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UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells

ABSTRACT: UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells

PROVIDER: PRJNA422467 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6377540_1.fastq.gz	Fastqsanger.gz
	SRR6377540_2.fastq.gz	Fastqsanger.gz
	SRR6377550_1.fastq.gz	Fastqsanger.gz
	SRR6377550_2.fastq.gz	Fastqsanger.gz
	SRR6377560.fastq.gz	Fastqsanger.gz

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UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [RNA-seq]

Project description:UTX is a histone H3 lysine 27 demethylase required for development. However, the mechanisms underlying developmental gene regulation by UTX are unclear. Here, we discovered a molecular interaction between UTX and 53BP1 that regulates gene expression in a human neurogenesis model. Human 53BP1 contains a UTX-binding site that diverges from its mouse homolog by 41%, and our data suggest that the UTX-53BP1 interaction is conserved in primates but not rodents. ChIP-Seq revealed that the genome-wide targets of UTX and 53BP1 overlap by 84%. We used CRISPR-Cas9 to generate mutations of 53BP1 and UTX in human embryonic stem cells, and found that both 53BP1 and UTX are required to promote the expression of hundreds of neurogenic genes during neural differentiation. Further, 53BP1 is required for human neural progenitor differentiation into neurons. Our findings suggest that the UTX-53BP1 interaction controls gene expression important for neural differentiation in humans.

2019-02-15 | GSE108115 | GEO

UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [ChIP-seq]

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UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [mouse RNA-seq]

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UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [ChIP-seq]

Project description:UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [ChIP-seq]

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UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [RNA-seq]

Project description:UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [RNA-seq]

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UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [mouse RNA-seq]

Project description:UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells [mouse RNA-seq]

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Phosphorylation of 53BP1 by ATM enforce neurodevelopmental programs in cortical organoids

Project description:53BP1 is a well-established DNA damage repair factor that has recently been shown to regulate gene expression and critically influence tumor suppression and neural development. For gene regulation, how 53BP1 is regulated remains unclear. Here, we showed that 53BP1-serine 25 phosphorylation by ATM is required for neural progenitor cell proliferation and neuronal differentiation in cortical organoids. 53BP1-serine 25 phosphorylation dynamics controls 53BP1 target genes for neuronal differentiation and function, cellular response to stress, and apoptosis. Beyond 53BP1, ATM is required for phosphorylation of factors in neuronal differentiation, cytoskeleton, p53 regulation, and ATM, BNDF, and WNT signaling pathways for cortical organoid differentiation. Overall, our data suggest that 53BP1 and ATM control key genetic programs required for human cortical development.

2024-08-11 | GSE231321 | GEO

UTX and 53BP1 co-regulate genetic programs for neural differentiation of human embryonic stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-15 | GSE108116 | GEO

Loss of UTX/KDM6A and the activation of FGFR3 converge to regulate differentiation gene expression programs in bladder cancer [ChIP-seq]

Project description:Bladder cancer prognosis is closely linked to the underlying differentiation state of the tumor, ranging from the less aggressive and most differentiated luminal tumors to the more aggressive and least differentiated basal tumors. Sequencing of bladder cancer has revealed that loss-of-function mutations in chromatin regulators and mutations that activate receptor tyrosine kinase (RTK) signaling frequently occur in bladder cancer. However, little is known as to whether and how these two types of mutations functionally interact or cooperate to regulate tumor growth and differentiation state. Here, we focus on loss of the histone demethylase UTX (also known as KDM6A) and activation of the RTK FGFR3, two events that commonly co-occur in muscle invasive bladder tumors. We show that UTX loss and FGFR3 activation cooperate to disrupt the balance of luminal and basal gene expression in bladder cells. UTX localized to enhancers surrounding many genes that are important for luminal cell fate, and supported the transcription of these genes in a catalytic-independent manner. In contrast to UTX, FGFR3 activation was associated with lower expression of luminal genes in tumors and FGFR inhibition increased transcription of these same genes in cell culture models. This suggests an antagonistic relationship between UTX and FGFR3. In support of this model, UTX loss-of-function potentiated FGFR3-dependent transcriptional effects and the presence of UTX blocked an FGFR3-mediated increase in the colony formation of bladder cells. Taken together, our study reveals how mutations in UTX and FGFR3 converge to disrupt bladder differentiation programs that could serve as a therapeutic target.

2020-09-15 | GSE157090 | GEO

Loss of UTX/KDM6A and the activation of FGFR3 converge to regulate differentiation gene expression programs in bladder cancer [RNA-seq]

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