|Chang, Perng kuang|
|Scharfenstein, Leslie - Les|
|Wei, Qijian - Mei mei|
Submitted to: Fungal Biology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 12/2/2011
Publication Date: 1/10/2012
Citation: Chang, P.-K., Scharfenstein, L.L., Ehrlich, K., Wei, Q., Bhatnagar, D., Ingber, B.F. 2012. Effects of laeA deletion on Aspergillus flavus conidial development and hydrophobicity may contribute to loss of aflatoxin production. Fungal Biology. 116:298-307. Interpretive Summary: The yellow green mold Aspergillus flavus is a major producer of the carcinogenic aflatoxins that pose a great risk to human and animal health. Aflatoxin production is known to be tightly linked to fungal development. To better understand the molecular mechanisms that underlie these two processes, we knocked out a critical regulatory gene that is involved in the production of many secondary metabolites. Impairment of this gene severely decreased expression of genes important for development and dissemination; it altered formation of conidiophores and elongation of conidial chains along with other physiological traits. This information, used along with other preventive strategies, may help to alleviate aflatoxin contamination of crops in the field.
Technical Abstract: The laeA gene encodes a nuclear protein that governs production of multiple fungal secondary metabolites. We examined the effects of laeA deletion in an Aspergillus flavus strain. Compared to wild type, expression of genes involved in secondary metabolism, conidiation and hydrophobicity was drastically reduced, but expression of genes involved in primary metabolism was decreased to a lesser extent. Dependent on medium composition, the laeA deletion strains exhibited varied morphological phenotypes. Asexual development such as formation of conidiophores and elongation of conidial chains was altered along with other physiological changes. Contrary to what was reported previously we found that the laeA deletion strains expressed low levels of aflR but were unable to produce aflatoxins or their precursors. The aforementioned defects were remediated in laeA addback strains. Our results suggest that loss of laeA exerts pleiotropic effects on expression of genes involved in development and secondary metabolite biosynthesis.