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J. Biol. Chem., Vol. 276, Issue 52, 48988-48996, December 28, 2001
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From the Candida albicans, normally a human
commensal, can cause fatal systemic infections under certain
circumstances. Its unique ability to switch from yeast to hyphal growth
in response to various environmental signals is inherent to its
pathogenicity. Filamentation is regulated by multiple pathways
including a Cph1-mediated mitogen-activated protein kinase
pathway, an Efg1-mediated cAMP/PKA pathway, and a
Cph2 pathway. To gain a general picture of how these various signaling
pathways regulate differential gene expression during filamentation, we
have constructed a partial C. albicans DNA array of 7,000 genes and used it to study the gene expression profiles using various
mutants and growth conditions. By combining this novel technology with
a new liquid medium in which cph1/cph1 is defective in
filamentation, previously identified differentially expressed genes
(ECE1, HWP1, HYR1,
RBT1, SAPs5-6, and RBT4) are found
to be regulated by all three pathways. In addition, two novel genes,
DDR48 and YPL184, have been found to be
differentially regulated during hyphal development and by all three
pathways. This suggests that distinct filamentation signaling pathways
converge to regulate a common set of differentially expressed genes. As one of the mechanisms for the observed convergence, we find that the
transcription of a key regulator, TEC1, is regulated by
Efg1 and Cph2. Importantly, most of the genes regulated by multiple filamentation pathways encode known virulence factors. Perhaps, C. albicans utilizes converging pathways to regulate its
vital virulence factors to ensure its survival and pathogenicity in various host environments.
DNA Array Studies Demonstrate Convergent Regulation of Virulence
Factors by Cph1, Cph2, and Efg1 in Candida albicans*
§,¶,
,
Department of Biological Chemistry,
University of California, Irvine, California 92697-1700 and
** Beckman Coulter, Inc., Advanced Technology Center,
Fullerton, California 92834-3100
*
This work was supported in part by Burroughs Wellcome,
University of California Universitywide AIDS Research Program Grant R00-1-058, and National Institutes of Health Grant GM55155.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Predoctoral fellow of a training grant from the University of
California Systemwide Biotechnology Research and Education program.
To whom correspondence should be addressed. Tel.:
949-824-1137; Fax: 949-824-2688; E-mail: h4liu@uci.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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