Abstract
The human fungal pathogen Candida albicans is a dimorphic opportunistic pathogen that colonises most of the human population without creating any harm. However, this fungus can also cause life-threatening infections in immunocompromised individuals. The ability to successfully colonise different host niches is critical for establishing infections and pathogenesis. C. albicans can live and divide in various morphological forms critical for its survival in the host. Indeed, C. albicans can grow as both yeast and hyphae and can form biofilms containing hyphae. The transcriptional regulatory network governing the switching between these different forms is complex but well understood. In contrast, non-DNA based epigenetic modulation is emerging as a crucial but still poorly studied regulatory mechanism of morphological transition. This review explores our current understanding of chromatin-mediated epigenetic regulation of the yeast to hyphae switch and biofilm formation. We highlight how modification of chromatin structure and non-coding RNAs contribute to these morphological transitions.
Highlights
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III-like enzyme dicer (Dcr) and the PIWI domain-containing protein Argonaute (Ago) are at the core of the RNA interference (RNAi) machinery and responsible for the generation of the three major branches of small non-coding RNAs (ncRNAs)—short interference RNAs, micro RNAs and PIWI-interacting RNAs—that differ in their biogenesis and mechanisms of action (Figure 4)
An increasing body of evidence demonstrates that chromatin modifiers and chromatin remodelers modulate the gene expression programmes associated with the yeast to hyphae switch and with biofilm formation, two interconnected processes playing important roles for host adaption and pathogenesis, as well as the white-opaque switch (Figure 6)
Summary
Epigenetics is a popular term first defined by Conrad Waddington in the early 1940s as "the process by which the genotype brings the phenotype into being" [1]. Post-translation modifications of histone proteins and their effect on gene expression are often described as an epigenetic regulatory mechanism. Riggs’ definition excludes the role of non-coding RNAs (ncRNAs) in transcription and other DNA-based organisms To overcome this conundrum, Adrian Bird redefined epigenetics as "the structural adaptation of chromosomal regions to register, signal or perpetuate altered activity states" [3]. At euchromatic transcriptionally active regions, genes promoters are assembled into a chromatin state containing acetylated histones that are tri-methylated on H3K4. The post-translation modification of histone proteins is a dynamic and reversible process catalysed by "writer" and "eraser" enzymes that add and remove epigenetic marks. Histone marks can be recognised by "reader" proteins, which can influence chromatin dynamics and function via promoting or blocking the recruitment of transcription factors and/or other chromatin-modifying factors (Figure 2B) [41]. Bromodomain-containing proteins bind acetylated histones, chromodomain containing proteins recognise specific methylation marks and the YEATS domain recognises the crotonyl marks [42]
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