The root-knot nematode effector Mi2G02 hijacks a host plant trihelix transcription factor to promote nematode parasitism

Root-knot nematodes (RKNs) cause huge agricultural losses every year. They secrete a repertoire of effectors to facilitate parasitism through the induction of plant-derived giant feeding cells, which serve as their sole source of nutrients. However, the mode of action of these effectors and host targeted proteins remain largely unknown. In this study, we investigated the role of the effector Mi2G02 in Meloidogyne incognita parasitism. Host-derived Mi2G02 RNA interference in Arabidopsis thaliana affects giant cells development, whereas the ectopic expression of Mi2G02 promotes root growth and increases plant susceptibility to M. incognita. We used various combinations of approaches to study the specific interactions between Mi2G02 and A. thaliana GT-3a, a trihelix transcription factor. GT-3a knockout in A. thaliana affected feeding site development, resulting in the production of fewer egg masses, whereas GT-3a overexpression in A. thaliana increased susceptibility to M. incognita and also root growth. Moreover, we highlight the role of Mi2G02 in maintaining GT-3a protein stabilization by inhibiting the 26S proteasome-dependent pathway, leading to a suppression of TOZ and RAD23C expression, promoting nematodes parasitism. Thus, this work enhances our understanding of the manipulation of the role and regulation of a transcription factor by a pathogen effector through interfering proteolysis pathway to reprogram genes expression for nematode feeding cells development.