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Unravelling the pathobiological role of the fungal KEOPS complex in Cryptococcus neoformans

ABSTRACT: Unravelling the pathobiological role of the fungal KEOPS complex in Cryptococcus neoformans

PROVIDER: PRJNA859376 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20274736_1.fastq.gz	Fastqsanger.gz
	SRR20274736_2.fastq.gz	Fastqsanger.gz
	SRR20274737_1.fastq.gz	Fastqsanger.gz
	SRR20274737_2.fastq.gz	Fastqsanger.gz
	SRR20274738_1.fastq.gz	Fastqsanger.gz

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Unravelling the pathobiological role of the fungal KEOPS complex in Cryptococcus neoformans

Project description:The kinase, putative endopeptidase and other peptides of small size (KEOPS) complex plays critical cellular functions in eukaryotes, but its pathobiological roles remains elusive in fungal pathogens. Here we comprehensively analyze the pathobiological functions of the KEOPS complex in fungal meningoencephalitis pathogen Cryptococcus neoformans. The cryptococcal KEOPS complex appears to have a linear arrangement of Pcc1-Kae1-Bud32-Cgi121, supported by physical interaction between Pcc1-Kae1, Kae1-Bud32, and Bud32-Cgi121, but does not have Gon7 ortholog, which is the part of the S. cerevisiae KEOPS complex. Deletion of PCC1, KAE1, and BUD32 causes severe growth defects with perturbed cell cycle control.

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Systematic Profiling of Essential Fungal Transcription Factors Uncovers Ezt1 as a Central Pathobiological and Morphogenic Regulator in Cryptococcus neoformans [ChIP-Seq]

Project description:Cryptococcus neoformans is a global fungal pathogen that causes fatal cryptococcosis, underscoring the urgent need for novel therapeutics given the limitations of current antifungals. Here, we systematically investigate essential transcription factors (TFs) in C. neoformans, focusing on their roles in growth and their potential as drug targets. We developed experimental pipelines to assess growth requirement, essentiality, and function using conditional gene expression, constitutive overexpression, and random spore analysis. Through these systematic analyses, we identify one quasi-essential (growth-required but non-essential) TF, Fhl1, and 13 essential TFs, including three (Ezt1, Ezt2 and Cbf1) that are highly divergent from counterparts in other eukaryotes. Notably, Ezt1 emerged as a central TF regulating over 1,200 genes, controlling growth, antifungal drug and stress responses, sexual development, and virulence. Collectively, our findings define the essential TF landscape of C. neoformans and provide a framework for leveraging these regulators, particularly Ezt1, to develop targeted therapies for cryptococcosis.

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Project description:Casein kinase 2 (CK2) is a potential therapeutic target for several human diseases due to its crucial roles in growth, differentiation, and metabolic homeostasis. This study delves into the role of the CK2 complex in Cryptococcus neoformans, a key fungal pathogen causing meningitis. In C. neoformans, the CK2 complex is made up of a main catalytic subunit (Cka1) and two regulatory subunits (Ckb1 and Ckb2). The primary role of Cka1 is as a protein kinase, while Ckb1/2 assist in various cellular functions. Triple mutants without all three subunits exhibited more pronounced defects than mutants lacking only Cka1, hinting at potential independent functions of Ckb1/2. In animal studies, mutants without these subunits showed a sharp decline in virulence. Moreover, CK2 disruption affected many effector proteins and disrupted key signaling pathways crucial for the pathogenicity of C. neoformans. Overall, the findings highlight the importance of the CK2 complex in fungal biology and its potential as a target for new antifungal treatments.

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