抗凋亡基因抑制酵母冷誘導的細胞凋亡及其調控機制.pdf

1、y738157論文題目[理塑一丫738176洳專：J學位論文⑧浙江大學碩士論文AbstractColdandapoptosisaretightlycorrelatedandtheresearchoncold—inducedapoptosishasbecomeoneofthemostimportantfieldsinthetransplantationmedicineareaThesignaltransductioninvolvedint

2、hecoldinducedapoptosisisanfractuous，eithermediatedormodulatedbyreactiveoxygenspecies(ROS)，Ca2，F(xiàn)e“andcold—relevantgenesinvivoHoweverlittleisknownaboutthesituationintheyeastAsyeasthasbeenextensivelycharacterizedbothbiochem

3、icallyandgeneticallywithitsgenetictractability，ithasbeenusedextensivelyasmodelsforgeneticanalysisofvariouscomplexpathwaysandprocesses，includingcelldivision，transcriptionandreceptormediatedsignaltransductionWetransformeda

4、ntiapoptoticgenesBcl2，CED9andPpBI1intotheyeasttoevaluatetheirfunctionofresistancetocoldstressTheresultsareasfonows：(1)Coldinducedapoptosisinyeastcells，moreover，yeastcellsdisplayrepresentivefeaturessuchaschromatincondensa

5、tion，DNAfragmentationandchromatinmargination(2)TheexpressionofBcl一2，CED一9andPpBI1significantlyinhibitscoldinducedapoptosisintheyeast(3)ROSandCa2actasintracellularsecondmessagertoinducecellapoptosisThepotentialmolecularme

6、chanismofcoldinducedcellapoptosisandhowBcl2，CED一9andPpBmfightsagainstcoldstessintheyeastisassociatedwiththeincreaseinintracellularROSandCa2inducedbycoldTheexpressionofPpBI1inhibitstheincreaseinintracellularC一，thusaUeviat

7、escellinjuriesinducedbyCa“(4)ColdinducedanincreaseinintracellularROS，howeveritCallnotbeinhibiteddirectlybytheexpressionofPpBl1InordertofurtherinvestigatetheroleofROSintheprocessofcold—inducedapoptosisandthemechanismofant

8、iapoptoticmembersmediatingROS，weusedwildstrainCY4andgshlmutantstrainCY8toinvestigatetheroleofPpBmmediatingROSResultsshowedthatexpressionofPpBmcouldrestorethegrowthofCY8andsignificantlyinhibitcoldinducedcellapoptosiswhena

9、ddingexogenousGSH，howeverexpressionofPpBI1couldnotrestorethegrowthofCY8andinhibitcold—inducedcellapoptosiswithoutexogenousGSHThesedatasuggestthepathwayofPpBI1againstROSstressisassociatedwithGSHdirectlyorindirectlyKeyword