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IRF4 genome wide binding and transciptomic profile in 501Mel melanoma cell line

ABSTRACT: IRF4 genome wide binding and transciptomic profile in 501Mel melanoma cell line

PROVIDER: PRJNA705651 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13811831_1.fastq.gz	Fastqsanger.gz
	SRR13811831_2.fastq.gz	Fastqsanger.gz
	SRR13811832_1.fastq.gz	Fastqsanger.gz
	SRR13811832_2.fastq.gz	Fastqsanger.gz
	SRR13811833_1.fastq.gz	Fastqsanger.gz

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IRF4 genome wide binding and transciptomic profile in 501Mel melanoma cell line

Project description:To map genome wide binding sites of IRF4, we performed ChIP-seq against eGFP tagged IRF4 in human melanoma cells. To assess whether IRF4 binding influences its target gene expression, RNA-seq was performed after siRNA mediated depletion of IRF4 in 501Mel cells. Subsequently, target genes of IRF4 obtained from ChIP-seq and RNA-seq studies were used to interrogate melanocyte meQTL and identified 131 candidate downstream target CpGs of IRF4, which were validated by cis-/trans-meQTL mediation analysis, suggesting transcription factor mediated expression changes reflected in methylation changes.

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BATF3-dependent IRF4 binding inhibits FOXP3 in differentiating Tregs

Project description:BATF3 has been shown to inhibit FOXP3 expression in differentiating CD4 T cells, however, the role of IRF4 in this inhibition is unexplored. IRF4 binds DNA weakly on its own and requires interactions with other transcription factors. We investigated how BATF3/IRF4 interactions are necessary for IRF4 binding and BATF3-mediated FOXP3 inhibition.

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Project description:An IRF4 de novo mutation affecting the DNA binding domain of encoded IRF4 protein (mutDBD) was identified in a patient presenting with combined immunodeficiency. The patient exhibited profound susceptibility to opportunistic infections notably Pneumocystis jirovecii and humoral immunodeficiency caused by a failure of terminal B cell differentiation. A heterozygous IRF4 missense variant resulting in a phenylalanine-to-leucine replacement within the interferon activation domain of the encoded IRF4 protein (mutIAD) was identified in three patients from a multigenerational family suffering from a novel autosomal dominant disease predominantly presenting as a hypogammaglobulinemia with recurrent infections. In this experiment we aimed to investigate the effect of the two different mutations on IRF4 genomic binding.

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Project description:Disease-causing mutations in genes encoding transcription factors (TF) are frequent in hematopoietic malignancies and might affect TF-interactions with respective DNA-binding motifs. Here, we report the characterization of a recurrent somatic mutation c.295T>C in the IRF4 gene in classic Hodgkin lymphoma (cHL) leading to a C99R exchange. IRF4-C99R is located in the center of the IRF4 alpha3-recognition helix contacting the DNA 5´-GAAA-3´ IRF consensus sequence. IRF4-C99R fundamentally alters IRF4 DNA-binding, combining loss-of-binding at canonical IRF motifs and neomorph gain-of-binding at canonical and non-canonical IRF composite elements (CEs), in particular AP-1-IRF-CEs (AICEs). In line, IRF4-C99R profoundly impairs IRF4-dependent plasma cell induction, and specifically up-regulates degenerate-AICE-dependent distinct cHL disease-characteristic genes. These data document an unprecedented mutation-induced shift of TF binding specificity and its impact for lymphoma pathogenesis and TF modulation.

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