Abstract
Human fungal pathogens, such as Candida albicans, Aspergillus fumigatus and Cryptococcus neoformans, are a public health problem, causing millions of infections and killing almost half a million people annually. The ability of these pathogens to colonise almost every organ in the human body and cause life-threating infections relies on their capacity to adapt and thrive in diverse hostile host-niche environments. Stress-induced genome instability is a key adaptive strategy used by human fungal pathogens as it increases genetic diversity, thereby allowing selection of genotype(s) better adapted to a new environment. Heterochromatin represses gene expression and deleterious recombination and could play a key role in modulating genome stability in response to environmental changes. However, very little is known about heterochromatin structure and function in human fungal pathogens. In this review, I use our knowledge of heterochromatin structure and function in fungal model systems as a road map to review the role of heterochromatin in regulating genome plasticity in the most common human fungal pathogens: Candida albicans, Aspergillus fumigatus and Cryptococcus neoformans.
Highlights
IntroductionHuman fungal pathogens are a leading cause of human mortality worldwide and kill almost
Human fungal pathogens are a leading cause of human mortality worldwide and kill almost2 million people every year [1]
The 35S and 5S genes are separated by two non-transcribed spacers (NTS), known as intergenic spacers (IGS), that contain three conserved elements: (i) an origin of replication, (ii) a replication fork blocking site (RFB) whose function is to avoid collision between replication and transcription machineries and (iii) a non-coding RNA promoter (E-pro) whose activity can be silenced by Sir2 [41,47,48]
Summary
Human fungal pathogens are a leading cause of human mortality worldwide and kill almost. During colonisation and infection of the host, human fungal pathogens encounter many different host environments to which they must adapt rapidly. They must adapt to grow at high temperature (i.e., fever) and they must survive the dramatic environmental changes following engulfment by macrophages and neutrophils of the host immune system. The importance of stress-induced genome instability has emerged as a key adaptive mechanism of human fungal pathogens [4]. 2019, 10, 855 years, the importance of stress-induced genome instability has emerged as a2 of adaptive mechanism of human fungal pathogens [4]. Variation can drive improved fitness [7,11,12,13,14,15]
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