Normal adaptation of Candida albicans to the murine gastrointestinal tract requires Efg1p-dependent regulation of metabolic and host defense genes

  1. Get@NRC: Normal adaptation of Candida albicans to the murine gastrointestinal tract requires Efg1p-dependent regulation of metabolic and host defense genes (Opens in a new window)
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Journal titleEukaryotic Cell
Pages3749; # of pages: 13
SubjectDNA binding protein; EFG1 protein, Candida albicans; fungal protein; superoxide dismutase; transcription factor; transcriptome; animal; article; Bagg albino mouse; Candida albicans; cecum; DNA microarray; fungal gene; fungus hyphae; gastrointestinal tract; gene expression; gene expression regulation; genetics; growth, development and aging; host pathogen interaction; ileum; lipid metabolism; metabolism; microbiology; mouse; physiology; upregulation; Animals; Candida albicans; Cecum; DNA-Binding Proteins; Fungal Proteins; Gastrointestinal Tract; Gene Expression; Gene Expression Regulation, Fungal; Genes, Fungal; Host-Pathogen Interactions; Hyphae; Ileum; Lipid Metabolism; Mice; Mice, Inbred BALB C; Oligonucleotide Array Sequence Analysis; Superoxide Dismutase; Transcription Factors; Transcriptome; Up-Regulation; Candida albicans; Murinae; Mus
AbstractAlthough gastrointestinal colonization by the opportunistic fungal pathogen Candida albicans is generally benign, severe systemic infections are thought to arise due to escape of commensal C. albicans from the gastrointestinal (GI) tract. The C. albicans transcription factor Efg1p is a major regulator of GI colonization, hyphal morphogenesis, and virulence. The goals of this study were to identify the Efg1p regulon during GI tract colonization and to compare C. albicans gene expression during colonization of different organs of the GI tract. Our results identified significant differences in gene expression between cells colonizing the cecum and ileum. During colonization, efg1- null mutant cells expressed higher levels of genes involved in lipid catabolism, carnitine biosynthesis, and carnitine utilization than did colonizing wild-type (WT) cells. In addition, during laboratory growth, efg1- null mutant cells grew to a higher density than WT cells. The efg1- null mutant grew in depleted medium, while WT cells could grow only if the depleted medium was supplemented with carnitine, a compound that promotes the metabolism of fatty acids. Altered gene expression and altered growth capability support the ability of efg1- cells to hypercolonize naïve mice. Also, Efg1p was shown to be important for transcriptional responses to the stresses present in the cecum environment. For example, during colonization, SOD5, encoding a superoxide dismutase, was highly upregulated in an Efg1p-dependent manner. Ectopic expression of SOD5 in an efg1- null mutant increased the fitness of the efg1- null mutant cells during colonization. These data show that EFG1 is an important regulator of GI colonization. © American Society for Microbiology. All Rights Reserved.
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AffiliationNational Research Council Canada (NRC-CNRC); NRC Biotechnology Research Institute (BRI-IRB)
Peer reviewedYes
NPARC number21269733
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Record identifier14854058-cb1e-45b8-804c-bac4199a5bc0
Record created2013-12-13
Record modified2016-05-09
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