Genetic Characterization of smg-8 Mutants Reveals No Role in C. elegans Nonsense Mediated Decay 英文参考文献.docVIP

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Genetic Characterization of smg-8 Mutants Reveals No Role in C. elegans Nonsense Mediated Decay 英文参考文献.doc

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Genetic Characterization of smg-8 Mutants Reveals No Role in C. elegans Nonsense Mediated Decay 英文参考文献

GeneticCharacterizationofsmg-8MutantsRevealsNo RoleinC.elegansNonsenseMediatedDecay JacquelineRosains,SusanE.Mango* DepartmentofMolecularandCellularBiology,HarvardUniversity,Cambridge,Massachussetts,UnitedStatesofAmerica Abstract The nonsense mediated decay (NMD) pathway degrades mRNAs bearing premature translation termination codons. In mammals,SMG-8hasbeenimplicatedintheNMDpathway,inpartbyitsassociationwithSMG-1kinase.Hereweusefour independentassaystoshowthatC.eleganssmg-8isnotrequiredtodegradenonsense-containingmRNAs.Weexaminethe geneticrequirementforsmg-8todestabilizetheendogenous,naturalNMDtargetsproducedbyalternativesplicingofrpl- 7a and rpl-12. We test smg-8 for degradation of the endogenous, NMD target generated by unc-54(r293), which lacks a normalpolyadenylationsite.Weprobetheeffectofsmg-8ontheexogenousNMDtargetproducedbymyo-3::GFP ,which carriesalong39untranslatedregionthatdestabilizesmRNAs.NoneoftheseknownNMDtargetsisinfluencedbysmg-8 mutations. In addition, smg-8 animals lack classical Smg mutant phenotypes such as a reduced brood size or abnormal vulva.Weconcludethatsmg-8isunlikelytoencodeacomponentcriticalforNMD. Citation:RosainsJ,MangoSE(2012)GeneticCharacterizationofsmg-8MutantsRevealsNoRoleinC.elegansNonsenseMediatedDecay.PLoSONE7(11):e49490. doi:10.1371/journal.pone.0049490 Editor:GeorgStoecklin,GermanCancerResearchCenter,Germany ReceivedJune5,2012;AcceptedOctober12,2012;PublishedNovember16,2012 Copyright: ?2012 Rosains,Mango.This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding: SEM received funding from the National Institutes of Health NIH (GM056264), the John D. and Catherine T. MacArthur Foundation and Harvard University.JRreceivedfundingfromHarvardUniversity.Thefundershadnoroleinstudydesign,datacollectionandanalysis,decisiontopublish,orpreparation ofthemanuscript. Co