IIGB researchers have now revealed a new molecular mechanism for resistance and susceptibility to a common fungus that causes wilt in susceptible tomato plants. Study results appeared Oct. 16, 2014 in PLOS Pathogens.

Katherine Borkovich, an IIGB professor of plant pathology and the chair of the Department of Plant Pathology and Microbiology, and colleagues started with two closely related tomato cultivars: “Moneymaker” is susceptible to the wilting fungus Fusarium oxysporum whereas “Motelle” is resistant. In their search for what makes the two different, the researchers focused on microRNAs, small molecules that act by regulating the expression of a variety of genes, including genes involved in plant immunity.

They treated roots from the two cultivars with water or with a solution containing F. oxysporum and looked for microRNAs that were increased in response to the fungus in Moneymaker (where they would inhibit resistance genes) or decreased in Motelle (where they would allow expression of resistance genes). They identified two candidate microRNAs whose levels went down in Motelle after treatment with the fungus.

Because microRNAs inhibit their targets by binding to them, computer searches can find target genes with complementary sequences. Such an “in silico” search for targets of the two microRNAs identified four candidates in the tomato genome, and all four resembled known plant resistance genes.

To test whether up-regulation of the target genes was indeed what made Motelle resistant, Borkovich and her colleagues employed a virus-induced gene silencing (VIGS) system that can down-regulate specific genes in tomato. After exposure to F. oxysporum, disease symptoms, including leaf wilting, were seen in VIGS Motelle plants that silenced any one of the four genes. Although the symptoms were not as severe as in Moneymaker plants, this suggested that all four targets contribute to resistance.

Borkovich was joined in the research by Shouqiang Ouyang (first author of the research paper), Gyungsoon Park, Hagop S. Atamian, Jason Stajich and Isgouhi Kaloshian at UC Riverside; and Cliff S. Han at Los Alamos National Laboratory.