Candida albicans SET1 encodes a histone 3 lysine 4 methyltransferase that contributes to the pathogenesis of invasive candidiasis

Molecular Microbiology
Suresh Babu RamanCornelius J Clancy

Abstract

Candida albicans causes diverse mucosal and systemic diseases. Although this versatility likely depends upon carefully co-ordinated gene expression, epigenetic regulation in C. albicans remains poorly characterized. Screening a genomic expression library, we identified C. albicans Set1p as an immunogenic protein with homology to a lysine histone methyltransferase of Saccharomyces cerevisiae. In this study, we demonstrated that total immunoglobulin, IgG and IgM titers against a unique Set1p N-terminal fragment were significantly higher among patients with disseminated candidiasis (DC) or oropharyngeal candidiasis than controls. Disruption of SET1 resulted in complete loss of methylation of histone 3 at lysine residue 4, hyperfilamentous growth under embedded conditions, less negative cell surface charges and diminished adherence to epithelial cells, effects that were reversed upon gene re-insertion at a disrupted locus. During murine DC, the null mutant was associated with prolonged survival and lower tissue burdens. Taken together, our findings suggest that SET1 regulates multiple processes important to the pathogenesis of candidiasis. The Set1p N-terminal fragment does not exhibit significant homology to eukaryotic or microbia...Continue Reading

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Citations

Sep 6, 2011·Biochimica Et Biophysica Acta·Jessica Lopes da Rosa, Paul D Kaufman
Oct 2, 2015·Briefings in Functional Genomics·Matthew Z Anderson, Richard J Bennett
Jun 1, 2016·Frontiers in Microbiology·Verónica Freire-BenéitezAlessia Buscaino
Nov 11, 2016·PLoS Pathogens·Karl KuchlerNeeraj Chauhan
Dec 3, 2015·The Journal of Microbiology·Jueun KimJung-Shin Lee

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