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J Bacteriol, June 1998, p. 3031-3038, Vol. 180, No. 12
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

The Developmentally Regulated alb1 Gene of Aspergillus fumigatus: Its Role in Modulation of Conidial Morphology and Virulence

Huei-Fung Tsai,1 Yun C. Chang,1 Ronald G. Washburn,2 Michael H. Wheeler,3 and K. J. Kwon-Chung1,*

Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 208921; Section of Infectious Diseases, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina 270062; and Cotton Pathology Research Unit, Southern Crops Research Laboratory, USDA Agricultural Research Service, College Station, Texas 778453

Received 12 February 1998/Accepted 14 April 1998

Aspergillus fumigatus, an important opportunistic pathogen which commonly affects neutropenic patients, produces conidia with a bluish-green color. We identified a gene, alb1, which is required for conidial pigmentation. The alb1 gene encodes a putative polyketide synthase, and disruption of alb1 resulted in an albino conidial phenotype. Expression of alb1 is developmentally regulated, and the 7-kb transcript is detected only during the conidiation stage. The alb1 mutation was found to block 1,3,6,8-tetrahydroxynaphthalene production, indicating that alb1 is involved in dihydroxynaphthalene-melanin biosynthesis. Scanning electron microscopy studies showed that the alb1 disruptant exhibited a smooth conidial surface, whereas complementation of the alb1 deletion restored the echinulate wild-type surface. Disruption of alb1 resulted in a significant increase in C3 binding on conidial surfaces, and the conidia of the alb1 disruptant were ingested by human neutrophils at a higher rate than were those of the wild type. The alb1-complemented strain producing bluish-green conidia exhibited inefficient C3 binding and neutrophil-mediated phagocytosis quantitatively similar to those of the wild type. Importantly, the alb1 disruptant had a statistically significant loss of virulence compared to the wild-type and alb1-complemented strains in a murine model. These results suggest that disruption of alb1 causes pleiotropic effects on conidial morphology and fungal virulence.

* Corresponding author. Mailing address: NIH/NIAID, Building 10, Room 11C304, 10 Center Dr., MSC 1882, Bethesda, MD 20892-1882. Phone: (301) 496-1602. Fax: (301) 402-1003. E-mail: June_Kwon-Chung{at}NIH.GOV.

J Bacteriol, June 1998, p. 3031-3038, Vol. 180, No. 12
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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