The evolutionarily conserved ESRE stress response network is activated by ROS and mitochondrial damage.

ABSTRACT:

Background

Mitochondrial dysfunction causes or contributes to a wide variety of pathologies, including neurodegenerative diseases, cancer, metabolic diseases, and aging. Cells actively surveil a number of mitochondrial readouts to ensure that cellular homeostasis is maintained.

Results

In this article, we characterize the role of the ethanol and stress response element (ESRE) pathway in mitochondrial surveillance and show that it is robustly activated when the concentration of reactive oxygen species (ROS) in the cell increases. While experiments were mostly performed in Caenorhabditis elegans, we observed similar gene activation profile in human cell lines. The linear relationship between ROS and ESRE activation differentiates ESRE from known mitochondrial surveillance path

SUBMITTER: Tjahjono E 

PROVIDER: S-EPMC7322875 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature