Distinct Roles for VeA and LaeA in Development and Pathogenesis of<i>Aspergillus flavus</i>

<jats:title>ABSTRACT</jats:title><jats:p><jats:italic>Aspergillus flavus</jats:italic>, a mycotoxigenic filamentous fungus, colonizes several important agricultural crops, such as maize and peanuts. Two proteins, VeA and LaeA, known to form a nuclear complex in<jats:italic>Aspergillus nidulans</jats:italic>have been found to positively regulate developmental processes in several<jats:italic>Aspergillus</jats:italic>species. Here, an examination of near-isogenic<jats:italic>A. flavus</jats:italic>mutants differing in copy number of<jats:italic>veA</jats:italic>and<jats:italic>laeA</jats:italic>alleles (0, 1, or at least 2 each) revealed critical roles for VeA and LaeA in<jats:italic>A. flavus</jats:italic>development and seed colonization. In contrast to the wild type, both null mutants were unable to metabolize host cell lipid reserves and were inhibited by oleic acid in growth assays. The copy number of LaeA but not VeA appeared critical for a density-dependent sclerotial-to-conidial shift, since the multicopy<jats:italic>laeA</jats:italic>(MC<jats:italic>laeA</jats:italic>) strain produced relatively constant sclerotial numbers with increasing population size rather than showing the decrease in sclerotia seen in both the wild-type and MC<jats:italic>veA</jats:italic>strains. The MC<jats:italic>veA</jats:italic>-<jats:italic>laeA</jats:italic>strain yielded an intermediate phenotype. This study revealed unique roles of VeA and LaeA in seed pathogenesis and fungal biology, distinct from their cooperative regulatory functions in aflatoxin and sclerotial development.</jats:p>