Location: Crop Improvement and Protection ResearchTitle: Secreted in xylem (SIX) 6 mediates Fusarium oxysporum f. sp. fragariae race 1 avirulence to strawberry cultivars with FW1 resistance
|DILLA-ERMITA, CHRISTINE - University Of California|
|PINCOT, DOMINIQUE - University Of California|
|FAMULA, RANDY - University Of California|
|COLE, GLENN - University Of California|
|KNAPP, STEVE - University Of California|
Submitted to: Fungal Genetics Conference/Asilomar
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/2022
Publication Date: 3/15/2022
Citation: Dilla-Ermita, C., Goldman, P.H., Anchieta, A.G., Pincot, D.D., Famula, R.A., Cole, G.S., Knapp, S.J., Klosterman, S.J., Henry, P.M. 2022. Secreted in xylem (SIX) 6 mediates Fusarium oxysporum f. sp. fragariae race 1 avirulence to strawberry cultivars with FW1 resistance. Fungal Genetics Conference, March 15-19, 2022, Pacific Grove, California.
Technical Abstract: Fusarium wilt of strawberry is an economically important disease caused by Fusarium oxysporum f. sp. fragariae (Fof). The dominant locus for resistance to Fusarium wilt, FW1, is currently deployed in strawberry cultivars and prevents disease caused by Fof ‘race 1’ isolates. However, we previously discovered Fof ‘race 2’ isolates that could overcome FW1-mediated resistance and remained highly virulent on cultivars with FW1. We hypothesized that FW1 functioned in a gene-for-gene interaction with an unknown avirulence gene (AvrFW1) expressed by Fof race 1 and absent in Fof race 2. If true, identifying the AvrFW1 gene would enable surveillance for race 2 isolates and provide crucial insight into the durability of FW1-mediated resistance. To test this hypothesis, we identified 21 gene homologs (out of 85,846 total homologs) present in 24 Fof race 1 genomes and absent in 3 Fof race 2 genomes. Only one of these homologs was up-regulated during plant infection. This gene had a secretion signal and was homologous to a known effector, secreted in xylem 6 (SIX6), and shared 100% sequence identity among all race 1 isolates. SIX6 was considered the only strong candidate for AvrFW1 and thus was knocked out by homologous recombination in two Fof race 1 isolates. All SIX6 knockout transformants (n = 6) gained virulence on FW1/fw1 cultivars, whereas ectopic transformants and the wildtype strain remained avirulent. Intriguingly, FW1/fw1 strawberry cultivars remained quantitatively less susceptible than fw1/fw1 cultivars to the knockout strains. To evaluate the relationship between FW1 and quantitative resistance to the knockout strain, seedlings from a segregating FW1/fw1 × fw1/fw1 population were: 1) genotyped for a SNP at the FW1 locus that is highly associated with resistance, and 2) tested for susceptibility to a SIX6 knockout strain or the wildtype. All FW1/fw1 seedlings were resistant to the wildtype, whereas 86% of FW1/fw1 seedlings were susceptible to the knockout transformant. Curiously, 14% of seedlings with the FW1/fw1 genotype were tolerant to the knockout strain; tolerance was not observed from any fw1/fw1 seedlings. These results support the conclusion that SIX6 is an avirulence factor interacting with a resistance gene at FW1. Additional experiments are necessary and underway to assess whether additional host and/or pathogen genes are involved in in the resistance phenotype.