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Summary  To defend against pathogens, plants have developed a complex immune system, which recognizes the pathogen effectors and mounts defence responses. In this study, the p33 protein of  Citrus tristeza virus  (CTV), a viral membrane‐associated effector, was used as a molecular bait to explore virus interactions with host immunity. We discovered that  Citrus macrophylla  miraculin‐like protein 2 (CmMLP2), a member of the soybean Kunitz‐type trypsin inhibitor family, targets the viral p33 protein. The expression of  CmMLP2  was up‐regulated by p33 in the citrus phloem‐associated cells. Knock‐down of the  MLP2  expression in citrus plants resulted in a higher virus accumulation, while the overexpression of  CmMLP2  reduced the infectivity of CTV in the plant hosts. Further investigation revealed that, on the one hand, binding of CmMLP2 interrupts the cellular distribution of p33 whose proper function is necessary for the effective virus movement throughout the host. On the other hand, the ability of CmMLP2 to reorganize the endomembrane system, amalgamating the endoplasmic reticulum and the Golgi apparatus, induces cellular stress and accumulation of the reactive oxygen species, which inhibits the replication of CTV. Altogether, our data suggest that CmMLP2 employs a two‐way strategy in defence against CTV infection.

plant biotechnology journal

Citrus miraculin‐like protein hijacks a viral movement‐related p33 protein and induces cellular oxidative stress in defence against  Citrus tristeza virus