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CRISPR/Cas9 mediated intersectional knockout of GSK3b in D2 receptor expressing mPFC neurons reveals contributions to emotional regulation

ABSTRACT: CRISPR/Cas9 mediated intersectional knockout of GSK3b in D2 receptor expressing mPFC neurons reveals contributions to emotional regulation

PROVIDER: PRJNA580259 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10360338_1.fastq.gz	Fastqsanger.gz
	SRR10360338_2.fastq.gz	Fastqsanger.gz
	SRR10360339_1.fastq.gz	Fastqsanger.gz
	SRR10360339_2.fastq.gz	Fastqsanger.gz
	SRR10360340_1.fastq.gz	Fastqsanger.gz

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CRISPR/Cas9 mediated intersectional knockout of GSK3b in D2 receptor expressing mPFC neurons reveals contributions to emotional regulation

Project description:Comparison of ribosome associated RNA between mPFC D2 neurons that lack Gsk3β with Controls

2020-08-14 | GSE139564 | GEO

Prefrontal D2- dopamine receptor deactivates top-down inhibitory control by regulating striatal cholinergic interneurons

Project description:Inhibitory control is a core cognitive function preventing the expression of maladaptive behaviors. This function is overridden in mental illnesses including bipolar disorder, autism spectrum disorders and schizophrenia, causing maladaptive psychomotor agitation. We developed intersectional CRISPR/Cas9 targeting approaches in adult mice to identify receptor/circuit selective mechanisms responsible for inactivation of inhibitory control in two models of amphetamine-induced psychomotor agitation. Inactivation of dopamine D2-receptors in the medial-prefrontal cortex (mPFC) abolished amphetamine-induced: psychomotor agitation, motor sensitization, and cAMP-associated transcriptome changes in the striatum. Further characterization using intersectional projection preparations indicate that these deficits implicate D2-receptors expressed on projection neurons innervating cholinergic interneurons of the dorsomedial striatum (DMS). Trans-synaptic targeting of acetylcholine production in DMS neurons receiving these projections restored psychomotor agitation in mice lacking mPFC D2- receptor expression. These findings identify a circuit by which activation of cortical D2-receptor circumvent an acetylcholine-mediated inhibition of DMS functions by the mPFC to promote psychomotor activation.

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GSK3B shRNA in Panc-1 xenografts

Project description:The Panc-1 human pancreatic cancer line (ATCC) was constructed to stably express control or GSK3B shRNA. Control or GSK3B shRNA expressing Panc-1 cells were implanted subcutaneously into the flanks of 3-5 week old, female, athymic nude mice. Tumors were grown to at least 250mm3. Tumor tissue was microdissected for further analysis. We compared control shRNA (n=4) to GSK3B shRNA (n=3) Panc-1 xenografts. The array data with simple statistical calculations are also provided in a supplementary Excel workbook, with probe-set annotation that we used at the time (users may want newer annotation). We compared xenografts of Panc-1 (Human pancreatic carcinoma cell line, grown in mice) stably expressing GSK3B shRNA (n=3) to similar xenografts with control shRNA (n=4). Xenografts were grown in the flanks of female, athymic nude mice until they reached at least 250mm3. Tumor tissue was microdissected for further analysis. mRNA abundance assays were performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets.

2014-01-09 | E-GEOD-35351 | biostudies-arrayexpress

GSK3B shRNA in Panc-1 xenografts

2014-01-09 | GSE35351 | GEO

CRISPR-Cas9-Mediated Intersectional Knockout of Glycogen Synthase Kinase 3β in D2 Receptor-Expressing Medial Prefrontal Cortex Neurons Reveals Contributions to Emotional Regulation.

Project description:Glycogen synthase kinase 3β (GSK3β) activity is regulated by dopamine D2 receptor signaling and can be inhibited by psychoactive drugs in a D2 receptor-dependent manner. However, GSK3β is ubiquitously expressed in the brain, and D2 receptor-expressing cells are distributed as a mosaic in multiple cortical regions. This complicates the interrogation of GSK3β functions in cortical D2 cells in a circuit-defined manner using conventional animal models. We used a CRISPR-Cas9-mediated intersectional approach to achieve targeted deletion of GSK3β in D2-expressing neurons of the adult medial prefrontal cortex (mPFC). Isolation and analysis of ribosome-associated RNA specifically from mPFC D2 neurons lacking GSK3β demonstrated large-scale translatome alterations. Deletion of GSK3β in mPFC D2 neurons revealed its contribution to anxiety-related, cognitive, and social behaviors. Our results underscore the viability of an intersectional knockout approach to study functions of a ubiquitous gene in a network-defined fashion while uncovering the contribution of GSK3β expressed in mPFC D2 neurons in the regulation of behavioral dimensions related to mood and emotions. This advances our understanding of GSK3β action at a brain circuit level and can potentially lead to the development of circuit selective therapeutics.

| S-EPMC7307679 | biostudies-literature

A Novel role for GSK3B as a modulator of Drosha Microprocessor activity and microRNA biogenesis

Project description:Regulation of microRNA (miR) biogenesis is complex and stringently controlled. Here we identify the kinase GSK3B as an important modulator of global miR biogenesis at microprocessor level. Repression of GSK3B activity reduces Drosha activity towards pri-miRs, leading to accumulation of unprocessed pri-miRs and reduction of pre-miRs and mature miRs without altering levels or cellular localisationof miR biogenesisproteins. Conversly, GSK3B activation increases Drosha activityand mature miR accumulation. GSK3B achieves this through promoting Drosha:cofactor and Drosha:pri-miR interactions: it binds to DGCR8 and p72 in the Microprocessor, an effect dependent of RNA. Indeed GSK3B itself can immunoprecipitate pri-miRs, suggesting possible RNA binding capacity. Kinase assays identify the mechanism for GSK3B-enhansed Drosha activity, which requires GSK3B nuclear localisation, as phosphorylation of Drosha at s300 and/or s302 confirmed by enhanced Drosha activity and association with cofactors, and increased abundance of mature microRNAs in the presence of phospho-mimetic Drosha. Functional implicatons of GSK3B-enhanced miR biogenesis are illustrated by increased levels of GSK3B-upregulatd miR targets following GSK3B inhibition. These data, the first link GSK3B with the miR cascade in humans, hilight a novel pro-biogenesis role for GSK3B in increasing miR biogenesis as a component of the Microprocessor complex with wide ranging consiquences.

2016-05-20 | GSE81141 | GEO

VTA and NAC labeled ribosome from mPFC

Project description:Projection-dependent ribosome profling from mouse mPFC. Ribosome from NAC- and VTA- projecting mPFC cells were immunoprecipited using GFP-trap (Chromotech). Translating mRNA was isolated and analyzed

2017-09-15 | GSE101185 | 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

Expression data from Drd2+ cells of mouse mPFC

Project description:The heterogeneity of cortical dopamine D2 receptor expressing cells is not well characterized We performed microarrays to study expression of all the transcriprts specifically from Drd2+ neurons of mouse mPFC. For this we immunoprecipitated ribosomes from mPFC of D2Cre::RiboTag mouse, where ribosomal subunit Rpl22 is tagged with HA epitope specifically in Drd2+ neurons

2018-06-16 | GSE115887 | GEO

Proteomic profiling of astrocytic O-GlcNAc transferase related proteins in the mPFC

Project description:Our research showed that astrocytic OGT could influence the expression of proteins in the mPFC. Most of these altered proteins participate in metabolic process, transferase activity, and biosynthetic process. GFAP, an astrocyte maker, was increased after OGT deletion. These results provide a framework for further study on the role of astrocytic OGT/O-GlcNAcylation in the mPFC.

2021-11-02 | PXD026887 | Pride

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