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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: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE291413 | GEO | 2025/03/14

REPOSITORIES: GEO

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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:GRHL and PGR control WNT4 expression in the mammary gland via 3D looping of conserved and species-specific enhancers [ATAC-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: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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Gene expression of RonTK-/- mammary glands compared to RonTK+/+ controls during development

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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:Primary mammary gland stromal fibroblasts from pubertal SHARPIN-deficient cpdm/cpdm -mice and their littermate controls

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Gene expression of RonTK-/- mammary glands compared to RonTK+/+ controls during development

Project description:RON WT and RON KO at 5, 6, 7 week virgin mammary glands In the study, we demonstrated that RON regulates mammary gland branching morphogenesis in pubertal development associated with changes in gene expression. Keywords: Pubertal mammary glands In the study, we hybridized RNA from 5, 6, 7 week old virgin female RON WT and KO mammary glands to Affymetrix GeneChip Mouse Genome 430 2.0 Array

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Project description:The identification of genes driving organ development is central to understanding which signaling pathways drive the pathogenesis of various diseases including cancer. This dataset depicts the proteomic changes observed in C57BL/6J mice expressing wild-type or 3SA-phospho mutant versions of the Bcl-2-associated death promoter, BAD. This data shows that BAD regulates postnatal mammary gland morphogenesis in puberty. Three conserved serine residues on BAD are co-ordinately phosphorylated to regulate its activity. Non-phosphorylated BAD mutant delayed pubertal ductal elongation. This defect was specific to the epithelial compartment as transplant and ex vivo organoid assays of mutant epithelium recapitulated decreased tubule migration. Proteomic signature between BAD+/+ and phosphomutant BAD-3SA mammary glands identified differences in actin-binding and focal adhesion components. Mechanistically, non-phosphorylated BAD impedes protein translation, specifically in protrusions, through aberrant hypophosphorylated 4E-BP1. These findings reveal a critical enhancement of localized translation for efficient pubertal-mammary-gland morphogenesis and identifies BAD as a novel regulator of this process.

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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.

2009-10-23 | GSE18704 | GEO

Open chromatin and single-cell sequencing analysis reveals the contribution of Wnt4-lineage cells and the importance of chromatin regulators in renal tubular and interstitial differentiation

Project description:Although Wnt4 is an early marker of nephron differentiation, how Wnt4-lineage cells differentiate into the renal interstitium and other cells types is unclear. Cell fate, proliferation, migration, and differentiation are controlled by precise spatiotemporal gene expression programs that are coordinately regulated by cell-cycle, lineage-specific transcription and chromatin regulatory factors. However, little is known about the roles of epigenetic/chromatin regulators in renal tubular and interstitial differentiation and diseases. We deleted the chromatin regulator Brg1 in Wnt4-expressing cells and FACS-purified Wnt4-lineage cells of wild-type and Brg1-deficient kidneys. We then carried out assay for transposase-accessible chromatin sequencing (ATAC-seq) to determine how Brg1-deficiency alters chromatin accessibility. We further performed single-cell RNA sequencing (scRNA-seq) to define the population and the effects of Brg1-deficiency in the differentiation of Wnt4-lineage cells. Our ATAC-seq analysis shows that Brg1-deficiency alters accessibility at thousands of active enhancers harboring motifs for an array of transcription factors. Unbiased scRNA-seq analyses identify 35 clusters of Wnt4-descendant cells and uncover novel cell types and genes that have so far not been linked to Wnt4-lineage cells. Brg1-deficiency leads to increased endothelial, stromal, and smooth-muscle cells and decreased nephron tubular cells. In Brg1-deficient kidneys, the expression of Pttg1 and proliferation are increased in Wnt4-expressing precursors, which cannot transition to a characteristic tubular state and appear to undergo fibrosis. Our results provide crucial insight into chromatin remodeling events and Wnt4-lineage cell-associated gene expression dynamics, highlighting the importance of chromatin regulators in controlling the differentiation of these cells and the expression of disease-associated genes.

2022-04-08 | GSE199188 | GEO

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