Candida albicans is a leading fungal colonizer in the human microbiome and acts as an opportunistic pathogen. When there is disruption to its residing environment, C. albicans can switch from commensal (budding) to a pathogenic (hyphal) morphology. Hyphal growth in C. albicans is documented to be induced by a range of factors. It has long been known that a highly potent inducer of this transition is serum, which contains many components including bacterial peptidoglycan (PG) fragments. Thus, interactions between bacteria and fungi contribute to an enhanced disease state during immune incompetence; however, it is unclear the extent to which C. albicans can utilize PG fragments to foster growth and pathogenesis. Here we show that the initiation of hyphal growth varies depending on the PG fragment being introduced. Transcriptional analysis using qRT-PCR was carried out to identify if well-known hyphae specific genes (HSGs) are upregulated during hyphal morphogenesis. We found that only specific PG fragments induce hyphal growth via transcriptional regulation of select HSGs, suggesting specific chemical characteristics of PGs are responsible for this result. In tandem, we have developed a novel fungal cell wall labelling method as a means to visualize this hyphal response using fluorescent microscopy. Together these results suggest that opportunistic microbes such as C. albicans have developed processes to recognize, respond, and utilize surrounding byproducts of co-colonizing organisms, providing insight into this complex relationship and new possible mechanisms to target for the development of novel antifungals.
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Williams et al. (2024) studied this question.
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