Yeast caspase 1 suppresses the burst of reactive oxygen species and maintains mitochondrial stability in Saccharomyces cerevisiae

TL;DR

This study reveals that yeast caspase 1 (Yca1) suppresses mitochondrial reactive oxygen species burst and maintains mitochondrial integrity in Saccharomyces cerevisiae, highlighting its protective role against oxidative stress.

Contribution

It demonstrates that yeast caspase 1 is involved in oxidative stress response by reducing ROS burst and preserving mitochondrial function, a novel function beyond apoptosis.

Findings

Yca1 deletion increases mitochondrial ROS during stress.

Yca1 helps maintain mitochondrial activity under oxidative conditions.

Yca1 delays mitochondrial damage during ROS burst.

Abstract

Caspases are a family of cysteine proteases that play essential roles during apoptosis, and we presume some of them may also protect the cell from oxidative stress. We found that the absence of yeast caspase 1(Yca1)in Saccharomyces cerevisiae leads to a more intense burst of mitochondrial reactive oxygen species (ROS) In addition, compared to wild type yeast cells, the ability of yca1 mutant cells to maintain mitochondrial activity is significantly reduced after either oxidative stress treatment or aging. During mitochondrial ROS burst, deletion of the yca1 gene delayed structural damage of a green fluorescent protein (GFP) reporter bound in the inner mitochondrial membrane. This work implies that yeast caspase 1 is closely connected to the oxidative stress response. We speculate that Yca1 can discriminate proteins damaged by oxidation and accelerate their hydrolysis to attenuate the ROS burst.