Regulation of antibiotic tolerance in Mycobacterium abscessus by proteolytic signaling

NIH RePORTER · NIH · R21 · $241,375 · view on reporter.nih.gov ↗

Abstract

ABSTRACT: Nontuberculous mycobacteria (NTM) infections such as Mycobacterium abscessus (Mabs) are a growing health concern, particularly in older and immunocompromised patient populations, and are among the most difficult bacterial infections to eradicate. Thus, there remains a critical need to understand the mechanisms enabling Mabs to survive prolonged exposure to lethal antibiotics. The central hypothesis of this proposal is that antibiotic tolerance is a regulated process, controlled by pathways that sense discrete stresses, and transduce signals leading to a coordinated cellular response that mitigates antibiotic cytotoxicity. In our preliminary data we present the results of a Tn-Seq screen to identify genes contributing to antibiotic tolerance. We now propose to use cutting-edge proteomics to study several proteases that were identified in the Tn-Seq screen.

Key facts

NIH application ID
10953347
Project number
1R21AI185949-01
Recipient
UNIVERSITY OF CALIFORNIA AT DAVIS
Principal Investigator
Bennett Penn
Activity code
R21
Funding institute
NIH
Fiscal year
2024
Award amount
$241,375
Award type
1
Project period
2024-06-01 → 2026-04-30