The function of Fig1, a transmembrane protein of the low-affinity calcium uptake system (LACS) in fungi, was examined for its role in the growth and development of the plant pathogen Fusarium graminearum. The Delta fig1 mutants failed to produce mature perithecia, and sexual development was halted prior to the formation of perithecium initials. The loss of Fig1 function also resulted in a reduced vegetative growth rate. Macroconidium production was reduced 70-fold in the Delta fig1 mutants compared to the wild type. The function of the high-affinity calcium uptake system (HACS), comprised of the Ca2+ channels Mid1 and Cch1, was previously characterized for F. graminearum. To better understand the roles of the LACS and the HACS, Delta fig1 Delta mid1, Delta fig1 Delta cch1, and Delta fig1 Delta mid1 Delta cch1 double and triple mutants were generated, and the phenotypes of these mutants were more severe than those of the Delta fig1 mutants. Pathogenicity on wheat was unaffected for the Delta fig1 mutants, but the Delta fig1 Delta mid1, Delta fig1 Delta cch1, and Delta fig1 Delta mid1 Delta cch1 mutants, lacking both LACS and HACS functions, had reduced pathogenicity. Additionally, Delta fig1 mutants of Neurospora crassa were examined and did not affect filamentous growth or female fertility in a Delta fig1 mating type A strain, but the Delta fig1 mating type a strain failed to produce fertile fruiting bodies. These results are the first report of Fig1 function in filamentous ascomycetes and expand its role to include complex fruiting body and ascus development.
