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Inhibition of the Chromatin Remodeling Factor NURF Rescued Sterility by a Clinic Variant of NuRD [RNA-seq]

ABSTRACT: The nucleosome remodeling and deacetylase (NuRD) complex is essential for gene expression and cell fate determination, and missense mutations of NuRD caused neurodevelopmental diseases. However, the molecular pathogenesisof clinic NuRD variants is unknown. Here, we introduced a clinic CHD3(L915F) variant into C. elegans homolog LET-418, impairing germline and vulva development and ultimately causing animal sterility. Our ATAC-seq and RNA-seq analyses revealed that this variant generated an abnormal open chromatin structure and disrupted the expression of developmental genes. Through genetic suppressor screens, we uncovered that intragenic mutations, likely renovating NuRD activity, restored animal viability. We also found that intergenic mutations in nucleosome remodeling factor NURF that counteracts NuRD rescued abnormal chromatin structure, gene expression, and animal sterility. We propose that two antagonistic chromatin-remodeling factors coordinate to establish the proper chromatin status and transcriptome and that inhibiting NURF may provide insights for treatment of NuRD mutation-related diseases.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE243398 | GEO | 2023/09/21

REPOSITORIES: GEO

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Inhibition of the Chromatin Remodeling Factor NURF Rescued Sterility by a Clinic Variant of NuRD [ATAC-seq]

Project description:The nucleosome remodeling and deacetylase (NuRD) complex is essential for gene expression and cell fate determination, and missense mutations of NuRD caused neurodevelopmental diseases. However, the molecular pathogenesisof clinic NuRD variants is unknown. Here, we introduced a clinic CHD3(L915F) variant into C. elegans homolog LET-418, impairing germline and vulva development and ultimately causing animal sterility. Our ATAC-seq and RNA-seq analyses revealed that this variant generated an abnormal open chromatin structure and disrupted the expression of developmental genes. Through genetic suppressor screens, we uncovered that intragenic mutations, likely renovating NuRD activity, restored animal viability. We also found that intergenic mutations in nucleosome remodeling factor NURF that counteracts NuRD rescued abnormal chromatin structure, gene expression, and animal sterility. We propose that two antagonistic chromatin-remodeling factors coordinate to establish the proper chromatin status and transcriptome and that inhibiting NURF may provide insights for treatment of NuRD mutation-related diseases.

2023-09-21 | GSE243397 | GEO

Inhibition of the Chromatin Remodeling Factor NURF Rescued Sterility by a Clinic Variant of NuRD

Project description:Inhibition of the Chromatin Remodeling Factor NURF Rescued Sterility by a Clinic Variant of NuRD

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Inhibition of the Chromatin Remodeling Factor NURF Rescued Sterility by a Clinic Variant of NuRD [ATAC-seq]

Project description:Inhibition of the Chromatin Remodeling Factor NURF Rescued Sterility by a Clinic Variant of NuRD [ATAC-seq]

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Inhibition of the Chromatin Remodeling Factor NURF Rescued Sterility by a Clinic Variant of NuRD [RNA-seq]

Project description:Inhibition of the Chromatin Remodeling Factor NURF Rescued Sterility by a Clinic Variant of NuRD [RNA-seq]

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Project description:GFI is a DNA binding transcriptional repressor that regulates myeloid differentiation. Here, we show that GFI1 interacts with the chromodomain helicase CHD4 and other components of the nucleosome remodeling and deacetylase (NuRD) complex. Our data demonstrated that GFI1 and GFI1/CHD4 complexes occupy sites of open chromatin enriched for histone marks associated with active transcription or different sets of genes that are either enriched for IRF1 or SPI-1 consensus binding sites. In addition, our study provided evidence that GFI1 affects the chromatin remodeling activity of the NuRD complex. Overall, our results indicate that GFI1/CHD4 complexes control chromatin openness and histone modifications differentially to regulate target genes, which govern the immune response, nucleosome organization, or metabolic processes.

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Comparison of the composition and interaction partners of the Nucleosome Remodeling and Deacetylase (NuRD) complex in cancer cells

Project description:The Nucleosome Remodeling and Deacetylase (NuRD) complex is essential for normal development in metazoans and has direct implications in a range of human diseases. Amongst all classes of chromatin remodeling complexes, the NuRD complex has been the most recalcitrant to analysis. This is, in part, due to difficulties with producing the intact complex recombinantly. Using affinity-purification followed by mass spectrometry, we determined the stoichiometry of the NuRD complex from three cancer cell lines representing three different human tissues. We also analysed the data to determine the interactome of the NuRD complex and identified potential NuRD interactors.

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2013-10-31 | E-GEOD-44773 | biostudies-arrayexpress

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Project description:Dynamic changes of histone epigenetic modifications and chromatin structure represent an universal mechanism by which cells adapt their transcriptional response to rapidly changing environmental conditions. During neuronal development, extensive chromatin remodeling takes place allowing the transition of pluripotent cells into differentiated neurons. Here we report that the ATP-dependent chromatin remodeling complex NuRD, which couples ATP-dependent nucleosome sliding with histone deacetylase activity, is a major remodeling complex in embryonic brain and plays an instructive role during mouse neuronal development. Importantly, the ATPase subunits of NuRD complex CHD3, CHD4 and CHD5 undergo a functional switch, thereby regulating distinct aspects of neuronal differentiation and migration in a sequential and mostly non-overlapping manner. We conclude that the recruitment of NuRD complexes containing specific CHDs to gene promoters and enhancers plays an instructive role in brain development. Gene expression analysis was performed in the mouse embryonic cortex at three developmental stages: E12.5, E15.5 and E18.5 using total RNA obtained from four embryos for each time point.

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