Candidate genes at the Rmi1 locus for resistance to Meloidogyne incognita in soybean

Abstract Key message The RKN resistance locus Rmi1 was fine-mapped to two genes on chromosome 10, a glycosyl hydrolase family 9 β-1, 4-endoglucanase gene and a type I pectin methylesterase gene. Abstract Root-knot nematodes (Meloidogyne spp. ) are a serious threat to soybean production in the southeast USA, with yield losses of more than 165 million in 2023. Development and deployment of resistant soybean cultivars is the most effective strategy for managing these nematode pests; however, the identity of the resistance genes and underlying mechanism of resistance remains obscure. An additive resistance gene, Resistance to M. incognita-1 (Rmi1), to the predominant species, was first identified in soybean cultivar Forrest but never mapped to a genomic region. Multiple mapping studies have identified a major quantitative trait locus (QTL) with additive action on chromosome 10. In this study, a population consisting of 170 F 2: 3 families derived from a cross of Bossier (susceptible) × Forrest (resistant) was initially used to confirm that Rmi1 is in the chromosome 10 QTL. Subsequently, 884 F 5: 6 recombinant inbred lines (RILs) derived from the same cross were used to fine-map the Rmi1 causal gene (s) to two genes – a β-1, 4-endoglucanase (Glyma. 10G017000, EG) and a pectin methylesterase/methylesterase inhibitor (Glyma. 10G017100, PME1). Both gene candidates have the potential to play a role in the resistance response to M. incognita. Both gene promoters harbor SNPs and indels and the encoded proteins exhibit amino acid polymorphisms, including a premature stop in PME1 of resistant soybeans. Additionally, both genes show a higher expression level in susceptible roots compared to resistant roots in the absence of infection. This suggests that Rmi1 may confer one or more pre-existing differences related to cell wall modification in soybean roots, ultimately leading to a decrease in susceptibility.