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Genome wide map of Runx3, Brn3a binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

ABSTRACT: Genome wide map of Runx3, Brn3a binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

PROVIDER: PRJNA1064151 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27512113_1.fastq.gz	Fastqsanger.gz
	SRR27512113_2.fastq.gz	Fastqsanger.gz
	SRR27512114_1.fastq.gz	Fastqsanger.gz
	SRR27512114_2.fastq.gz	Fastqsanger.gz
	SRR27512115_1.fastq.gz	Fastqsanger.gz

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Genome wide map of Runx3, Brn3a binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

Project description:We isolated E12.5 TrkC neurons and profiled Runx3, Brn3a binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons by Cut&Run

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Genome wide map of Runx3, Brn3a, Islet1 binding, chromatin accessibility (ATAC) and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

Project description:We isolated E11.5 TrkC neurons and profiled chromatin accessibility (ATAC), Runx3, Brn3a, Islet1 binding and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons by Cut&Run

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Genome wide map of Runx3, Brn3a, Islet1 binding, chromatin accessibility (ATAC) and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

Project description:Genome wide map of Runx3, Brn3a, Islet1 binding, chromatin accessibility (ATAC) and Histone H3 acetylated on lysine 27 (H3K27Ac) during early development of DRG TrkC neurons

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Project description:We isolated E11.5 TrkC neurons and profiled ATAC and H3K27ac genomic regions

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Novel role of TrkC in diabetic nephropathy and cross-talk of TrkC with insulin-related signaling

Project description:Diabetic nephropathy is a major cause of end-stage renal disease. Kidney podocytes play a central role in the pathogenesis of diabetic nephropathy. With their intercellular contacts they assemble part of the kidney filter. Many molecular mechanisms of the pathogenesis of diabetic nephropathy are not elucidated and targeted therapies are lacking. Nephron-specific TrkCknockout (TrkC-KO) and TrkC overexpressing mice exhibit features of diabetic nephropathy such as enlarged glomeruli with mesangial proliferation, basement membrane thickening, albuminuria and podocyte loss when aging. Insulin-like growth factor 1 receptor (Igf1R)- associated gene expression was regulated in TrkC-KO mice glomeruli by qPCR. Phosphoproteins associated with insulin, erb-b2 receptor tyrosine kinase (Erbb) and Toll-like receptor signaling were enriched in lysates of podocytes treated with the TrkC ligand neurotrophin-3(Nt-3) in a mass spectrometry analysis. Activation of TrkC by Nt-3 resulted in phosphorylation of the Igf1R on activating tyrosine residues in podocytes. Our results identify TrkC to be a potentially targetable mediator of diabetic nephropathy.

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H3 lysine 4 is acetylated at active gene promoters and is regulated by H3 lysine 4 methylation.

Project description:Methylation of histone H3 lysine 4 (H3K4me) is an evolutionarily conserved modification whose role in the regulation of gene expression has been extensively studied. In contrast, the function of H3K4 acetylation (H3K4ac) has received little attention because of a lack of tools to separate its function from that of H3K4me. Here we show that, in addition to being methylated, H3K4 is also acetylated in budding yeast. Genetic studies reveal that the histone acetyltransferases (HATs) Gcn5 and Rtt109 contribute to H3K4 acetylation in vivo. Whilst removal of H3K4ac from euchromatin mainly requires the histone deacetylase (HDAC) Hst1, Sir2 is needed for H3K4 deacetylation in heterochomatin. Using genome-wide chromatin immunoprecipitation (ChIP), we show that H3K4ac is enriched at promoters of actively transcribed genes and located just upstream of H3K4 tri-methylation (H3K4me3), a pattern that has been conserved in human cells. We find that the Set1-containing complex (COMPASS), which promotes H3K4me2 and -me3, also serves to limit the abundance of H3K4ac at gene promoters. In addition, we identify a group of genes that have high levels of H3K4ac in their promoters and are inadequately expressed in H3-K4R, but not in set1? mutant strains, suggesting that H3K4ac plays a positive role in transcription. Our results reveal a novel regulatory feature of promoter-proximal chromatin, involving mutually exclusive histone modifications of the same histone residue (H3K4ac and H3K4me).

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H3 Lysine 4 Is Acetylated at Active Gene Promoters and Is Regulated by H3 Lysine 4 Methylation

Project description:Methylation of histone H3 lysine 4 (H3K4me) is an evolutionarily conserved modification whose role in the regulation of gene expression has been extensively studied. In contrast, the function of H3K4 acetylation (H3K4ac) has received little attention because of a lack of tools to separate its function from that of H3K4me. Here we show that, in addition to being methylated, H3K4 is also acetylated in budding yeast. Genetic studies reveal that the histone acetyltransferases (HATs) Gcn5 and Rtt109 contribute to H3K4 acetylation in vivo. Whilst removal of H3K4ac from euchromatin mainly requires the histone deacetylase (HDAC) Hst1, Sir2 is needed for H3K4 deacetylation in heterochomatin. Using genome-wide chromatin immunoprecipitation (ChIP), we show that H3K4ac is enriched at promoters of actively transcribed genes and located just upstream of H3K4 tri-methylation (H3K4me3), a pattern that has been conserved in human cells. We find that the Set1-containing complex (COMPASS), which promotes H3K4me2 and -me3, also serves to limit the abundance of H3K4ac at gene promoters. In addition, we identify a group of genes that have high levels of H3K4ac in their promoters and are inadequately expressed in H3-K4R, but not in set1 mutant strains suggesting that H3K4ac plays a positive role in transcription. Our results reveal a novel regulatory feature of promoter-proximal chromatin, involving mutually exclusive histone modifications of the same histone residue (H3K4ac and H3K4me).

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The interactomes of RUNX1 and RUNX3 from Mus musculus T cells

Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.

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