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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
Author(s) -
Guaragnella Nicoletta,
Passarella Salvatore,
Marra Ersilia,
Giannattasio Sergio
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.07.044
Subject(s) - yeast , programmed cell death , cytochrome c , chemistry , biochemistry , acetic acid , microbiology and biotechnology , reactive oxygen species , cytochrome , apoptosis , biology , enzyme
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.