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Applied and Environmental Microbiology, December 2008, p. 7607-7612, Vol. 74, No. 24
0099-2240/08/$08.00+0     doi:10.1128/AEM.01743-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Identification and Characterization of the Asperthecin Gene Cluster of Aspergillus nidulans{triangledown} ,{dagger}

Edyta Szewczyk,1,{ddagger} Yi-Ming Chiang,2,3 C. Elizabeth Oakley,1,§ Ashley D. Davidson,1 Clay C. C. Wang,3,4* and Berl R. Oakley1*

Department of Molecular Genetics, Ohio State University, 484 West 12th Avenue, Columbus, Ohio 43210,1 Graduate Institute of Pharmaceutical Science, Chia Nan University of Pharmacy and Science, Tainan 71710, Taiwan, Republic of China,2 Department of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles, California 90089,3 Department of Chemistry, College of Letters, Arts, and Sciences, University of Southern California, Los Angeles, California 900894

Received 29 July 2008/ Accepted 20 October 2008

The sequencing of Aspergillus genomes has revealed that the products of a large number of secondary metabolism pathways have not yet been identified. This is probably because many secondary metabolite gene clusters are not expressed under normal laboratory culture conditions. It is, therefore, important to discover conditions or regulatory factors that can induce the expression of these genes. We report that the deletion of sumO, the gene that encodes the small ubiquitin-like protein SUMO in A. nidulans, caused a dramatic increase in the production of the secondary metabolite asperthecin and a decrease in the synthesis of austinol/dehydroaustinol and sterigmatocystin. The overproduction of asperthecin in the sumO deletion mutant has allowed us, through a series of targeted deletions, to identify the genes required for asperthecin synthesis. The asperthecin biosynthesis genes are clustered and include genes encoding an iterative type I polyketide synthase, a hydrolase, and a monooxygenase. The identification of these genes allows us to propose a biosynthetic pathway for asperthecin.

* Corresponding author. Mailing address for Clay C. C. Wang: Department of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California, 1985 Zonal Ave., Los Angeles, CA 90089. Phone: (323) 442-1670. Fax: (323) 442-1390. E-mail: clayw{at}usc.edu. Present address for Berl R. Oakley: Department of Molecular Biosciences, University of Kansas, 1200 Sunnyside Ave., Lawrence, KS 66045. Phone: (785) 864-8170. Fax: (785) 864-5294. E-mail: boakley2{at}ku.edu

{triangledown} Published ahead of print on 31 October 2008.

{dagger} Supplemental material for this article may be found at http://aem.asm.org/.

{ddagger} Present address: Research Center for Infectious Diseases, Röntgenring 11, D-97070 Würzburg, Germany.

§ Present address: Department of Molecular Biosciences, University of Kansas, 1200 Sunnyside Ave., Lawrence, KS 66045.

Applied and Environmental Microbiology, December 2008, p. 7607-7612, Vol. 74, No. 24
0099-2240/08/$08.00+0     doi:10.1128/AEM.01743-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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