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White-Brown switching controls phenotypic plasticity and virulence of Candida auris [1]

ABSTRACT: White-Brown switching controls phenotypic plasticity and virulence of Candida auris [1]

PROVIDER: PRJNA1169345 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR30893449_1.fastq.gz	Fastqsanger.gz
	SRR30893449_2.fastq.gz	Fastqsanger.gz
	SRR30893450_1.fastq.gz	Fastqsanger.gz
	SRR30893450_2.fastq.gz	Fastqsanger.gz

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White-Brown switching controls phenotypic plasticity and virulence of Candida auris [2]

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White-Brown switching controls phenotypic plasticity and virulence of Candida auris [3]

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Project description:White-Brown switching controls phenotypic plasticity and virulence of Candida auris [2]

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KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells

Project description:Vascular smooth muscle cells (VSMCs) within atherosclerotic lesions undergo a phenotypic switching in a KLF4-dependent manner. Glycolysis plays important roles in transdifferentiation of somatic cells, however, it is unclear whether and how KLF4 mediates the link between glycolytic switch and VSMCs phenotypic transitions. Here, we show that KLF4 upregulation accompanies VSMCs phenotypic switching in atherosclerotic lesions. KLF4 enhances the metabolic switch to glycolysis through increasing PFKFB3 expression. Inhibiting glycolysis suppresses KLF4-induced VSMCs phenotypic switching, demonstrating that glycolytic shift is required for VSMCs phenotypic switching. Mechanistically, KLF4 upregulates expression of circCTDP1 and eEF1A2, both of which cooperatively promote PFKFB3 expression. TMAO induces glycolytic shift and VSMCs phenotypic switching by upregulating KLF4. Our study indicates that KLF4 mediates the link between glycolytic switch and VSMCs phenotypic transitions, suggesting that a previously unrecognized KLF4-eEF1A2/circCTDP1-PFKFB3 axis plays crucial roles in VSMCs phenotypic switching.

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Transcriptional Signatures Predict Phenotypic Variations of Candida auris

Project description:Transcriptomic analysis of different Candida auris clinical isolates with distinct antifungal susceptibility profiles.

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Discovery of a "White-Gray-Opaque" Tristable Phenotypic Switching System in Candida Albicans: Roles of Non-Genetic Diversity in Host Adaption

Project description:The capacity of the commensal yeast Candida albicans to grow in several forms, referred to as phenotypic plasticity, is critical for its survival, and abilities to thrive and cause infection in the human host. In this study, we report a novel phenotype of C. albicans, referred as the “gray” phenotype. The gray cell type, together with the previously discovered “white” and “opaque” cell types, forms a tristable phenotypic switching system. The three phenotypes differ in cellular and colony appearance, global transcriptional profiles, secreted aspartyl proteinase (Sap) activities and virulence in different infection models. The addition of the gray cell type to the phenotypic transition systems may enhance fitness and confers an adaptive advantage for C. albicans in the host. We further demonstrate that two key regulators of white-opaque switching, Wor1 and Efg1, are not required for maintenance of the gray phenotype, suggesting that a different regulatory circuitry may be involved in the regulation of gray cell formation. Our study provides an example of multiple stable and heritable switching systems, indicating that the regulation of morphological forms to adapt to environmental changes could be much more elaborate than previously thought. total RNA profiles of 24h old white, gray and opaque cell types

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