Present address: Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213, USA.
Candida albicans transcription factor Rim101 mediates pathogenic interactions through cell wall functions
Article first published online: 10 JUL 2008
© 2008 The Authors. Journal compilation © 2008 Blackwell Publishing Ltd
Volume 10, Issue 11, pages 2180–2196, November 2008
How to Cite
Nobile, C. J., Solis, N., Myers, C. L., Fay, A. J., Deneault, J.-S., Nantel, A., Mitchell, A. P. and Filler, S. G. (2008), Candida albicans transcription factor Rim101 mediates pathogenic interactions through cell wall functions. Cellular Microbiology, 10: 2180–2196. doi: 10.1111/j.1462-5822.2008.01198.x
- Issue published online: 13 OCT 2008
- Article first published online: 10 JUL 2008
- Received 7 March, 2008; revised 11 May, 2008; accepted 22 June, 2008.
pH-responsive transcription factors of the Rim101/PacC family govern virulence in many fungal pathogens. These family members control expression of target genes with diverse functions in growth, morphology and environmental adaptation, so the mechanistic relationship between Rim101/PacC and infection is unclear. We have focused on Rim101 from Candida albicans, which we find to be required for virulence in an oropharyngeal candidiasis model. Rim101 affects the yeast–hypha morphological transition, a major virulence requirement in disseminated infection models. However, virulence in the oropharyngeal candidiasis model is independent of the yeast–hypha transition because it is unaffected by an nrg1 mutation, which prevents formation of yeast cells. Here we have identified Rim101 target genes in an nrg1Δ/Δ mutant background and surveyed function using an overexpression-rescue approach. Increased expression of Rim101 target genes ALS3, CHT2, PGA7/RBT6, SKN1 or ZRT1 can partially restore pathogenic interaction of a rim101Δ/Δ mutant with oral epithelial cells. Four of these five genes govern cell wall structure. Our results indicate that Rim101-dependent cell wall alteration contributes to C. albicans pathogenic interactions with oral epithelial cells, independently of cell morphology.