說明成果講稿2013abstract book the1st annual symposium for research oriented elite program

THE1STANNUALSYMPOSIUMFORRESEARCHORIENTEDELITEPROGRAMKeynoteMolecularMechanismsofChromosomeHongtaoYu*(UniversityofTexasSouthwesternMedicalCenter,UnitedStates)Accuratechromosomesegregationrequiresthecoordinationbetweenthedissolutionofsister-chromatidcohesionandtheestablishmentofproperkinetochore–microtubuleattaent.Duringmitosis,sister-chromatidcohesionatcentromeresenablesthebi-orientationofandtensionacrosssisterkinetochores.Wehaveshownthecomplexbetweenshugoshinandproteinphosphatase2A(Sgo1–PP2A)localizestocentromeresinmitosis,bindstocohesininareactionrequiringCdk-dependentphosphorylationofSgo1,dephosphorylatescohesin-boundsororin,andprotectsacentromericpoolofcohesinfrommitotickinasesandthecohesininhibitorWapl.ThecentromericlocalizationofSgo1requireshistoneH2Aphosphorylation(pH2A)bythekinaseBub1.CohesinandpH2AspecifytwodistinctpoolsofSgo1–PP2Aatinnercentromeresandkinetochores,respectively.KinetochoretensiontriggersSgo1dephosphorylationandredistributesSgo1frominnercentromerestokinetochores.Cleavageofcentromericcohesinbyseparaseallowssisterchromatidsconnectedtomicrotubulesfromopposingpolestobeevenlypartitionedintodaughtercells. pleteSgo1redistributioncauseschromosomenondisjunction.Therefore,theBub1-mediatedpH2Amarkinstallsatension-sensitive,Sgo1-basedmolecularswitchforchromosomesegregation.、Keynote sticity:FromSynapsetoMu-mingPoo*(InstituteofNeuroscience,AcademyofSciences,)Thecognitivefunctionsofthebrain,suchaslearningandmemory,dependontheabilityofneuralcircuitstochangetheirpropertiesofManyoftheseuse-dependentchanges(“sticity”)occuratsynapses,wheresignalsaretransmittedbetweennervecells(neurons).Dependingonthepatternofneuronalactivities,repetitivesynaptictransmissioncouldcauselong-termpotentiation(LTP)orlong-termdepression()ofthesynapseinitsefficacyforfuturetransmission.Iwillsummarizeourstudiesonhowthetimingofneuronalactivities(es)inthepre-andpost-synapticneuronsdetermineswhetherasynapseundergoesLTPor,aphenomenonknownas“eTiming-Dependentsticity”(STDP),andhowSTDPmayprovidethemechanismforcodingandstoringtheinformationonthetemporalsequenceandintervalofsensorysignals,twokeyelementsofepisodicmemory.Iwillalsodiscussingeneraltheideathatneuralsticityisthemainfactorthatshapesthedevelopmentofneuralcircuits,andthatneuralsticityoffersthepotentialforfunctionalrecoveryfrominjuriesanddiseasesoftheadultbrain.Finally,toarguethathighercognitivefunctionsinhumanssuchself-awarenessmayoriginatefromexperience-dependentneuralsticity,Iwillpresentourrecentfindingsshowingthatmirrorself-recognition,acognitivefunctionknowntobelimitedonlytohumansandgreatapes,couldbeacquiredbyrhesusmonkeysfollowingtrainingforvisual-somatosensoryassociation.SEPTEMBER

SESSION e KeynoteLectureDr.HongtaoYu S1:DNAandHistoneStructure PosterSession1(OddNumbers) S2:CellBiology Group S3:nt S4:MetabolismandStressResponse S5:SyntheticBiology PosterSession2(EvenNumbers) InformaltalkwithDr.YuandDr.Poo GameTimeSEPTEMBER KeynoteLectureDr.Mu-mingPoo Presentationof ConcludingRemarksandShuttlebusheadingtotheholeavesat7:00pm,Sep.20thfromthegateoftheNewLifeScienceShuttlebusheadingbacktoschoolleavesat10:30am,Sep.22ndfromthereceptionofthehoPROGRAMSATURDAY,SEPTEMBER21, e KeynoteDr.HongtaoMolecularmechanismsofchromosome S1:DNAandHistoneXiaoweiHistonechaperonespt16regulatessir-mediatedepigeneticsilencinginSaccharomycescerevisiaeMoSinglenucleotidepolymorphismrelatedDnasehypersensitivitysiteSinglenucleotidepolymorphismrelatedDnasehypersensitivitysiteandal tionusingCRISPR-Cas9system PosterSession1(Odd S2:CellXinAna3isanovelconservedproteinrequiredforcentrioleduplicationorintegrityAnzhimir-28*regulationinbcellXiangyuIdentificationofdownstreameffectorsofRIPK3-MLKLdependentnecrosisbynon-naturalaminoacidphotocrosslinker Group S3:ntYanNovelysissystemfordynamicrootAnRanAsmallmoleculedisturbsrootdevelopmentinArabidopsisYaoIdentificationofproteinsassociatedwithEin2–thekeyproteininvolvedinethylenesignalingpathway Coffee S4:MetabolismandStressTianMrap2isnotregulatedtranscriptionallybyenergystate,butAgrpSiyangMeasurementofadrenalactivityinfivecaptiveprimateZidongSpatialdistributiondynamicsofp53inresponseto Coffee S5:SyntheticWeiyueEngineeringmicrobialPuZheng,ShuaixingHe,HuanWang,HaoranAromaticsbusted：Acomprehensiveandtativedetectionfor PosterSession2(Even InformaltalkwithDr.YuandDr. GameSUNDAY,SEPTEMBER22, KeynoteDr.Mu-ming sticity:Fromsynapseto Presentationof ConcludingRemarksand CheckingStudentSession:DNAandHistoneHistoneChaperoneSpt16RegulatesSir-MediatedEpigeneticSilencinginSaccharomycesXiaoweiYan(嚴(yán)筱溦)*(CollegeofLifeSciences,PekingUniversity,),QingLi(CollegeofLifeSciences,PekingUniversity,)Epigeneticinheritanceofthesilentchromatin,alsotermedasheterochromatin,iscriticalforthemaintenanceofgeneexpressionpatternsandgenomeintegrity.InSaccharomycescerevisiae,theformationandspreadingoftheheterochromatinattheHMmatinglociaredependentonthestepwisepolymerizationoffoursilentinformationregulatorproteins(Sir1p,Sir2p,Sir3pandSir4p).However,howtheSirproteinsarerecruitedduringtheassemblyofheterochromatinremainslargelyunknown.HereweshowthathistonechaperoneSPT16isrequiredfortheheterochromatinsilencingintheabsenceofSIR1.WefoundthatmutationsinSPT16severelyexacerbatethesilencingdefectsinsir1mutantcells.Moreover,thebindingofSir2-4proteinstoHMlocisignificantlyreducedinspt16sir1doublemutantcells.Agreewiththat,theacetylationof16onH4(H4K16Ac)issignificantlyincreasedintheseregions.Interestingly,mutationsinSPT16incombinationwithdeletionsofCAC1andRTT106,twootherhistonechaperones,leadtocompleylossofsilencingattheHMloci.TheseresultsrevealanovelroleforSpt16inheterochromatinsilencinganddemonstratethathistonechaperones,agroupofkeyyersinnucleosomeassembly,arerequiredfortherecruitmentofSir2-4proteinsontochromatinintheformationofheterochromatin.SingleNucleotidePolymorphismRelatedDnaseHypersensitivitySiteandAltionUsingCRISPR-Cas9SystemMoZhao(趙墨)*(CollegeofLifeSciences,PekingUniversity,),JonathanFlint(NuffieldDepartmentofMedicine,UniversityofOxford,UnitedKingdom)Ineukaryote’sgenome,therearecertainregionsthatshowhighersensitivitytoDNaseI.Thesehypersensitiveregionsarethuscalled“DNaseHypersensitivitySite”(DHS).DHSaremarkersoftranscriptionalactivityandcis-regulatoryelementsincludingenhancers,insulatorsandsilencers.GenomicsequencingandDNasesequencingdatashowedthat,in8inbredstrainsofMusmusculus,DHSvarybetweenstrains.Moreover,asmallportionofvariableDHSiscorrelatedwithsinglenucleotidepolymorphism(SNP)withinthem.Basedonthesefacts,weproposedthattheSNPmightbethecausalfactorofDHSvariation.Toverifythishypothesis,wentousetheclusteredregularlyinterspacedpalindromicrepeats/CRISPR-associatedproteins(CRISPR-Cas9)systemtochangeSNPinmiceEScells,andtestifDHSappear/disappearaccordingly.Mycontributionstothisprojectareasthefollowing:BeforeIjoinedin,morethan100candidatesofDHSsitethatcorrelatewithnearby/withinSNPweredetectedbycomputationalmethod.UsingUCSCgenomebrowserandourownsequencingdatabase,Ivalidatedandshortlistedthesecandidates.Afterbeingvalidated,IdesignedandorderedspecificoligosfortheCRISPR-Cas9systemtowork.Ialsodidtheconstructionandvalidationofallthesmids(8intotal).ThesignificanceofmyworkistoprovidedeeperunderstandingoftranscriptionalfactorbindingandregulationoftranscriptionalStudentSession:CellAna3IsaNovelConservedProteinRequiredforCentrioleDuplicationorXinGu(古欣)*(CollegeofLifeSciences,PekingUniversity,),DavidM.Glover’slab(DepartmentofGenetics,UniversityofCambridge,UnitedKingdom)Centriolesaremicrotubule-basedstructuresthatareessentialfortheformationofcentrosomesandcilia.Centriolenumberistightlyregulatedandgeneticscreenhasrevealedseveralproteinsinwormsareessentialforcentrioleduplication.Ana3isoneofthenovelproteinsrecentlyidentifiedimportantforcentrioleduplication,however,itscellularlocalizationandexactfunctionarelargelyunknown.Ana3depletionledtoasignificantreductionofthenumberofcentriolesinculturedDrosophilacells.SimilarresultswerefoundfortestescellsofAna3mutantflies,indicatingitsessentialfunctionincentrioleduplicationorintegrity.Live-imagingoftheembryosandimmune-stainingofthetestesofGFP-Ana3transgenicfliesrevealedAna3chimericproteinlocalizedincentrosomeduringallphasesofmitosisandmeiosis.Usingsuper-resolutionmicroscopy,thelocalizationofexon1ofAna3wasfoundtolieinthe“core”regionofcentrosome,consistentwithitsessentialfunctionsincentrioleduplication.Interestingly,theCterminusofAna3humanhomologue,Rotatin,islocatedoutofthe“core”region,suggestingdistinctfunctionsfordifferents.MassspectralysishasidentifiedAna3existinginacomplexwithReductionofCnn4(Rcd4)fromculturedDrosophilacells.FunctionalknockingdownofRcd4andAna3bothledtoreductionofcentriolenumber,albeitAna3knockingdownhasamoredramaticeffect,indicatingAna3mightworkupstreamofRcd4.mir-28*RegulationinBCellAnzhiYao(姚安之)*(YuanpeiCollege,PekingUniversity,),CatherineYan(BethIsraelDeaconessMedicalCenter,andtheHarvardStemCellInstitute,UnitedStates)Oncogenicc-Mycexpressioncontributestomanytypesofcancers,includingB-lymphoma.MicroRNAs(miRs)whichcandown-regulatec-Mycexpressionmaybethepotentialtargetsofcancertherapies.miR-28isexpressedinnormalhumanfollicularandcentroblasticBcellsubsets,andisshowntobedownregulatedindiffuselargeBcelllymphoma(DLBCL).Itsoverexpressioninvivohasbeenshowntodelaytumordevelopmentyetpromotetumormetastasis.Recently,wegeneratedaconditionalapproachinmicetospecificallyinactivatec-Mycinna?venormalandlymphoma-proneBcells.Preliminarily,usingaqPCRbasedmiRNAlibraryscreen,weidentifiedmiR-28*tobeconstitutivelyupregulatedinnaiveBcellsdeficientforc-Myc,andisconverselydown-regulatedinc-Myc-activatedBcellsandBlymphomas,suggestiveofanotpreviouslydefinepotentialinverserelationshipbetweenmiR28*andc-Mycexpressionoraction.ThefocusofmyprojectistoinvestigatethemolecularinterybetweenmiR-28*andc-Myc,whichfocusontheimpactofmiR28*onc-Mycexpression,andtheproliferativesurvivalandmigration/metastasisofc-MycactivatedBcellsandBlymphomas.IdentificationofDownstreamEffectorsofRIPK3-MLKLDependentNecrosisbyNon-NaturalAminoAcidPhotocrosslinkerXiangyuZhang(張翔宇)*(CollegeofLifeSciences,PekingUniversity, ),ZhirongShen(NationalInstituteofBiologicalSciences,),XiaodongWang(NationalInstituteofBiologicalSciences,)Necrosis,likeapoptosis,canbeexecutedbyregulatedmechanisms.Thereceptor-inctingserine-threoninekinase3(RIP3)andthemixedlineagekinase -likeprotein(MLKL)aretwokeysignalingmoleculesintheTNF-αinducednecrosispathway.InordertoinvestigatehowRIPK3/MLKLcomplexfunctionstocausedownstreamexcutionofnecrosis,weapplygeneticallyencoded,highlyefficientproteinphotocrosslinkingprobe,DiZPK,toprofiletheinvivodownstreameffectorsofRIPK3andMLKL.ForRIPK3crosslinkassay,IconstructedHelastablecelllineover-expressedwithDiZPK-tRNAandDiZPK-tRNAsynthase.Transientco-transfectionofRIP3mutantsconstructtogetherwithPyl-tRS(DiZPK-tRNAandDiZPK-tRNAsynthase)showsagelshiftofRIP3protein,whichindicatesthattherearepotentialnovelinctingproteinswerecrosslinkedwithRIP3.ForMLKLcrosslinkassay,IconstructedX21MLKLknockoutcelllineviaCRISPR/Cas9system,whichcouldbetransfectedwithMLKL-DiZPKmutantstoscreenforpotentialinctingproteinsofMLKL.IfthesubsequentexperimentresultsofInmunnoprecipitateandMassspectrometrypresentedfunctionalcandidates,itwouldprovideamuchdeeperunderstandingofsignalingandexecutivemechanismofRIP3/MLKLinnecrosis.StudentSession:ntNovelysisSystemforDynamicRootYanGong(龔龑)*(CollegeofLifeSciences,PekingUniversity, ),TakehikoOgura(GregorMendelInstitute,Austria),WolfgangBusch(GregorMendelInstitute,Austria)ntrootgravitropismresponseisessentialforwaterandnutrientsabsorption.Todate,bytraditionalforwardgeneticsusingmodelntArabidopsisthaliana,theoutlineofthegeneregulatorynetworkforgravitropismresponsehasbeendepicted,butthedetailsarestillunclear.Weaimtounderstandthedynamicprocessofrootgravitropismandidentifynovelcomponentsofgravitropismresponseinrootsbycombiningautomaticimagingsystemandgenomewideassociatestudy(GWAS).IncooperationwithDr.EdgarSpalding,weperformedhigh-throughputautomaticimagingtoysisrootgravitropismresponseutilizing232A.thaliananaturalaccessions.Aftergravityreverse,about40,000imagesofsinglentwerecreatedbyadurationof8hoursat4minutesinterval.Thoseimagesareappliedtoautomatedimageprocessingtoaccurayfyroottipanglechange.ThesedatahadbeenusedtoconductGWAStofindgenomicregionsthatwereassociatedwithrootgravitropismresponse.Wefoundseveralgenesinproximityofsignificantlyassociatedregions.Usingpublicdatabasesoflargescaletranscriptome,weselectedhighlyconfidentgenesshowingconsistentexpressionprofileswiththeknowngravitropismresponsivegenes,includinganalpha/beta-hydrolasessuperfamilyprotein.Wearecurrentlyinvestigatingthesegenesbyphenotypicstudyofmutantlinesandnaturalaccessions,expressionexaminationandbiochemicalcharacterization.ASmallMoleculeDisturbsRootDevelopmentinArabidopsisAnranLi(李安然)*(CollegeofLifeSciences,PekingUniversity,),HongweiGuo(CollegeofLifeSciences,PekingUniversity,)Usingachemicalbiologyscreeningapproach,ourlabidentifiedasmallchemicalmolecule,Ket,whichcanspecificallyinhibittheethylenetripleresponseintherootofetiolatedseedlingsofArabidopsisthaliana.Accordingtoprimaryresult,Ketcaneffectivelypromotetherootelongationofeto1-2(ethyleneoverproduction1-2)whichdemonstrateaconstitutivelyethylenetripleresponseintheabsenceofexogenousethylene.Next,wewilltakeadeeplookintothemechanismofhowthissmallchemicalaffectstherootelongationusingbothmolecularandbiochemicalmethods.What’smore,Ketwasreportedtobeanon-steroidalanti-infltorydrug(NSAID)inhuman,whichcaninhibitjasmonatebiosynthesisinnt.SofurtherresearchneedtobedonetorevealtheroleofKetonethylene-inducedinhibitionofrootgrowthandjasmonatebiosynthesis.IdentificationofProteinsAssociatedwithEIN2–TheKeyProteinInvolvedinEthyleneSignalingPathwayYaoXiao(肖瑤)*(CollegeofLifeSciences,PekingUniversity,),HongweiGuo(CollegeofLifeSciences,PekingUniversity,)EIN2(Ethylene-insensitive2)isanessentialtransducerinethylenesignalingpathway,bridgingthesignalingfromERtonucleustoregulatethedownstreamtranscriptionalfactorEIN3/EIL1.LossoffunctionofEIN2causestotallyinsensitivetoethylenetreatmentwhiledoublemutantein3eil1remainspartialresponsestoethylene,whichremindsustoinvestigateproteinsassociatedwithEIN2(E2APs)toexpandourknowledgeofethylenesignalingtransduction.Currently,identificationofE2APswasfacilitatedbyutilizingGFPantibodytoimmunoprecipitateGFP-taggedEIN2fromtheectopicexpressionseedlings,andsubsequentlyidentifyingtheco-immunoprecipitatedproteinsbyLC-MS.ImainlyfocusedontheE2APswhichmayfunctioninreactiveoxygenspeciesandphosphatidatesignalingpathway.TheinctionoftheseE2APswereselectedtobefurtherconfirmedbyreversedCo-IP.Interestingly,wefoundthatacollectionofE2APscaninctwithdifferentEIN2processingproducts,indicatingthediversityofEIN2functioninethylenesignalingmightberelatedtodifferentE2APs.StudentSession:MetabolismandStressMrap2IsNotRegulatedTranscriptionallybyEnergyState,ButAgrpTianLu(陸天)*(CollegeofLifeSciences,PekingUniversity, ),MariaJoachim(Harvardmedicalschool,ChildrenHospitalBoston,Endocrinology,UnitedStates),JosephAMajzoub(Harvardmedicalschool,ChildrenHospitalBoston,Endocrinology,UnitedStates)Themelanocortinreceptor(MCR)familyconsistsoffiveG-proteincoupledreceptors.Amongall,MC3RandMC4Rarebothhighlyexpressedinbrainandhaveimportantfunctionsinmetabolism.AlthoughMRAP2(Melanocortin2receptor-accessoryprotein)wasfoundtobindtoandmodulatethefunctionofMC2R(Chanetal,2009PNAS),itsfunctionwasnotknown.AsaietalfoundthatMrap2increasesαMSHsignalingviaMC4Rfive-fold(Asaietal2013).Onanad-libdiet,youngMrap2KOmicedevelopobesitywithnormalfoodintake,whereasolderMrap2KOmicehavemorefoodintakethanWTmice.ThisindicatesthatMrap2mayhaveimportantfunctioninregulatingenergybalance,possiblyinvolvingmodulationoftheefficiencywithwhichingestedfoodisusedtogenerateenergyinyounganimals,aswellasregulationoffoodintakeinolderanimals.BecauseMrap2hassuchalargeeffectonMC4Rsignaling,itispossiblethatthechangesinMrap2expressionmayyanimportantroleinregulationofenergybalance.Forthisreason,weexaminedMrap2mRNAcontentinthemousebrainindifferentstatesofenergybalance,todeterminewhetherMrap2mRNAcontentmightyaroleinregulatingenergybalance.Wesetupthreegroupsofmice:Ad-lib,fastingandrefed,fiedtheenergybalanceofeachgroupandfound1)AgrpandCrhmRNAareincreasedbyfasting,2)POMCmRNAisnotaffectedbyfasting,3)InHT&Pons,Mrap2andMC4RmRNAisnotsignificantlydecreasedbyappetiteTheregulationofMrap2mRNAinPVNmaybeindiscerniblebyqPCRbecausetherearemanysitesofhypothalamicMrap2expression,bothwithinandoutsideofMc4rneurons,andMrap2maybeaffectedbyenergybalanceonlyinMc4rneurons.WecoustructedtheMc4r-2a-cremiceandcharacterizeitslocalizationandbodyweightfornextstudy.Furtherexperimentswillbeinsituhybridizationtoseetheregulationinpreciseregion.MeasurementofAdrenalActivityinFiveCaptivePrimateSiyangXia(夏思楊)*(CollegeofLifeSciences,PekingUniversity,),MengYao(CollegeofLifeSciences,PekingUniversity,)Inmls,understressfulsituations,adrenalactivityareusuallystrengthened,amajorresultofwhichistheincreasesecretionofglucocorticoid,includingcortisolandcorticosterone,intoblood,andfurtherintofecesafterchemicalmodificationinliver.Therefore,theconcentrationofthesehormonesandtheirmetabolites,whichcouldbemeasuredbyEnzymeImmunoassay(EIA),hasbeenusedasasignalofthestressstatusoftheanimal.Basedon863fecalsamplesfrom6primatespecies(Presbytisfrancoisi,Cercopithecusneglectus,Aesfusciceps,Rhinopithecusbieti,Lemurcatta,Saimirisciureus)collectedinBeijingZooin9months,thisprojecthopetocompare5activity,aswellasthepossiblerelatednessbetweenstressresponseandphylogeniesinprimates.Sofar,theEIAmeasurementshavebeenestablished.However,nosolidconclusionshavebeenreachedyet,asthemeasurementsarestillinprogress.SpatialDistributionDynamicsofp53inResponsetoZidongZhang(張子棟)*(CollegeofLifeSciences,PekingUniversity, ),ChaoTang(CenterforTheoreticalBiology,PekingUniversity, Recentlyithasbeendiscoveredthatthep53levelpresentseitheroscillatoryorsustainedpatterninresponsetodifferentintensitiesofstress,thusinitiatingdifferentcellresponsessuchascellcyclearrestorapoptosisrespectively.Howeveritisnoticeablethatp53functioninavarietyofwaysincludingregulatinggeneexpressionaswellasinducingapoptosisinmitochondriathroughprotein-proteininction,indicatingthatthespatialdistributionofp53betweennucleus,cytosmandmitochondriamayalsobeimportantincellfatedecision.Sowetrytocharacterizethespatialdynamicsofp53inresponsetodifferentstressusingmicroscopyorotherexperimentalwaysaswellastheoreticalmodeling.Alsowewanttoperturbthespatialdistributionofp53usinglightsensitivesysteminordertounderstandhowthespatialdynamicsofp53regulatescellresponses.StudentSession:SyntheticBiologyEngineeringMicrobialConsortiaWeiyueJi(吉瑋玥)*(CollegeofLifeSciences,PekingUniversity,),QiOuyang(CollegePhysics,PekingUniversity,),WendellLim(DepartmentofCellularandMolecularPharmacology,DepartmentofBiochemistryandBiophysics,UniversityofCalifornia,SanFrancisco,UnitedStates)Microbialconsortia,referringtoagroupofmultipleinctingmicrobialpopulations,areubiquitousinnature.Forexample,microbialcommunitiesexistbothinhumangutandsoil,whichaidineverythingfromnutritionproductiontoimmunityanddefense.Learningfromnaturalmicrobialconsortia,therefore,enablebiologiststoutilizingthiscommunitystructureofmicroorganismtodesignandconstructionnovelandmorecomplexfunctions.Oneoftheadvantageofmulticellularityisscaling-upofsyntheticgenecircuits.However,howtoreliablydesignanddistributethecircuitsinmicrobialconsortiawithlimitednumberofwell-behavedgeneticmodulesandwiringquorum-sensingmoleculeremainanissue.HereweproposeaformalizeddesignprocessandasaproofofprincipledesignanE.coliconsortiumthatperformsXORfunction,atypicalcomplexcomputingoperation.Anotherthingaboutmulticellularityisspecifictargeting.Commonlybacterialpopulationsarecontrolledusingindiscriminate,broadrangeantibiotics,thoughthis“kill-all”approachkillsbeneficialorganismandencouragestheformationof strains.Herewewouldliketotakeadvantageofanaturalhorizontalgenetransfermechanismsinbacteria,conjugation,andanewlydevelopedRNAi-likerepressionsystem,CRISPRi,toselectivelyregulategeneexpressionintargetedstrainswithinacomplexmicrobialcommunity.AromaticsBusted：AComprehensiveandtativeDetectionforPuZhen(鄭璞)*(CollegeofLifeSciences,PekingUniversity, ),ShuaixingHe(何帥欣)*(CollegeofLifeSciences,PekingUniversity, ),HaoranXue(薛浩然)*(CollegeofLifeSciences,PekingUniversity, ),HuangWang(王歡)*(CollegeofLifeSciences,Peking ),QiOuyang(CollegeofPhysics,PekingUniversity, Aromaticpollutionis ingaworldwideconcern,andmonitoringaromaticsremainschallenging.Notingtheabundantgenomicdataofprokaryotesfromaromatics-richenvironment,PekingiGEMappliedpartminingtothegeneticrepertoiretodevelopacomprehensivesetofbiosensorsforaromatics.Thetranscriptionalregulatorsforeachtypicalclassofaromaticcompoundswerebioinformaticallydeterminedandpromoterengineeringandproteinengineeringwereperformedtotunetheirfunction.Toexpandthedetectionrange,enzymesinupperpathways,workingasplug-ins,werecoupledwithbiosensorstodegradearomaticstodetectablecompounds.Forenvironmentaldetection,weconstructthebandpassfiltertodetectacertainrangeofconcentration.Responsesofbiosensorsequippedwithband-passfiltercanrobustlyreflecttheconcentrationofenvironmentalsamples.PekingiGEMhasremarkablyenrichedthelibraryofbiosensorsforaromaticsandenabledtativedetectionforenvironmentalmonitoring.Thesebiosensorswillbealsopotentformetabolicengineeringandwell-characterizedsyntheticbiological(PosterNumberPosterAGeneticScreeninDrosophilaforGenes ctingwithXingchenLiu(劉星晨)*(CollegeofLifeSciences,Peking FOXPfamilyproteins,functioningastranscriptionfactorsregulatinggeneexpression,arecrucialforcertaindevelopmentalprocessesinhuman.Loss-of-functionofFoxP1,2iscausativeofspeechdisordersandmentaldisabilities.ThemainaimofmyprojectistoobtainabetterunderstandingofgeneticinctionpartnerswithFoxP.WewilluseDrosophilatoperformthesestudies,asitprovidesaninvivomodeltogainabetterunderstandingofmolecularmechanismsbehindFoxPinctionnetwork.2IsoformsofFoxPinDrosophilaareover-expressedineyes,whichresultsingeneticallysensitizedroughandirregularommatidiastructure.TodeterminewhichgenesinctwithFoxP,wecomparetheeyemorphologyofFoxPover-expressionlines,withindividualsinwhichbothFoxPareover-expressedandcertaingenesaredown-regulatedusingRNAi.Amongthegeneswehavescreened,Ptip,Hth,SpoonbillandCG5708arefoundtobepotentialinctionpartnerswithFoxP.ThecharacterizationofthesepartnerswouldlusmoreaboutthepossibleregulatorsofFoxPaswellaspossibleinctorswhichwouldbecandidatestoyasimilarrolesintheneurobiologyofbraindevelopment.BiologicalDetectionofEndocrineDisruptingChemicalsand ysisofHermaphroditicSpeciesSensitivityGeSong(宋戈)*(CollegeofLifeSciences,PekingUniversity,),JianyingHu(CollegeofUrbanandEnvironmentalSciences,PekingUniversity,)Therehasbeenincreasingconcernthatchemicalsintheenvironmentmaymimicthenaturalhormoneestrogen,andtherebydisruptnormalendocrinefunctionsofhumansandwildlifespecies.Manyestrogeniccompounds,suchaso,p’-DDT,NP,BPA,havebeendetectedinwaterofYangtzeRiver,andthedevelopmentandreproductiveoflocalfishspecies,includingsturgeon(Acipensersinensis),canbeeasilyinfluenced.SincesturgeonislistedasagradeIprotectedanimalin ,studiesontheirsensitivityisnecessary.Inthisstudy,weusedyeasttwo-hybridsystemtoinvestigatethebindingabilityof9naturalandsyntheticchemicalswiththeestrogenreceptor(ER)ofsturgeon.ThebindingabilitiesofthesechemicalstoERsofsturgeonwerecomparedwiththatofMedaka,amodelspecies,throughLowestObservedEffectConcentration(LOEC).Theresultsshowedthatsturgeonestrogenreceptoris2to4timesmoresensitivethanthatofMedaka.Furtherstudieswillbedoneusingfishcells,i.e.celltransfection,inwhichtheconditionisnearertotherealone.Theaimoftheresearchistofindtheevidenceofcausalrelationshipbetweenenvironmentalpollutionandthereductionofsturgeon,theendangeredspecies.ResearchontheEnvironmentalFactorsInfluencingPersistenceofE.JinYang(楊津)*(CollegeofLifeSciences,PekingUniversity, ),FanBai(BiodynamicOpticalImagingCenter,PekingUniversity)Bacterialpersistenceisastateinwhichafractionofcellssurvivesantibioticprocessing.,cellswithpersistencemaynotbeuniformlydistinctfromthesiblingswhofailtosurvive.Recentstudiesshowedthat“persisters”arequiteheterogeneousintheirmechanismtosurviveinsteadoftotallydormantaswebelievedbefore,andthatthequalityofbeingpersistentmayresultfromstochasticalexpressionofsomeparticulargenes.Ourresearchthusfocusesontheenvironmentalfactors,suchasUV,smalldoseofantibioticsandROS,whichcouldmoreorlessregulatethepersistenceofE.colitoantibiotics.In