Effect of RP58 deletion on neural cell transcriptional programs
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE121260 | GEO | 2021/05/24
REPOSITORIES: GEO
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Project description:Effect of RP58 deletion on neural cell transcriptional programs
| PRJNA496494 | ENA
Project description:The investigate the loss-of fucntion azf1 suppressive mutations to the sef1-deleted transcriptional netwrok in L. kluyveri, we analyzed the gene expression profiles in response to azf1 deletion under fermentative and respiratory conditions and foucsed on the compensatory effects on gene expression to sef1 deletion.
2022-04-12 | GSE200532 | GEO
Project description:To predict Rp58-regulated gene involved in myogenesis, RNA profiling experiments were performed, comparing RNA derived from C2C12 with or without expressing shRNA for Rp58. As a result, 271 genes were upregulated in C2C12 stably expressing shRNA-Rp58 cells compared with control C2C12 cells. As Rp58 is repressor in C2C12, we hypothesized that Rp58 regulates gene cluster which expression is downregulated in accordance with Rp58 expression and myogenesis progression. In this regard, we also characterized dynamic gene expression patterns during myogenesis by microarray at 4 different stage (GM, day 0, 2, 4) of C2C12 myogenesis assays and found that 399 genes expression is characterized as downregulation pattern during myogenesis. Importantly, this down regulation gene set and upregulated genes by shRNA for Rp58 were highly overlapped. Keywords: time course, shRNA
2009-07-31 | GSE12993 | GEO
Project description:To predict RP58-regulated genes involved in skeletal myogenesis, RNA profiling experiments were performed, comparing RNA derived from skeletal muscle tissue of a RP58+/+ mouse to that from a RP58 knockout (KO) mouse at E18.5. Importantly, well-known dominant-negative inhibitors of muscle differentiation, the Id family of genes (Id1/Id2/Id3), were upregulated in the RP58 KO muscle. On the contrary, a number of muscle differentiation-related genes, such as Ckm, troponin and Myosin, were downregulated in the same sample. These results indicate that the repressor protein RP58 is important for muscle terminal differentiation, possibly suppressing the gene expression of muscle differentiation genes such as the Ids. Keywords: Knockout tissue
2009-07-31 | GSE16595 | GEO
Project description:Appropriate number of neurons and glial cells is generated from neural stem cells (NSCs) by the regulation of cell cycle exit and subsequent differentiation. Although the regulatory mechanism remains obscure, Id (inhibitor of differentiation) proteins are known to contribute critically to NSC proliferation by controlling cell cycle. Here we report that a transcriptional factor, RP58, negatively regulates all 4 Id genes (Id1-Id4) in developing cerebral cortex. Consistently, Rp58 knockout (KO) mice demonstrated enhanced astrogenesis accompanied with an excess of NSCs. These phenotypes were mimicked by the overexpression of all Id genes in wild-type cortical progenitors. Furthermore, Rp58 KO phenotypes were rescued by the knockdown of all Id genes in mutant cortical progenitors but not by the knockdown of each single Id gene. Finally, we determined p57 as an effector gene of RP58-Id-mediated cell fate control. These findings establish RP58 as a novel key regulator that controls the self-renewal and differentiation of NSCs and restriction of astrogenesis by repressing all Id genes during corticogenesis.
2014-12-08 | GSE34327 | GEO
Project description:To predict RP58-regulated genes involved in skeletal myogenesis, RNA profiling experiments were performed, comparing RNA derived from skeletal muscle tissue of a RP58+/+ mouse to that from a RP58 knockout (KO) mouse at E18.5. Importantly, well-known dominant-negative inhibitors of muscle differentiation, the Id family of genes (Id1/Id2/Id3), were upregulated in the RP58 KO muscle. On the contrary, a number of muscle differentiation-related genes, such as Ckm, troponin and Myosin, were downregulated in the same sample. These results indicate that the repressor protein RP58 is important for muscle terminal differentiation, possibly suppressing the gene expression of muscle differentiation genes such as the Ids. Keywords: Knockout tissue Skeletal muscles of WT and RP58 KO mice (E18.5 diaphragm) were dissected under a microscope and RNA was extracted using ISOGEN (Nippongene). After EtOH precipitation, RNA was dissolved into DEPC-DW and its concentration was determined. Microarray analysis - cRNA was synthesized. 10 ug of cRNA were hybridized to Affymetrix mouse 430A 2.0 arrays. Signal intensities were calculated using the RMA method. MAPPFinder (www.genmapp.org) was used to integrate expression data with known pathways.
2009-07-31 | E-GEOD-16595 | biostudies-arrayexpress
Project description:To predict Rp58-regulated gene involved in myogenesis, RNA profiling experiments were performed, comparing RNA derived from C2C12 with or without expressing shRNA for Rp58. As a result, 271 genes were upregulated in C2C12 stably expressing shRNA-Rp58 cells compared with control C2C12 cells. As Rp58 is repressor in C2C12, we hypothesized that Rp58 regulates gene cluster which expression is downregulated in accordance with Rp58 expression and myogenesis progression. In this regard, we also characterized dynamic gene expression patterns during myogenesis by microarray at 4 different stage (GM, day 0, 2, 4) of C2C12 myogenesis assays and found that 399 genes expression is characterized as downregulation pattern during myogenesis. Importantly, this down regulation gene set and upregulated genes by shRNA for Rp58 were highly overlapped. Experiment Overall Design: C2C12 murine skeletal muscle cells were purchased from American Type Experiment Overall Design: culture Collection (ATCC). These cells were mainteined in GM (DMEM Experiment Overall Design: supplemented with 10% FBS). Cells were grown in GM and after reaching Experiment Overall Design: counfluence, the medium was switched to DM (DMEM supplemented with 2% hourse serum) and further incubated. The medium was changed every 2 days. Culture was performed by using within five passages cells. For the experiment of shRNA for Rp58, transfection was performed by using Lipofectamin 2000 (Invitrogen). Stable transfectants were obtained by selection of the transfected C2C12 cells for two weeks. Experiment Overall Design: Microarray analysis - RNA was isolated as described from C2C12, and cRNA was synthesized. 10 ug of cRNA were hybridized to Affymetrix mouse 430 2.0 arrays. Intensity values were quantified using RMA algorithm. Experiment Overall Design: MAPPFinder (www.genmapp.org) was used to integrate expression data with known pathways.
2009-08-09 | E-GEOD-12993 | biostudies-arrayexpress
Project description:The early onset of microglia activation in the Rp58 hetero-KO mice raised the possibility that chronic inflammation in the brain was induced by mutation even in the early life stage. To test this possibility, we examined gene expression profiles in the hippocampus of the Rp58 hetero-KO and the control wild-type mice in adulthood and old age months. Among the genes whose expression level was down-regulated in the aged wild-type mice, 341 genes were down-regulated in the adulthood Rp58 hetero-KO mice when both were compared with the adulthood wild-type mice. Conversely, the expression levels of 103 genes were up-regulated both in the adulthood Rp58 hetero-KO and the aged wild-type mice. In the pathway enrichment analysis, these 103 up-regulated genes included Cxcl10, Oas2, Oas1a, and Oasl2, which are associated with a pathway of immune response interferon gamma action on extracellular matrix and cell differentiation.
2022-07-16 | GSE207955 | GEO
Project description:Appropriate number of neurons and glial cells is generated from neural stem cells (NSCs) by the regulation of cell cycle exit and subsequent differentiation. Although the regulatory mechanism remains obscure, Id (inhibitor of differentiation) proteins are known to contribute critically to NSC proliferation by controlling cell cycle. Here we report that a transcriptional factor, RP58, negatively regulates all 4 Id genes (Id1-Id4) in developing cerebral cortex. Consistently, Rp58 knockout (KO) mice demonstrated enhanced astrogenesis accompanied with an excess of NSCs. These phenotypes were mimicked by the overexpression of all Id genes in wild-type cortical progenitors. Furthermore, Rp58 KO phenotypes were rescued by the knockdown of all Id genes in mutant cortical progenitors but not by the knockdown of each single Id gene. Finally, we determined p57 as an effector gene of RP58-Id-mediated cell fate control. These findings establish RP58 as a novel key regulator that controls the self-renewal and differentiation of NSCs and restriction of astrogenesis by repressing all Id genes during corticogenesis. Sample RNAs were obtained from E16.5 Rp58 KO mouse cerebral cortex or control cortex. Two independent total RNA samples from each mouse strain were mixed and purified using the RNeasy Mini Kit (Qiagen). Oligonucleotide microarray analysis was performed using Panorama Micro Array gene expression chips, each containing approx 22000 probe sets (Sigma-Aldrich) according to the manufacturer's instructions.
2014-12-08 | E-GEOD-34327 | biostudies-arrayexpress
Project description:ELAV/Hu factors are conserved RNA binding proteins that play diverse roles in mRNA processing and regulation. The founding member, Drosophila Elav, was recognized as a vital neural factor 35 years ago. Nevertheless, still little is known about its impacts on the transcriptome, and potential functional overlap with its paralogs. Building on our recent findings that neural-specific lengthened 3' UTR isoforms are co-determined by ELAV/Hu factors, we address their impacts on splicing. While only a few splicing targets of Drosophila are known, we find that ectopic expression of the three family members (Elav, Fne and Rbp9) induces overlapping changes to hundreds of cassette exon and dozens of alternative last exon (ALE) splicing events. Reciprocally, double mutants of elav/fne, but not elav alone, have opposite effects on both classes of regulated mRNA processing events in the larval CNS. While manipulation of Drosophila ELAV/Hu factors induces both exon skipping and inclusion, motif analysis indicates their major direct effects are to suppress cassette exon usage. Moreover, the roles of ELAV/HU factors in global promotion of distal ALE splicing are mechanistically linked to terminal 3' UTR extensions in neurons, since both involve local suppression of proximal polyadenylation signals via ELAV/Hu binding sites downstream of cleavage sites. The phenotypic impact of combined ELAV/Hu activities in neural mRNA processing is overt, since fne loss strongly enhances neuronal differentiation phenotypes in elav mutants. Finally, we provide evidence for conservation in mammalian neurons, which undergo broad programs of distal ALE and APA lengthening, linked to ELAV/Hu motifs downstream of regulated polyadenylation sites. Overall, ELAV/Hu proteins orchestrate multiple conserved programs of neuronal mRNA processing by suppressing alternative exons and polyadenylation sites.
2021-02-23 | GSE164129 | GEO