Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 4/11/2018
Publication Date: N/A
Technical Abstract: Fusarium consists of over 200 phylogenetically distinct species, many of which cause important crop diseases and/or produce mycotoxins and other secondary metabolites (SMs). Some fusaria also cause opportunistic infections in humans and other animals. To investigate the distribution of biosynthetic gene clusters (clusters) responsible for synthesis of mycotoxins and other SMs, we conducted phylogenomic analyses of 343 genome sequences that represent 26 single and multi-species lineages of Fusarium. Using antiSMASH and OrthoFinder, we identified 15,647 putative clusters, and observed tremendous variation in presence and absence of homologous clusters among the genomes. We noted three patterns of cluster distribution: limited, wide and sporadic. Among the clusters identified in the genomes were 192 that are likely to be responsible for the synthesis of sphinganine-analog metabolites (SAMs), a class of metabolites that disrupt sphingolipid metabolism and that include fumonisin mycotoxins. We based the identification of the SAM clusters on the presence within a putative cluster of genes encoding three enzymes that we predict are required for synthesis of all SAMs: a reducing polyketide synthase, an amino transferase, and a dehydrogenase. Phylogenetic analyses resolved the putative SAM clusters into six homolog groups: the fumonisin cluster and clusters SAM1 – SAM5. We propose that each of these six clusters confers the ability to synthesize a family of structurally distinct SAMs. Our analyses also suggest that some SAM clusters have undergone horizontal transfer among Fusarium species, and indicate that two or more SAM clusters occur in some Fusarium genomes. In addition, SAM clusters tend to have limited and/or sporadic distributions among Fusarium. The SM products of clusters SAM1 – SAM5 are not known, but we predict that SAM5 is responsible for synthesis of 2-Amino-14, 16-dimethyloctadecan-3-ol, a SAM previously reported in F. avenaceum. The somewhat common occurrence of SAM clusters among the 343 Fusarium genomes suggests that the ability to disrupt sphingolipid metabolism provides an ecological advantage to many but not all fusaria.