Expression microarray analysis of pubertal mouse mammary gland development
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE6453 | GEO | 2007/05/01
SECONDARY ACCESSION(S): PRJNA98655
REPOSITORIES: GEO
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Project description:The aim was to carry out global analysis of gene expression changes occurring in the normal pubertal mouse mammary gland from the appearance to the regression of terminal end buds. Experiment Overall Design: 5 time points were chosen for analysis: 3wk, 4wk, 5wk, 6wk and 7wk. Each time point was analysed in triplicate with the exception of the 5wk time point which was analysed in duplicate. Total: 14 samples. Each sample was prepared from a pool of RNA from mammary glands of a minimum of three mice.
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Project description:The pituitary gland exhibits sex differences in its function. Diseases associated with dysregulation of the pituitary are also sex-biased in prevalence. Previous qPCR profiling of puberty-related genes in the pituitary gland revealed increasingly sex-biased expression of genes profiled across pubertal transition. Here, we performed small RNA-seq on total RNA extracted from C57BL/6J mouse pituitary gland of both sexes mice at 4 ages spanning pubertal transition (postnatal days 12, 22, 27, 32) (6 replicates per sex at each age) to examine microRNA (miRNA) regulation of sex differences in gene expression observed. Total RNA was sent to SickKids TCAG core to construct small RNA-seq libraries using NEBNext Small RNA Library Prep Kit according to manufacterer’s protocol. Resulting single-end libraries were sequenced at TCAG core on the Illumina HiSeq 2500 v4 flow cell with SR50 bp. Data obtained was processed using miRDeep2 pipeline to align small RNA-seq reads to the mouse genome (mm10) and to filter for miRNAs.
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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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Project description:The pituitary gland exhibits sex differences in its function. Diseases associated with dysregulation of the pituitary are also sex-biased in prevalence. Previous qPCR profiling of puberty-related genes in the pituitary gland revealed increasingly sex-biased expression of genes profiled across pubertal transition. Here, we performed 3’-UTR-seq on pituitary gland from both sexes of C57BL/6J mice at 5 ages spanning pubertal transition (postnatal days 12, 22, 27, 32, 37) (6 replicates per sex at each age) to examine genome-wide sex-biased trends in gene expression and potential regulatory mechanisms of these sex differences. QuantSeq 3’mRNA-seq libraries were constructed from total RNA using an automated method with Agilent NGS Workstation. Resulting single-end libraries were sequenced at SickKids TCAG core on the Illumina v4 flow cell with SR50 bp cycles extended to 68 bp. A customized pipeline was developed and used for analysis of reads obtained (see paper for details). Processed reads were mapped to mouse genome (mm10).
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Project description:Peri-pubertal High-Fat Diet Promotes c-Myc Stabilization in Mammary Gland Epithelium
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Project description:Perinatal exposure to bisphenol A (BPA) has been shown to cause aberrant mammary gland morphogenesis and mammary neoplastic transformation. Yet, the underlying mechanism is poorly understood. We tested the hypothesis that mammary glands exposed to BPA during a susceptible window may lead to its susceptibility to tumorigenesis through a stem-cell mediated mechanism. We exposed 21-day-old Balb/c mice to BPA by gavage (25 µg/kg/day) during puberty for 3 weeks, and a subset of animals were further challenged with one oral dose (30 mg/kg) of 7,12-dimethylbenz[a]anthracene (DMBA) at 2 months of age. Primary mammary cells were isolated at 6 weeks, and 2 and 4 months of age for mammary stem cell (MaSC) quantification and function analysis. Pubertal exposure to the low-dose BPA increased lateral branches and hyperplasia in adult mammary glands and caused an acute increase of MaSC in 6-week-old glands and a delayed increase of luminal progenitors in 4-month-old adult gland. Most importantly, pubertal BPA exposure altered the function of MaSC from different age groups, causing pre-neoplastic lesions in their regenerated glands similar to those induced by DMBA exposure, which indicates that MaSCs are susceptible to BPA-induced transformation. Deep sequencing analysis on MaSC-enriched mammospheres identified a set of aberrantly expressed genes associated with pre-neoplastic lesions in human breast cancer patients. Thus, our study for the first time shows that pubertal BPA exposure altered MaSC gene expression and function such that they induced early neoplastic transformation.
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Project description:Primary mammary gland stromal fibroblasts from pubertal SHARPIN-deficient cpdm/cpdm -mice and their littermate controls
2016-12-15 | GSE83795 | GEO
Project description:Dietary fat consumption during rapid mammary gland developing period such as peri-pubertal maturation or pregnancy increases the risk for breast cancer. However, the molecular mechanism underlying this observation is not well elucidated. To provide mechanistic insight, we examined gene expression profile in mouse mammary epithelial cells (MMECs) exposed to high-fat diet (HFD) or control diet (CD). Trp53-/- female mice were treated with experimental diets for 5 weeks during the peri-puberty period (3 to 8 weeks of age). This treatment induced insignificant difference in body weight between mice exposed to HFD and CD. Gene Set Enrichment Analysis (GSEA) predicted elevated expression of c-Myc target genes when exposed to HFD. Consistently, we detected marked elevation of c-Myc protein and prolongation of its half-life in MMECs exposed to HFD suggesting that HFD increased its stability. Additionally, we observed increased phosphorylation at c-MycS62 with concomitant increase in ERK phosphorylation. HFD rendered Trp53-/- MMECs more colonogenic and spherogenic, which was antagonized by a c-Myc inhibitor. Oleic acid the main fatty acid constituent of the HFD and TAK-875 an agonist for G protein-coupled receptor 40 (a receptor for oleic acid) as well enhanced c-Myc stabilization and MMECs proliferation. Collectively, these data suggest that HFD exerts its effect on MMECs through the stabilization of an oncoprotein, deciphering a novel mechanism whereby dietary fat promotes mammary carcinogenesis.
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Project description:Mammary gland development is a complex and dynamic process that occurs mainly postnatally. Ductal elongation and branching morphogenesis are regulated by a plethora of factors, including cytokines, hormones, growth factors and the extracellular matrix. Gas6 is a secreted gamma-carboxylated protein that binds to a family of receptors tyrosine kinase receptors known as the TAMR family (Tyro3, Axl, Mer). Gas6 function in developmental processes has been shown in nervous, reproductive and immune systems. In this study, we found that Gas6 is highly expressed in virgin adult mammary glands but declines during pregnancy and lactation. Specifically, Gas6 is highly expressed in luminal and basal mammary epithelial cells during puberty and adulthood, while TAMR expression is low. Mammary whole mount analysis revealed that Gas6 germline deletion does not impact ductal elongation, branching morphogenesis or terminal end bud formation. Masson's trichrome staining showed that collagen deposition is similar in Gas6-/- mice as compared to wildtype mice. Gas6-/- mammary glands presented an organized luminal and myoepithelial bilayer of cells, and the proportion of mammary stem cells was unchanged in Gas6-/- mammary glands as compared to wildtype. Finally, proliferation of epithelial cells and macrophage number were similar in both groups. These studies suggest that Gas6 is not essential for pubertal mammary gland development in nulliparous mice.
| S-EPMC6289431 | biostudies-literature