About the project
The stress adaptation of Mycobacterium tuberculosis, the causative agent of tuberculosis, is a crucial aspect of its persistence within the host. Toxin-antitoxin (TA) systems have emerged as important players in the ability of M. tuberculosis to survive and persist under stressful conditions. These TA systems consist of a toxin, which has a detrimental effect on bacterial cells, and its cognate antitoxin, which neutralises the toxin's activity. In the context of M. tuberculosis, these TA systems contribute to the bacterium's ability to endure various stressors, such as nutrient deprivation, immune responses, and exposure to antibiotics. By entering a reversible state of dormancy, known as persistence, M. tuberculosis can withstand adverse conditions and evade the host immune system. TA systems are involved in regulating this switch to persistence and are crucial for the survival and long-term persistence of M. tuberculosis within host tissues. Understanding the mechanisms underlying stress adaptation and the role of TA systems in M. tuberculosis persistence can offer valuable insights into developing novel therapeutic strategies to combat tuberculosis, including targeting these systems to enhance the effectiveness of existing drugs and prevent the emergence of drug-resistant strains.
Funding
This work is funded by the School of Life Sciences (University of Westminster) Research Startup Fund.
Contact
For further information contact the Principal Investigator Dr. Beth Sawyer at [email protected].