A high-frequency single nucleotide polymorphism in the MtrB sensor kinase in clinical strains of Mycobacterium tuberculosis alters its biochemical and physiological properties

The DNA polymorphisms found in clinical strains of Mycobacterium tuberculosis drive altered physiology, virulence, and pathogenesis in them. Although the lineages of these clinical strains can be traced back to common ancestor/s, there exists a plethora of difference between them, compared to those...

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Bibliographic Details
Published in:PloS one 2021-09, Vol.16 (9), p.e0256664-e0256664
Main Authors: Waturuocha, Uchenna Watson, P. J., Athira, Singh, Krishna Kumar, Malhotra, Vandana, Krishna, M. S, Saini, Deepak Kumar
Format: Article
Language:English
Subjects:
Analysis
Biology and Life Sciences
Cell division
Cell size
Cloning
Deoxyribonucleic acid
Diagnosis
DNA
Drug resistance
E coli
Gene expression
Genetic aspects
Kinases
Mutation
Mycobacterium tuberculosis
Nucleotides
Pathogenesis
Pathogens
Phosphorylation
Physiology
Plasmids
Polymorphism
Proteins
Research and Analysis Methods
Sensors
Signal transduction
Single nucleotide polymorphisms
Single-nucleotide polymorphism
Strains (organisms)
Tuberculosis
Virulence
Zoology
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Summary:The DNA polymorphisms found in clinical strains of Mycobacterium tuberculosis drive altered physiology, virulence, and pathogenesis in them. Although the lineages of these clinical strains can be traced back to common ancestor/s, there exists a plethora of difference between them, compared to those that have evolved in the laboratory. We identify a mutation present in ~80% of clinical strains, which maps in the HATPase domain of the sensor kinase MtrB and alters kinase and phosphatase activities, and affects its physiological role. The changes conferred by the mutation were probed by in-vitro biochemical assays which revealed changes in signaling properties of the sensor kinase. These changes also affect bacterial cell division rates, size and membrane properties. The study highlights the impact of DNA polymorphisms on the pathophysiology of clinical strains and provides insights into underlying mechanisms that drive signal transduction in pathogenic bacteria.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0256664