Rapid evolution of an adaptive multicellular morphology of Candida auris during systemic infection.
Bing. Jian J; Guan. Zhangyue Z; Zheng. Tianhong T; Ennis. Craig L CL; Nobile. Clarissa J CJ; Chen. Changbin C; Chu. Haiqing H; Huang. Guanghua G
Key Findings
- Candida auris rapidly evolves a multicellular, aggregative shape during systemic infection in mice
- Aggregates gather in the brain and outcompete single‑cell yeast forms
- De novo point mutations in cell‑division and cell‑wall genes drive the aggregative phenotype
- Aggregates are more resistant to the host antimicrobial peptide LL‑37 and PACAP
Practical Outcomes
- For most biohackers, this research doesn’t change any daily health or longevity practices. It mainly warns that this pathogen can become more drug‑resistant, but it offers no new supplement or protocol to apply.
Summary
The study shows that the fungus Candida auris can quickly change into a clumped‑together form inside mice, especially in the brain, and this clumped form is harder for the body’s natural antimicrobial peptide LL‑37 to kill. The change happens because of new genetic mutations that affect how the fungus grows and divides.
Abstract
Candida auris has become a serious threat to public health. The mechanisms of how this fungal pathogen adapts to the mammalian host are poorly understood. Here we report the rapid evolution of an adaptive C. auris multicellular aggregative morphology in the murine host during systemic infection. C. auris aggregative cells accumulate in the brain and exhibit obvious advantages over the single-celled yeast-form cells during systemic infection. Genetic mutations, specifically de novo point mutations in genes associated with cell division or budding processes, underlie the rapid evolution of this aggregative phenotype. Most mutated C. auris genes are associated with the regulation of cell wall integrity, cytokinesis, cytoskeletal properties, and cellular polarization. Moreover, the multicellular aggregates are notably more recalcitrant to the host antimicrobial peptides LL-37 and PACAP relative to the single-celled yeast-form cells. Overall, to survive in the host, C. auris can rapidly evolve a multicellular aggregative morphology via genetic mutations.
Study Information
pubmed
2024
2024-03-16T00:00:00.000Z
10.1038/s41467-024-46786-8
42
88