Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Testosterone-dependent and independent transcriptional networks in the hypothalamus of Gpr54 and Kiss1 knockout male mice

ABSTRACT: Humans and mice with loss of function mutations in GPR54 (KISS1R) or kisspeptin (KISS1) do not progress through puberty, caused by a failure to release GnRH. The transcriptional networks regulated by these proteins in the hypothalamus have yet to be explored by genome-wide methods. Using micro-dissected hypothalamic tissues to isolate RNA from our mice, we first set out to define the transcriptional differences among the wild type and knockout mice. Since the GPR54-kisspeptin axis is subject to hormonal feedback and the knockout mice are pre-pubertal, we also tested the hormonal dependence/independence of each differentially expressed transcript. To avoid variation in gene expression due to fluctuations in the levels of circulating hormones during the female estrous cycle, only male mice were used in this study. 17 samples were successfully hybridized; 4 GKO, 5 KKO, 3 WT 3 weeks old, 5 WT 6 weeks old. We compared GKO to KKO, GKO to WT, KKO to WT and all KO to all WT.

ORGANISM(S): Mus musculus

SUBMITTER: Steven McKinney

PROVIDER: E-GEOD-28383 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The testosterone-dependent and independent transcriptional networks in the hypothalamus of Gpr54 and Kiss1 knockout male mice are not fully equivalent.

Prentice Leah M LM d'Anglemont de Tassigny Xavier X McKinney Steven S Ruiz de Algara Teresa T Yap Damian D Turashvili Gulisa G Poon Steven S Sutcliffe Margaret M Allard Pat P Burleigh Angela A Fee John J Huntsman David G DG Colledge William H WH Aparicio Samuel A J SA

BMC genomics 20110428

<h4>Background</h4>Humans and mice with loss of function mutations in GPR54 (KISS1R) or kisspeptin do not progress through puberty, caused by a failure to release GnRH. The transcriptional networks regulated by these proteins in the hypothalamus have yet to be explored by genome-wide methods.<h4>Results</h4>We show here, using 1 million exon mouse arrays (Exon 1.0 Affymetrix) and quantitative polymerase chain reaction (QPCR) validation to analyse microdissected hypothalamic tissue from Gpr54 and ...[more]

PMID: 21527035

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Project description:The overall goal of the study was to use in vivo data combined with functional genomics to define gene expression signatures representative of a spectrum of HSV CNS infections. Innate immune deficiencies result in a spectrum of severe clinical outcomes following infection. In particular, there is a strong association between loss of the signal transducer and activator of transcription (Stat) pathway, breach of the blood-brain barrier (BBB), and virus-induced neuropathology. The gene signatures that characterize resistance, disease, and mortality in the virus-infected nervous system have not been defined. Herpes simplex virus type 1 (HSV-1) is commonly associated with encephalitis in humans, and humans and mice lacking Stat1 display increased susceptibility to HSV central nervous system (CNS) infections. In this study, two HSV-1 strains were used, KOS (wild type [WT]), and Δvhs, an avirulent recombinant lacking the virion host shutoff (vhs) function. In addition, two mouse strains were used: strain 129 (control) and a Stat1-deficient (Stat1(-/-)) strain. Using combinations of these virus and mouse strains, we established a model of infection resulting in three different outcomes: viral clearance without neurological disease (Δvhs infection of control mice), neurological disease followed by viral clearance (Δvhs infection of Stat1(-/-) mice and WT infection of control mice), or neurological disease followed by death (WT infection of Stat1(-/-) mice). Through the use of functional genomics on the infected brain stem and liver, we determined gene signatures that were representative of the three infection outcomes. Gender matched, 6- to 8- week old immunocompetent, control 129S6 and 129S6 Stat1 knockout mice were infected corneally with 2x10^6 PFU of either wild type HSV-1, a vhs-null HSV virus, or mock-infected. Brain stems and liver of individual mice were isolated at days 1, 3, 5 and 7 post-inoculation for microarray analysis. For microarray analysis, samples were collected from n=2 animals (1 male, 1 female) per mouse strain and virus strain for each time point. Equal masses of tissue were pooled from two mock-infected mice per time point and run on microarray.

Dataset Information

Testosterone-dependent and independent transcriptional networks in the hypothalamus of Gpr54 and Kiss1 knockout male mice

Publications

The testosterone-dependent and independent transcriptional networks in the hypothalamus of Gpr54 and Kiss1 knockout male mice are not fully equivalent.

Similar Datasets

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