Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA214090 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Developmental gene expression is defined through cross-talk between the function of transcription factors and epigenetic status including histone modification. Although several known transcription factors play crucial roles in mammalian sex determination, how chromatin regulation contributes to this process is unknown. We observed male-to-female sex reversal in mice lacking the H3K9 demethylase Jmjd1a, and found that Jmjd1a directly regulates expression of the mammalian Y chromosome sex-determining gene Sry, by regulating H3K9me2 marks. These studies reveal a pivotal role for epigenetic regulation in mammalian sex determination, and provide new impetus for identifying additional causes of disorders of sex determination by environmental factors. Gene expression patterns were measured in gonadal somatic cells of Jmjd1a mutant and control embryos at E11.5. Three biological replicates were performed in each group.
2013-08-03 | E-GEOD-49513 | biostudies-arrayexpress
Project description:Developmental gene expression is defined through cross-talk between the function of transcription factors and epigenetic status including histone modification. Although several known transcription factors play crucial roles in mammalian sex determination, how chromatin regulation contributes to this process is unknown. We observed male-to-female sex reversal in mice lacking the H3K9 demethylase Jmjd1a, and found that Jmjd1a directly regulates expression of the mammalian Y chromosome sex-determining gene Sry, by regulating H3K9me2 marks. These studies reveal a pivotal role for epigenetic regulation in mammalian sex determination, and provide new impetus for identifying additional causes of disorders of sex determination by environmental factors.
2013-08-03 | GSE49513 | GEO
Project description:Sex differences in liver gene expression are dictated by sex-differences in circulating growth hormone (GH) profiles. Presently, the pituitary hormone dependence of mouse liver gene expression was investigated on a global scale to discover sex-specific early GH response genes that might contribute to sex-specific regulation of downstream GH targets and to ascertain whether intrinsic sex-differences characterize hepatic responses to plasma GH stimulation. RNA expression analysis using 41,000-feature microarrays revealed two distinct classes of sex-specific mouse liver genes: genes subject to positive regulation (class-I) and genes subject to negative regulation by pituitary hormones (class-II). Genes activated or repressed in hypophysectomized (Hypox) mouse liver within 30-90min of GH pulse treatment at a physiological dose were identified as direct targets of GH action (early response genes). Intrinsic sex-differences in the GH responsiveness of a subset of these early response genes were observed. Notably, 45 male-specific genes, including five encoding transcriptional regulators that may mediate downstream sex-specific transcriptional responses, were rapidly induced by GH (within 30min) in Hypox male but not Hypox female mouse liver. The early GH response genes were enriched in 29 male-specific targets of the transcription factor Mef2, whose activation in hepatic stellate cells is associated with liver fibrosis leading to hepatocellular carcinoma, a male-predominant disease. Thus, the rapid activation by GH pulses of certain sex-specific genes is modulated by intrinsic sex-specific factors, which may be associated with prior hormone exposure (epigenetic mechanisms) or genetic factors that are pituitary-independent, and could contribute to sex-differences in predisposition to liver cancer or other hepatic pathophysiologies.
2010-01-27 | GSE17644 | GEO
Project description:Adipocyte differentiation has been shown to require iron, but the underlying mechanism remains unclear. We have previously reported that iron supply through ferritinophagy is associated with demethylation of the repressive histone mark H3K9me2 in the differentiation-associated genes, which is mediated by the histone demethylase JMJD1A. To examine how JMJD1A regulates the gene expression program during adipocyte differentiation, in this study we peformed H3K9me2 CUT&Tag analysis using 3T3-L1 pre-adipocytes with Jmjd1a knockdown.
2025-04-29 | GSE284471 | GEO
Project description:The Hypoxia-Inducible Factors induce the expression of the histone demethylases JMJD1A (KDM3A) and JMJD2B (KDM4B), linking the hypoxic tumor microenvironment to epigenetic mechanisms that may foster tumor progression. Using transcript profiling, we have identified genes that are regulated by JMJD1A and JMJD2B in both normoxic and hypoxic conditions in SKOV3ip.1 ovarian cancer cells. This dataset includes expression data obtained from exposing ovarian cancer cells to hypoxia in combination with siRNA-mediated knockdown of the hypoxia-inducible histone demethylases JMJD1A and JMJD2B. These data were used to both identify functional overlap between each histone demethylase, as well as identify effectors of tumor growth mediated by JMJD2B (KDM4B) in normoxia and hypoxia.
2017-03-13 | GSE66894 | GEO
Project description:Analysis of gene expresssion altered upon knockdown of histone demethylase JMJD1A in human prostate cancer cells. The objective is to elucidate the transcriptional programs that are controlled by JMJD1A in human prostate cancer.
2015-09-08 | GSE70498 | GEO
Project description:The histone demethylase JMJD1A（Jumoji domain containing 1A） is overexpressed in multiple cancers and promotes cancer progression. However, the role and mechanism of JMJD1A in gastric cancer remains poorly understood.Here, we found that JMJD1A could suppress gastric cancer cell proliferation, migration, invasion and xenograft tumor growth. Using RNA sequencing, we identified RUNX3 as a novel target gene of JMJD1A.
2020-02-12 | GSE145105 | GEO
Project description:Analysis of gene expresssion altered upon knockdown of histone demethylase JMJD1A in human prostate cancer cells. The objective is to elucidate the transcriptional programs that are controlled by JMJD1A in human prostate cancer. CWR22Rv1 prostate cancer cells were transduced with lentiviral particles encoding control pLKO.1 or JMJD1A shRNA (shJMJD1A). After 48 h, total RNAs were collected for the microarray analysis to determine the differentially expressed genes between Rv1 pLKO.1 and Rv1 shJMJD1A samples.
2015-09-08 | E-GEOD-70498 | biostudies-arrayexpress
Project description:Mitochondria play a vital role in non-shivering thermogenesis in both brown and subcutaneous white adipose tissues (BAT and scWAT, respectively). However, specific regulatory mechanisms driving mitochondrial function in these tissues have been unclear. Here we demonstrate that prolonged activation of β-adrenergic signaling induces epigenetic modifications in scWAT, specifically targeting the enhancers for the mitochondria master regulator genes Pgc1a/b. This is mediated at least partially through JMJD1A, a histone demethylase that in response to β-adrenergic signals, facilitates H3K9 demethylation of the Pgc1a/b enhancers, promoting mitochondrial biogenesis and the formation of beige adipocytes. Disruption of demethylation activity of JMJD1A in mice impairs activation of Pgc1a/b driven mitochondrial biogenesis and limits scWAT beiging, contributing to reduced energy expenditure, obesity, insulin resistance, and metabolic disorders. Notably, JMJD1A demethylase activity is not required for Pgc1a/b dependent thermogenic capacity of BAT especially during acute cold stress, emphasizing the importance of scWAT thermogenesis in overall energy metabolism.
2024-03-12 | GSE236724 | GEO
Project description:Protein kinase A promotes beige adipogenesis downstream from β-adrenergic receptor signaling by phosphorylating proteins, including histone H3 lysine 9 (H3K9) demethylase JMJD1A. To ensure homeostasis, this process needs to be reversible however, this step is not well understood. We show that myosin phosphatase target subunit 1- protein phosphatase 1β (MYPT1-PP1β) phosphatase activity is inhibited via PKA-dependent phosphorylation, which increases phosphorylated JMJD1A and beige adipogenesis. Mechanistically, MYPT1-PP1β depletion resulted in JMJD1A-mediated H3K9 demethylation and activation of the Ucp1 enhancer/promoter regions. Interestingly, MYPT1-PP1β also dephosphorylates myosin light chain which regulates actomyosin tension-mediated activation of YAP/TAZ which directly stimulates Ucp1 gene expression. Preadipocyte specific Mypt1 deficiency increases cold tolerance with higher Ucp1 levels in subcutaneous white adipose tissues compared to control mice, confirming this regulatory mechanism in vivo. Thus, we have uncovered new regulatory cross-talk involved in beige adipogenesis that coordinates epigenetic regulation with direct activation of the mechano-sensitive YAP/TAZ transcriptional co-activators.
2022-09-01 | GSE202505 | GEO