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ARS Home » Southeast Area » New Orleans, Louisiana » Southern Regional Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #302669

Title: Transcriptomic profiles of Aspergillus flavus CA42, a strain that produces small sclerotia, by decanal treatment and after recovery

item Chang, Perng Kuang
item Scharfenstein, Leslie
item Mack, Brian
item Yu, Jiujiang
item Ehrlich, Kenneth

Submitted to: Fungal Genetics and Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/15/2014
Publication Date: 7/25/2014
Citation: Chang, P.-K., Scharfenstein, L.L., Mack, B.M., Yu, J., Ehrlich, K. 2014. Transcriptomic profiles of Aspergillus flavus CA42, a strain that produces small sclerotia, by decanal treatment and after recovery. Fungal Genetics and Biology. 68:39-47.

Interpretive Summary: Plant volatiles from cotton leaf, corn and soybean are able to inhibit Aspergillus flavus growth and/or aflatoxin production. To better understand volatile-fungus interactions we investigated how decanal, a cotton volatile, affected genome-wide gene expression of an A. flavus isolate that produces small sclerotia (S strain). We compared transcriptomic profiles of control, treated, and after recovery, which represent various developmental stages. Decanal treatment of the S strain A. flavus yielded fluffy variants. Gene ontology analyses showed that decanal treatment enriched cellular carbohydrate metabolism including aflatoxin biosynthesis and that cellular components affected were mainly associated with cell wall. The induced fluffy phenotype was related to lower transcript abundance of several genes associated with development of conidiophores. Transcriptional activation of genes in the aflatoxin and kojic acid gene clusters was correlated with expression of laeA, a regulatory gene of secondary metabolism. The study further identified candidate genes involved in vegetative growth, asexual development, and aflatoxin biosynthesis not previously known, which may aid in the efforts in the elimination and reduction of aflatoxin contamination of crops.

Technical Abstract: Aspergillus flavus is a ubiquitous saprophyte and is capable of producing many secondary metabolites including the carcinogenic aflatoxins. The A. flavus population that produces small sclerotia (S strain) has been implicated as the culprit for persistent aflatoxin contamination of crops in fields. We investigated how the plant volatile decanal, a C10 fatty aldehyde, affected the growth and development of the S strain A. flavus. Decanal treatment yielded fluffy variants lacking sclerotia and conidia and exhibiting a dosage-dependent radial colony growth. We used RNA-Seq analysis to examine transcriptomic changes induced by decanal and after recovery. Mature sclerotia contained only 80% of the total combined transcripts in comparison to 94% for the decanal treated culture. Gene ontology (GO) analysis showed that decanal treatment enriched oxidoreductase activity, and cellular carbohydrate metabolism, alcohol metabolism and aflatoxin biosynthesis. Affected cellular components were primarily associated with cell wall. The recovered culture resumed sclerotial production. Moreover, its GO functional categories significantly overlapped with those of the untreated sclerotial culture. Cellular components involved are mainly integral constituents to membrane. Five of the functions enriched, oxidoreductase activity, monooxygenase activity, electron carrier activity, heme binding, and iron binding are found in the normal sclerotial culture. The results suggested that decanal halted development at the vegetative state rendering the fungus unable to produce conidia and sclerotia. The induced fluffy phenotype could be related to lower transcript abundance of flbB, flbD, and flbE but not related to veA expression. Increased abundance of the laeA transcript in the treated culture was correlated with early transcriptional activation aflatoxin and kojic acid biosynthesis gene clusters. Expression profiles revealed subtle differences in timing of activation of the respective 55 secondary metabolite gene clusters.