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Transcription profiling of mouse liver from adults who differ in expression of Regulator of sex-limitation genes.

ABSTRACT: Regulator of sex-limitation (rsl) is a recessive mouse phenotype in which the otherwise male-specific sex-limited protein (Slp) gene is expressed in females. Positional cloning in rsl mice led to the identification of mutations in two neighboring KRAB zinc finger transcriptional repressors, Rsl1 and Rsl2, and BAC transgenic rescue experiements verified their ability to repress male-specific genes in the liver. Microarrays were used here to expand the list of Rsl-target genes in mouse liver. Enrichment of genes involved in intermediary metabolism among those responsive to Rsl suggest a role for Rsl1/2 in metabolic homeostasis in the mouse. Experiment Overall Design: Total RNA was extracted from livers of adult male and female wild type, rsl-null and transgenic mice that overexpress Rsl1 or Rsl2, specifically in the liver. Equivalent amounts of RNA were pooled from five or more mice per sex and genotype. Two pools per sex and genotype were hybridized to the Affymetrix Mouse Genome 430 2.0 array.

ORGANISM(S): Mus musculus

SUBMITTER: Christopher Krebs

PROVIDER: E-GEOD-12712 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from liver of adult mice that differ in expression of Regulator of sex-limitation genes.

Project description:Regulator of sex-limitation (rsl) is a recessive mouse phenotype in which the otherwise male-specific sex-limited protein (Slp) gene is expressed in females. Positional cloning in rsl mice led to the identification of mutations in two neighboring KRAB zinc finger transcriptional repressors, Rsl1 and Rsl2, and BAC transgenic rescue experiements verified their ability to repress male-specific genes in the liver. Microarrays were used here to expand the list of Rsl-target genes in mouse liver. Enrichment of genes involved in intermediary metabolism among those responsive to Rsl suggest a role for Rsl1/2 in metabolic homeostasis in the mouse. Keywords: sex comparison and genetic modification

2008-09-10 | GSE12712 | GEO

Expression data from white adipose tissue of adult mice with mutations in Regulator of sex-limitation genes

Project description:Regulator of sex-limitation (rsl) is a recessive mouse phenotype in which the otherwise male-specific sex-limited protein (Slp) gene is expressed in females. Positional cloning in rsl mice led to the identification of mutations in two neighboring KRAB zinc finger transcriptional repressors, Rsl1 and Rsl2, and BAC transgenic rescue experiements verified their ability to repress male-specific genes in the liver. Microarrays were used here to identify RSL-sensitive genes in mouse abdominal white adipose tissue. Experiment type: sex comparison and genetic modification Total RNA was extracted from abdominal white adipose tissue of adult male and female wild type and Rsl-null mice. Equivalent amounts of RNA were pooled from five mice per sex and genotype. Two pools per sex and genotype were hybridized to the Affymetrix Mouse Genome 430 2.0 PM Array Strip.

2013-07-23 | E-GEOD-49075 | biostudies-arrayexpress

Expression data from white adipose tissue of adult mice with mutations in Regulator of sex-limitation genes

2013-07-23 | GSE49075 | GEO

Sex-dependent and HNF4alpha-dependent Mouse Liver Gene Expression

Project description:A series of dual-channel gene expression profiles obtained using Rosetta/Agilent Whole Mouse Genome oligonucleotide microarrays, 4 x 44K format, was used to identify sex-dependent and HNF4alpha-dependent differences in gene expression in adult mouse liver. This series is comprised of four sex-genotype combinations: adult male wild-type liver (M-WT), adult female wild-type liver (F-WT), adult male liver-specific HNF4alpha knockout liver (M-KO) and adult female liver-specific HNF4alpha knockout liver (F-KO). Four pools, each comprised of 4 randomly selected individual liver RNAs, were prepared for each sex-genotype combination. The pools were paired randomly to generate 4 separate experimental comparisons: M-WT:F-WT (first array comparison), M-WT:M-KO (second array comparison), F-WT:F-KO (third array comparison), and M-KO:F-KO (fourth array comparison). A total of 4994 HNF4alpha-dependent genes were identified, of which ~1000 fewer genes responded to the loss of HNF4alpha in female liver as compared to male liver. Moreover, 90% of the genes showing sex-specific expression in the liver were shown to lose sex specificity in HNF4alpha-deficient liver. Keywords: genetic knockout and sex response

2008-03-21 | GSE10390 | GEO

Gene expression profiling of Male and Female adult mouse liver using RNA-seq

Project description:Liver sex-specific long noncoding RNAs (lncRNAs) were identified based on three pools of male and three pools of female ribosomal RNA-depleted total liver RNAs, as well as three pools of male and three pools of female ribosomal RNA-depleted nuclear liver RNAs from CD-1 mice. This dataset is part of a larger study, entitled "Sex-biased lncRNAs inversely correlate with sex-opposite gene co-expression networks in Diversity Outbred mouse liver", Endocrinology (2019) 160:989-1007, PMID:30840070.

2020-05-22 | GSE109621 | GEO

RNA-seq gene expression profiling of livers from CD1 mice treated with adeno-associated virus encoding constitutively active STAT5b (AAV8-STAT5ca)

Project description:PolyA-selected nuclear RNA isolated from livers of adult male mice administered AAV8-STAT5ca was analyzed by RNA-seq to determine the impact of constitutive STAT5 activation on the expression of sex-biased genes in male mouse liver. This is part of a study entitled 'Constitutively active STAT5b feminizes mouse liver gene expression', where delivery of constitutively active STAT5 (STAT5CA) to male mouse liver was shown to induce widespread feminization of the liver, with extensive induction of female-biased genes and repression of male-biased genes, largely mimicking results obtained when male mice are given GH as a continuous infusion. Many of the STAT5CA-responding genes were associated with nearby (< 50 kb) sites of STAT5 binding to liver chromatin, supporting the proposed direct role of persistently active STAT5 in continuous GH-induced liver feminization. The feminizing effects of STAT5CA were dose-dependent; moreover, at higher levels, STAT5CA overexpression resulted in some histopathology, including hepatocyte hyperplasia, and increased karyomegaly and multinuclear hepatocytes. Together, these findings establish that the persistent activation of STAT5 by GH that characterizes female liver is by itself sufficient to account for the sex-dependent expression of a majority of hepatic sex-biased genes.

2022-04-04 | GSE196015 | GEO

RNA-seq gene expression profiling of livers from C57Bl/6 mice treated with adeno-associated virus encoding constitutively active STAT5b (AAV8-STAT5ca)

Project description:PolyA-selected total RNA isolated from livers of adult male mice administered AAV8-STAT5ca was analyzed by RNA-seq to determine the impact of constitutive STAT5 activation on the expression of sex-biased genes in male mouse liver. This is part of a study entitled 'Constitutively active STAT5b feminizes mouse liver gene expression', where delivery of constitutively active STAT5 (STAT5CA) to male mouse liver was shown to induce widespread feminization of the liver, with extensive induction of female-biased genes and repression of male-biased genes, largely mimicking results obtained when male mice are given GH as a continuous infusion. Many of the STAT5CA-responding genes were associated with nearby (< 50 kb) sites of STAT5 binding to liver chromatin, supporting the proposed direct role of persistently active STAT5 in continuous GH-induced liver feminization. The feminizing effects of STAT5CA were dose-dependent; moreover, at higher levels, STAT5CA overexpression resulted in some histopathology, including hepatocyte hyperplasia, and increased karyomegaly and multinuclear hepatocytes. Together, these findings establish that the persistent activation of STAT5 by GH that characterizes female liver is by itself sufficient to account for the sex-dependent expression of a majority of hepatic sex-biased genes.

2022-04-04 | GSE196014 | GEO

Naïve and LCMV Cl13 infected liver tissue of ERT2 AlbCre Ifnar1 fl/fl mice

Project description:Age- and sex-matched (male, 2-3 months old) ERT2 AlbCre Ifnar fl/fl and ERT2 AlbCre Ifnar +/+ mice were injected intraperitoneally with 40 mg/kg tamoxifen for 5 consective days. Mice were then intravenously infected with 2x10^6 focus forming units of LCMV Cl13 and liver tissue of either genotype was harvested 1.5 days post infection and analyzed for transcriptomic changes (n = 3). Liver tissue of uninfected animals of both genotypes was harvested as control (n = 3).

2019-12-05 | GSE117237 | GEO

Neurofibromatosis type 1-dependent alterations in mouse microglia function are not cell-intrinsic

Project description:We previously discovered a sex-by-genotype defect in microglia function using a germline heterozygous knockout mouse model of Neurofibromatosis type 1 (Nf1+/- mice), in which only microglia from male Nf1+/- mice exhibited defects in purinergic signaling. Herein, we leveraged an unbiased proteomic approach to demonstrate that male, but not female, heterozygous Nf1+/- microglia exhibit differences in protein expression, which largely reflect pathways involved cytoskeletal organization. In keeping with potential defects in cytoskeletal function, only male Nf1+/- microglia had reduced process arborization and surveillance capacity. Next, to determine whether these microglial defects were cell autonomous or reflected adaptive responses to Nf1 heterozygosity in other cells in the brain, we generated conditional microglia Nf1-mutant knockout mice by intercrossing Nf1flox/flox with Cx3cr1-CreER mice (Nf1flox/wt; Cx3cr1-CreER mice, Nf1MG+/- mice). Surprisingly, neither male nor female Nf1MG+/- mouse microglia had impaired process arborization or surveillance capacity. In contrast, when Nf1 heterozygosity was generated in neurons, astrocytes and oligodendrocytes by intercrossing Nf1flox/flox with hGFAP-Cre mice (Nf1flox/wt; hGFAP-Cre mice, Nf1GFAP+/- mice), the microglia defects found in Nf1+/- mice were recapitulated. Collectively, these data reveal that Nf1+/- sexually dimorphic microglia abnormalities are likely not cell-intrinsic properties, but rather reflect a response to Nf1 heterozygosity in other brain cells.

2023-05-10 | PXD035881 | Pride

Small RNA-seq of adult male and female mouse liver

Project description:Total RNA-seq analysis of mouse liver RNA following locked nucleic acids (LNAs) treatment to identify mRNA targets of mmu-miR-802-5p and mmu-miR-1948-5p in vivo. These datasets are part of a study where we used small RNA sequencing to discover 24 sex-biased mouse liver miRNAs, and then investigated the roles of two of these miRNAs in GH-regulated liver sex differences. Studies in pre-pubertal and young adult mice, and in mice where pituitary hormones are ablated or where sex-specific hepatic GH signaling is dysregulated, demonstrated that the male-biased miR-1948 and the female-biased miR-802 are both regulated by sex-specific pituitary GH secretory patterns, acquire sex specificity at puberty, and are dependent on the GH-activated transcription factor STAT5 for their sex-specific expression. Both miRNAs are within genomic regions characterized by sex-biased chromatin accessibility. miR-1948, a novel, uncharacterized miRNA, has essential features for correct Drosha/Dicer processing, generates a bona fide mature miRNA with strong strand bias for the 5p arm, and is bound by Argonaute in liver tissue, as is miR-802. In vivo studies using inhibitory locked nucleic acid sequences revealed that miR-1948-5p preferentially represses female-biased mRNAs and induces male-biased mRNAs in male liver, and conversely, miR-802-5p preferentially represses male-biased mRNAs and increases levels of female-biased mRNAs in female liver. Cytochrome P450 mRNAs were strongly enriched as targets of both miRNAs. Thus, miR-1948-5p and miR-802-5p are functional components of the GH regulatory network that shapes sex-differential gene expression in mouse liver.

2018-01-25 | GSE103879 | GEO

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