Molecular Mechanism Of TYLCV Induced Whitefly Effector Bep1 In Regulation Of Plant Immunity

Around 80% of known plant viruses are vector-borned.Emergence of insect-transmitted plant viruses over the past years has caused reduced agricultural productivity.Plant insect-borne diseases are highly dependent on virus-insect-plant tripartite interaction,which is involved in arms race of signal recognition and counter recognition among them.Host immune systems mount insect-pathogen double challenges when pathogen-carrier insect infests.Plants have evolved a sophisticated defensive system,including immunity,to protect themselves from invaders.Plants percept pathogens or insects and consequently trigger immune responses to defend,and in turn,pathogens and insects have evolved mechanisms to overcome these immune defenses.Early response to herbivores begins with PRR perception of damage patterns.Danger-associated molecular patterns(DAMPs)and pathogen-associated molecular patterns(PAMPs)have been characterized as pattern-triggered plant immunity(PTI)in plants.Activation of several MAPKs are early signaling response following perception of PAMPs or DAMPs.Subsequently,MAPKs phosphorylate their substrates,and thus trigger downstream responses,including production of reactive oxygen species(ROS),callose deposition,and induction of defense genes.Several distinct MAPK cascades in plant and animal have been implicated in the regulation of defense against pathogens.To overcome plant immune defenses,insects have evolved strategies including effector salivation to inhibit insects triggered immunity.However,what's biological roles of MAPK in plant response agaisnt hemipterans such as whitefly and the mechanisms of insect effector in immune system are still elusive.Here we first found that infestation of whitefly triggers plant MAPKs(mitogen-activated protein kinase)activation in unique mode differ from chewing insects.The activation of MAPKs then trigger defense pathway including callose deposition.Upon whitefly infestation,the expression level of AtPEPR1 that encoded a receptor to recognize DAMP was heavily induced within half a hour.It raised the possibility of PEPR signaling are involved in host immune response against whitefly infestation.The activation of MAPKs and callose deposition induced by whitefly are similar with Pep1 treatment raise a propose that Pep1 treatment can mimic the whitefly infestation in the defense response.Then we found that MPK3 and MPK6 are negative regulator in the defense response to whitefly.The mpk3 and mpk6 mutants are more attractive to whitefly and showed lower resistance level.MPK4 are positive regulator to fine-tune the immune response.From transcriptome analysis of TYLCV infected whitefly,we found 28 candiated effectors in the screening of whitefly saliva protein.The Bep1 protein can effective inhibit the defense gene PDF1.2 expression induced by whitefly infestation.The interation between Bep1 and WRKY33 competitive inhibit the combine of WRKY33 and MPK6.The whitefly effector Bep1 effected MAPK3 and MAPK6 therefore inactivates early immune signaling.This immune alternation by Bep1 affects whitefly feeding behavious thereby leading a possible enhancing of viral transmission.This discovery represents the first evidence of MAPK cascade in defense against whitefly infestation and a novel mechanism of immune suppression on targeting host MAPK components by a effector protein.Our data present a novel biochemical activity for a whitefly and counter-host defense mechanism of whitefly effector.This study enrichs our understanding on virus-plant-whitefly tripartite interaction.Our research will be helpful to making effective strategies in the protection of crops from both insects and disease infection.