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Lactate sensing drives fungal immune evasion

ABSTRACT: Lactate sensing drives fungal immune evasion

PROVIDER: PRJEB13396 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1354030.fastq.gz	Fastqsanger.gz
	ERR1354040.fastq.gz	Fastqsanger.gz
	ERR1354031.fastq.gz	Fastqsanger.gz
	ERR1354041.fastq.gz	Fastqsanger.gz
	ERR1354032.fastq.gz	Fastqsanger.gz

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Lactate sensing drives fungal immune evasion

Project description:Experiment Description RNA sequencing was performed on Candida albicans wild type cells (SC5314) grown to exponential phase on YNB Lactate, YNB Glucose, or YNB Glucose plus Lactate, and compared to exponential Candida albicans crz1 cells grown on YNB Glucose or YNB Glucose plus Lactate. Three independent experiments were performed.

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Epitope shaving and fungal immune evasion – culture supernatants

Project description:The cell wall provides a major physical interface between fungal pathogens and their mammalian host. This extracellular armour is critical for fungal cell homeostasis and survival. Yet essential cell wall moieties, such as β-1,3-glucan, are recognised as pathogen-associated molecular patterns (PAMPs) that activate immune-mediated clearance mechanisms. We have reported that the opportunistic human fungal pathogen, Candida albicans, masks β-1,3-glucan following exposure to lactate, hypoxia or iron depletion. However, the precise mechanism(s) by which C. albicans masks β-1,3-glucan have remained obscure. Here, we performed proteomic analysis of supernatants harvested from C. albicans cells grown in hypoxia or lactate compared to glucose-grown controls to identify mechanisms driving β-1,3-glucan masking.

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Project description:The cell wall provides a major physical interface between fungal pathogens and their mammalian host. This extracellular armour is critical for fungal cell homeostasis and survival. Yet essential cell wall moieties, such as β-1,3-glucan, are recognised as pathogen-associated molecular patterns (PAMPs) that activate immune-mediated clearance mechanisms. We have reported that the opportunistic human fungal pathogen, Candida albicans, masks β-1,3-glucan following exposure to lactate, hypoxia or iron depletion. However, the precise mechanism(s) by which C. albicans masks β-1,3-glucan have remained obscure. Here, we performed proteomic analysis of cell walls from C. albicans cells grown in hypoxia or lactate compared to glucose-grown controls to identify mechanisms driving β-1,3-glucan masking.

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Lactate signalling regulates fungal β-glucan masking and immune evasion.

Project description:As they proliferate, fungi expose antigens at their cell surface that are potent stimulators of the innate immune response, and yet the commensal fungus Candida albicans is able to colonize immuno competent individuals. We show that C. albicans may evade immune detection by presenting a moving immunological target. We report that the exposure of β-glucan, a key pathogen-associated molecular pattern (PAMP) located at the cell surface of C. albicans and other pathogenic Candida species, is modulated in response to changes in the carbon source. Exposure to lactate induces β-glucan masking in C. albicans via a signalling pathway that has recruited an evolutionarily conserved receptor (Gpr1) and transcriptional factor (Crz1) from other well-characterized pathways. In response to lactate, these regulators control the expression of cell-wall-related genes that contribute to β-glucan masking. This represents the first description of active PAMP masking by a Candida species, a process that reduces the visibility of the fungus to the immune system.

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Temporally-coordinated bivalent histone modifications of BCG1 enable fungal invasion and immune evasion

Project description:Bivalent histone modifications, including functionally opposite H3K4me3 and H3K27me3 marks simultaneously on the same nucleosome, control various cellular processes by fine-tuning the gene expression in eukaryotes. However, the role of bivalent histone modifications in fungal virulence remains elusive. Here, we report that bivalent chromatin modification of BCG1 (bivalent chromatin-marked gene1) is critical for Fusarium graminearum (Fg) successfully invading the host plant. By mapping the genome-wide landscape of H3K4me3 and H3K27me3 dynamic modifications in Fg during invasion, we identified the infection-related bivalent chromatin-marked genes (BCGs). BCG1, which encodes a xylanase containing a novel G/Q-rich motif, possessed the highest bivalent modification. We showed that the G/Q-rich motif of BCG1 is required for its xylanase activity and is essential for the full virulence of Fg. Intriguingly, this G/Q-rich motif can be recognized by pattern-recognition receptors (PRRs) to trigger plant immunity. Therefore, Fg tightly regulates BCG1 expression during different infection stages. During initial infection stages, Fg employs H3K4me3 modification to induce BCG1 expression required for host cell wall degradation. Upon breaching the cell wall barrier, this active chromatin state was reset to bivalency by co-modifying with H3K27me3, which enables epigenetic silencing of BCG1 to escape from host immune surveillance. Collectively, our study highlights how fungal pathogens deploy bivalent epigenetic modification to achieve temporally-coordinated activation and suppression of a critical fungal gene, thereby facilitating successful infection and host immunity evasion. This SuperSeries is composed of the SubSeries listed below.

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