Invited Presenter

Elizabeth K. Brauer ^1,2, Whynn Bosnich ¹, Kirsten Holy ¹, Indira Thapa ¹, Srinivasan Krishnan ³, Moatter Syed ^1,2, Melissa Bredow ^4,a, Amanda Sproule ¹, Monique Power ^1,2, Anne Johnston ¹, Michel Cloutier ¹, Naveen Haribabu ⁵, Izhar U.H. Khan ¹, Jean-Simon Diallo ⁵, Jacqueline Monaghan ⁴, Denise Chabot ¹, David P. Overy ¹, Rajagopal Subramaniam ¹, Miguel Piñeros ^3,6, Barbara Blackwell ¹ and Linda J. Harris ¹
1. Ottawa Research and Development Centre, Agriculture and Agri-Food Canada, Ottawa, ON, Canada, K1A 0C6
2. Department of Biology, University of Ottawa, Ottawa, ON, Canada
3. Boyce Thompson Institute for Plant Research, Cornell University, Ithaca, NY 14853
4. Biology Department, Queen’s University, Biological Sciences Complex, 116 Barrie St, Kingston, ON, Canada, K7L 3N6
5. Ottawa Hospital Research Institute, 501 Smyth Road, Ottawa, Ontario K1H 8L6, Canada
6. Robert W. Holley Center for Agriculture and Health, United States Department of Agriculture–Agricultural Research Service, Cornell University, Ithaca, NY 14853
a. Present address: Department of Plant Pathology and Microbiology, Iowa State University, Ames IA 50011
Corresponding Author: Elizabeth Brauer, elizabeth.brauer@agr.gc.ca

Elizabeth Brauer

Fusarium graminearum produces secondary metabolite virulence factors during infection to overcome host defenses and survive in a nutrient-poor environment. We recently identified a cyclic lipopeptide produced by Fusarium graminearum called gramillin which is a virulence factor in maize silks but not in wheat spikes. Gramillin is toxic to maize but not to wheat cells, though the mechanism for gramillin toxicity is unknown. Our work indicates that gramillin targets plant membranes which it disrupts ion homeostasis causing necrosis and cell death. In artificial membranes, gramillin functions as a cation-conducting ionophore, and in leaf mesophyll cells, gramillin causes plasma membrane depolarization and K⁺ leakage. Gramillin’s toxic effect on plant membranes extends across monocots and dicots where it also induces cellular stress responses including a ROS burst. Its virulence function extends to promoting infection in barley spikes and Arabidopsis seedlings where it suppresses callose formation and promotes expression of secondary metabolite biosynthetic genes.  Gramillin-induced ROS bursts in the plant are dependent on the stress response genes ILK1 and RBOHD. During infection, RBOHD and ILK1 suppress callose production and enhance fungal virulence gene expression, leading to plant susceptibility. We conclude that gramillin’s ionophore activity is detected by plants and that gramillin targets plant membrane responses to promote susceptibility to the F. graminearum fungal pathogen.