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GAC1, a gene encoding a putative GTPase-activating protein, regulates bikaverin biosynthesis in Fusarium verticillioides

     Department of Plant Pathology and Microbiology, The Program for the Biology of Filamentous Fungi, Texas A&M University, College Station, Texas 77843-2132

Jillian A. Brown
Courtney B. Williams
Lorena L. Canales

     Bioenvironmental Sciences Program, Department of Plant Pathology and Microbiology, Texas A&M University, College Station, Texas 77843-2132

Won-Bo Shim ¹

     Department of Plant Pathology and Microbiology, The Program for the Biology of Filamentous Fungi, Texas A&M University, College Station, Texas 77843-2132

Fusarium verticillioides (teleomorph Gibberella moniliformis) is an ascomycete known to produce a variety of secondary metabolites, including fumonisins, fusaric acid and bikaverin. These metabolites are synthesized when the fungus is under stress, notably nutrient limitations. To date we have limited understanding of the complex regulatory process associated with fungal secondary metabolism. In this study we generated a collection of F. verticillioides mutants by using REMI (restriction enzyme mediated integration) mutagenesis and in the process identified a strain, R647, that carries a mutation in a gene designated GAC1. Mutation in the GAC1 locus, which encodes a putative GTPase activating protein, resulted in the increased production of bikaverin, suggesting that GAC1 is negatively associated with bikaverin biosynthesis. Complementation of R647 with the wild-type GAC1 gene restored the bikaverin production level to that of the wild-type progenitor, demonstrating that gac1 mutation was directly responsible for the overproduction of bikaverin. We also demonstrated that AREA, encoding global nitrogen regulator, and PKS4, encoding polyketide synthase, are downstream genes that respectively are regulated positively and negatively by GAC1. Our results suggest that GAC1 plays an important role in signal transduction regulating bikaverin production in F. verticillioides.

Key words: restriction enzyme mediated integration, secondary metabolism, signal transduction