SMG-1 and mTORC1 Act Antagonistically to Regulate Response to Injury and Growth in Planarians 英文参考文献.docVIP

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SMG-1 and mTORC1 Act Antagonistically to Regulate Response to Injury and Growth in Planarians 英文参考文献.doc

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SMG-1 and mTORC1 Act Antagonistically to Regulate Response to Injury and Growth in Planarians 英文参考文献

SMG-1andmTORC1ActAntagonisticallytoRegulate ResponsetoInjuryandGrowthinPlanarians CristinaGonza′lez-Este′vez1*,DanielA.Felix1,MatthewD.Smith1,JordiPaps2,SimonJ.Morley3, VictoriaJames4,TysonV.Sharp4,A.AzizAboobaker1* 1CentreforGeneticsandGenomics,UniversityofNottingham,QueensMedicalCentre,Nottingham,UnitedKingdom,2DepartmentofZoology,UniversityofOxford, Oxford, United Kingdom, 3Department of Biochemistry, School of Life Sciences, University of Sussex, Brighton, United Kingdom, 4School of Biomedical Sciences, UniversityofNottinghamMedicalSchool,Nottingham,UnitedKingdom Abstract Planarianflatwormsareabletoboth regeneratetheirwholebodiesandcontinuouslyadapttheirsizetonutrientstatus. Tightcontrolofstemcellproliferationanddifferentiationduringtheseprocessesisthekeyfeatureofplanarianbiology. Hereweshowthattheplanarianhomologofthephosphoinositide3-kinase-relatedkinase(PIKK)familymemberSMG-1and mTORcomplex1componentsarerequiredforthistightcontrol.Lossofsmg-1resultsinahyper-responsivenesstoinjury and growth and the formation of regenerative blastemas that remain undifferentiated and that lead to lethal ectopic outgrowths.Invasivestemcellhyper-proliferation,hyperplasia,hypertrophy,anddifferentiationdefectsarehallmarksofthis uncontrolled growth. These data imply a previously unappreciated and novel physiological function for this PIKK family member.IncontrastwefoundthatplanarianmembersofthemTORcomplex1,torandraptor,arerequiredfortheinitial responsetoinjuryandblastemaformation.Doublesmg-1RNAiexperimentswithtororraptorshowthatabnormalgrowth requiresmTORsignalling.Wealsofoundthatthemacroliderapamycin,anaturalcompoundinhibitorofmTORC1,isableto increasethesurvivalrateofsmg-1RNAianimalsbydecreasingcellproliferation.OurfindingssupportamodelwhereSmg-1 actsasanovelregulatorofboththeresponsetoinjuryandgrowthcontrolmechanisms.Ourdatasuggestthepossibility thatthismaybebysuppressingmTORsignalling.CharacterisationofboththeplanarianmTORC1signallingcomponents andanotherPIKKfamilymemberaske