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Candida Albicans mutant LC-MSMS

ABSTRACT: Candida albicans is a common resident of humans that colonizes multiple body sites in most healthy individuals (e.g., the gut), but can rapidly proliferate and initiate specific microbial programs to cause infections in immunocompromised hosts. However, the molecular mechanisms underlying its commensal-pathogenic switch have not been fully elucidated. Here, we demonstrate that the mitochondrial protein Mcu1, associated with TCA cycle enzymes, plays a crucial role in sensing N-acetylglucosamine (GlcNAc), a key host intestinal signal, and regulates phenotypic switching in C. albicans. Disruption of Mcu1 or key TCA cycle enzymes impairs the ability of mutant strains to utilize GlcNAc as a carbon source, blocks white-opaque switching in vitro, and reduces intestinal colonization in vivo. We further demonstrated that Mcu1 modulates the mitochondrial redox state, which thereby influences respiratory metabolism, including TCA cycle. Furthermore, Mcu1 regulates white-GUT switching by regulating the expression of Wor1, the master transcriptional regulator of white-opaque switching. Since GUT cells represent a colonization-specific morphology that supports commensalism, our findings indicate that Mcu1 and TCA cycle enzymes cooperatively regulate the commensal-pathogenic switch in C. albicans.

INSTRUMENT(S):

ORGANISM(S): Candida Albicans (yeast)

TISSUE(S): Cell Culture

SUBMITTER: MINGYANG Ma

LAB HEAD: Guanghua Huang

PROVIDER: PXD071309 | Pride | 2026-01-20

REPOSITORIES: Pride

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			Action	DRS
	MCU1-1.d.zip	Other
	MCU1-2.d.zip	Other
	MCU1-3.d.zip	Other
	MCU1-4.d.zip	Other
	WT-1.d.zip	Other

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