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GRHL and PGR control WNT4 expression in the mammary gland via 3D looping of conserved and species-specific enhancers [ATAC-Seq]

ABSTRACT: GRHL and PGR control WNT4 expression in the mammary gland via 3D looping of conserved and species-specific enhancers [ATAC-Seq]

PROVIDER: PRJNA1233316 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR32612952_1.fastq.gz	Fastqsanger.gz
	SRR32612952_2.fastq.gz	Fastqsanger.gz
	SRR32612953_1.fastq.gz	Fastqsanger.gz
	SRR32612953_2.fastq.gz	Fastqsanger.gz

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GRHL and PGR control WNT4 expression in the mammary gland via 3D looping of conserved and species-specific enhancers [4C-Seq]

Project description:GRHL and PGR control WNT4 expression in the mammary gland via 3D looping of conserved and species-specific enhancers [4C-Seq]

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GRHL and PGR control WNT4 expression in the mammary gland via 3D looping of conserved and species-specific enhancers [4C-Seq]

Project description:This dataset belongs to a study in which we functionally dissect the cis-acting enhancer network and spatiotemporal transcriptional mechanisms that regulate WNT4 expression in the mouse mammary gland and the human breast. As part of these efforts, we performed 4C chromatin conformation capture in BC44 and HC11 (two mouse mammary epithelial cell lines) using the Wnt4 promoter as a viewpoint.

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GRHL and PGR control WNT4 expression in the mammary gland via 3D looping of conserved and species-specific enhancers [ATAC-Seq]

Project description:This dataset belongs to a study in which we functionally dissect the cis-acting enhancer network and spatiotemporal transcriptional mechanisms that regulate WNT4 expression in the mouse mammary gland and the human breast. As part of these efforts, we characterized the chromatin accessibility landscape in the pubertal mouse mammary gland. For this, we FACS sorted basal, luminal and stromal cell populations and performed bulk ATAC-seq analysis

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Genome-wide binding sites of Progesterone receptor (PGR) isoforms PGR-A and PGR-B during differentiation of human endometrial stromal cells

Project description:We report the genome-wide binding sites of PGR-A and PGR-B at 2h of in vitro differentiation of human endometrial stromal cells that express either PGR-A or PGR-B. Progesterone, acting through the progesterone receptors (PGRs), is one of the most critical regulators of endometrial differentiation, known as decidualization, which is a key step toward the establishment of pregnancy. Yet a long-standing unresolved issue in uterine biology is the precise roles played by the major PGR isoforms, PGR-A and PGR-B, during decidualization in the human. Our approach, expressing PGR-A and PGR-B individually after silencing endogenous PGRs in human endometrial stromal cells (HESC), enabled the analysis of the roles of these isoforms separately as well as jointly by ChIP-seq and gene-expression analysis. In order to study the cistromes of PGR-A and PGR-B at 2h of in vitro differentiation of human endometrial stromal cells, we generated primary cultures of human endometrial stromal cells expressing flag tagged PGR-A and PGR-B individually after silencing endogenous PGRs. Input DNA was used as the reference sample.

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Gene expression profiles of Wnt4 high and Wnt4 low populations of murine islets at postnatal day 1 (P1).

Project description:To find the differences between β cells expressing Wnt4 and those that do not express it (or express it at low levels) at neonatal stage, murine islets at postnatal day 1 (P1) were collected. Based on a reporter expressing Cre recombinase from the Wnt4 locus, we observed that Wnt4 expression starts in a small subset of β cells at embryonic day (E) 18.5. At neonatal stages, around 50% of β cells express Wnt4 at P0 and most of cells express it by P5. We collected Wnt4 high and Wnt4 low islet cells by FACS and compared their gene expression profile. Wnt4 high islet cell population showed a significant increase of β-cell maturation and function related genes, including transcription factors such as Pdx1 and Nkx6.1, insulin 2, glucokinase (Gck), and the glucose transporter Slc2a2. On the contrary, Wnt4 low islet cell population showed significant increasing of proliferation markers such as Pcna, Mki67 and the positive cell cycle regulators Ccnd1, Ccnd3, Ccna2, Cdk1, Cdk2 and Cdk6. Taken together, these results show that Wnt4 expression is higher in more mature but less proliferative β cells.

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Project description:Progesterone receptor (PGR) is essential for various functions in the female reproductive tract, especially ovulation in the ovary. PGR consists of two main isoforms, PGR-A and PGR-B, that possess different expression patterns and are responsible for various unique roles in different tissue contexts. While both are present in the reproductive tract, PGR-A is the only one known to be essential for ovulation while PGR-B plays a lesser role in the reproductive tract. However, the specific roles of PGR isoforms on gene expression in peri-ovulatory granulosa cells have not been previously investigated in detail. In this study, we identified the unique role of PGR-A and PGR-B in peri-ovulatory granulosa cells through RNA-seq of knockout mouse models for total PGR (PGR KO) or specific isoforms (PGR-A KO and PGR-B KO)

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WNT4 is required for ovarian follicle development and female fertility

Project description:To study the physiological role of WNT4 in the postnatal ovary, a mouse strain bearing a floxed Wnt4 allele was created and mated to the Amhr2tm3(cre)Bhr strain to target deletion of Wnt4 to granulosa cells. Wnt4flox/-;Amhr2tm3(cre)Bhr/+ mice had significantly reduced ovary weights and produced smaller litters (P<0.05). Serial follicle counting demonstrated that, while Wnt4flox/-;Amhr2tm3(cre)Bhr/+ mice were born with a normal ovarian reserve and maintained normal numbers of small follicles until puberty, they had only 25.2% of the normal number of healthy antral follicles. Some Wnt4flox/-;Amhr2tm3(cre)Bhr/+ mice had no antral follicles or corpora lutea and underwent premature follicle depletion. RTPCR analyses of Wnt4flox/-;Amhr2tm3(cre)Bhr/+ granulosa cells and cultured granulosa cells that overexpress WNT4 demonstrated that WNT4 regulates the expression of Star, Cyp11a1 and Cyp19, steroidogenic genes previously identified as downstream targets of the WNT signaling effector CTNNB1. WNT4- and CTNNB1-overexpressing cultured granulosa cells were analyzed by microarray for alterations in gene expression, which showed that WNT4 also regulates a series of genes involved in late follicle development and the cellular stress response via the WNT/CTNNB1 signaling pathway. Together, these data indicate that WNT4 is required for normal antral follicle development, and may act by regulating granulosa cell functions including steroidogenesis.

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PGR-B is responsible for a proliferative gene signature in ovarian neoplasia in PGR-B expressing mice.

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2020-09-10 | GSE137499 | GEO

Role of LDB1 in the transition from chromatin looping to transcription activation

Project description:Many questions remain about how close association of genes and distant enhancers occurs and how this is linked to transcription activation. In erythroid cells, LDB1 is recruited to the β-globin locus via LMO2 and is required for looping of the β-globin locus control region (LCR) to the active β-globin promoter. We show that the LDB1 dimerization domain (DD) is necessary and, when fused to LMO2 is sufficient, to completely restore LCR-promoter looping and transcription in LDB1 depleted cells. The looping function of the DD is unique and irreplaceable by heterologous dimerization domains. Dissection of the DD revealed distinct functional properties of conserved subdomains. Notably, a conserved helical region (DD4/5) is dispensable for LDB1 dimerization and chromatin looping but essential for transcriptional activation. DD4/5 is required for the recruitment of the co-regulators FOG1 and NuRD complex. Lack of DD4/5 alters histone acetylation and RNA polymerase II recruitment and results in failure of the locus to migrate to the nuclear interior as normally occurs during erythroid maturation. These results uncouple enhancer-promoter looping from nuclear migration and transcription activation and reveal new roles for LDB1in these processes. RNA-seq in LDB1 knockdown, LDB1 delta4/5 construct, LDB1 full-length construct, and control in induced MEL cells; three replicates each.

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