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Neuro-specific HuR-deficient mice spontaneously develop motor neuron disease

ABSTRACT: To study the neuron-specific function of HuR, we generated inducible, neuron-specific HuR-deficient mice of both sexes. These mice developed a phenotype consisting of poor balance, decreased movement, and decreased strength Genome-wide microarray and RT-PCR analysis further indicated that HuR deficiency in neurons resulted in altered expression of genes in the brain involved in cell growth The additional enriched GO terms in the brain tissues of neuron-specific HuR-deficient mice were largely related to inflammation, including interferon-induced genes and complement components.

ORGANISM(S): Mus musculus

PROVIDER: GSE112678 | GEO | 2018/04/05

REPOSITORIES: GEO

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Neuro-specific HuR-deficient mice spontaneously develop motor neuron disease

Project description:Neuro-specific HuR-deficient mice spontaneously develop motor neuron disease

| PRJNA448705 | ENA

Expression date from WT RAW264.7 and HuR-deficient RAW264.7 stimulated with poly(I:C) using lipofectamine

Project description:HuR-deficient cells showed the decreased expression of genes involved in chemotaxis, cell proliferation and signal transduction. We used microarray to detail the global gene expression of HuR-deficient cell after poly(I:C) stimulation.

2018-04-01 | GSE103459 | GEO

Neuron-Specific HuR-Deficient Mice Spontaneously Develop Motor Neuron Disease.

Project description:Human Ag R (HuR) is an RNA binding protein in the ELAVL protein family. To study the neuron-specific function of HuR, we generated inducible, neuron-specific HuR-deficient mice of both sexes. After tamoxifen-induced deletion of HuR, these mice developed a phenotype consisting of poor balance, decreased movement, and decreased strength. They performed significantly worse on the rotarod test compared with littermate control mice, indicating coordination deficiency. Using the grip-strength test, it was also determined that the forelimbs of neuron-specific HuR-deficient mice were much weaker than littermate control mice. Immunostaining of the brain and cervical spinal cord showed that HuR-deficient neurons had increased levels of cleaved caspase-3, a hallmark of cell apoptosis. Caspase-3 cleavage was especially strong in pyramidal neurons and ? motor neurons of HuR-deficient mice. Genome-wide microarray and real-time PCR analysis further indicated that HuR deficiency in neurons resulted in altered expression of genes in the brain involved in cell growth, including trichoplein keratin filament-binding protein, Cdkn2c, G-protein signaling modulator 2, immediate early response 2, superoxide dismutase 1, and Bcl2. The additional enriched Gene Ontology terms in the brain tissues of neuron-specific HuR-deficient mice were largely related to inflammation, including IFN-induced genes and complement components. Importantly, some of these HuR-regulated genes were also significantly altered in the brain and spinal cord of patients with amyotrophic lateral sclerosis. Additionally, neuronal HuR deficiency resulted in the redistribution of TDP43 to cytosolic granules, which has been linked to motor neuron disease. Taken together, we propose that this neuron-specific HuR-deficient mouse strain can potentially be used as a motor neuron disease model.

| S-EPMC6008238 | biostudies-literature

Transcriptome comparison of white adipose tissue between control and adipose specific HuR knockout mice

Project description:Human antigen R (HuR) is a member of the Hu family of RNA-binding proteins and is involved in many physiological processes. To investigate the role of adipose HuR, we generate adipose-specific HuR knockout (HuRAKO) mice. As compared with control mice, HuRAKO mice show obesity when induced with a high-fat diet, along with insulin resistance, glucose intolerance, hypercholesterolemia and increased inflammation in adipose tissue. The obesity of HuRAKO mice is attributed to adipocyte hypertrophy in white adipose tissue due to decreased expression of adipose triglyceride lipase (ATGL), a critical lipase involved in lipolysis. HuR positively regulates ATGL expression by promoting the mRNA stability and translation of ATGL. Consistently, the expression of HuR in adipose tissue is reduced in obese humans, which is associated with reduced ATGL expression. This study suggests that adipose HuR may be a critical regulator of ATGL expression and lipolysis and thereby controls obesity and metabolic syndrome.

2019-04-23 | GSE130147 | GEO

Title: RNA-seq analysis of mRNA profiles in the livers of HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice fed with an MCD for 3 weeks.

Project description:ionPurpose: The goal of this study is to investigate how HuR regulates NASH progression. Methods: The hepatic mRNA profiles of HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice (n=3 for each group) fed with an MCD for 3 weeks were generated by deep sequencing using an Illumina Novaseq platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.p6) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of hepatic mRNA profiles in HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice fed with an MCD for 3 weeks, generated by RNA-seq technology. Our results show that 353 genes were upregulated and 422 genes were downregulated. Gene Ontology (GO) analysis showed that genes related to leukocyte migration, leukocyte chemotaxis, cell chemotaxis, neutrophil migration and Fc receptor signaling pathway were significantly decreased, which contributes to the protective effects of NASH progression in HKO mice.

2023-06-17 | GSE152670 | GEO

RNA Immunoprecipitation-sequencing from mouse liver using HuR antibody

Project description:We report the HuR-RNA interactions in the liver by performing RNA-immunoprecipitation sequencing (RIP-seq). RIP-seq was performed in healthy livers of wildtype (WT) mice using a HuR antibody. We found that 1380 cytoplasmic-target mRNAs bound to HuR, as assessed by the comparison between the HuR-specific antibody and the IgG control

2021-09-15 | GSE143703 | GEO

Developmental Cytoplasmic-to-Nuclear Translocation of RNA-Binding Protein HuR Is Required for Adult Neurogenesis

Project description:Although neurogenesis in the adult brain recapitulates processes that occur during embryonic development, adult neurogenesis exhibits distinct characteristics from its embryonic counterpart. However, the intrinsic mechanism underlying the differential regulation of neurogenesis between these two stages remains unclear. Herein, we show that the ablation of RNA-binding protein HuR in neural stem cells (NSCs) impairs adult, but not embryonic, neurogenesis. HuR is predominantly expressed in the cytoplasm of embryonic NSCs but translocates into the nucleus of adult NSCs. Transcriptomic analysis of HuR-deficient adult NSCs revealed that nuclear HuR primarily regulates alternative splicing of numerous premRNA transcripts, including focal adhesion kinase (FAK). HuR-deficient adult NSCs generate increased FAK mRNA isoforms with shorter 5’ UTRs, leading to enhanced FAK mRNA translation and hyperactivated FAK signaling, and inhibition of FAK ameliorates defective adult neurogenesis and impaired hippocampus-dependent learning in HuR-deficient mice. Taken together, these findings reveal novel mechanistic insights into the differential regulation of embryonic and adult neurogenesis through developmental cytoplasmic-to-nuclear translocation of HuR in NSCs.

2019-11-04 | GSE137323 | GEO

RNA binding protein HuR protects against NAFLD by suppressing long noncoding RNA H19 expression

Project description:NAFLD has become the most common chronic liver disease worldwide. Human antigen R (HuR), an RNA-binding protein, is an important post-transcriptional regulator. HuR has been reported as a key player in regulating lipid homeostasis in the liver and adipose tissues by using tissue-specific HuR knockout mice. However, the underlying mechanism by which hepatocyte-specific HuR regulates hepatic lipid metabolism under metabolic stress remains unclear and is the focus of this study.

2022-12-01 | GSE213215 | GEO

Sequencing of liver RNA from HuR WT and HuR KO mice

Project description:Sequencing of liver RNA from HuR WT and HuR KO mice

| PRJNA600219 | ENA

HuR- dependent regulation of mRNA splicing is essential for the B cell antibody response [Ribo-Seq]

Project description:Post-transcriptional regulation of mRNA by the RNA binding protein HuR is required in B cells for the germinal centre reaction and for the production of class-switched antibodies in response to T-independent antigens. Transcriptome-wide examination of RNA isoforms, abundance and translation in HuR-deficient B cells, together with direct measurements of HuR-RNA interaction, revealed that HuR-dependent mRNA splicing affects hundreds of transcripts including the dihydrolipoyl succinyltransferase (Dlst), a subunit of the aketoglutaratedehydrogenase (aKGDH) enzyme. In the absence of HuR, defective mitochondrial metabolism results in high levels of reactive oxygen species and B cell death. Our study shows how post-transcriptional processes control the balance of energy metabolism required for B cell proliferation and differentiation. Sequencing analysis of ribosome protected RNA fragments in ex vivo or LPS-activated splenic B cells was performed using ARTseqM-bM-^DM-" Ribosome Profiling Kit - Mammalian (Epicentre, RPHMR12126) and Illumina platform. Splenic B cells come from HuRf/f control or HuR cKO mice. 4-5 biological replicates per genotype and condition.

2015-02-13 | E-GEOD-62134 | biostudies-arrayexpress

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