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Expression data from E10 cells with miR-129 over-expression

ABSTRACT: miRNAs are known to regulate gene expression by suppressing translation, but there is also a wealth of data showing that they can act as critical regulators of mRNA stability of their targets. In this experiment, we analyzed the mRNA expression profiles of E10 with high expression of miR-129 as compared to control cells to identify miR-129 targets. E10 cells infected with miR-129 over-expressing lentivirus or the control lentivirus were cultured for 48 hours. More than 80% of cells were infected. Total RNA samples were isolated using Trizol (invitrogen), and subjected to labeling, fragmentation and hybridization, according to manufacturer’s protocols. Mouse Genome 430 2.0 Array (Affymetrix) was used for mRNA expression profiling.

ORGANISM(S): Mus musculus

PROVIDER: GSE15121 | GEO | 2010/01/01

SECONDARY ACCESSION(S): PRJNA114875

REPOSITORIES: GEO

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Expression data from E10 cells with miR-129 over-expression

Project description:miRNAs are known to regulate gene expression by suppressing translation, but there is also a wealth of data showing that they can act as critical regulators of mRNA stability of their targets. In this experiment, we analyzed the mRNA expression profiles of E10 with high expression of miR-129 as compared to control cells to identify miR-129 targets. E10 cells infected with miR-129 over-expressing lentivirus or the control lentivirus were cultured for 48 hours. More than 80% of cells were infected. Total RNA samples were isolated using Trizol (invitrogen), and subjected to labeling, fragmentation and hybridization, according to manufacturer’s protocols. Mouse Genome 430 2.0 Array (Affymetrix) was used for mRNA expression profiling. We compared the mRNA expression profiles between cells infected with miR-129 expressing lentivirus and the cells infected with control lentivirus

2009-12-31 | E-GEOD-15121 | biostudies-arrayexpress

miR-129-3p control cilia assembly by regulating CP110 and actin dynamics [miR-129-3p overexpression]

Project description:Primary cilium serves as a cellular “antenna” to sense environmental signals. Ciliogenesis requires the removal of CP110 to convert the mother centriole into the basal body. Actin dynamics is also critical for cilia formation. How these distinct processes are properly regulated remains unknown. Here we show that miR-129-3p, a microRNA conserved in the vertebrates, controlled cilia assembly by down-regulating both CP110 and four proteins critical for actin dynamics, Arp2, Toca1, abLIM1, and abLIM3. Consistently, blocking miR-129-3p repressed cilia formation in cultured mammalian cells, whereas its overexpression potently induced ciliogenesis in proliferating cells and extraordinary cilia elongation. Moreover, inhibition of miR-129-3p in zebrafish embryos suppressed cilia assembly in the Kupffer’s vesicle and pronephric duct, leading to developmental abnormalities including curved body, pericardial oedema, and randomised left-right patterning. Our results thus unravel a novel mechanism that orchestrates both the centriole-to-basal body transition and subsequent cilia assembly via microRNA-mediated posttranscriptional regulations. We want to find the targets of miR-129-3p by overexpressing miR-129-3p oligo or control oligo in hTERT-RPE1 cells. Through microarray analysis we could check the downregulated genes and these genes might be the targets of miR-129-3p.

2012-06-01 | GSE34846 | GEO

MiR-129-5p downregulates HuD expression impairing neuritogenesis in Amyotrophic Lateral Sclerosis

Project description:Amyotrophic lateral sclerosis (ALS) involves the degeneration of brain and spinal cord motor neurons. Mutations in Superoxide Dismutase 1 (SOD1), TAR DNA-binding protein 43 (TDP-43) and Fused-in-Sarcoma (FUS) account for 20-30 % of the familial ALS (fALS) cases. The RNA-binding proteins TDP-43 and FUS function in mRNA and miRNA biogenesis. MiRNAs are required for survival of neurons and deregulation of miRNA expression has been reported in several neurodegenerative disorders. Here, we report the dysregulation of DROSHA, DGCR8, and DICER in human neuroblastoma SH-SY5Y cells expressing the ALS-associated SOD1(G93A) mutant protein. MiRNA profiling in SH-SY5Y/SOD1(G93A) cells and transgenic SOD1(G93A) mice revealed upregulation of miR-129-5p at the early stage of disease. Moreover, miR-129-5p is also upregulated in lymphocytes of sporadic ALS patients. We demonstrate that miR-129-5p targets ELAVL4/HuD mRNA by binding to its 3’ UTR, which reduces HuD expression and impairs differentiation and neurite outgrowth. Conversely, treatment with an antagomir or complementation with HuD protein restores neuritogenesis. Collectively, our study identifies miR-129-5p and HuD as key regulators of neuronal differentiation and as potential therapeutic targets for ALS.

2018-02-01 | GSE94379 | GEO

miR-129-3p control cilia assembly by regulating CP110 and actin dynamics [miR-129-3p overexpression]

Project description:Primary cilium serves as a cellular M-bM-^@M-^\antennaM-bM-^@M-^] to sense environmental signals. Ciliogenesis requires the removal of CP110 to convert the mother centriole into the basal body. Actin dynamics is also critical for cilia formation. How these distinct processes are properly regulated remains unknown. Here we show that miR-129-3p, a microRNA conserved in the vertebrates, controlled cilia assembly by down-regulating both CP110 and four proteins critical for actin dynamics, Arp2, Toca1, abLIM1, and abLIM3. Consistently, blocking miR-129-3p repressed cilia formation in cultured mammalian cells, whereas its overexpression potently induced ciliogenesis in proliferating cells and extraordinary cilia elongation. Moreover, inhibition of miR-129-3p in zebrafish embryos suppressed cilia assembly in the KupfferM-bM-^@M-^Ys vesicle and pronephric duct, leading to developmental abnormalities including curved body, pericardial oedema, and randomised left-right patterning. Our results thus unravel a novel mechanism that orchestrates both the centriole-to-basal body transition and subsequent cilia assembly via microRNA-mediated posttranscriptional regulations. We want to find the targets of miR-129-3p by overexpressing miR-129-3p oligo or control oligo in hTERT-RPE1 cells. Through microarray analysis we could check the downregulated genes and these genes might be the targets of miR-129-3p. RPE1 cells were transfected with control (Ctrl) or miR-129-3p (M129) oligo for 72h, and harvested for RNA extraction and hybridization on Affymetrix microarrays. Two samples: RPE1-Ctrl, RPE1-M129

2012-05-31 | E-GEOD-34846 | biostudies-arrayexpress

Src modulates its oncogenic signaling via regulation of miRNA-129-3p [microRNA]

Project description:To address the molecular mechanisms underlying c-Src-induced cell transformation, we previously developed a model system using Csk-deficient fibroblasts that can be transformed by wild-type c-Src. In this study, we applied this system for the analysis of the potential contribution of mRNA and miRNA to c-Src-induced cell transformation. We found miR-129-3p was downregulated in c-Src-induced cell transformation in a Dox-inducible expression system via c-Src, c-Yes, and Fer.

2019-12-08 | GSE121853 | GEO

Src modulates its oncogenic signaling via regulation of miRNA-129-3p [mRNA]

2019-12-08 | GSE121852 | GEO

Overexpression of miR-129-5p in thyroid carcinoma cells

Project description:TCP1 papillary thyroid carcinoma cells were plated at 100,000 cells/well in a 6-well plate and transfected with 10nM of a synthetic pre-miR-129-5p or a negative pre-miRNA using Lipofectamine RNAiMAX reagent. RNA samples were harvested at 24 and 48 hours post-transfection.

2011-12-06 | GSE19933 | GEO

Mus musculus

Project description:Expression data from E10 cells with miR-129 over-expression

| PRJNA114875 | ENA

Effects of miR-20b and miR-363-5p transfection

Project description:microRNA and mRNA profiling by array for carcinoma cell line E10 after transfection with miR-20b or miR-363-5p

2013-07-01 | E-MTAB-1395 | biostudies-arrayexpress

Ribosome profiling of early zebrafish embryos -- miRNA-mediated regulation during embryogenesis causes translational repression before mRNA decay

Project description:MicroRNAs regulate gene expression through deadenylation, repression and mRNA decay. However, the contribution of each mechanism in non-steady-state situations remains unclear. We monitored the impact of miR-430 on ribosome occupancy of endogenous mRNAs in wild type and dicer mutants lacking mature miR-430. Our results indicate that miR-430 reduces the number of ribosomes on target mRNAs before causing mRNA decay. Translational repression occurs before complete deadenylation, and disrupting deadenylation using an internal poly(A) tail did not block target repression. Finally, we observe that ribosome density along the length of the target mRNA remains constant, suggesting that translational repression occurs by reducing the initiation rate rather than reducing elongation or causing ribosomal drop-off. In summary, our results show that miR-430 regulates translation initiation before inducing mRNA decay.

2012-03-15 | GSE34743 | GEO

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