Silencing <i>SmD1</i> in Solanaceae alters susceptibility to root-knot nematodes

<jats:title>Summary</jats:title><jats:p>Root-knot nematodes (RKNs) are among the most damaging pests of agricultural crops. Indeed, <jats:italic>Meloidogyne</jats:italic> is an extremely polyphagous genus of nematodes that can infect thousands of plant species. A few genes for resistance (R-genes) to RKNs suitable for use in crop breeding have been identified, and new virulent strains and species of nematode emerge rendering these R-genes ineffective. Effective parasitism is dependent on the secretion, by the RKN, of effectors targeting plant functions, which mediate the reprogramming of root cells into specialised feeding cells. These cells, the giant cells, are essential for RKN development and reproduction. The EFFECTOR 18 protein (EFF18) from <jats:italic>M. incognita</jats:italic> interacts with the spliceosomal protein SmD1 in Arabidopsis, disrupting its function in alternative splicing regulation and modulating the giant cell transcriptome. We show here that EFF18 is a conserved RKN-specific effector. We also show here that EFF18 effectors also target SmD1 in <jats:italic>Nicotiana benthamiana</jats:italic> and <jats:italic>Solanum lycopersicum</jats:italic>. The alteration of <jats:italic>SmD1</jats:italic> expression by virus-induced gene silencing (VIGS) in Solanaceae affects giant cell formation and nematode development. Thus, <jats:italic>SmD1</jats:italic> is a susceptibility gene and a promising target for the development of broad resistance, especially in Solanaceae, for the control of <jats:italic>Meloidogyne</jats:italic> spp.</jats:p>