RNA-seq dataset of the estrogen-dependent regulation of the transcriptome in mouse mammary gland epithelial organoids
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PROVIDER: PRJNA1269599 | ENA |
REPOSITORIES: ENA
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Project description:This GSE covered two different but complementary works on mouse mammary epithelial organoids. The first one is a publication from 2025 in Data in Brief entitled "RNA-seq dataset of the estrogen-dependent regulation of the transcriptome in mouse mammary gland epithelial organoids”. The second one is a publication from 2026 in Scientific Reports entitled “The mTOR signalling pathway regulates key steps of mammary gland organoid genesis in a temporal manner”. The mammary gland development in utero and during life is strongly regulated by hormones. We first studied the impact of estradiol during 11 days in culture and performed bulk mRNA sequencing to better understand the impact of estrogen signalling on the mammary epithelial cell transcriptome. Besides, the development of the gland is also a complex process that evolves throughout life. In developmental assays, the mechanistic target of rapamycin (mTOR) was shown to be a regulator of cellular lineage determination and branching morphogenesis, acting in a time-dependent manner to control these processes. We treated our organoids with Torin 1 at two different growing points and used bulk mRNA sequencing to demonstrate the regulatory functions of mTOR in controlling mammary epithelial cells’ capacity to generate organoids. Altogether, these two datasets help understand the function of the mammary gland. They can be reanalyzed and combined with recent single-cell RNA-seq data to better understand the role of the estrogen receptor and the mTOR signalling pathway in the functions of the gland in physiological conditions, such as lactation or pathological conditions, such as breast cancer.
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Project description:Both ovarian and pituitary hormones are required for the pubertal development of the mouse mammary gland. Estradiol directs ductal elongation and branching within the adipose stroma of the adolescent mouse mammary gland, while progesterone leads to tertiary branching and alveolar development. The purpose of this investigation was to identify the estrogen-responsive genes that are associated with estrogen-stimulated ductal elongation and branching in the mouse mammary gland in the absence of other ovarian hormones. We also wanted to determine if estrogen-responsive gene regulation at early stages of ductal elongation (ie. when ductal growth was minimal) was similar to those regulated after significant ductal elongation had occurred. To identify estrogen-regulated genes, ovariectomized prepubertal mice were exposed to 17beta-estradiol for four weeks, and mammary gland global gene expression analyzed by microarray analysis at various points during this time course. We determined that while many genes are regulated in all weeks of treatment, there remained a subset of genes that was uniquely regulated at each time-point. This observation was reflected in the biological functions of these genes; some categories were represented in all weeks of treatment while others were specific to only certain time-points. We have also identified estradiol-responsive genes in the mouse mammary gland that co-express with Estrogen Receptor alpha in human breast cancer, which may represent novel effectors of estrogen action and/or biomarkers for the progression of estrogen-dependent cancers and other estrogen-driven diseases.
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Project description:Both ovarian and pituitary hormones are required for the pubertal development of the mouse mammary gland. Estradiol directs ductal elongation and branching within the adipose stroma of the adolescent mouse mammary gland, while progesterone leads to tertiary branching and alveolar development. The purpose of this investigation was to identify the estrogen-responsive genes that are associated with estrogen-stimulated ductal elongation and branching in the mouse mammary gland in the absence of other ovarian hormones. We also wanted to determine if estrogen-responsive gene regulation at early stages of ductal elongation (ie. when ductal growth was minimal) was similar to those regulated after significant ductal elongation had occurred. To identify estrogen-regulated genes, ovariectomized prepubertal mice were exposed to 17beta-estradiol for four weeks, and mammary gland global gene expression analyzed by microarray analysis at various points during this time course. We determined that while many genes are regulated in all weeks of treatment, there remained a subset of genes that was uniquely regulated at each time-point. This observation was reflected in the biological functions of these genes; some categories were represented in all weeks of treatment while others were specific to only certain time-points. We have also identified estradiol-responsive genes in the mouse mammary gland that co-express with Estrogen Receptor alpha in human breast cancer, which may represent novel effectors of estrogen action and/or biomarkers for the progression of estrogen-dependent cancers and other estrogen-driven diseases. Experiment Overall Design: For each time-course experiment, one frozen #4 mammary gland was individually pulverized from four to five animals per treatment group, then homogenized in 3mL Trizol (Invitrogen, Carlsbad, CA) and RNA was prepared according to the manufacturerâ??s protocol. The RNA from individual animals was then pooled for each treatment group (four to five animals per group) and further purified using the QIAGEN (Valencia, CA) RNeasy Mini kit (Cat. No. 74104) clean-up protocol. Experiment Overall Design: Gene expression analysis was conducted using Agilent Mouse Oligo arrays (pattern number 011978) (Agilent Technologies, Palo Alto, CA). Total RNA was amplified using the Agilent Low RNA Input Fluorescent Linear Amplification Kit protocol. Starting with 500ng of total RNA, Cy3 or Cy5 labeled cRNA was produced according to manufacturerâ??s protocol. For each two color comparison, 750ng of each Cy3 and Cy5 labeled cRNAs were mixed and fragmented using the Agilent In Situ Hybridization Kit protocol. In each case, samples from estradiol-treated animals were co-hybridized with the day 7 placebo sample. Due to the rapid increase in adiposity in the mammary fat pad in the ovariectomized placebo-treated mice in days 14 and 28, the day 7 placebo sample was used as a control for all estradiol treated samples to avoid any variation due to this biological difference. Hybridizations were performed for 17 hours in a rotating hybridization oven using the Agilent 60-mer oligo microarray processing protocol. Slides were washed as indicated in this protocol and then scanned with an Agilent Scanner. Data was obtained using the Agilent Feature Extraction software (v7.5), using defaults for all parameters. Experiment Overall Design: The Agilent Feature Extraction Software performed error modeling, adjusting for additive and multiplicative noise. The resulting data were processed using the Rosetta Resolver® system (version 7.1) (Rosetta Biosoftware, Kirkland, WA).
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