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.