ChIP-seq of MOZ (Flag-V5-BIO tagged) in mouse mouse craniofacial development
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ABSTRACT:
PROVIDER: PRJNA555849 | ENA |
REPOSITORIES: ENA
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Project description:Carboxy-terminally tagged MOZ (Flag-V5-BIO tagged) was detected by ChIP-seq using anti-V5 antibody (Sigma, A7345) to precipitate chromatin associated with MOZ
2019-07-23 | GSE134607 | GEO
Project description:Distribution of MOZ (KAT6A) in the genome and effects of MOZ on gene expression during mouse craniofacial development
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Project description:Monocytic leukemia Zinc finger protein (MOZ) is a MYST-type acetyltransferase involved in chromosomal translocation in acute myelogenous leukemia (AML) and myelodysplastic syndrome. MOZ is established as essential for hematopoiesis; however, the role of MOZ in AML has not been addressed. We propose that MOZ is critical for AML development induced by MOZ-TIF2 fusions. Moz-deficient hematopoietic stem/progenitor cells (HSPCs) expressing MOZ-TIF2 could form colonies in vitro but could not induce AML in mice. By contrast, Moz was dispensable for colony formation by HOXA9-transduced cells and AML development caused by HOXA9 and MEIS1, suggesting a specific requirement for MOZ in AML induced by MOZ/MLL-fusions. Expression of the of Meis1, but not Hoxa9, was reduced in Moz-deficient MOZ-TIF2 AML cells. AML development induced by MOZ-TIF2 was rescued by introducing Meis1 into Moz-deficient cells carrying MOZ-TIF2. Meis1 deletion impaired MOZ-TIF2-mediated AML development. Active histone modifications were also severely reduced at the Meis1 locus in Moz-deficient MOZ-TIF2 AML cells. These results suggest that endogenous MOZ is critical for MOZ-fusion-induced AML development and maintains active chromatin signatures at target gene loci.
2022-07-24 | GSE208741 | GEO
Project description:Analysis of the expression of KH2 embryonic stem cells inducibly expressing V5 tagged Sox17 protein. Results provide information on the endodermal gene expression program activated after Sox17 expression in ES cells.
2013-04-23 | GSE43233 | GEO
Project description:Analysis of the expression of KH2 embryonic stem cells inducibly expressing V5 tagged Sox17 protein. Results provide information on the endodermal gene expression program activated after Sox17 expression in ES cells. Total RNA extracted from 48 hours doxycycline induced compaired to non-induced Sox17-V5 expressing ES cells
2013-04-23 | E-GEOD-43233 | biostudies-arrayexpress
Project description:Genomic locations of V5-tagged budding yeast Rif1 (including wilt-type and designer mutants) were analysed by ChIP-Seq. Mutants tested were rif1-7A and rif1-7E, in which Ser/Thr residues in the cluster of SQ/TQ sites were mutated to Ala or Glu, respectively. We also tested tested rif1-∆594, in which the C-terminal 594 amino acids were deleted.
2023-11-19 | E-MTAB-13452 | biostudies-arrayexpress
Project description:Trichormus variabilis V5 strain:V5 Genome sequencing and assembly
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Project description:Purpose: The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) of U251 cells with endogenous Gcn5 depletion and reconstituted expression of WT Flag-rGcn5 or Flag-rGcn5 Y645A / endogenous DLST depletion and reconstituted expression of WT V5-rDLST or V5-rDLST R224A/K226E Transcriptomes. And quantitatively analyze the cell signaling pathways that regulated by the studied mutants. Methods: total mRNA was extracted from U251 cells with endogenous Gcn5 depletion and reconstituted expression of WT Flag-rGcn5 or Flag-rGcn5 Y645A / endogenous DLST depletion and reconstituted expression of WT V5-rDLST or V5-rDLST R224A/K226E.llumina compatible libraries were prepared by using the KAPA Stranded mRNA-Seq Library Preparation Kit for Illumina® platforms (KAPA Biosystems). In brief, 250 ng of total RNA was enriched for poly-A-tailed mRNA by using Kapa’s mRNA Capture beads. Poly-A-enriched RNA was fragmented to a median size of 150 bp by using chemical fragmentation and converted into double-stranded cDNA with dUTP incorporated into the second cDNA strand. The ends of the double-stranded cDNA were polished, 5’-phosphorylated, and 3’-A-tailed for the ligation of indexed adapters. Adapter-ligated DNA fragments were amplified by 8 cycles of PCR. The strand with incorporated dUTP was not amplified. The resulting libraries were quantified by qPCR and assessed for size distribution by using the 4200 TapeStation (Agilent Technologies), and then multiplexed, 4 per pool, and sequenced on the Illumina’s NextSeq500 by using the mid-output, 75-bp paired-end read format. Results: Using an optimized data analysis workflow, we mapped about 50 million sequence reads per sample to the human genome and quantified the expression of protein coding genes in the U251 cells of WT Gcn5 and Gcn5 Y645A mutant/WT DLST and DLST R224A/K226E mutant. Altered expression of 3 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Conclusions: Our study represents the first detailed analysis of U251 cells with endogenous Gcn5 depletion and reconstituted expression of WT Flag-rGcn5 or Flag-rGcn5 Y645A / endogenous DLST depletion and reconstituted expression of WT V5-rDLST or V5-rDLST R224A/K226E Transcriptomes. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that Gcn5 Y45A mutant and DLST R224A/K226E mutant, which reduce histone H3 K79 succinylation, can regulate several cell signaling pathways that important for cancer cell proliferation.
2017-12-13 | GSE98050 | GEO
Project description:V5 tagged Elf5.
2018-09-07 | GSE119657 | GEO
Project description:Human acetyltransferases MOZ and MORF are implicated in chromosomal translocations associated with aggressive leukemias. Oncogenic translocations involve the far amino terminus of MOZ/MORF, the function of which remains unclear. Here, we identified and characterized two structured winged helix domains, WH1 and WH2, in MORF and MOZ. WHs bind DNA in a cooperative manner, with WH1 specifically recognizing unmethylated CpG sequences. Structural and genomic analyses show that the DNA binding function of WHs targets MORF/MOZ to gene promoters, stimulating transcription and H3K23 acetylation, and WH1 recruits oncogenic fusions to HOXA genes that trigger leukemogenesis. Cryo-EM, NMR, mass spectrometry and mutagenesis studies provide mechanistic insight into the DNA-binding mechanism, which includes the association of WH1 with the linker DNA and binding of WH2 to the dyad of the nucleosome, with the latter being further modulated by the neighboring domain DPF and autoacetylation of MORF. The discovery of WHs in MORF and MOZ and their DNA binding functions could open a new avenue in developing therapeutics to treat diseases associated with aberrant MOZ/MORF acetyltransferase activities.
2023-03-11 | PXD036192 | Pride