The filamentous fungus Aspergillus flavus is a plant and human pathogen predominantly found in the soil as spores or sclerotia and is capable of producing various secondary metabolites (SM) such as the carcinogenic mycotoxin aflatoxin. Recently, we have discovered a novel nuclear chromatin binding complex (KERS) that contains the JARID1-type histone demethylase KdmB, a putative cohesion acetyl transferase EcoA, a class I type histone deacetylase RpdA and the PHD ring finger reader protein SntB in the model filamentous fungus Aspergillus nidulans. Here, we show the presence of the KERS complex in A. flavus by immunoprecipitation-coupled mass spectrometry and constructed kdmBΔ and rpdAΔ strains to study their roles in fungal development, SM production and histone post-translational modifications (HPTMs). We found that KdmB and RpdA couple the regulation of SM gene clusters with fungal light-responses and HPTMs. KdmB and RpdA have opposing roles in light-induced asexual conidiation, while both factors are positive regulators of sclerotia development through the nsdC and nsdD pathway. KdmB and RpdA are essential for the productions of aflatoxin (similar to findings for SntB) as well as cyclopiazonic acid, ditryptophenaline and leporin B through controlling the respective SM biosynthetic gene clusters. We further show that both KdmB and RpdA regulate H3K4me3 and H3K9me3 levels, while RpdA also acts on H3K14ac levels in nuclear extracts. Therefore, the chromatin modifiers KdmB and RpdA of the KERS complex are key regulators for fungal development and SM metabolism in A. flavus.

Fusarium head blight (FHB) is one of the most devastating diseases of cereal crops, causing severe reduction in yield and quality of grain worldwide. In the United States, the major causal agent of FHB is the mycotoxigenic fungus, Fusarium graminearum. The contamination of grain with mycotoxins, including deoxynivalenol and zearalenone, is a particularly serious concern due to its impact on the health of humans and livestock. For the past few decades, multidisciplinary studies have been conducted on management strategies designed to reduce the losses caused by FHB. However, effective management is still challenging due to the emergence of fungicide-tolerant strains of F. graminearum and the lack of highly resistant wheat and barley cultivars. This review presents multidisciplinary approaches that incorporate advances in genomics, genetic-engineering, new fungicide chemistries, applied biocontrol, and consideration of the disease cycle for management of FHB.

Phytopathogenic Alternaria species are renown for production of toxins that contribute to virulence on host plants. Typically, these toxins belong to well-known secondary metabolite chemical classes including polyketides, non-ribosomal peptides and terpenes. However, the purported host toxin brassicicolin A produced by A. brassicicola is an isocyanide, a chemical class whose genetics and encoding gene structure is largely unknown. The chemical structure of brassicicolin A shows it to have similarity to the recently characterized fumicicolins derived from the Aspergillus fumigatus isocyanide synthase CrmA. Examination of the A. brassicicola genome identified AbcrmA, a putative homolog with 64% identity to A. fumigatus CrmA. Deletion of AbcrmA resulted in loss of production of brassicicolin A. Contrary to reports that brassicicolin A is a host-specific toxin, the ΔAbcrmA mutants were equally virulent as the wildtype on Brassica hosts. However, in line with results of A. fumigatus CrmA generated metabolites, we find that brassicicolin A increased 360-fold under copper limited conditions. Also, like A. fumigatus CrmA derived metabolites, we find brassicicolin A to be a broad-spectrum antimicrobial. We speculate that CrmA-like isocyanide synthase products provide the producing fungi a fitness advantage in copper depleted environments.