About

B. Gillian Turgeon is a Professor and Section Head of Plant Pathology and Plant-Microbe Biology within the School of Integrative Plant Science at Cornell University. Her research focuses on the discovery of attributes that distinguish pathogens from non-pathogens and symbionts from pathogens or non-pathogens, which is a central goal in plant pathology. Her work overlaps with the study of fungal reproductive strategies, emphasizing recognition issues involved in cellular communication and interaction between fungi and their plant hosts. This research aims to understand how cells recognize self from non-self, facilitating either mutualistic associations or disease causation. Her practical research includes understanding how fungi travel via spore dissemination, with the goal of developing global solutions for preventing plant disease. She applies a broad range of classical genetic, molecular genetic, genomic, biochemical, and cytological tools in her studies, utilizing three model fungi: Cochliobolus heterostrophus, Setosphaeria turcica, and Fusarium graminearum/Gibberella zeae, which are pathogens of corn, wheat, barley, and rice. Her contributions to the field have been recognized through her election as a Fellow of the American Academy of Microbiology in 2013. She holds a Doctorate from the University of Dayton and C.F. Kettering Research Institute, a Master of Science from Carleton University, and a Bachelor of Science from Carleton University. Her research interests include fungal pathogens of cereals, fungal genomics, and secondary metabolites.

Research topics

• Genetics
• Biology
• Biochemistry
• Chemistry
• Evolutionary biology
• Microbiology
• Ecology

Selected publications

• Additional file 3 of Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  Figshare · 2026-01-01

  articleOpen access

  Supplementary Material 3.

  PublisherDOI

• Additional file 3 of Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  Figshare · 2026-01-01

  articleOpen access

  Supplementary Material 3.

  PublisherDOI

• Additional file 1 of Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  Figshare · 2026-01-01

  articleOpen access

  Supplementary Material 1.

  PublisherDOI

• Additional file 2 of Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  Figshare · 2026-01-01

  articleOpen access

  Supplementary Material 2.

  PublisherDOI

• Additional file 1 of Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  Figshare · 2026-01-01

  articleOpen access

  Supplementary Material 1.

  PublisherDOI

• Additional file 2 of Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  Figshare · 2026-01-01

  articleOpen access

  Supplementary Material 2.

  PublisherDOI

• Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  Figshare · 2026-01-01

  otherOpen access

  Abstract Background Fumonisins are among the mycotoxins of most concern to food safety and are structurally similar to AAL toxins, a family of host selective toxins. Together, these two toxin families are produced by ecologically diverse species in three fungal classes: AAL toxins by Alternaria arborescens in class Dothideomycetes and fumonisins by Aspergillus species in class Eurotiomycetes and by Fusarium and Tolypocladium species in class Sordariomycetes. Although structural similarities suggest that AAL toxins and fumonisins have a common biogenic origin, the evolutionary origins and relationships of their biosynthetic genes are not clear. Results Here, we used BLAST, comparative genomic, phylogenetic, and functional analyses to identify and characterize homologs of the fumonisin biosynthetic gene (FUM) cluster in fungi. Our analyses identified FUM cluster homologs in A. arborescens and in species of Aspergillus, Bipolaris, Fusarium, and Tolypocladium. The results also suggest that the FUM cluster likely evolved from an ancestral cluster with 11 FUM genes through multiple mechanisms, including (1) vertical transmission, (2) acquisition of additional genes by some cluster lineages, (3) duplication of individual FUM genes, and (4) either horizontal transfer of the cluster from the Sordariomycetes to the Dothideomycetes or duplication and differential loss. Overall, our results suggest that the AAL toxin and FUM clusters share a common evolutionary origin and indicate that structural variation of the chemical products of AAL toxins and fumonisins has resulted from variation in FUM gene content and function. Conclusions The presence of FUM clusters in relatively few classes of fungi with distinct lifestyles (plant versus insect/animal pathogens) suggests an important role of FUM metabolites in diverse fungal-host interactions. This study advances our understanding of the role of specific FUM genes in toxin biosynthesis and will improve our ability to detect and predict the ability of fungi found in food and animal feed to synthesize these mycotoxins.

  PublisherDOI

• Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  Figshare · 2026-01-01

  otherOpen access

  Abstract Background Fumonisins are among the mycotoxins of most concern to food safety and are structurally similar to AAL toxins, a family of host selective toxins. Together, these two toxin families are produced by ecologically diverse species in three fungal classes: AAL toxins by Alternaria arborescens in class Dothideomycetes and fumonisins by Aspergillus species in class Eurotiomycetes and by Fusarium and Tolypocladium species in class Sordariomycetes. Although structural similarities suggest that AAL toxins and fumonisins have a common biogenic origin, the evolutionary origins and relationships of their biosynthetic genes are not clear. Results Here, we used BLAST, comparative genomic, phylogenetic, and functional analyses to identify and characterize homologs of the fumonisin biosynthetic gene (FUM) cluster in fungi. Our analyses identified FUM cluster homologs in A. arborescens and in species of Aspergillus, Bipolaris, Fusarium, and Tolypocladium. The results also suggest that the FUM cluster likely evolved from an ancestral cluster with 11 FUM genes through multiple mechanisms, including (1) vertical transmission, (2) acquisition of additional genes by some cluster lineages, (3) duplication of individual FUM genes, and (4) either horizontal transfer of the cluster from the Sordariomycetes to the Dothideomycetes or duplication and differential loss. Overall, our results suggest that the AAL toxin and FUM clusters share a common evolutionary origin and indicate that structural variation of the chemical products of AAL toxins and fumonisins has resulted from variation in FUM gene content and function. Conclusions The presence of FUM clusters in relatively few classes of fungi with distinct lifestyles (plant versus insect/animal pathogens) suggests an important role of FUM metabolites in diverse fungal-host interactions. This study advances our understanding of the role of specific FUM genes in toxin biosynthesis and will improve our ability to detect and predict the ability of fungi found in food and animal feed to synthesize these mycotoxins.

  PublisherDOI

• Distribution and shared evolutionary history of the Fumonisin and AAL toxin biosynthetic gene clusters

  BMC Genomics · 2026-01-21

  articleOpen access
  PublisherDOI

• <i>Cochliobolus miyabeanus</i> species-specific identification using nonribosomal peptide synthetase (NRPS) and polyketide synthase (PKS)-encoding genes associated with virulence to rice

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-23

  preprintOpen accessSenior authorCorresponding

  Abstract Cochliobolus miyabeanus causes brown spot disease of rice. For necrotrophic Cochliobolus spp., some small molecule products of nonribosomal peptide synthetases (NRPS) and polyketide synthases (PKS) are known pathogenicity and/or virulence factors, often acting in a host-specific manner. Previous whole genome analyses across Cochliobolus species identified 11 NRPS- and 21 PKS - encoding genes in C. miyabeanus . First purpose of the current study was to examine the effect of deletion of ten of the discontinuously distributed genes (corresponding to JGI protein IDs 4446, 5802, 6546, 7015, 9064, 41693, 41753, 83551, 98843 and 107726) on virulence of C . miyabeanus to rice. A second purpose, based on results of the first, was to develop a PCR method to specifically identify C. miyabeanus and to distinguish it from other closely related Cochliobolus spp. We show that deletion of seven of the genes resulted in mutants that were reduced in virulence compared to the wild-type strain WK1C. Wild-type developed large dark brown necrotic lesions surrounded by chlorotic halos, while the mutants produced smaller, light brown spots with chlorosis. These results suggest that the products of these genes contribute to brown spot disease. In addition, we identified PKS and NPS SNPs that discriminate between C. miyabeanus and other species of Cochliobolus .

  PublisherOA PDFDOI

Recent grants

• Secondary Metabolite Niches: Whole Genome Functional Analysis of Non-Ribosomal Peptide Synthetases

  NSF · $571k · 2006–2010

Frequent coauthors

• O. C. Yoder

  Plant (United States)

  114 shared

• Shunwen Lu

  Agricultural Research Service

  67 shared

• Scott Kroken

  60 shared

• Scott Baker

  Environmental Molecular Sciences Laboratory

  53 shared

• Harold Kistler

  University of Minnesota

  50 shared

• Liane Rosewich Gale

  University of Minnesota

  43 shared

• Karen Hilburn

  43 shared

• Kye-Yong Seong

  Twin Cities Orthopedics

  42 shared

Labs

• Turgeon LabPI

Awards & honors

• Fellow, American Academy of Microbiology 2013