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Juan Antonio Garcia

Juan Antonio Garcia

JuanAntonioGarcia,GroupLeaderofCentroNacionaldeBiotecnologia.Hisgroupareinterestedinvirus-hostinteractionsthatcanhelptodefinevirushostrange.Thegrouphavedemonstratedthatsinglealterationsinthe6K1andCIproteins(correspondingtothecleavagesiterecognizedbytheviralproteaseNIainthePPVpolyprotein)areinvolvedinalternativehostadaptationofatypicalPPVisolatestoNicotianabenthamianaandPrunusavium.Theseresultssuggestthatfineregulationofpolyproteinprocessingmightdependonspecifichostfactorsandcontributetoadaptationtospecifichosts.BystudyingresistanceofArabidopsisthalianaandChenopodiumfoetidumtocherrystrainPPVisolates,weshowedthatdefectsininteractionsbetweentranslationinitiationfactorsandpotyviralproteinsmightnotonlypreventinfectioninresistantvarietiesofsusceptiblehostspecies,butalsocontributetonon-hostresistance.Thegroupalsodemonstratedthatself-cleavageofPPVP1isnegativelyregulatedbyitshighlydisorderedN-terminalregionandreliesonaspecifichostfactorforitsactivation.Basedontheseresults,thegroupspeculatethath

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Juan Antonio Garcia,Group Leader of Centro Nacional de Biotecnologia.His group are interested in virus-host interactions that can help to define virus host range. The group have demonstrated that single alterations in the 6K1 and CI proteins (corresponding to the cleavage site recognized by the viral protease NIa in the PPV polyprotein) are involved in alternative host adaptation of atypical PPV isolates to Nicotiana benthamiana and Prunus avium. These results suggest that fine regulation of polyprotein processing might depend on specific host factors and contribute to adaptation to specific hosts. By studying resistance of Arabidopsis thaliana and Chenopodium foetidum to cherry strain PPV isolates, we showed that defects in interactions between translation initiation factors and potyviral proteins might not only prevent infection in resistant varieties of susceptible host species, but also contribute to non-host resistance. The group also demonstrated that self-cleavage of PPV P1 is negatively regulated by its highly disordered N-terminal region and relies on a specific host factor for its activation. Based on these results, the group speculate that host-dependent regulation of P1/HCPro protease processing evolved to attenuate virus virulence and thus alleviate antiviral responses.