Knock‐out of metacaspase and/or cytochrome c results in the activation of a ROS‐independent acetic acid‐induced programmed cell death pathway in yeast

To gain further insight into yeast acetic acid‐induced programmed cell death (AA‐PCD) we analyzed the effects of the antioxidant N ‐acetyl‐ l ‐cysteine (NAC) on cell viability, hydrogen peroxide (H 2 O 2 ) production, DNA fragmentation, cytochrome c (cyt c ) release and caspase‐like activation in wild type (wt) and metacaspase and/or cyt c ‐lacking cells. We found that NAC prevents AA‐PCD in wt cells, by scavenging H 2 O 2 and by inhibiting both cyt c release and caspase‐like activation. This shows the occurrence of a reactive oxygen species (ROS)‐dependent AA‐PCD. Contrarily no NAC dependent change in AA‐PCD of mutant cells was detectable, showing that a ROS‐independent AA‐PCD can also occur.