Summary
Sclerotinia sclerotiorum
, a predominately necrotrophic fungal pathogen with a broad host range, causes a significant yield‐limiting disease of soybean called Sclerotinia stem rot. Resistance mechanisms against this pathogen in soybean are poorly understood, thus hindering the commercial deployment of resistant varieties. We used a multiomic approach utilizing
RNA
‐sequencing, gas chromatography–mass spectrometry‐based metabolomics and chemical genomics in yeast to decipher the molecular mechanisms governing resistance to
S. sclerotiorum
in soybean. Transcripts and metabolites of two soybean recombinant inbred lines, one resistant and one susceptible to
S. sclerotiorum
were analysed in a time course experiment. The combined results show that resistance to
S. sclerotiorum
in soybean is associated in part with an early accumulation of
JA
‐Ile ((+)‐7‐iso‐jasmonoyl‐L‐isoleucine), a bioactive jasmonate, increased ability to scavenge reactive oxygen species, and importantly, a reprogramming of the phenylpropanoid pathway leading to increased antifungal activities. Indeed, we noted that phenylpropanoid pathway intermediates, such as 4‐hydroxybenzoate, cinnamic acid, ferulic acid and caffeic acid, were highly accumulated in the resistant line.
In vitro
assays show that these metabolites and total stem extracts from the resistant line clearly affect
S. sclerotiorum
growth and development. Using chemical genomics in yeast, we further show that this antifungal activity targets ergosterol biosynthesis in the fungus, by disrupting enzymes involved in lipid and sterol biosynthesis. Overall, our results are consistent with a model where resistance to
S. sclerotiorum
in soybean coincides with an early recognition of the pathogen, leading to the modulation of the redox capacity of the host and the production of antifungal metabolites.