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RA and BMP4 cooperate with p63 to alter chromatin dynamics during surface epithelial commitment

ABSTRACT: RA and BMP4 cooperate with p63 to alter chromatin dynamics during surface epithelial commitment

PROVIDER: PRJNA491197 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7211490_1.fastq.gz	Fastqsanger.gz
	SRR7211490_2.fastq.gz	Fastqsanger.gz
	SRR7211491_1.fastq.gz	Fastqsanger.gz
	SRR7211491_2.fastq.gz	Fastqsanger.gz
	SRR7211492_1.fastq.gz	Fastqsanger.gz

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RA and BMP4 cooperate with p63 to alter chromatin dynamics during surface epithelial commitment

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

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Retinoic acid and BMP4 cooperate with p63 to alter chromatin dynamics during surface epithelial commitment.

Project description:Human embryonic stem cell (hESC) differentiation promises advances in regenerative medicine1-3, yet conversion of hESCs into transplantable cells or tissues remains poorly understood. Using our keratinocyte differentiation system, we employ a multi-dimensional genomics approach to interrogate the contributions of inductive morphogens retinoic acid and bone morphogenetic protein 4 (BMP4) and the epidermal master regulator p63 (encoded by TP63)4,5 during surface ectoderm commitment. In contrast to other master regulators6-9, p63 effects major transcriptional changes only after morphogens alter chromatin accessibility, establishing an epigenetic landscape for p63 to modify. p63 distally closes chromatin accessibility and promotes accumulation of H3K27me3 (trimethylated histone H3 lysine 27). Cohesin HiChIP10 visualizations of chromosome conformation show that p63 and the morphogens contribute to dynamic long-range chromatin interactions, as illustrated by TFAP2C regulation11. Our study demonstrates the unexpected dependency of p63 on morphogenetic signaling and provides novel insights into how a master regulator can specify diverse transcriptional programs based on the chromatin landscape induced by exposure to specific morphogens.

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Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation

Project description:Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation. Keywords: Notch1, p63, keratinocyte differentiation, gene expression profiling

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BMP4-directed trophoblast differentiation of human embryonic stem cells is mediated through a ΔNp63+ cytotrophoblast stem cell state

Project description:We show that FCM-BMP4-treated hESC differentiate into bona fide CTB by direct comparison to primary human placental tissues and isolated CTB through gene expresson profiling. We have compared gene expression profiling of FCM-BMP4-treated hESC to a panel of fetal tissues and first trimester tissues. Moreover, we have analysed the expression profiles of cells after shRNA knock-down of p63 compared to Scramble upon BMP4 treatment. Difference in expression between CTB trimester 1 / trimester 3 and PSC were compared the difference between FCM-BMP4-treated hESC and PSC at each time point collected.

2013-11-05 | E-GEOD-49354 | biostudies-arrayexpress

Circulating endoglin induces hypertension via the upregulated expression of BMP4

Project description:Endoglin is a membrane glycoprotein primarily expressed by the vascular endothelium and involved in cardiovascular diseases. Upon the proteolytic processing of the membrane-bound protein, a circulating form of endoglin (soluble endoglin, sEng) can be released, and high levels of sEng have been observed in several endothelial-related pathological conditions, where it appears to contribute to endothelial dysfunction. Preeclampsia is a multisystem disorder of high prevalence in pregnant women characterized by the onset of high blood pressure and often associated with increased levels of sEng. Although a pathogenic role for sEng involving hypertension has been reported in several animal models of preeclampsia, the exact molecular mechanisms implicated remain to be identified. To search for sEng-induced mediators, we have analyzed the protein secretome of human endothelial cells in the presence of sEng. We find that sEng induces the expression of BMP4 in endothelial cells, as evidenced by their proteomic signature, gene transcript levels and BMP4 promoter activity. A mouse model of preeclampsia with high sEng plasma levels (sEng+) showed increased levels of BMP4 transcripts in lungs and increased circulating BMP4, compared to those of control animals. In addition, after crossing female wild type with male sEng+ mice, hypertension appears 18 days after mating, precisely coinciding with the appearance of high plasma levels of BMP4. Also, serum levels of sEng and BMP4 are positively correlated in pregnant women with and without preeclampsia. Interestingly, sEng-induced arterial pressure elevation in sEng+ mice was abolished in the presence of the BMP4 inhibitor noggin, suggesting that BMP4 is a downstream mediator of sEng. These results provide a better understanding on the role of sEng in the pathobiology of preeclampsia and other cardiovascular diseases, where sEng levels are increased.

2020-04-23 | PXD016228 | Pride