxicity Screening of Inhibitors Targeting Intracellular Mycobacterium tuberculosis
Published on: April 5, 2017
Mycobacterium tuberculosis ftsH expression in response to stress and viability
Manjot Kiran1, Ashwini Chauhan, Renata Dziedzic
1Biochemistry Department, The University of Texas Health Science Center at Tyler, 11937 US Hwy 271, Tyler, TX 75708, USA.
Tuberculosis (Edinburgh, Scotland)
|December 17, 2009
Summary
Mycobacterium tuberculosis FtsH protease is upregulated during stress, enhancing resistance to reactive oxygen intermediates. Overexpression of FtsH delays growth and reduces FtsZ levels, suggesting a role in stress response and cell division regulation.
Area of Science:
- Microbiology
- Molecular Biology
- Protease Function
Background:
- FtsH is a crucial membrane-bound protease involved in protein degradation.
- Mycobacterium tuberculosis (Mtb) pathogenesis involves complex stress response mechanisms.
Purpose of the Study:
- To investigate the role of Mtb FtsH in stress response.
- To determine the effect of FtsH expression on Mtb viability and FtsZ levels.
Main Methods:
- Gene expression analysis of ftsH under various stress conditions.
- Phenotypic analysis of Mtb strains with altered ftsH expression.
- Quantification of FtsZ protein levels.
Main Results:
- Mtb ftsH expression is upregulated by reactive oxygen and nitrogen intermediates (ROI/RNI) and during macrophage infection.
- Overexpression of ftsH confers resistance to ROI but leads to delayed growth and reduced viability.
- FtsH overexpression results in decreased intracellular FtsZ levels.
Conclusions:
- Mtb FtsH acts as a stress-response protein, aiding in coping with ROI.
- FtsH may play a regulatory role in FtsZ levels, impacting cell division in Mtb.
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