The Mi-EFF1/Minc17998 effector interacts with the soybean GmHub6 protein to promote host plant parasitism by Meloidogyne incognita

Background: Meloidogyne incognita is the most frequently reported species from the root-knot nematode (RKN) complex responsible for causing damage in several different crops worldwide. The interaction between M. incognita and host plants involves the secretions of molecular factors from the nematode, which mainly suppress the defense response and promote plant parasitism. On the other hand, several plant elements are associated with the immune defense system that opposes nematode infection. Results: In this study, the interaction of the Mi-EFF1/Minc17998 effector with the soybean GmHub6 (Glyma.17G099100; TCP14) protein was identified and characterized in vitro and in vivo . Data showed that the GmHub6 gene is upregulated by M. incognita infection in a nematode-resistant soybean cultivar (PI595099) compared to a susceptible cultivar (BRS133). Accordingly, the Arabidopsis thaliana AtHub6 mutant line (AT3G47620, orthologous gene of GmHub6 displayed normal vegetative development of the plant but was more susceptible to M. incognita . Thus, since the soybean and A. thaliana Hub6 proteins are TEOSINTE BRANCHED/CYCLOIDEA/PCF (TCP) transcription factors involved in plant development and morphogenesis modulation, flowering time regulation, and the activation of the plant immune system, our data suggest that the interaction of Mi-EFF1/Minc17998 and Hub6 proteins is associated with an increase in plant susceptibility to nematode infection during parasitism. It is suggested that this interaction may prevent the nuclear localization or disturb the activity of GmHub6 as a typical transcription factor modulating the cell cycle of the plant, avoid the activation of the host’s defense response, and successfully promote parasitism. Conclusion: Our findings indicate the potential of the Mi-EFF1/Minc17998 effector for the development of biotechnological tools based on the approaches of RNA interference and GmHub6 gene overexpression for RKN control.