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Applied and Environmental Microbiology, September 2008, p. 5674-5685, Vol. 74, No. 18
0099-2240/08/$08.00+0     doi:10.1128/AEM.00565-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Morphological Transitions Governed by Density Dependence and Lipoxygenase Activity in Aspergillus flavus{triangledown} ,{dagger}

S. Horowitz Brown,1 R. Zarnowski,2 W. C. Sharpee,1 and N. P. Keller1,2*

Department of Plant Pathology,1 Department of Medical Microbiology and Immunology, University of Wisconsin—Madison, 1550 Linden Dr., Madison, Wisconsin 53706-15982

Received 9 March 2008/ Accepted 10 July 2008

Aspergillus flavus differentiates to produce asexual dispersing spores (conidia) or overwintering survival structures called sclerotia. Results described here show that these two processes are oppositely regulated by density-dependent mechanisms and that increasing the cell density (from 101 to 107 cells/plate) results in the lowest numbers of sclerotial and the highest numbers of conidial. Extract from spent medium of low-cell-density cultures induced a high-sclerotium-number phenotype, whereas high-cell-density extract increased conidiation. Density-dependent development is also modified by changes in lipid availability. Exogenous linoleic acid increased sclerotial production at intermediate cell densities (104 and 105 cells/plate), whereas oleic and linolenic acids inhibited sclerotium formation. Deletion of Aflox encoding a lipoxygenase (LOX) greatly diminished density-dependent development of both sclerotia and conidia, resulting in an overall increase in the number of sclerotia and a decrease in the number of conidia at high cell densities (>105 cells/plate). Aflox mutants showed decreased linoleic acid LOX activity. Taken together, these results suggest that there is a quorum-sensing mechanism in which a factor(s) produced in dense cultures, perhaps a LOX-derived metabolite, activates conidium formation, while a factor(s) produced in low-density cultures stimulates sclerotium formation.


* Corresponding author. Mailing address: 3476 Microbial Science Building, Department of Medical Microbiology and Immunology and Department of Plant Pathology, UW—Madison, 1550 Linden Dr., Madison, WI 53706. Phone: (608) 262-9795. Fax: (608) 262-8418. E-mail: npk{at}plantpath.wisc.edu

{triangledown} Published ahead of print on 25 July 2008.

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


Applied and Environmental Microbiology, September 2008, p. 5674-5685, Vol. 74, No. 18
0099-2240/08/$08.00+0     doi:10.1128/AEM.00565-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.




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