ArticleJournal of bacteriology1999
PHR1 and PHR2 of Candida albicans encode putative glycosidases required for proper cross-linking of beta-1,3- and beta-1,6-glucans.
Article in Journal of bacteriology, 1999. 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, 187 citations in OpenAlex.
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- The association of DNase I with antimicrobial photodynamic therapy affects Candida albicans gene expression and promotes immunomodulatory effects in mice with candidiasis.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025Article
- β-1,6-Glucan plays a central role in the structure and remodeling of the bilaminate fungal cell wall.eLife · 2024Article
- Regulation of candidalysin underlies Candida albicans persistence in intravascular catheters by modulating NETosis.PLoS pathogens · 2024Article
- Structural diversification of fungal cell wall in response to the stress signaling and remodeling during fungal pathogenesis.Physiology and molecular biology of plants : an international journal of functional plant biology · 2024Review
- Transcriptional expression ofMicrobiology spectrum · 2024Article
- Baicalin promotes β-1,3-glucan exposure inFrontiers in cellular and infection microbiology · 2024Article
- Review
- A glycosylated Phr1 protein is induced by calcium stress and its expression is positively controlled by the calcium/calcineurin signaling transcription factor Crz1 in Candida albicans.Cell communication and signaling : CCS · 2023Article
- Molecular association ofFrontiers in cellular and infection microbiology · 2023Review
- Associations of Rap1 with Cell Wall Integrity, Biofilm Formation, and Virulence in Candida albicans.Microbiology spectrum · 2022Article
- Nature of β-1,3-Glucan-Exposing Features on Candida albicans Cell Wall and Their Modulation.mBio · 2022Article
- Biomarkers of caspofungin resistance inVirulence · 2022Article
- Characterization ofCell surface (Amsterdam, Netherlands) · 2022Article
32 more citing papers are in PubMed but not listed here.
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Authors and funding
1 author at 1 institution in 1 country.
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Abstract
PHR1 and PHR2 encode putative glycosylphosphatidylinositol-anchored cell surface proteins of the opportunistic fungal pathogen Candida albicans. These proteins are functionally related, and their expression is modulated in relation to the pH of the ambient environment in vitro and in vivo. Deletion of either gene results in a pH-conditional defect in cell morphology and virulence. Multiple sequence alignments demonstrated a distant relationship between the Phr proteins and beta-galactosidases. Based on this alignment, site-directed mutagenesis of the putative active-site residues of Phr1p and Phr2p was conducted and two conserved glutamate residues were shown to be essential for activity. By taking advantage of the pH-conditional expression of the genes, a temporal analysis of cell wall changes was performed following a shift of the mutants from permissive to nonpermissive pH. The mutations did not grossly affect the amount of polysaccharides in the wall but did alter their distribution. The most immediate alteration to occur was a fivefold increase in the rate of cross-linking between beta-1,6-glycosylated mannoproteins and chitin. This increase was followed shortly thereafter by a decline in beta-1,3-glucan-associated beta-1, 6-glucans and, within several generations, a fivefold increase in the chitin content of the walls. The increased accumulation of chitin-linked glucans was not due to a block in subsequent processing as determined by pulse-chase analysis. Rather, the results suggest that the glucans are diverted to chitin linkage due to the inability of the mutants to establish cross-links between beta-1,6- and beta-1,3-glucans. Based on these and previously published results, it is suggested that the Phr proteins process beta-1,3-glucans and make available acceptor sites for the attachment of beta-1,6-glucans.
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