January 25 2006
9:30 LSB 2320

Abstract:

The molecular genetics of both plant host resistance and fungal virulence can be studied using Fusarium wilt disease of Arabidopsis. The mechanisms responsible for resistance to the soil-borne vascular pathogen Fusarium oxysporum can be defined using Arabidopsis mutants and natural variation in Arabidopsis ecotypes.

To varying degrees, Arabidopsis ecotypes display race-specific resistance to three forma specialis (f.) of F. oxysporum. Resistance to f. matthioli is oligogenic. Six dominant RESISTANCE TO FUSARIUM OXYSPORUM (RFO) loci significantly contribute to resistance in the Arabidopsis Col-0 ecotype relative to Ty-0 ecotype. We cloned RFO1, the gene with the strongest effect. Interestingly, RFO1 resistance is not race specific because RFO1 also confers resistance to f. conglutinans and f. raphani. Resistance provided by three other Col-0 RFO loci is dependent on RFO1. RFO1 is the WALL-ASSOCIATED KINASE-LIKE KINASE 22 (WAKL22) and identifies a novel type of dominant resistance gene, a non-LRR receptor-like kinase.

Because f. conglutinans isolates are readily transformed by Agrobacterium tumefaciens, genetic manipulation of the fungal pathogen has been made routine. In a pilot screen of ~3,500 insertion mutants, we isolated 40 mutants that displayed robust growth on minimal medium but attenuated virulence on Arabidopsis. One of these mutants 1T2 also displayed reduced conidiation and reduced hyphal branching, phenotypes exhibited by fga1 and fgb1, which are deficient for the alpha and beta subunit of a heterotrimeric G protein, respectively. Both F. oxysporum mutants fga1 and fgb1 were also shown by others to have attenuated virulence. However, heterotrimeric G protein signaling and the candidate gene that is responsible for the 1T2 phenotypes have not been previously associated.