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Transcritpional profiling of unstimulated and Candida albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

ABSTRACT: Transcritpional profiling of unstimulated and Candida albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

PROVIDER: PRJNA434710 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6751070.fastq.gz	Fastqsanger.gz
	SRR6751071.fastq.gz	Fastqsanger.gz
	SRR6751062.fastq.gz	Fastqsanger.gz
	SRR6751072.fastq.gz	Fastqsanger.gz
	SRR6751063.fastq.gz	Fastqsanger.gz

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Transcritpional profiling of unstimulated and Candida albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils

Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, if and how neutrophils cell-intrinsically titrate their inflammatory response remains unknown. Here, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, neutrophils rely on a direct PU.1 repressor function as rheostat of the inflammatory chromatin state, safeguarding their epigenome from undergoing uncontrolled activation prior to pathogenic stimulation.

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Genome-wide binding profiles of PU.1 in unstimulated and Candida albicans stimulated HoxER-PU.1 WT neutrophils

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Chromatin accessibility in C. albicans stimulated HoxER-PU.1 WT and HoxER-PU.1 KO neutrophils and DMSO, TSA or Entinostat treated HoxER-PU.1 WT neutrophils

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Genome-wide binding profiles of JUNB in unstimulated HoxER-PU.1 WT and PU.1 KO neutrophils

Project description:Genome-wide binding profiles of JUNB in unstimulated HoxER-PU.1 WT and PU.1 KO neutrophils

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Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, neutrophil-intrinsic mechanisms adjusting an appropriate inflammatory response are unknown. Herein, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, PU.1 acts as rheostat of the inflammatory chromatin state, safeguarding the neutrophil epigenome from undergoing uncontrolled activation prior to pathogenic stimulation.

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