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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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