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Genome-wide mapping of Nup98HoxA9- and Crm1-binding sites in ES cell lines.

ABSTRACT: We used ChIP-seq to examine the genome-wide binding of Nup98-HoxA9 and Crm1 in ES cells. Our analysis revealed that Nup98-HoxA9 is highly and preferentially targeted to specific chromatin sites, particularly near Hox cluster regions where the export factor Crm1 is originally prebound.

ORGANISM(S): Mus musculus

PROVIDER: GSE68783 | GEO | 2016/01/04

REPOSITORIES: GEO

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Genome-wide mapping of Nup98HoxA9- and Crm1-binding sites in ES cell lines.

Project description:We used ChIP-seq to examine the genome-wide binding of Nup98-HoxA9 and Crm1 in ES cells. Our analysis revealed that Nup98-HoxA9 is highly and preferentially targeted to specific chromatin sites, particularly near Hox cluster regions where the export factor Crm1 is originally prebound. chromatin immunoprecipitation

2016-01-04 | E-GEOD-68783 | biostudies-arrayexpress

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Genome-wide mapping of SET-Nup214, mutant NPM1 (NPM1c), and CRM1-binding sites in human leukemia or mouse ES cell lines

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Genome-wide mapping of MLL1, CRM1, and NUP-fusion derivatives in human leukemia or mouse ES cell lines

Project description:We used ChIP-seq to examine the genome-wide binding of MLL1, CRM1, and NUP-fusions in human leukemia or mouse ES cell lines. Our analysis revealed that MLL1, CRM1, and NUP-fusions are preferentially co-localized on the genome.

2023-07-27 | GSE202837 | GEO

Genome-wide maps of NUP98 fusion and MLL1 co-bound targets and their chromatin state in NUP98 fusion transformed cells.

Project description:By performing biotin-mediated chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) for two different NUP98 fusions, we defined the genome-wide direct binding sites of NUP98-HOXA9 or NUP98-HOXD13. To test whether NUP98 fusions and Mll1 were recruited to the same region of Hox genes promoters, Mll1 ChIP-seq analysis was carried out in murine NUP98-HOXA9 transformed cells using an anti-Mll1n antibody. In agreement with our results showing that NUP98-HOXA9 interacts with MLL1 in NSL/MLL1 complex, Mll1 binding targets significantly overlap with that of NUP98-HOXA9 at promoter region and gene body region. Given that MOF and MLL1 work in concert to modify H4K16ac and H3K4me3 at promoters, we further test whether H3K4me3 and H4K16ac marks are associated with NUP98-HOXA9-bound targets in murine NUP98-HOXA9 transformed cells by anti-H3K4me3 and anti-H4K16ac ChIP-seq. Our data show that both H3K4me3 and H4K16ac mark presents on NUP98-HOXA9 binding targets at promoters, and this is in line with the coordination role in the activities between MOF-mediated H4K16 acetylation and MLL/SET-mediated H3K4 methylation. In summary, our results confirmed that NUP98-HOXA9 and Mll1 are recruited to the same Hox loci, and this recruitment is associated with activating epigenetic marks, supporting the notion of the association between NUP98 fusions and NSL/Mll1 complex, suggesting that the recruitment of NUP98 fusions to the Hox gene loci maybe through MLL1.

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CRM1 Exportome and nucleocytoplasmic partition

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2020-10-28 | GSE160186 | GEO

Gene expression profiling of human DLD-1 cells after block of CRM1 receptor with Leptomycin B inhibitor.

Project description:We used RNA-seq approach to define a contribution of mammalian export receptor CRM1 (Chromosomal Maintenance 1 or Exportin 1) into Tpr-dependent export of RNA molecules from the nucleus to the cytoplasm. Basket nucleoporin Tpr was AID-tagged and depleted through Auxin Induced Degradation system. Loss of Tpr led to rapid changes in gene expression profile, and gene expression changes were compared to GANP, NXF1, RanGAP1 (GSE132363) and CRM1 loss and inhibition, respectively. Altogether, we found a minimal subset of RNAs that are controlled both by Tpr nucleoporin and CRM1 receptor.

2020-06-15 | GSE148560 | GEO

Phase-separated nuclear bodies of nucleoporin fusions promote condensation of MLL1/CRM1 and rearrangement of 3D genome structure

Project description:We performed Hi-C to analyze the effect of NUP98-HOXA9 fusion on 3D chromatin structure of mouse embryonic stem cells (mESCs). Our analysis revealed that NUP98-HOXA9 induced a drastic alteration of high-order genome structure in a phase separation-dependent manner.

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