ArticleCellular microbiology2008
Candida albicans transcription factor Rim101 mediates pathogenic interactions through cell wall functions.
Article in Cellular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed.
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- Decoding the host-pathogen interspecies molecular crosstalk during oral candidiasis in humans: anFrontiers in genetics · 2023Article
- Reinforcement amid genetic diversity in the Candida albicans biofilm regulatory network.PLoS pathogens · 2023Article
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- Evolutionary Morphogenesis of Sexual Fruiting Bodies in Basidiomycota: Toward a New Evo-Devo Synthesis.Microbiology and molecular biology reviews : MMBR · 2022Review
- Improvement of laccase activity by silencing PacC in Ganoderma lucidum.World journal of microbiology & biotechnology · 2022Article
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- Nutritional immunity: targeting fungal zinc homeostasis.Heliyon · 2021Review
- Determining Aspergillus fumigatus transcription factor expression and function during invasion of the mammalian lung.PLoS pathogens · 2021Article
- An expanded cell wall damage signaling network is comprised of the transcription factors Rlm1 and Sko1 in Candida albicans.PLoS genetics · 2020Article
32 more citing papers are in PubMed but not listed here.
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8 authors.
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Abstract
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 nrg1Delta/Delta 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 rim101Delta/Delta 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.
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