Programmed Cell death occurs through different pathways in Saccharomyces cerevisiae

The unicellular budding yeastSaccharomyces cerevisiaecanundergo a programmed cell death (PCD) process which resembles mammalian apoptosis in both morphological and molecularaspects [1]. Due to the high degree of conservation of genesand pathways betweenS. cerevisiaeand higher eukaryotes, yeastis a favorite model organism to investigate how PCD occurs. By using an experimental system in which PCD is induced byacetic acid (AA-PCD), we have determined how cells die as afunction of time en route to AA-PCD and characterized theinterrelations among certain molecular processes and components [2]. Different yeast mutant cells were studied to under-stand the role of oxidative stress, cytochrome c and the metacaspase-encoding YCA1 gene in AA-PCD. We found that cell death can also occur without cytochrome c release and/orYCA1. Data show the existence of two AA-PCD pathways, one in which YCA1 acts upstream of cytochrome c release and cas-pase-like activity increase in a reactive oxygen species (ROS)-dependent manner and another in which cytochrome c releasedoes not occur and caspase-like activation occurs in a ROS-independent manner [3,4]. In these pathways mitochondriaappear to play crucial but different roles in cell death commit-ment. We aim to investigate the pivotal role of mitochondria as‘receivers, integrators and transmitters’ of death signals in PCDpathways, whose dysregulation underlies several human patholo-gies, such as neurodegeneration and cancer