Ménage à trois: how do Fusarium verticillioides and Sarocladium zeae compete and interact with each other in maize kernels?
Fusarium verticillioides (Fv) is a prevalent seed-borne maize endophyte capable of causing severe kernel rot and fumonisin mycotoxin contamination. Within maize kernels, Fv is primarily confined to the pedicel, while another co-occurring seed-borne fungal endophyte, Sarocladium zeae (Sz), is generally isolated in the endosperm and embryo. In vitro competition assays have indicated Sz can inhibit the growth of Fv. The two lactam-containing antibiotics produced by Sz, named pyrrocidine A and B, are associated with this inhibition of Fv. To explore the mechanism of antagonism, RNA-seq experiments were conducted by challenging the Fv with pyrrocidine B at subinhibitory concentrations. Among the most differentially expressed genes was FVEG_11089 (up-regulated 470-fold) that codes for an ABC transporter. Deletion of FVEG_11089 caused increased sensitivity of Fv to pyrrocidine B. The expression of FVEG_11089 is independent of its adjacent and similarly-induced transcription factor. Additionally, deletion of a PB-induced zinc-binding dehydrogenase gene in Fv led to >10-fold increase in fumonisin production compared to wild type. Hence, we theorize that FVEG_11089 functions in pyrrocidine B resistance by transporting the antibiotic out of the Fv cells. Exposure to pyrrocidine B may suppress fumonisin production and affect the pathogenicity of Fv. Further exploration of the antifungal resistance mechanisms addresses the overall competitive relationships of the two maize seed endophytes colonizing the same ecological niche and how they cope with xenobiotic challenges.