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G3 (Bethesda) DOI:10.1093/g3journal/jkab001

Comparative genomics of white and opaque cell states supports an epigenetic mechanism of phenotypic switching in Candida albicans.

Publication TypeJournal Article
Year of Publication2021
AuthorsBeekman, CN, Cuomo, CA, Bennett, RJ, Ene, IV
JournalG3 (Bethesda)
Date Published2021 02 09
KeywordsCandida albicans, Epigenesis, Genetic, Fungal Proteins, Gene Expression Regulation, Fungal, Gene Regulatory Networks, Genomics, Phenotype

Several Candida species can undergo a heritable and reversible transition from a 'white' state to a mating proficient 'opaque' state. This ability relies on highly interconnected transcriptional networks that control cell-type-specific gene expression programs over multiple generations. Candida albicans, the most prominent pathogenic Candida species, provides a well-studied paradigm for the white-opaque transition. In this species, a network of at least eight transcriptional regulators controls the balance between white and opaque states that have distinct morphologies, transcriptional profiles, and physiological properties. Given the reversible nature and the high frequency of white-opaque transitions, it is widely assumed that this switch is governed by epigenetic mechanisms that occur independently of any changes in DNA sequence. However, a direct genomic comparison between white and opaque cells has yet to be performed. Here, we present a whole-genome comparative analysis of C. albicans white and opaque cells. This analysis revealed rare genetic changes between cell states, none of which are linked to white-opaque switching. This result is consistent with epigenetic mechanisms controlling cell state differentiation in C. albicans and provides direct evidence against a role for genetic variation in mediating the switch.


Alternate JournalG3 (Bethesda)
PubMed ID33585874
PubMed Central IDPMC8366294
Grant ListR01 AI141893 / AI / NIAID NIH HHS / United States
R21 AI139592 / AI / NIAID NIH HHS / United States
U19 AI110818 / AI / NIAID NIH HHS / United States
P20 GM109035 / GM / NIGMS NIH HHS / United States
R01 AI081704 / AI / NIAID NIH HHS / United States