Rereplication in emi1-Deficient Zebrafish Embryos Occurs through a Cdh1-Mediated Pathway 英文参考文献.docVIP

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Rereplication in emi1-Deficient Zebrafish Embryos Occurs through a Cdh1-Mediated Pathway 英文参考文献.doc

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Rereplication in emi1-Deficient Zebrafish Embryos Occurs through a Cdh1-Mediated Pathway 英文参考文献

Rereplicationinemi1-DeficientZebrafishEmbryos OccursthroughaCdh1-MediatedPathway MaraE.Robu,YongZhang,JenniferRhodes* ImmuneCellDevelopmentandHostDefenseProgram,FoxChaseCancerCenter,TempleUniversityHealthSystem,Philadelphia,Pennsylvania,UnitedStatesofAmerica Abstract Disruptionof earlymitoticinhibitor 1(Emi1)interfereswithnormal cellcycleprogression andresultsin earlyembryonic lethalityinvertebrates.DuringSandG2phasestheubiquitinligasecomplexAPC/CisinhibitedbyEmi1protein,thereby enablingtheaccumulationofCyclinsAandBsotheycanregulatereplicationandpromotethetransitionfromG2phaseto mitosis,respectively.DepletionofEmi1preventsmitoticentryandcausesrereplicationandanincreaseincellsize.Inthis study, we show that the developmental and cell cycle defects caused by inactivation of zebrafish emi1 are due to inappropriateactivationofAPC/CthroughitscofactorCdh1.Inhibiting/slowingprogressionintoS-phasebydepletingCdt1, anessentialreplicationlicensingfactor,partiallyrescuedemi1deficiency-inducedrereplicationandtheincreasedcellsize. Thecellsizeeffectwasenhancedbyco-depletionofcellsurvivalregulatorp53.Thesedatasuggestthattheincreasedsizeof emi1-deficient cells is either directly or indirectly caused by the rereplication defects. Moreover, enforced expression of CyclinApartiallyablatedtherereplicatingpopulationinemi1-deficientzebrafishembryos,consistentwiththeroleofCyclin Ainoriginlicensing.ForcedexpressionofCyclinBpartiallyrestoredtheG1population,inagreementwiththeestablished roleofCyclinBinmitoticprogressionandexit.However,expressionofCyclinBalsopartiallyinhibitedrereplicationinemi1- deficient embryos, suggesting a role for Cyclin B in regulating replication in this cellular context. As Cyclin A and B are substrates for APC/C-Cdh1 - mediated degradation, andCdt1 is under control of Cyclin A, these data indicate that emi1 deficiency-induceddefectsinvivoareduetothedysregulationofanAPC/C-Cdh1molecularaxis. Citation: Robu ME, Zhang Y,RhodesJ (2012) Rereplication in emi1-Deficient