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RORα coordinates thalamic and cortical maturation to instruct barrel cortex development.

ABSTRACT: The retinoic acid orphan receptor alpha (RORα) is well known for its role in cerebellar development and maturation as revealed in the stagerrer (Stg) mutant mouse line. However it’s potential involvement for the development of other brain regions has not been assessed. Here we describe a new role of RORα in the development of the thalamic and cortical circuits that leads to the assembly of columnar barrel structures in the primary somatosensory cortex. Microarray analyses comparing gene expression in the thalamus and cortex of the Stg, showed a down-regulation of genes that have been involved in the control of TCA or cellular maturation of layer IV neurons. Overall, our study outlines a new role of RORα for the coordinated maturation of the thalamus and cortex during early postnatal life, and shows that it is required to initiate the transcription of genes involved in barrel formation.

ORGANISM(S): Mus musculus

PROVIDER: GSE80317 | GEO | 2017/09/30

SECONDARY ACCESSION(S): PRJNA318576

REPOSITORIES: GEO

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Mus musculus

Project description:RORα coordinates thalamic and cortical maturation to instruct barrel cortex development.

| PRJNA318576 | ENA

The identification of genes altered by RORα in progression of non-alcoholic steatohepatitis (NASH)

Project description:Purpose: To identify the target genes of RORα associated with development of NASH Methods: RNA isolation for sequencing analysis from liver tissues of High fat diet (HFD)-fed RORα-LKO and RORα f/f mice and mRNA-sequencing Conclusion: When calcuated by dividing the normalized read count of HFD-fed RORα-LKO by that of RORαf/f,.there are 8505 genes altered by RORα deletion (cut-off, 0.8-fold, 1.5-fold).

2019-12-03 | GSE90844 | GEO

RORɣt and RORα Signature Genes in Human Th17 Cells

Project description:In an effort to study gene expression modulated by RORɣt and RORα in human Th17 cells, global gene expression of human CD4 T cells activated under Th17 skewing conditions was profiled by RNA sequencing. RORɣt and RORα signature genes were identified in these Th17 cells treated with specific siRNAs to knock down RORɣt or RORα expression. In addition, selective small molecule RORɣt modulators were also utilized as pharmacological tools in RORɣt signature gene identification.

2017-09-14 | GSE103844 | GEO

Cortical, hippocampal and thalamic whole genome transcriptome data from controls and G72 schizophrenia mice of both sexes

Project description:G72 transgenic (TG, transgenic mice carrying the G72/G30 locus) and wildtype (WT) mice with a CD1 background were used for transcriptome data acquisition. Importantly, three different brain regions, i.e., the retrosplenial cortex, the hippocampus and thalamus, of animals from both sexes were investigated. In total, eight WT control animals (four ♂, age: 23.14 ± 0.00 wks; four ♀, age: 23.46 ± 0.11 wks) and eight G72 transgenic mice (four ♂, age: 23.14 ± 0.00 wks; four ♀, age: 23.14 ± 0.00 wks) were used for dissection of the cortex, thalamus and hippocampus for subsequent transcriptome analysis. Our data allow new insight into relevant alterations in gene transcript levels in G72 mice and allow the reader/user to carry out additional complex analyses to characterize potential sex-, age- and brain-region-specific profiles in gene expression and related pathways. These analyses could trigger biomarker identification and drug research and development in schizophrenia research in the future.

2023-12-01 | E-MTAB-13547 | biostudies-arrayexpress

RORα is critical for mTORC1 activity in T cell-mediated colitis [ChIP-seq]

Project description:Inflammatory bowel disease (IBD) is multi-factorial chronic intestinal inflammation driven by pathogenic T cells. The mechanisms underlying colitis pathogenicity and anti-TNF therapy resistance are not fully understood. Here we demonstrate that RORα is highly expressed in active UC patients, particularly in those non-responsive to anti-TNF treatment. Rorα deficient CD4+ T cells could not induce severe gut inflammation in a T cell transfer colitis model. Mechanistically, RORα regulated T cell infiltration in colon by promoting T cell migration and inhibiting T cell apoptosis. Meanwhile, genome-wide occupancy and transcriptome analysis revealed that RORα promoted mTORC1 activation. mTORC1 signaling, also hyperactivated in active UC patients, was necessary for T cell-mediated colitis.

2021-07-28 | GSE168217 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [RNA-seq]

2021-07-28 | GSE168216 | GEO

A genetically defined mPFC-thalamic circuit underlies pain chronicity

Project description:Chronic pain is a major health care problem with great social and economic consequences. Although the medial prefrontal cortex (mPFC) and the thalamus have been implicated in regulating pain, whether and how these regions may involve in pain chronification process have remained largely unknown. Here, we show that Foxp2+ neurons in mPFC, which are corticothalamic (CT) neurons representing the major mPFC output to thalamus, are deactivated in chronic inflammatory pain. Interestingly, prolonged, but not short-term, inactivation of the Foxp2+ neurons in mPFC increases the sensitivity to noxious stimulations. Conversely, chemogenetic activation of this neuronal cluster induces robust antinociceptive effects in both naïve mice and mice with chronic inflammatory pain. Furthermore, we found that the mPFC Foxp2+ neurons project to several thalamic relay nuclei and that activation of the mPFC to the parataenial nucleus of thalamus (PTN) circuit relieves pain. Finally, RNA-seq of the mPFC Foxp2+ neurons revealed that many genes related to neuronal activity are dysregulated in mice with chronic inflammatory pain. Collectively, our studies revealed that Foxp2+ neurons in mPFC that project to thalamus play a critical role in somatosensory processing and pain chronification.

2023-09-16 | GSE243136 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [16S rRNA-seq]

2021-07-28 | GSE168218 | GEO

Inhibition of nuclear receptor RORα attenuates cartilage damage in osteoarthritis by modulating IL-6/STAT3 pathwa

Project description:Osteoarthritis is characterized by cartilage destruction, chronic inflammation, and subchondral sclerosis. Evidence showed that nuclear receptor family is closely associated with cartilage damage in an unclear molecular mechanism. Here, we investigated the role and molecular mechanism of the retinoic acid receptor-related orphan receptor-α (RORα), an important member of nuclear receptor, in regulating cartilage degradation and osteoarthritis pathogenesis. Investigation to osteoarthritis clinical specimen showed that the degree of RORα elevation is positively correlated with the severity of osteoarthritis and cartilage damage. In an in vivo osteoarthritis models induced by anterior crucial ligament transaction, intraarticularly injection of siRora adenovirus reversed the cartilage damage. RORα knock-down increased the protein expression level of anabolic factor such as type II collagen, Aggrecan, and decreased the expression of catabolic factor. RNA-seq data suggested IL-6/STAT3 pathway is significantly down-regulated. Mechanistically, RORα knock-down decreased the expression level of both IL-6 and phosphorylated STAT3. RORα exerted its effect on IL-6/STAT3 signaling in two different ways, which includes interaction with STAT3 and IL6 promoter. Taken together, our findings indicated the pivotal role of RORα/IL-6/STAT3 axis in osteoarthritis progression and confirmed RORα knock-down exerted therapeutic effect in human chondrocyte thus providing a potential drug target in osteoarthritis therapy.

2021-04-20 | GSE172291 | GEO

A Thalamic Orphan Receptor Drives Variability in Short Term Memory

Project description:Working memory is a form of short-term memory that involves maintaining and updating task relevant information toward goal-directed pursuits. Classical models posit persistent activity in prefrontal cortex (PFC) as a primary neural correlate, but emerging views suggest additional mechanisms may exist. We screened ~200 genetically diverse mice on a working memory task and identified a genetic locus on Chromosome 5 that contributes to a substantial proportion (17%) of the phenotypic variance. Within the locus, we identified a gene encoding an orphan G-protein coupled receptor, Gpr12, which is sufficient to drive substantial and bi-directional changes in working memory. Molecular, cellular, and imaging studies revealed that Gpr12 enables high thalamus-PFC synchrony to support memory maintenance and choice accuracy. These findings identify a novel orphan receptor as a potent modifier of short-term memory, and supplement classical PFC-based models with an emerging thalamus-centric framework for the mechanistic understanding of working memory.

2020-10-01 | GSE156836 | GEO

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