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Expression data from liver of adult mice that 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. Keywords: sex comparison and genetic modification

ORGANISM(S): Mus musculus

PROVIDER: GSE12712 | GEO | 2008/09/10

SECONDARY ACCESSION(S): PRJNA112645

REPOSITORIES: GEO

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Transcription profiling of mouse liver from adults who 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. 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.

2008-10-25 | E-GEOD-12712 | biostudies-arrayexpress

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

2013-07-23 | GSE49075 | 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

Stomatin-like protein 2 induces metastasis by regulating the expression of a rate-limiting enzyme of the hexosamine biosynthetic pathway in pancreatic cancer

Project description:Stomatin-like protein 2 (SLP-2) is associated with poor prognosis in several types of cancer, including pancreatic cancer; however, the molecular mechanism of its involvement remains elusive. This study aimed to elucidate the role of this protein in the development of pancreatic cancer. Human pancreatic cancer cell lines AsPC-1 and PANC-1 were transfected by a vector expressing SLP-2 shRNA. Analyses of cell proliferation, migration, invasion, chemosensitivity, and glucose uptake were performed, while a mouse xenograft model was used to evaluate the functional role of SLP-2 in pancreatic cancer. Immunohistochemical analysis was retrospectively performed on human tissue samples to compare expression between the primary site (n=279) and the liver metastatic site (n=22). Furthermore, microarray analysis was conducted to identify genes correlated with SLP-2. In vitro analysis demonstrated that cells in which SLP-2 was suppressed showed reduced cell motility and glucose uptake, while in vivo analysis showed a dramatic decrease in the number of liver metastases. Immunohistochemistry revealed that SLP-2 was elevated in liver metastatic sites. Microarray analysis indicated this protein regulated the expression of glutamine-fructose-6-phosphate transaminase 2 (GFPT2), a rate-limiting enzyme of the hexosamine biosynthesis pathway. SLP-2 contributes to the malignant character of pancreatic cancer by inducing liver metastasis. Cell motility and glucose uptake may be induced via the hexosamine biosynthesis pathway, through the expression of GFPT2. This reveals a new mechanism of liver metastasis and implies that SLP-2 and its downstream pathway could provide novel therapeutic targets for pancreatic cancer.

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Identification of Hnf6 binding sites in male and female mouse liver

Project description:∼40,000 HNF6 binding sites were identified in mouse liver chromatin, including several thousand sites showing significant differences in level of HNF6 binding between male and female mouse liver. These sex-biased HNF6 binding sites showed strong enrichment for sex-biased DNase hypersensitive sites and for proximity to genes showing local sex-biased chromatin marks and a corresponding sex-biased expression. ~90% of genome-wide CUX2 binding sites identified previously in female mouse liver (Conforto TL, Zhang Y, Sherman J, Waxman DJ., Mol Cell Biol. 2012;32(22):4611-4627) were also bound by HNF6, giving evidence for genome-wide competition between HNF6 and CUX2 for chromatin binding in female mouse liver. These HNF6/CUX2 common binding sites were enriched for genomic regions more accessible in male than in female mouse liver chromatin, and showed strongest enrichment for male-biased genes, suggesting HNF6 displacement by CUX2 as a mechanism to explain the observed CUX2 repression of male-biased genes in female liver. However, HNF6 binding was sex-independent at a majority of its binding sites, and peak regions of HNF6 binding were frequently associated with co-binding by multiple other liver transcription factors, consistent with HNF6 playing a global regulatory role in both male and female liver.

2015-07-28 | GSE60014 | GEO

Genome-wide maps of histone modifications in male and female mouse liver

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2013-07-03 | GSE44571 | 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

Sex-specific early growth hormone responses in mouse liver (Mus musculus)

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

4C-seq analysis of interactions with promoters and enhancers nearby five sex-specific genes, in male and female mouse liver

Project description:Sequencing files provided here include 4C-seq experiments for a total of 6 viewpoints neighboring 5 highly sex-biased genes in mouse liver. These files are part of a larger study ("CTCF and Cohesin link sex-biased distal regulatory elements to sex-biased gene expression in mouse liver"), where we compare CTCF and cohesin binding in male and female mouse liver as well as differences in chromatin conformation (DNA looping).

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

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