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Infection and Immunity, July 1999, p. 3193-3198, Vol. 67, No. 7
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Unanticipated Heterogeneity in Growth Rate and Virulence among Candida albicans AAF1 Null Mutants

Günter Rieg,1 Yue Fu,1 Ashraf S. Ibrahim,1 Xiang Zhou,1 Scott G. Filler,1,2 and John E. Edwards Jr.1,2,*

Division of Infectious Diseases, St. John's Cardiovascular Research Center, Department of Medicine, Harbor-UCLA Research and Education Institute, Torrance, California 90502,1 and UCLA School of Medicine, Los Angeles, California 900242

Received 8 February 1999/Returned for modification 29 March 1999/Accepted 2 April 1999

The disruption of a specific gene in Candida albicans is commonly used to determine the function of the gene product. We disrupted AAF1, a gene of C. albicans that causes Saccharomyces cerevisiae to flocculate and adhere to endothelial cells. We then characterized multiple heterozygous and homozygous mutants. These null mutants adhered to endothelial cells to the same extent as did the parent organism. However, mutants with presumably the same genotype revealed significant heterogeneity in their growth rates in vitro. This heterogeneity was not the result of the transformation procedure per se, nor was it caused by differences in the expression or function of URA3, a marker used in the process of gene disruption. The growth rate among the different heterozygous and homozygous null mutants was positively correlated with in vivo virulence in mice. It is possible that the variable phenotypes of C. albicans were due to mutations outside of the AAF1 coding region that were introduced during the gene disruption process. These results indicate that careful phenotypic characterization of mutants of C. albicans generated through targeted gene disruption should be performed to exclude the introduction of unexpected mutations that may influence pathogenicity in mice.

* Corresponding author. Mailing address: Division of Infectious Diseases, St. John's Cardiovascular Research Center, Harbor-UCLA Research and Education Institute, Bldg. RB2, 1124 West Carson St., Torrance, CA 90502. Phone: (310) 222-3813. Fax: (310) 782-2016. E-mail: Edwards{at}HUMC.EDU.

Infection and Immunity, July 1999, p. 3193-3198, Vol. 67, No. 7
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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