Fusarium wilt disease caused by the soil-borne pathogen Fusarium oxysporum f. sp. lycopersici (Fol) is a major threat in tomato-producing regions that can lead to acute yield losses. Host resistance as compared to other control strategies provides an effective and reliable means to contain the spread of the pathogen. Given that genes that confer resistance to all the three known Fol races are single dominant genes, there is a risk of resistance breakdown by the mutating pathogen. Furthermore, in the face of imminent race 4 emergence, building a quantitative and durable resistance shield by pyramiding novel resistant genes in commercial cultivars becomes pertinent. S. pennellii has been previously identified as a repository for resistant genes to Fol3 and recently, two novel loci mapped at chromosomes 3 and 10 were identified from two accessions- LA 1522 and LA 750 respectively using bulk segregant analysis QTL seq. Preliminary analysis was conducted to develop molecular markers for both chromosomes and validate their co-segregation with the region of introgression associated with resistance. We found co-segregating markers for resistance harbored by chromosome 3 and designated the locus as I8. This marker therefore constitutes additional genomic resources for marker-assisted selection of this trait. Although we found markers that co-segregate with resistance on chromosome 10, we provide initial evidence that this resistance is the same with the I6 locus previously identified on chromosome 10 and derived from LA 716 while complementary phenotypic screens showed partial penetrance of this locus. Together, these resistance loci (I6 and I8) could constitute a qualitative shield against the pathogen in commercial cultivars. Efforts are underway to fine map these loci and characterize them under field conditions and against other previously known races.
