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Role of SRF in activity-regulated transcription in the striatum of the brain

ABSTRACT: Ablation of the Srf gene in dopaminoceptive neurons of the brain was performed using the Cre/loxP system, with the recombinase expressed from a BAC-derived Drd1a promoter. Our goal was to analyze how loss of SRF will affect acitivity-regulated transcription induced by strong stimulation, i.e. cocaine. Keywords: Treatment x Genotype

ORGANISM(S): Mus musculus

PROVIDER: GSE10870 | GEO | 2009/04/30

SECONDARY ACCESSION(S): PRJNA107375

REPOSITORIES: GEO

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Role of SRF in activity-regulated transcription in the striatum of the brain

Project description:Ablation of the Srf gene in dopaminoceptive neurons of the brain was performed using the Cre/loxP system, with the recombinase expressed from a BAC-derived Drd1a promoter. Our goal was to analyze how loss of SRF will affect acitivity-regulated transcription induced by strong stimulation, i.e. cocaine. Keywords: Treatment x Genotype Animals were injected i.p. with either 25 mg/kg cocaine or saline and sacrificed after one hour by cervical dislocation. Expression profiling was performed using total RNA isolated from the striatum.

2010-03-04 | E-GEOD-10870 | biostudies-arrayexpress

Effects of CaMKIV loss on cocaine-induced gene expression in the striatum

2008-09-10 | GSE10869 | GEO

Transcription profiling of mouse with abalated dopaminoceptive neurons to examine the effects of CaMKIV loss on cocaine-induced gene expression in the striatum

Project description:Ablation of the Camk4 gene in dopaminoceptive neurons of the brain was performed using the Cre/loxP system, with the recombinase expressed from a BAC-derived Drd1a promoter. Our goal was to analyze how loss of CaMKIV will affect acitivity-regulated transcription induced by strong stimulation, i.e. cocaine. Experiment Overall Design: Animals were injected i.p. with either 25 mg/kg cocaine or saline and sacrificed after one hour by cervical dislocation. Expression profiling was performed using total RNA isolated from the striatum.

2008-10-25 | E-GEOD-10869 | biostudies-arrayexpress

Effect of loss of CREB and CREM on cocaine-induced gene expression in the striatum

Project description:Ablation of the Creb1 gene in forebrain neurons was performed using the Cre/loxP system, with the recombinase expressed from the Camk2alfa promoter. Mice were crossed into the Crem KO background to prevent compensation of CREB loss by CREM overexpression. Our goal was to analyze how loss of CREB will affect acitivity-regulated transcription induced by strong stimulation, i.e. cocaine. Keywords: Treatment x Genotype

2008-04-03 | GSE8948 | GEO

Transcription profiling of mouse Serum response factor (Srf) conditional knockout in the mouse liver

Project description:Serum response factor (SRF) is a transcription factor that binds to the serum response element (SRE) of genes that are expressed in response to mitogens. SRF plays essential roles in muscle and nervous system development; however, little is known about the role of SRF during liver growth and function. To examine the function of SRF in the liver, we generated mice in which the Srf gene was specifically disrupted in hepatocytes. The survival of mice lacking hepatic SRF activity was lower than that of control mice; moreover, surviving mutant mice were smaller and had lower blood glucose and triglyceride levels compared with control mice. Srf-deficient livers were also smaller than control livers, hepatocyte morphology was abnormal, and liver-cell proliferation and viability was compromised. Gene array and quantitative RT-PCR analysis of SRF depleted livers revealed a reduction in mRNAs encoding components of the growth hormone/IGF1 pathway, cyclins, several metabolic regulators, and cytochrome p450 enzymes. Conclusion: SRF is essential for hepatocyte proliferation and survival, liver function, and control of postnatal body growth by regulating hepatocyte gene expression. Experiment Overall Design: Total RNA was harvested from the following sources and used for Affymetrix array analysis following manufacturer defined protocols: Experiment Overall Design: control liver (Srf loxP/+ AlfpCre): 3 male mice (3 weeks old) Experiment Overall Design: mutant liver (Srf loxP/loxP AlfpCre): 3 male mice (3 weeks old), tissue used lacked Srf

2009-03-07 | E-GEOD-13333 | biostudies-arrayexpress

Vascular smooth muscle selective deletion of Srf

Project description:Previous efforts to conditionally delete the Srf transcription factor in smooth muscle lineages were met with early demise of the mouse due to a gastrointestinal (GI) obstruction phenotype. We have developed a new, more VSMC selective Cre recombinase mouse (Itga8-CreERT2), that circumvents the GI phenotype thus affording the opportunity to evaluate, in an unambiguous manner, VSMC phenotypes where Srf is reduced. The mice live for at least 6 months post-tamoxifen and here we report the first RNA-seq experiments in mouse aortic SMC where Srf is reduced.

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Effect of loss of CREB and CREM on kainate-induced gene expression in the hippocampus (MG-U74C).

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Effect of loss of CREB and CREM on kainate-induced gene expression in the hippocampus (MG-U74B).

2008-04-03 | GSE8946 | GEO

Effect of loss of CREB and CREM on kainate-induced gene expression in the hippocampus (MG-U74A).

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PF4-Cre mediated deletion of SRF in murine megakaryocytes.

Project description:Srf is a MADS-box transcription factor that is critical for muscle differentiation. Its function in hematopoiesis has not yet been revealed. Mkl1, a cofactor of Srf, is part of the t(1;22) translocation in acute megakaryoblastic leukemia, and plays a critical role in megakaryopoiesis. In order to test the role of Srf in megakaryocyte development, we crossed Pf4-Cre mice, which express Cre recombinase in cells committed to the megakaryocytic lineage, to SrfF/F mice in which functional Srf is no longer expressed after Cre-mediated excision. Pf4-Cre/SrfF/F (KO) mice are born with normal mendelian frequency, but have significant macrothrombocytopenia with approximately 50% reduction in platelet count. In contrast, the BM has increased numbers and percentages of CD41+ megakaryocytes (WT: 0.41+/-0.06%; KO: 1.92+/-0.12%) with significantly reduced ploidy. KO mice show significantly increased megakaryocyte progenitors in the BM by both FACS analysis and CFU-Mk. Megakaryocytes lacking Srf have abnormal stress fiber and demarcation membrane formation and platelets lacking Srf have abnormal actin distribution. In vitro and in vivo assays reveal platelet function defects in KO mice. Critical actin cytoskeletal genes are downregulated in KO megakaryocytes. Thus, Srf is required for normal megakaryocyte maturation and platelet production, due at least in part, to regulation of cytoskeletal genes. C-kit+CD41+ megakaryocyte progenitors from PF4-Cre/SRF C57BL/6 SRF WT (3) and C57BL/6 SRF KO (3) mice were sorted by flow cytometry and cultured for three days in thrombopoietin.

2010-07-13 | E-GEOD-21859 | biostudies-arrayexpress

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