Loss of hif-1 promotes resistance to the exogenous mitochondrial stressor ethidium bromide in Caenorhabditis elegans

• DOI: 10.1186/s12860-016-0112-x
• Publication Date: 2016-09-12T21:01:52Z
• Authors: Muntasir Kamal; Dayana R. D’Amora; Terrance J. Kubis...
• Keywords: Ethidium bromide

Mitochondrial dysfunction is one of the leading causes neurological disorders in humans. perturbations lead to adaptive mechanisms that include HIF-1 stabilization, though consequences increased levels following mitochondrial stress remain poorly understood. Using Caenorhabditis elegans, we show a hif-1 loss-of-function mutation confers resistance towards toxin ethidium bromide (EtBr) and suppresses EtBr-induced production ROS. In mammals, PD-related gene DJ-1 known act as redox sensor confer protection against antioxidants inhibitors. A deletion mutant C. elegans homolog djr-1.1 also showed EtBr. Furthermore, our data implicates p38 MAP kinase an indispensable factor for survival both mutants. We propose activates pathways are antagonistic conferring EtBr toxicity blocking activity may promote cells with compromised function.