affects the virulence of and the uptake of multiple carbon sources present in different host niches.

BACKGROUND

is a commensal yeast that may cause life-threatening infections. Studies have shown that the cytochrome b-c1 complex subunit 7 gene () of encodes a protein that forms a component of the mitochondrial electron transport chain complex III, making it an important target for studying the virulence of this yeast. However, to the best of our knowledge, the functions of have not yet been characterized.

METHODS

A knockout strain was constructed using SN152, and BALb/c mice were used as model animals to determine the role of in the virulence of . Subsequently, the effects of on mitochondrial functions and use of carbon sources were investigated. Next, its mutant biofilm formation and hyphal growth maintenance were compared with those of the wild type. Furthermore, the transcriptome of the mutant was compared with that of the WT strain to explore pathogenic mechanisms.

RESULTS

Defective reduced recruitment of inflammatory cells and attenuated the virulence of infection . Furthermore, the mutant influenced the use of multiple alternative carbon sources that exist in several host niches (GlcNAc, lactic acid, and amino acid, etc.). Moreover, it led to mitochondrial dysfunction. Furthermore, the knockout strain showed defects in biofilm formation or the maintenance of filamentous growth. The overexpression of cell-surface-associated genes (, , , and ) can restore defective virulence phenotypes and the carbon-source utilization of .

CONCLUSION

This study provides new insights into the mitochondria-based metabolism of , accounting for its virulence and the use of variable carbon sources that promote to colonize host niches.