Monitoring Nociception by Analyzing Gene Expression Changes in the Central Nervous System of Mice
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Four Unique Interneuron Populations Reside in Neocortical Layer 1
The Journal of Neuroscience, January 2, 2019 • 39(1):125–139 • 125 Systems/Circuits Four Unique Interneuron Populations Reside in Neocortical Layer 1 X Benjamin Schuman,1* XRobert P. Machold,1* Yoshiko Hashikawa,1 Ja´nos Fuzik,1 Gord J. Fishell,2 and X Bernardo Rudy1,3 1Neuroscience Institute, New York University, New York, New York 10016, 2Harvard Medical School and the Stanley Center at the Broad, Cambridge, Massachusetts 02142, and 3Department of Anesthesiology, Perioperative Care and Pain Medicine, New York University School of Medicine, New York, New York 10016 Sensory perception depends on neocortical computations that contextually adjust sensory signals in different internal and environmen- tal contexts. Neocortical layer 1 (L1) is the main target of cortical and subcortical inputs that provide “top-down” information for context-dependent sensory processing. Although L1 is devoid of excitatory cells, it contains the distal “tuft” dendrites of pyramidal cells (PCs) located in deeper layers. L1 also contains a poorly characterized population of GABAergic interneurons (INs), which regulate the impact that different top-down inputs have on PCs. A poor comprehension of L1 IN subtypes and how they affect PC activity has hampered our understanding of the mechanisms that underlie contextual modulation of sensory processing. We used novel genetic strategies in male and female mice combined with electrophysiological and morphological methods to help resolve differences that were unclear when using only electrophysiological and/or morphological approaches. We discovered that L1 contains four distinct popula- tions of INs, each with a unique molecular profile, morphology, and electrophysiology, including a previously overlooked IN population (named here “canopy cells”) representing 40% of L1 INs. -
Single-Cell Rnaseq Reveals Seven Classes of Colonic Sensory Neuron
Gut Online First, published on February 26, 2018 as 10.1136/gutjnl-2017-315631 Neurogastroenterology ORIGINAL ARTICLE Gut: first published as 10.1136/gutjnl-2017-315631 on 26 February 2018. Downloaded from Single-cell RNAseq reveals seven classes of colonic sensory neuron James R F Hockley,1,2 Toni S Taylor,1 Gerard Callejo,1 Anna L Wilbrey,2 Alex Gutteridge,2 Karsten Bach,1 Wendy J Winchester,2 David C Bulmer,1 Gordon McMurray,2 Ewan St John Smith1 ► Additional material is ABSTRact pathways to the central nervous system (CNS).1 In published online only. To view Objective Integration of nutritional, microbial and the colorectum, sensory innervation is organised please visit the journal online (http:// dx. doi. org/ 10. 1136/ inflammatory events along the gut-brain axis can alter into two main pathways: thoracolumbar (TL) spinal gutjnl- 2017- 315631). bowel physiology and organism behaviour. Colonic afferents projecting via the lumbar splanchnic sensory neurons activate reflex pathways and give nerve (LSN) and lumbosacral (LS) spinal afferents 1Department of Pharmacology, University of Cambridge, rise to conscious sensation, but the diversity and projecting via the pelvic nerve (PN) that are respon- Cambridge, UK division of function within these neurons is poorly sible for transducing conscious sensations of full- 2Neuroscience and Pain understood. The identification of signalling pathways ness, discomfort, urgency and pain, in addition to Research Unit, Pfizer, contributing to visceral sensation is constrained by a reflex actions.2 Cambridge, UK paucity of molecular markers. Here we address this by Visceral sensory afferents act to maintain many comprehensive transcriptomic profiling and unsupervised aspects of GI physiology, such as continence and Correspondence to James R F Hockley, Department clustering of individual mouse colonic sensory neurons. -
F2RL2 Antibody Cat
F2RL2 Antibody Cat. No.: 56-323 F2RL2 Antibody F2RL2 Antibody immunohistochemistry analysis in formalin fixed and paraffin embedded human heart tissue followed by peroxidase conjugation of the secondary antibody and DAB staining. Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human This F2RL2 antibody is generated from rabbits immunized with a KLH conjugated IMMUNOGEN: synthetic peptide between 21-50 amino acids from the N-terminal region of human F2RL2. TESTED APPLICATIONS: IHC-P, WB For WB starting dilution is: 1:1000 APPLICATIONS: For IHC-P starting dilution is: 1:10~50 PREDICTED MOLECULAR 43 kDa WEIGHT: September 25, 2021 1 https://www.prosci-inc.com/f2rl2-antibody-56-323.html Properties This antibody is purified through a protein A column, followed by peptide affinity PURIFICATION: purification. CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated PHYSICAL STATE: Liquid BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: F2RL2 Proteinase-activated receptor 3, PAR-3, Coagulation factor II receptor-like 2, Thrombin ALTERNATE NAMES: receptor-like 2, F2RL2, PAR3 ACCESSION NO.: O00254 GENE ID: 2151 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References Coagulation factor II (thrombin) receptor-like 2 (F2RL2) is a member of the large family of 7-transmembrane-region receptors that couple to guanosine-nucleotide-binding proteins. -
Supplemental Figure 1. Vimentin
Double mutant specific genes Transcript gene_assignment Gene Symbol RefSeq FDR Fold- FDR Fold- FDR Fold- ID (single vs. Change (double Change (double Change wt) (single vs. wt) (double vs. single) (double vs. wt) vs. wt) vs. single) 10485013 BC085239 // 1110051M20Rik // RIKEN cDNA 1110051M20 gene // 2 E1 // 228356 /// NM 1110051M20Ri BC085239 0.164013 -1.38517 0.0345128 -2.24228 0.154535 -1.61877 k 10358717 NM_197990 // 1700025G04Rik // RIKEN cDNA 1700025G04 gene // 1 G2 // 69399 /// BC 1700025G04Rik NM_197990 0.142593 -1.37878 0.0212926 -3.13385 0.093068 -2.27291 10358713 NM_197990 // 1700025G04Rik // RIKEN cDNA 1700025G04 gene // 1 G2 // 69399 1700025G04Rik NM_197990 0.0655213 -1.71563 0.0222468 -2.32498 0.166843 -1.35517 10481312 NM_027283 // 1700026L06Rik // RIKEN cDNA 1700026L06 gene // 2 A3 // 69987 /// EN 1700026L06Rik NM_027283 0.0503754 -1.46385 0.0140999 -2.19537 0.0825609 -1.49972 10351465 BC150846 // 1700084C01Rik // RIKEN cDNA 1700084C01 gene // 1 H3 // 78465 /// NM_ 1700084C01Rik BC150846 0.107391 -1.5916 0.0385418 -2.05801 0.295457 -1.29305 10569654 AK007416 // 1810010D01Rik // RIKEN cDNA 1810010D01 gene // 7 F5 // 381935 /// XR 1810010D01Rik AK007416 0.145576 1.69432 0.0476957 2.51662 0.288571 1.48533 10508883 NM_001083916 // 1810019J16Rik // RIKEN cDNA 1810019J16 gene // 4 D2.3 // 69073 / 1810019J16Rik NM_001083916 0.0533206 1.57139 0.0145433 2.56417 0.0836674 1.63179 10585282 ENSMUST00000050829 // 2010007H06Rik // RIKEN cDNA 2010007H06 gene // --- // 6984 2010007H06Rik ENSMUST00000050829 0.129914 -1.71998 0.0434862 -2.51672 -
Edinburgh Research Explorer
Edinburgh Research Explorer International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list Citation for published version: Davenport, AP, Alexander, SPH, Sharman, JL, Pawson, AJ, Benson, HE, Monaghan, AE, Liew, WC, Mpamhanga, CP, Bonner, TI, Neubig, RR, Pin, JP, Spedding, M & Harmar, AJ 2013, 'International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands', Pharmacological reviews, vol. 65, no. 3, pp. 967-86. https://doi.org/10.1124/pr.112.007179 Digital Object Identifier (DOI): 10.1124/pr.112.007179 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Pharmacological reviews Publisher Rights Statement: U.S. Government work not protected by U.S. copyright General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 1521-0081/65/3/967–986$25.00 http://dx.doi.org/10.1124/pr.112.007179 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:967–986, July 2013 U.S. -
Serotonin Receptor 3A Controls Interneuron Migration Into the Neocortex
ARTICLE Received 3 Sep 2014 | Accepted 9 Oct 2014 | Published 20 Nov 2014 DOI: 10.1038/ncomms6524 OPEN Serotonin receptor 3A controls interneuron migration into the neocortex Sahana Murthy1,2,*, Mathieu Niquille1,2,*, Nicolas Hurni1,2, Greta Limoni1,2, Sarah Frazer1,2, Pascal Chameau3, Johannes A. van Hooft3, Tania Vitalis4 & Alexandre Dayer1,2 Neuronal excitability has been shown to control the migration and cortical integration of reelin-expressing cortical interneurons (INs) arising from the caudal ganglionic eminence (CGE), supporting the possibility that neurotransmitters could regulate this process. Here we show that the ionotropic serotonin receptor 3A (5-HT3AR) is specifically expressed in CGE-derived migrating interneurons and upregulated while they invade the developing cortex. Functional investigations using calcium imaging, electrophysiological recordings and migra- tion assays indicate that CGE-derived INs increase their response to 5-HT3AR activation during the late phase of cortical plate invasion. Using genetic loss-of-function approaches and in vivo grafts, we further demonstrate that the 5-HT3AR is cell autonomously required for the migration and proper positioning of reelin-expressing CGE-derived INs in the neocortex. Our findings reveal a requirement for a serotonin receptor in controlling the migration and laminar positioning of a specific subtype of cortical IN. 1 Department of Mental Health and Psychiatry, University of Geneva Medical School, CH-1211 Geneva 4, Switzerland. 2 Department of Basic Neurosciences, University of Geneva Medical School, CH-1211 Geneva 4, Switzerland. 3 Swammerdam Institute for Life Sciences, Center for NeuroScience, University of Amsterdam, Sciencepark 904, 1098 XH Amsterdam, The Netherlands. 4 CNRS-UMR 8249, Brain Plasticity Unit, ESPCI ParisTech, 10 rue Vauquelin, 75005 Paris, France. -
Supplementary Data
Supplemental Data A novel mouse model of X-linked nephrogenic diabetes insipidus: Phenotypic analysis and therapeutic implications Jian Hua Li, Chung-Lin Chou, Bo Li, Oksana Gavrilova, Christoph Eisner, Jürgen Schnermann, Stasia A. Anderson, Chu-Xia Deng, Mark A. Knepper, and Jürgen Wess Supplemental Methods Metabolic cage studies. Animals were maintained in mouse metabolic cages (Hatteras Instruments, Cary, NC) under controlled temperature and light conditions (12 hr light and dark cycles). Mice received a fixed daily ration of 6.5 g of gelled diet per 20 g of body weight per day. The gelled diet was composed of 4 g of Basal Diet 5755 (Test Diet, Richmond, IN), 2.5 ml of deionized water, and 65 mg agar. Preweighted drinking water was provided ad libitum during the course of the study. Mice were acclimated in the metabolic cages for 1-2 days. Urine was collected under mineral oil in preweighted collection vials for successive 24 hr periods. Analysis of GPCR expression in mouse IMCD cells via TaqMan real-time qRT-PCR. Total RNA prepared from mouse IMCD tubule suspensions was reverse transcribed as described under Experimental Procedures. Tissues from ten 10-week old C57BL/6 WT mice were collected and pooled for each individual experiment. cDNA derived from 640 ng of RNA was mixed with an equal volume of TaqMan gene expression 2 x master mix (Applied Biosystems, Foster City, CA). 100 μl-aliquots of this mixture (corresponding to 80 ng of RNA) were added to each of the 8 fill ports of a 384-well plate of a mouse GPCR array panel (Applied Biosystems). -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
High Yield and Efficient Expression and Purification of the Human 5-HT3A Receptor
npg Acta Pharmacologica Sinica (2015) 36: 1024–1032 © 2015 CPS and SIMM All rights reserved 1671-4083/15 www.nature.com/aps Original Article High yield and efficient expression and purification of the human 5-HT3A receptor Zhong-shan WU1, 2, Zhi-cheng CUI3, Hao CHENG2, Chen FAN3, Karsten MELCHER4, Yi JIANG2, Cheng-hai ZHANG2, Hua-liang JIANG5, Yao CONG2, Qian LIU1, *, H Eric XU2, 4, * 1Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan 430074, China; 2VARI-SIMM Center, Center for Structure and Function of Drug Targets, CAS-Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China; 3National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201210, China; 4Laboratory of Structural Sciences, Van Andel Research Institute, Grand Rapids, MI 49503, USA; 5State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China Aim: To establish a method for efficient expression and purification of the human serotonin type 3A receptor (5-HT3A) that is suitable for structural studies. Methods: Codon-optimized cDNA of human 5-HT3A was inserted into a modified BacMam vector, which contained an IgG leader sequence, an 8×His tag linked with two-Maltose Binding Proteins (MBP), and a TEV protease cleavage site. The BacMam construct was used to generate baculoviruses for expression of 5-HT3A in HEK293F cells. The proteins were solubilized from the membrane with the detergent C12E9, and purified using MBP affinity chromatography. -
Prox1regulates the Subtype-Specific Development of Caudal Ganglionic
The Journal of Neuroscience, September 16, 2015 • 35(37):12869–12889 • 12869 Development/Plasticity/Repair Prox1 Regulates the Subtype-Specific Development of Caudal Ganglionic Eminence-Derived GABAergic Cortical Interneurons X Goichi Miyoshi,1 Allison Young,1 Timothy Petros,1 Theofanis Karayannis,1 Melissa McKenzie Chang,1 Alfonso Lavado,2 Tomohiko Iwano,3 Miho Nakajima,4 Hiroki Taniguchi,5 Z. Josh Huang,5 XNathaniel Heintz,4 Guillermo Oliver,2 Fumio Matsuzaki,3 Robert P. Machold,1 and Gord Fishell1 1Department of Neuroscience and Physiology, NYU Neuroscience Institute, Smilow Research Center, New York University School of Medicine, New York, New York 10016, 2Department of Genetics & Tumor Cell Biology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, 3Laboratory for Cell Asymmetry, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan, 4Laboratory of Molecular Biology, Howard Hughes Medical Institute, GENSAT Project, The Rockefeller University, New York, New York 10065, and 5Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 Neurogliaform (RELNϩ) and bipolar (VIPϩ) GABAergic interneurons of the mammalian cerebral cortex provide critical inhibition locally within the superficial layers. While these subtypes are known to originate from the embryonic caudal ganglionic eminence (CGE), the specific genetic programs that direct their positioning, maturation, and integration into the cortical network have not been eluci- dated. Here, we report that in mice expression of the transcription factor Prox1 is selectively maintained in postmitotic CGE-derived cortical interneuron precursors and that loss of Prox1 impairs the integration of these cells into superficial layers. Moreover, Prox1 differentially regulates the postnatal maturation of each specific subtype originating from the CGE (RELN, Calb2/VIP, and VIP). -
Integrative Differential Expression and Gene Set Enrichment Analysis Using Summary Statistics for Scrna-Seq Studies
ARTICLE https://doi.org/10.1038/s41467-020-15298-6 OPEN Integrative differential expression and gene set enrichment analysis using summary statistics for scRNA-seq studies ✉ Ying Ma 1,7, Shiquan Sun 1,7, Xuequn Shang2, Evan T. Keller 3, Mengjie Chen 4,5 & Xiang Zhou 1,6 Differential expression (DE) analysis and gene set enrichment (GSE) analysis are commonly applied in single cell RNA sequencing (scRNA-seq) studies. Here, we develop an integrative 1234567890():,; and scalable computational method, iDEA, to perform joint DE and GSE analysis through a hierarchical Bayesian framework. By integrating DE and GSE analyses, iDEA can improve the power and consistency of DE analysis and the accuracy of GSE analysis. Importantly, iDEA uses only DE summary statistics as input, enabling effective data modeling through com- plementing and pairing with various existing DE methods. We illustrate the benefits of iDEA with extensive simulations. We also apply iDEA to analyze three scRNA-seq data sets, where iDEA achieves up to five-fold power gain over existing GSE methods and up to 64% power gain over existing DE methods. The power gain brought by iDEA allows us to identify many pathways that would not be identified by existing approaches in these data. 1 Department of Biostatistics, University of Michigan, Ann Arbor, MI 48109, USA. 2 School of Computer Science, Northwestern Polytechnical University, Xi’an, Shaanxi 710072, P.R. China. 3 Department of Urology, University of Michigan, Ann Arbor, MI 48109, USA. 4 Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA. 5 Section of Genetic Medicine, Department of Medicine, University of Chicago, Chicago, IL 60637, USA. -
A Comprehensive Network and Pathway Analysis of Human Deafness Genes
Otology & Neurotology 34:961Y970 Ó 2013, Otology & Neurotology, Inc. A Comprehensive Network and Pathway Analysis of Human Deafness Genes *Georgios A. Stamatiou and †Konstantina M. Stankovic *Department of Otolaryngology, Hippokration General Hospital, University of Athens, Athens, Greece; and ÞDepartment of Otology and Laryngology, Harvard Medical School and Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. Objective: To perform comprehensive network and pathway factor beta1 (TGFB1) for Group 1, MAPK3/MAPK1 MAP kinase analyses of the genes known to cause genetic hearing loss. (ERK 1/2) and the G protein coupled receptors (GPCR) for Study Design: In silico analysis of deafness genes using inge- Group 2, and TGFB1 and hepatocyte nuclear factor 4 alpha (HNF4A) nuity pathway analysis (IPA). for Group 3. The nodal molecules included not only those known Methods: Genes relevant for hearing and deafness were iden- to be associated with deafness (GPCR), or with predisposition to tified through PubMed literature searches and the Hereditary otosclerosis (TGFB1), but also novel genes that have not been Hearing Loss Homepage. The genes were assembled into 3 groups: described in the cochlea (HNF4A) and signaling kinases (ERK 1/2). 63 genes that cause nonsyndromic deafness, 107 genes that cause Conclusion: A number of molecules that are likely to be key nonsyndromic or syndromic sensorineural deafness, and 112 genes mediators of genetic hearing loss were identified through three associated with otic capsule development and malformations. Each different network and pathway analyses. The molecules included group of genes was analyzed using IPA to discover the most new candidate genes for deafness.