THE JOURNAL OF CELL BIOLOGY
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apoptosis inyeast Viral killertoxinsinducecaspase-mediated Weiler andSchmitt,2003),the (Martinac etal.,1990;Weiler2002;Breinig function byformingcation-specificplasmamembranepores zygocin, Introduction proteins ofthesecreted double- fied sofar,whichareallencodedbycytoplasmicpersisting three differentkillertoxins(K1,K2,andK28)havebeenidenti- and secretedby inhibitors ofproteinsynthesislikediphtheriatoxinproduced apoptosis (WeinrauchandZychlinsky, 1999). cerevisiae Wickner, 1996).Althoughmostviralkillertoxins,likethe 1997; SchmittandBreinig,2002).In receptor- protein toxinthatkillssusceptibleyeastcellsinatwo-step typically associatedwiththesecretionofaproteinorglyco- spread phenomenonamongagreatvarietyofyeastgeneraandis The productionofcytotoxicproteins(killertoxins)isawide- concentrations preventtheoccurrenceofanapoptoticcell killing mechanisms.Incontrast,hightoxin their primary significantlyin response, althoughallthreetoxinsdiffer (K1, K28, andzygocin)induceanapoptoticyeastcell that moderatedosesofthreevirallyencodedkillertoxins (ROS) arekeyregulatorsofthisprocess.Here,weshow 2 1 Jochen Reiter, pore-forming toxinslike the G1/Sboundary(Schmittetal.,1996;Eisfeld2000). secretion pathwayinreverse,andinducesacellcyclearrest at susceptible cellsbyreceptor-mediatedendocytosis,travelsthe http://www.jcb.org/cgi/doi/10.1083/jcb.200408071 The JournalofCell Biology © blue agarplates;PS,phosphatidylserine; ROS,reactiveoxygenspecies. Abbreviations usedinthispaper:DHR, dihydrorhodamine;MBA,methylene Correspondence toManfredJ.Schmitt: [email protected]
Applied MolecularBiology, UniversityoftheSaarland,D-66041Saarbrücken,Germany Institute ofMolecularBiosciences,Karl-FranzensUniversity, A-8010Graz, Austria
TeRceelrUiest rs $8.00 TheRockefellerUniversity Press caspase (Yca1p)andcellularreactiveoxygenspecies factors suchasH n yeast,apoptoticcelldeathcanbetriggeredbyvarious
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2 , Vol. 31,2005353–358 168,No.3,January
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