( . ) is an opportunistic pathogen in humans and possesses a white-opaque heritable switching system. Wor1 is a master regulator of white-opaque switching and is essential for opaque cell formation in . . However, the regulatory network of Wor1 in white-opaque switching is still vague. In this study, we obtain a series of Wor1-interacting proteins using LexA-Wor1 as bait. Among these proteins, function unknown now 30 (Fun30) interacts with Wor1 and . Fun30 expression is upregulated in opaque cells at the transcriptional and protein levels. Loss of attenuates white-to-opaque switching, while ectopic expression of significantly increases white-to-opaque switching in an ATPase activity-dependent manner. Furthermore, upregulation is dependent on CO ; loss of , a key CO -sensing transcriptional regulator, abolishes upregulation. Interestingly, deletion of affects the expression regulation feedback loop. Thus, our results indicate that the chromatin remodeller Fun30 interacts with Wor1 and is required for expression and opaque cell formation.
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http://dx.doi.org/10.3724/abbs.2023031 | DOI Listing |
Microbiol Mol Biol Rev
June 2024
Department of Biology, University of Iowa, Iowa City, Iowa, USA.
SUMMARY remains a major fungal pathogen colonizing humans and opportunistically invading tissue when conditions are predisposing. Part of the success of was attributed to its capacity to form hyphae that facilitate tissue invasion. However, in 1987, a second developmental program was discovered, the "white-opaque transition," a high-frequency reversible switching system that impacted most aspects of the physiology, cell architecture, virulence, and gene expression of .
View Article and Find Full Text PDFBiophys J
June 2024
Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island. Electronic address:
Candida albicans, a prominent member of the human microbiome, can make an opportunistic switch from commensal coexistence to pathogenicity accompanied by an epigenetic shift between the white and opaque cell states. This transcriptional switch is under precise regulation by a set of transcription factors (TFs), with Enhanced Filamentous Growth Protein 1 (Efg1) playing a central role. Previous research has emphasized the importance of Efg1's prion-like domain (PrLD) and the protein's ability to undergo phase separation for the white-to-opaque transition of C.
View Article and Find Full Text PDFMol Microbiol
February 2024
College of Life Sciences, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, China.
bioRxiv
November 2023
Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence Rhode Island, 02912, USA.
, a prominent member of the human microbiome, can make an opportunistic switch from commensal coexistence to pathogenicity accompanied by an epigenetic shift between the white and opaque cell states. This transcriptional switch is under precise regulation by a set of transcription factors (TFs), with Enhanced Filamentous Growth Protein 1 (Efg1) playing a central role. Previous research has emphasized the importance of Egf1's prion-like domain (PrLD) and the protein's ability to undergo phase separation for the white-to-opaque transition of .
View Article and Find Full Text PDFGenetics
November 2023
Department of Microbiology and Immunology, University of California - San Francisco, San Francisco, CA 94143, USA.
Candida albicans, a normal member of the human microbiome and an opportunistic fungal pathogen, undergoes several morphological transitions. One of these transitions is white-opaque switching, where C. albicans alternates between 2 stable cell types with distinct cellular and colony morphologies, metabolic preferences, mating abilities, and interactions with the innate immune system.
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