Disruption of Vps4 and JNK Function in Drosophila Causes Tumour Growth 英文参考文献.docVIP

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Disruption of Vps4 and JNK Function in Drosophila Causes Tumour Growth 英文参考文献.doc

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Disruption of Vps4 and JNK Function in Drosophila Causes Tumour Growth 英文参考文献

DisruptionofVps4andJNKFunctioninDrosophila CausesTumourGrowth LinaM.Rodahl1,KaisaHaglund1,CatherineSem-Jacobsen1,FranzWendler2,Jean-PaulVincent2 ,Karine Lindmo1,TorErikRusten1,HaraldStenmark1* 1Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo and Institute for Cancer Research, the Norwegian Radium Hospital, Rikshospitalet University Hospital,Montebello,Oslo,Norway,2MRCNationalInstituteofMedicalResearch,MillHill,London,UnitedKingdom Abstract SeveralregulatorsofendocytictraffickinghaverecentlybeenidentifiedastumoursuppressorsinDrosophila.Theseinclude componentsoftheendosomalsortingcomplexrequiredfortransport(ESCRT)machinery.DisruptionofsubunitsofESCRT-I and –II leads to cell-autonomous endosomal accumulation of ubiquitinated receptors, loss of apicobasal polarity and epithelialintegrity,andincreasedcelldeath.HerewereportthatdisruptionoftheATPasedVps4,themostdownstream componentoftheESCRTmachinery,causesthesamearrayofcellularphenotypes.Wefindthatlossofepithelialintegrity andincreasedapoptosis,butnotlossofcellpolarity,requiretheactivationofJNKsignalling.AbrogationofJNKsignalling preventsapoptosisindVps4deficientcells.IndeeddoubledeficiencyindVps4andJNKsignallingleadstotheformationof neoplastic tumours. We conclude that dvps4 is a tumour suppressor in Drosophila and that JNK is central to the cell- autonomousphenotypesofESCRT-deficientcells. Citation: Rodahl LM, Haglund K, Sem-Jacobsen C, Wendler F, Vincent J-P, et al. (2009) Disruption of Vps4 and JNK Function in Drosophila Causes Tumour Growth.PLoSONE4(2):e4354.doi:10.1371/journal.pone.0004354 Editor:MikhailV.Blagosklonny,OrdwayResearchInstitute,UnitedStatesofAmerica ReceivedDecember17,2008;AcceptedDecember25,2008;PublishedFebruary4,2009 Copyright: ? 2009 Rodahl et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:K