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Cryptococcus neoformans strain:XL280

ABSTRACT: Chromatin remodeling complex SWI/SNF regulates hyphal cellular differentiation in Cryptococcus neoformans

PROVIDER: PRJNA534125 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8947060_1.fastq.gz	Fastqsanger.gz
	SRR8947060_2.fastq.gz	Fastqsanger.gz
	SRR8947070_1.fastq.gz	Fastqsanger.gz
	SRR8947070_2.fastq.gz	Fastqsanger.gz
	SRR8947061_1.fastq.gz	Fastqsanger.gz

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Transcription factor Znf2 coordinates with the chromatin remodeling SWI/SNF complex to regulate differentiation in Cryptococcus neoformans

Project description:Cellular differentiation is instructed by development regulators in coordination with chromatin remodeling complexes. Much information about their coordination comes from studies in the model ascomycetous yeasts. It is not clear, however, of the kind of information that can be extrapolated to species of other phyla in Kingdom Fungi. In the basidiomycete Cryptococcus neoformans, the transcription factor Znf2 controls yeast-to-hypha differentiation. Through a forward genetic screen, we identified the basidiomycete-specific factor Brf1 and discovered that it works together with Snf5 in the SWI/SNF chromatin remodeling complex in concert with existent Znf2 to execute cellular differentiation. We demonstrated that SWI/SNF assists Znf2 opening up the promoter regions of hyphal specific genes, including the ZNF2 gene itself. In addition, this complex supports Znf2 to fully associate with its target regions. Importantly, our findings revealed key differences in composition and biological function of the SWI/SNF complex in the two major phyla of Kingdom Fungi.

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Cryptococcus neoformans var. neoformans XL280

Project description:Cryptococcus neoformans var. neoformans XL280 Genome sequencing

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Project description:Cryptococcus neoformans var. neoformans XL280 Raw sequence reads

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Cryptococcus neoformans strain:XL280

Project description:Cryptococcus neoformans strain:XL280 Raw sequence reads

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Project description:We measured protein translation (by ribosome profiling) and RNA levels (by polyA-enriched RNA-seq) in Cryptococcus neoformans strain H99 and Cryptococcus neoformans strain JEC21. This is the first transcriptome-wide map of translation in this species complex.

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Project description:We investigated the effects of the hypoxia-mimetic CoCl2 on the gene expression of pathogenic fungus Cryptococcus neoformans. Keywords: compound treatment design

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Transcriptome analysis of pulmonary CCR2+ inflammatory monocytes challenged with Cryptococcus neoformans

Project description:The encapsulated yeast Cryptococcus neoformans can cause a fatal meningoencephalitis in immunocompromised patients. C. neoformans infection is acquired through the respiratory tract, but the cellular and molecular mechanisms of the pulmonary innate immune response are still not well defined. To investigate the response of CCR2+ inflammatory monocytes to C. neoformans, we compared the transcriptomes of CCR2+ inflammatory monocytes from the lungs of naïve versus infected mice.

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HDAC genes play distinct and redundant roles in Cryptococcus neoformans virulence

Project description:The human fungal pathogen Cryptococcus neoformans undergoes many phenotypic changes to promote its survival in specific ecological niches and inside the host. To explore the role of chromatin remodeling on the expression of virulence-related traits, we identified and deleted seven genes encoding predicted class I/II histone deacetylases (HDACs) in the C. neoformans genome. Our results identified the HDA1 HDAC gene as a central mediator controlling several cellular processes, including mating and virulence. A global gene expression profile comparing the hda1Δ mutant versus wild-type revealed altered transcription of specific genes associated with the most prominent virulence attributes in this fungal pathogen. This study directly correlates the effects of Class I/II HDAC-mediated chromatin remodeling on the marked phenotypic plasticity and virulence potential of this microorganism. Furthermore, our results provide insights into regulatory mechanisms involved in virulence gene expression that are likely shared with other microbial pathogens.

2018-06-06 | GSE109582 | GEO

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