Journal
MOLECULAR MICROBIOLOGY
Volume 97, Issue 1, Pages 125-138Publisher
WILEY
DOI: 10.1111/mmi.13014
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Funding
- National Library of Medicine Biomedical Informatics Training grant [5T15LM007443]
- National Institutes of Health [R01GM/AI55155, R01AI099190]
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The human fungal pathogen Candida albicans undergoes white-opaque phenotypic switching, which enhances its adaptation to host niches. Switching is controlled by a transcriptional regulatory network of interlocking feedback loops acting on the transcription of WOR1, the master regulator of white-opaque switching, but regulation of the network on the translational level is not yet explored. Here, we show that the long 5 untranslated region of WOR1 regulates the white-opaque phenotype. Deletion of the WOR1 5 UTR promotes white-to-opaque switching and stabilizes the opaque state. The WOR1 5 UTR reduces translational efficiency and the association of the transcript with polysomes. Reduced polysome association was observed for additional key regulators of cell fate and morphology with long 5 UTR as well. Overall, we find a novel regulatory step of white-opaque switching at the translational level. This translational regulation is implicated for many key regulators of cell fate and morphology in C.albicans.
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