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Myc and the Tip60 chromatin remodeling complex control neuroblast maintenance and polarity in Drosophila

ABSTRACT: Myc and the Tip60 chromatin remodeling complex control neuroblast maintenance and polarity in Drosophila

PROVIDER: PRJNA445881 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6904770_1.fastq.gz	Fastqsanger.gz
	SRR6904770_2.fastq.gz	Fastqsanger.gz
	SRR6904765_1.fastq.gz	Fastqsanger.gz
	SRR6904765_2.fastq.gz	Fastqsanger.gz
	SRR6904766_1.fastq.gz	Fastqsanger.gz

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Myc and the Tip60 chromatin remodeling complex control neuroblast maintenance and polarity in Drosophila

Project description:Stem cells establish cortical polarity and divide asymmetrically to simultaneously maintain themselves and generate differentiating offspring cells. Several chromatin modifiers have been identified as stemness factors in mammalian pluripotent stem cells, but whether these factors control stem cell polarity and asymmetric division has not been investigated so far. We addressed this question in Drosophila neural stem cells called neuroblasts. We identified the Tip60 chromatin remodeling complex and its interaction partner Myc to regulate target genes required for neuroblast maintenance. Knockdown of members of this complex results in loss of cortical polarity, symmetric neuroblast division and premature differentiation through nuclear entry of the transcription factor Prospero. We found that aPKC is the key target gene of Myc and the Tip60 complex subunit Domino regulating neuroblast polarity. Our transcriptome analysis further showed that Domino regulates the expression of mitotic spindle genes which were identified before as direct Myc targets. Our findings reveal an evolutionarily conserved functional link between Myc, the Tip60 complex and the molecular network controlling cell polarity and asymmetric cell division.

2018-07-06 | PXD009939 | Pride

Myc and the Tip60 chromatin remodeling complex control neuroblast maintenance and polarity in Drosophila.

Project description:Stem cells establish cortical polarity and divide asymmetrically to simultaneously maintain themselves and generate differentiating offspring cells. Several chromatin modifiers have been identified as stemness factors in mammalian pluripotent stem cells, but whether these factors control stem cell polarity and asymmetric division has not been investigated so far. We addressed this question in Drosophila neural stem cells called neuroblasts. We identified the Tip60 chromatin remodeling complex and its interaction partner Myc as regulators of genes required for neuroblast maintenance. Knockdown of Tip60 complex members results in loss of cortical polarity, symmetric neuroblast division, and premature differentiation through nuclear entry of the transcription factor Prospero. We found that aPKC is the key target gene of Myc and the Tip60 complex subunit Domino in regulating neuroblast polarity. Our transcriptome analysis further showed that Domino regulates the expression of mitotic spindle genes previously identified as direct Myc targets. Our findings reveal an evolutionarily conserved functional link between Myc, the Tip60 complex, and the molecular network controlling cell polarity and asymmetric cell division.

| S-EPMC6092623 | biostudies-literature

Myc and the Tip60 chromatin remodeling complex control neuroblast maintenance and polarity in Drosophila

Project description:Transcriptomic analyses of wild type and Domino knockdown 3rd instar larval neural cells

2018-05-15 | GSE112395 | GEO

Lysine acetyltransferase Tip60 is required for hematopoietic stem cells maintenance

Project description:Hematopoietic stem cells (HSC) have the potential to replenish the blood system for the lifetime of the organism. Their two defining properties, self-renewal and differentiation, are tightly regulated by the epigenetic machineries. Here, using conditional gene knockout models, we demonstrate a critical requirement of lysine acetyltransferase 5 (also known as Tip60) for murine HSC maintenance both in the embryonic and adult stages, which depends on its acetyltransferase activity. Genome-wide chromatin and transcriptome profiling revealed that Tip60 co-localizes with c-Myc and that Tip60 deletion suppress the expression of Myc target genes, which are associated with critical biological processes for HSC maintenance, cell-cycle and DNA repair. Notably, acetylated H2A.Z (acH2A.Z) was enriched at the Tip60-bound active chromatin and Tip60 deletion induced a robust reduction in the acH2A.Z / H2A.Z ratio. These results uncover a critical epigenetic regulatory layer for HSC maintenance through Tip60 dependent H2A.Z acetylation to activate Myc target genes.

2020-06-19 | GSE120705 | GEO

Lysine acetyltransferase Tip60 is required for hematopoietic stem cells maintenance

Project description:Lysine acetyltransferase Tip60 is required for hematopoietic stem cells maintenance

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Neuroblast-specific open chromatin allows the temporal transcription factor, Hunchback, to bind neuroblast-specific loci

Project description:Integration of spatial and temporal identity during Drosophila neurogenesis is due to spatial factors generating neuroblast-specific chromatin thereby biasing subsequent temporal transcription factor binding and producing neuroblast-specific neurons.

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Project description:TIP60 complex

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Unique structural features of the human NuA4/TIP60 acetyltransferase and chromatin remodeling complex

Project description:The human NuA4/TIP60 co-activator complex, a fusion of the yeast SWR1 and NuA4 complexes, both incorporates the histone variant H2A.Z into nucleosomes and acetylates histones H4/H2A/H2A.Z to play crucial roles regulating gene expression and maintaining genome stability. Our cryo-EM studies show that within the NuA4/TIP60 complex, the EP400 subunit serves as an architectural scaffold holding the different functional modules in specific positions and giving rise to a novel arrangement of the ARP module. EP400 interacts with the TRRAP subunit using a footprint that overlaps with that of the SAGA acetyltransferase complex, thereby preventing the formation of a hybrid complex. Loss of the TRRAP subunit leads to mislocalization of NuA4/TIP60, resulting in the redistribution of H2A.Z and its acetylation across the genome,emphasizing the dual functionality of NuA4/TIP60 as a single macromolecular assembly.

2024-08-08 | PXD053207 | Pride

Unique structural features of the human NuA4/TIP60 acetyltransferase and chromatin remodeling complex

Project description:The human NuA4/TIP60 co-activator complex, a fusion of the yeast SWR1 and NuA4 complexes, both incorporates the histone variant H2A.Z into nucleosomes and acetylates histones H4/H2A/H2A.Z to play crucial roles regulating gene expression and maintaining genome stability. Our cryo-EM studies show that within the NuA4/TIP60 complex, the EP400 subunit serves as an architectural scaffold holding the different functional modules in specific positions and giving rise to a novel arrangement of the ARP module. EP400 interacts with the TRRAP subunit using a footprint that overlaps with that of the SAGA acetyltransferase complex, thereby preventing the formation of a hybrid complex. Loss of the TRRAP subunit leads to mislocalization of NuA4/TIP60, resulting in the redistribution of H2A.Z and its acetylation across the genome, emphasizing the dual functionality of NuA4/TIP60 as a single macromolecular assembly.

2024-08-08 | PXD053209 | Pride

TIP60/KAT5 is required for the maintenance of homeostasis in hippocampal CA1

Project description:ChIP-Seq for H4K12ac from the hippocampal neuronal nuclei of Tip60 cKO and control mice.

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