title: Apoptosis in yeast: triggers, pathways, subroutines.
abstract: A cell's decision to die is controlled by a sophisticated network whose deregulation contributes to the pathogenesis of multiple diseases including neoplastic and neurodegenerative disorders. The finding, more than a decade ago, that baker's yeast (Saccharomyces cerevisiae) can undergo apoptosis uncovered the possibility to investigate this mode of programmed cell death (PCD) in a model organism that combines both technical advantages and a eukaryotic 'cell room.' Since then, numerous exogenous and endogenous triggers have been found to induce yeast apoptosis and multiple yeast orthologs of crucial metazoan apoptotic regulators have been identified and characterized at the molecular level. Such apoptosis-relevant orthologs include proteases such as the yeast caspase as well as several mitochondrial and nuclear proteins that contribute to the execution of apoptosis in a caspase-independent manner. Additionally, physiological scenarios such as aging and failed mating have been discovered to trigger apoptosis in yeast, providing a teleological interpretation of PCD affecting a unicellular organism. Due to its methodological and logistic simplicity, yeast constitutes an ideal model organism that is efficiently helping to decipher the cell death regulatory network of higher organisms, including the switches between apoptotic, autophagic, and necrotic pathways of cellular catabolism. Here, we provide an overview of the current knowledge about the apoptotic subroutine of yeast PCD and its regulation.
authors.affiliation: Institute of Molecular Biosciences, Karl-Franzens University, Graz, Austria.
authors.forename: D
authors.initials: D
authors.lastname: Carmona-Gutierrez
authors.forename: T
authors.initials: T
authors.lastname: Eisenberg
authors.forename: S
authors.initials: S
authors.lastname: Büttner
authors.forename: C
authors.initials: C
authors.lastname: Meisinger
authors.forename: G
authors.initials: G
authors.lastname: Kroemer
authors.forename: F
authors.initials: F
authors.lastname: Madeo
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D008247:Lysosomes / Q000378:metabolism; D008954:Models, Biological; D020675:Peroxisomes / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000166:cytology* / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*