Understanding the function of two tandemly duplicated immune receptor genes in disease resistance and its temperature sensitivity

Pathogens of Brassica species cause major crop losses around the world. Yellow wilt, caused by F. oxysporum, is one of the most serious diseases of vegetable brassicas worldwide. The phoma stem canker pathogen, L. maculans, of oilseed rape (Brassica napus) causes global losses of US$1 billion per year. Breeding for resistant cultivars is economically and environmentally the best strategy, especially for subsistence farmers, who cannot afford fungicides.
Resistance against both F. oxysporum and L. maculans is governed by major resistance (R) genes. The Japanese research team has identified the FocBr1 resistance locus against F. oxysporum. Point mutants are being characterised by the UK team; the first homozygous mutant obtained displays a dwarf phenotype. Susceptibility of these mutants to F. oxysporum would proof that it is the elusive R gene.
Temperature sensitivity of R gene-mediated resistance is of concern as the climate is changing. AtSNC1 is a central regulator of temperature sensitivity of R gene-mediated resistance in A. thaliana; mutations in snc1 result in a temperature-sensitive dwarf phenotype with constitutively upregulated immune responses. The putative B. rapa ortholog, BrSNC1, occurs in tandem with FocBr1. Point mutations in this gene are also being characterised by the UK team.
The wider context of these two genes within the immune network are also investigated by the participating Japanese and UK teams. The collective research findings will improve understanding of the immune network in Brassicaceae and contribute to resilient and increased crop production.