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0 reviewsAbstract27 The spread of insect-borne plant pathogens depends on their ability to manipulate the 28 behavior of their vectors. Some bacteria-infected plants become more attractive to vectors, 29 but the underlying mechanism remains poorly understood. Huanglongbing (HLB), a 30 devastating citrus disease, is primarily caused by the bacterium 'Candidatus Liberibacter 31 asiaticus' (CLas) and is transmitted by psyllid vectors. In this study, we identify that the 32 effector protein SDE5, secreted by CLas, inhibits the biosynthesis of volatile terpenoids in33 host citrus plants, thereby enhancing the attraction of psyllid vectors. Biochemically, SDE5 34 acts as an inhibitor of bacterial C-type lysozyme, promoting both CLas infection and35 psyllid vector attraction. Two plant U-box (PUB) E3 ligases, PUB10 and PUB21, could be 36 recruited by SDE5 to promote ubiquitination and proteasomal degradation of MYC2, the 37 key transcription factor in jasmonate signaling and terpene-based anti-herbivore defenses. 38 Additionally, SDE5 disrupts MYC2 dimerization, effectively attenuating its capacity to 39 activate terpene biosynthesis genes. This dual suppression function significantly reduces 40 volatile terpenoid emissions in SDE5-transgenic citrus lines, resulting in heightened psyllid 41 attraction and enhanced psyllid fitness. Conversely, the anti-proteolysis peptide 3-14 (APP 42 3-14), which stabilizes MYC2 protein and inhibits the HLB pathogen, increases the 43 emission of volatile terpenoids to repel psyllids. These findings provide a novel strategy 44 for disrupting mutualistic alliances between plant bacterial pathogens and insect vectors 45 through manipulating olfactory defense.46 Keywords: Huanglongbing, SDE5 effector, MYC2-mediated olfactory defense, anti47 proteolysis peptide, psyllid vector, pathogen-insect mutualism 48
