An ABC Transporter Mutation Is Correlated with Insect Resistance to Bacillus thuringiensis Cry1Ac Toxin 英文参考文献.docVIP
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An ABC Transporter Mutation Is Correlated with Insect Resistance to Bacillus thuringiensis Cry1Ac Toxin 英文参考文献
AnABCTransporterMutationIsCorrelatedwithInsect
ResistancetoBacillusthuringiensisCry1AcToxin
LindaJ.Gahan1,YannickPauchet2,HeikoVogel2,DavidG.Heckel2*
1Department of Biological Sciences, Clemson University, Clemson, South Carolina, United States of America, 2Department of Entomology, Max Planck Institute for
ChemicalEcology,Jena,Germany
Abstract
TransgeniccropsproducinginsecticidaltoxinsfromBacillusthuringiensis(Bt)arecommerciallysuccessfulinreducingpest
damage,yetknowledgeofresistancemechanismsthatthreatentheirsustainabilityisincomplete.Insectresistancetothe
pore-formingCry1Actoxiniscorrelatedwiththelossofhigh-affinity,irreversiblebindingtothemid-gutmembrane,butthe
genetic factors responsible for this change have been elusive. Mutations in a 12-cadherin-domain protein confer some
Cry1Acresistancebutdonotblockthistoxinbindingininvitroassays.Wesoughttoidentifymutationsinothergenesthat
mightberesponsibleforthelossofbinding.Weemployedamap-basedcloningapproachusingaseriesofbackcrosses
with1,060progenytoidentifyaresistancegeneinthecottonpestHeliothisvirescensthatsegregatedindependentlyfrom
thecadherinmutation.WefoundaninactivatingmutationoftheABCtransporterABCC2thatisgeneticallylinkedtoCry1Ac
resistanceandiscorrelatedwithlossofCry1Acbindingtomembranevesicles.ABCproteinsareintegralmembraneproteins
withmanyfunctions,includingexportoftoxicmoleculesfromthecell,buthavenotbeenimplicatedinthemodeofaction
of Bt toxins before. The reduction in toxin binding due to the inactivating mutation suggests that ABCC2 is involved in
membraneintegrationofthetoxinpore.OurfindingssuggestthatABCproteinsmayplayakeyroleinthemodeofaction
ofBttoxinsandthatABCproteinmutationscanconferhighlevelsofresistancethatcouldthreatenthecontinuedutilization
ofBt–expressingcrops.However,suchmutationsmayimposeaphysiologicalcostonresistantinsects,byreducingexport
of other toxins such as plant secondary compounds from the cell. This weakness could be exploited to manage this
mechanismofBtresistanceinthefield.
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