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RNA-seq analysis of the effects of single and compound deletion of Moz (Kat6a) and/or Dlx5 during mouse craniofacial development

ABSTRACT: RNA-seq analysis of the effects of single and compound deletion of Moz (Kat6a) and/or Dlx5 during mouse craniofacial development

PROVIDER: PRJNA555853 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9724210.fastq.gz	Fastqsanger.gz
	SRR9724220.fastq.gz	Fastqsanger.gz
	SRR9724230.fastq.gz	Fastqsanger.gz
	SRR9724240.fastq.gz	Fastqsanger.gz
	SRR9724250.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA-seq analysis of the effects of single and compound deletion of Moz (Kat6a) and/or Dlx5 during mouse craniofacial development

Project description:The purpose of these data is to investigate the genetic perturbations which underlie the cleft palate phenotype in Kat6a and Dlx5 mutant mouse embryos. The palate develops from the maxillary portion of the first pharyngeal arches, commencing between E10.5 and E11.5 of mouse gestation.

2019-07-23 | GSE134608 | GEO

Distribution of MOZ (KAT6A) in the genome and effects of MOZ on gene expression during mouse craniofacial development

Project description:Distribution of MOZ (KAT6A) in the genome and effects of MOZ on gene expression during mouse craniofacial development

| PRJNA555846 | ENA

The histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA-binding winged helix domainThe histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA-binding winged helix domain

Project description:The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrated that a winged helix domain at the N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A to unmethylated CpG islands (CGIs) genome wide. Mutation of the essential amino acids completely abrogates the enrichment of KAT6A at CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases

2023-01-14 | PXD034833 | Pride

RNA-seq profiling of mouse embryonic fibroblasts from Kat6a knockout and wildtype mice

Project description:Acetylation of histones by lysine acetyltransferases (KATs) is essential for transcriptional regulation of gene expression. The MYST family of KATs (KAT5-8) includes the oncogenes KAT6A (MOZ) and KAT6B (MORF/QKF). KAT6A has key roles in promoting cell proliferation through transcriptional activation of negative regulators of the Cdkn2a locus, which encode the tumor suppressors INK4A and ARF. To examine the loss of KAT6A function, mouse embryonic fibroblasts (MEFs) were isolated from E13.5 Kat6a+/+ and Kat6a–/– embryos and RNA-seq profiling was performed.

2018-08-03 | GSE108242 | GEO

ChIP-seq of MOZ (Flag-V5-BIO tagged) in mouse mouse craniofacial development

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

The genome wide mapping of H3K9 and H3K23 acetylation in Moz+/+ and Moz-/- MOZ-TIF2 AML cells

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

The histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA binding winged helix domain [RNA-seq]

Project description:The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrate that a winged helix (WH) domain at the very N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A with unmethylated CpG islands (CGIs) genome-wide. Mutation of the essential amino acids for DNA binding completely abrogates the enrichment of KAT6A at CGIs. In contrast, deletion of a second WH domain or the histone tail binding PHD fingers only subtly influences the binding of KAT6A to CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases.

2022-12-20 | GSE206273 | GEO

The histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA binding winged helix domain [ChIP-seq]

Project description:The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrate that a winged helix (WH) domain at the very N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A with unmethylated CpG islands (CGIs) genome-wide. Mutation of the essential amino acids for DNA binding completely abrogates the enrichment of KAT6A at CGIs. In contrast, deletion of a second WH domain or the histone tail binding PHD fingers only subtly influences the binding of KAT6A to CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases.

2022-12-20 | GSE206272 | GEO

ChIP-seq of MOZ (Flag-V5-BIO tagged) in mouse mouse craniofacial development

Project description:ChIP-seq of MOZ (Flag-V5-BIO tagged) in mouse mouse craniofacial development

| PRJNA555849 | ENA

Expression data from Lck-Dlx5 lymphoma

Project description:Lck-Dlx5 induces T-cell lymphoma but the mechanism is unknown. We used microarrays to detail the global programme of gene expression underlying Dlx5-induced T-cell lymphoma T-cells were isolated from Lck-Dlx5 mice, Lck-MyrAkt2 mice and Wild type littermates for RNA extraction and hybridization on Affymetrix microarrays.

2016-06-24 | E-GEOD-83685 | biostudies-arrayexpress

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