Notch3 Is Dispensable for Thymocyte β-Selection and Notch1-Induced T Cell Leukemogenesis 英文参考文献.docVIP
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Notch3 Is Dispensable for Thymocyte β-Selection and Notch1-Induced T Cell Leukemogenesis 英文参考文献
Notch3IsDispensableforThymocyteb-Selectionand
Notch1-InducedTCellLeukemogenesis
SaraSuliman1,2,JoanneTan1,2,KeliXu1,PhilaretosC.Kousis1,PaulE.Kowalski1,GregChang1,SeanE.
Egan1,3,CynthiaGuidos1,2
*
1Program inStem Cell and Developmental Biology, Hospital for Sick Children Research Institute, Toronto,Ontario, Canada, 2Department ofImmunology, Faculty of
Medicine,UniversityofToronto,Toronto,Ontario,Canada,3DepartmentofMolecularGenetics,FacultyofMedicine,UniversityofToronto,Toronto,Ontario,Canada
Abstract
Notch1(N1)signalinginducedbyintrathymicDelta-like(DL)ligandsisrequiredforTcelllineagecommitmentaswellasself-
+
renewalduring‘‘b-selection’’ofTCRb CD42CD82doublenegative3(DN3)Tcellprogenitors.However,over-expressionof
theN1intracellulardomain(ICN1)rendersN1activationligand-independentanddrivesleukemictransformationduringb-
selection.DN3progenitorsalsoexpressNotch3(N3)mRNA,andover-expressionofligand-independentmutantN3(ICN3)
influencesb-selectionanddrivesTcellleukemogenesis.However,theimportanceofligand-activatedN3inpromotingb-
selectionandICN1-inducedTcellleukemogenesishasnotbeenexamined.Toaddressthesequestionswegeneratedmice
lacking functional N3. We confirmed that DN3 progenitors express N3 protein using a N3-specific antibody. Surprisingly
however,N3-deficientDN3thymocyteswerenotdefectiveingeneratingDPthymocytesundersteadystateconditionsorin
morestringent competitionassays.TodetermineifN3 co-operates withN1toregulate b-selection, wegeneratedN1;N3
compound mutants. However, N3 deficiency did not exacerbate the competitive defect of N1+/2 DN3 progenitors,
demonstrating that N3 does not compensate for limiting N1 during T cell development. Finally, N3 deficiency did not
attenuateTcellleukemogenesisinducedbyconditionalexpressionof ICN1inDN3thymocytes.Importantly,weshowed
thatincontrasttoN1,N3hasalowbindingaffinityforDL4,themostabundantintrathymicDLligand.Thus,despitethe
profoundeffectsofectopicligand-independentN3activationonTcelldevelopmentandleukemogenesis,
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