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Transcription profiling of mouse developing kidney to investigate Wnt4-dependent gene expression (GUDMAP Series_id: 13)

ABSTRACT: Our laboratory's interest is in understanding the molecular principles that underlie the regional organization of the mammalian metanephric kidney. Our goal is to generate a detailed spatial map of the cellular expression of selected regulatory genes during mammalian kidney development. The goal of this study is to identify a population of genes that are enriched in the renal vesicle (RV) and its derivatives using Wnt4 mutants. Experiment Overall Design: Wnt4 is required for renal vesicle (RV) induction. Therefore, RV and the derivatives (s-shaped body and eventually the mature nephron) are missing in Wnt4 mutants. At E14.5, these structures are present in wildtype kidneys. Transcriptional profile comparison between E14.5 wildtype and Wnt4 mutants therefore identify genes expressed in the RV and derivatives. Minimally pooled kidney samples were used as single biological replicates. Total RNA was isolated from these pools and subjected to a single round of amplification for use on Affymetrix arrays.

ORGANISM(S): Mus musculus

SUBMITTER: Mehran Sharghi

PROVIDER: E-GEOD-6934 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling of mouse E14.5 Wnt4 mutants vs wild types

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Transcriptional comparison between whole kidneys from E14.5 Wnt4 mutants and wildtype mice (Mouse430_2 platform). (GUDMAP Series ID: 13)

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Project description:Our laboratory's interest is in understanding the molecular principles that underlie the regional organization of the mammalian metanephric kidney. Our goal is to generate a detailed spatial map of the cellular expression of selected regulatory genes during mammalian kidney development. The goal of this study is to identify genes expressed during the morphogenesis of the nephron. By profiling two specific developmental nephron structures, we expect to identify genes expressed in both, and unique to each, which suggests they may play a role in the underlying mechanism responsible for the morphogenesis. Experiment Overall Design: Two early nephron structures, the renal vesicle and the s-shaped body, and the collecting duct system, were microdissected from E14.5 kidneys based on morphological criteria. Antibody and lectin staining together with RT-PCR were used for identity verification and for exclusion of contamination by other tissues. Samples are minimally pooled for amplification. A biological replicate is a single minimally pooled sample. RNA isolated from the collected structures was put through two rounds of T7-driven amplification to obtain the microgram quantities of cRNA needed for hybridization to Affymetrix microarrays. Detection of genes previously shown to be expressed in these early structures, such as Wt1, Wnt4 and Pax8, validates the data from the screen. The collecting duct sample serves as a reference sample for comparing the renal vesicle and s-shaped body comparison in this study.

2008-06-14 | E-GEOD-6287 | biostudies-arrayexpress

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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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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

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

Cell intrinsic Wnt4 influences cDC fate determination to suppress Type 2 immunity

Project description:We demonstrate that Wnt4, a beta-catenin independent Wnt ligand, is produced by both hematopoietic and non-hematopoietic cells and is both necessary and sufficient for pre-cDC1/cDC1 maintenance. Whereas BM cDC precursors undergo phosphoJNK/c-Jun activation upon Wnt4 treatment, loss of cDC Wnt4 in CD11cCreWnt4flox/flox mice impaired differentiation of CD24+, Clec9A+, CD103+ cDC1 compared to CD11cCre controls. Conversely, sc-RNAseq analysis of BM revealed a 2-fold increase in cDC2 gene signature genes and flow cytometry demonstrated increased numbers of SIRP-α + cDC2 amid lack of Wnt4. Increased cDC2 numbers due to CD11c-restricted Wnt4 deficiency increased interleukin 5 production, group 2 innate lymphoid cell (ILC2) expansion, and host resistance to the hookworm parasite Nippostrongylus brasiliensis. Collectively, these data uncover a novel and unexpected role for Wnt4 in cDC subset differentiation and Type 2 immunity.

2019-08-01 | GSE131569 | GEO

Reduced WNT4 expression in normal skin fibroblasts leads to ‘Dupuytren-like’ changes in the transcriptome

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2024-07-01 | GSE269317 | GEO

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