Submitted to: Molecular Microbiology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 9/18/2006
Publication Date: 10/18/2006
Citation: Li, S., Myung, K., Guse, D., Donkin, B., Proctor, R., Grayburn, W.S., Calvo, A.M. 2006. FvVE1 regulates filamentous growth, the ratio of microconidia to macroconidia and cell wall formation in Fusarium verticillioides. Molecular Microbiology. 62(5):1418-1432. Interpretive Summary: The fungus Fusarium verticillioides can cause ear and stalk rot of maize and can produce the carcinogenic toxin fumonisin B1 in infected maize kernels. In an effort to reduce the toxin contamination and diseases on maize in the U.S., we are studying genes in the fungus that are involved in fumonisin production and growth. In this report, we examined the function of the F. verticillioides VEA gene by inactivating it and observing the resulting effects on growth and development of the fungus. Deletion of VEA caused profound alterations in the growth and spore production of F. verticillioides. These alterations could be reversed by osmotic stabilizers, chemicals that stabilize the flow of water between the interior of cells and their external environment. A better understanding of the genes that affect the growth of F. verticillioides may lead to novel strategies for controlling fumonisin contamination and ear and stalk rot of maize.
Technical Abstract: The gene, veA, coordinates asexual and sexual sporulation in the fungal species Aspergillus nidulans. Whether veA has the same role in morphogenesis in other fungi has not been investigated. In this work, we studied the role of the veA homolog, FvVEA, in the fungus Fusarium verticillioides. Deletion of FvVEA suppressed aerial hyphal growth and reduced colony surface hydrophobicity on solid media. In submerged cultures, FvVEA deletion caused loss of hyphal polarity, marked activation of conidiation, and yeast-like budding growth. In addition, FvVEA deletion markedly increased the ratio of macroconidia to microconidia. Supplementation of osmotic stabilizers restored wild-type phenotype to the deletion mutants, suggesting phenotypic alterations are related to cell wall defects. This is consistent with the hypersensitivity of FvVEA deletion mutants to the cell wall assembly disrupting agent SDS and with the 7% reduction in the mannoprotein content of mutants compared to the wild-type strain. However, no dramatic cell wall alterations were observed when mutants were examined by transmission electron microscopy. Our data strongly suggest that FvVEA is important for cell wall integrity, cell surface hydrophobicity, hyphal polarity and conidiation pattern.