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3. Improving the predictive power of mouse models

Author

Pera, Martin, Greene, Andy, Cardon, Lon, Carter, Gregory W., Chesler, Elissa J., Churchill, Gary, Kumar, Vivek, Lutz, Cathleen, Munger, Steven, Murray, Steve, O’Connell, Kristen, Reinholdt, Laura, and Rosenthal, Nadia A.

Published
2024
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4. The Ontology of Biological Attributes (OBA)—computational traits for the life sciences

Author

Stefancsik, Ray, Balhoff, James P, Balk, Meghan A, Ball, Robyn L, Bello, Susan M, Caron, Anita R, Chesler, Elissa J, de Souza, Vinicius, Gehrke, Sarah, Haendel, Melissa, Harris, Laura W, Harris, Nomi L, Ibrahim, Arwa, Koehler, Sebastian, Matentzoglu, Nicolas, McMurry, Julie A, Mungall, Christopher J, Munoz-Torres, Monica C, Putman, Tim, Robinson, Peter, Smedley, Damian, Sollis, Elliot, Thessen, Anne E, Vasilevsky, Nicole, Walton, David O, and Osumi-Sutherland, David

Subjects
Biological Sciences, Genetics, Networking and Information Technology R&D (NITRD), Human Genome, 2.5 Research design and methodologies (aetiology), Generic health relevance, Genome-Wide Association Study, Biological Science Disciplines, Phenotype, Biological Ontologies, Genetics & Heredity
Abstract

Existing phenotype ontologies were originally developed to represent phenotypes that manifest as a character state in relation to a wild-type or other reference. However, these do not include the phenotypic trait or attribute categories required for the annotation of genome-wide association studies (GWAS), Quantitative Trait Loci (QTL) mappings or any population-focussed measurable trait data. The integration of trait and biological attribute information with an ever increasing body of chemical, environmental and biological data greatly facilitates computational analyses and it is also highly relevant to biomedical and clinical applications. The Ontology of Biological Attributes (OBA) is a formalised, species-independent collection of interoperable phenotypic trait categories that is intended to fulfil a data integration role. OBA is a standardised representational framework for observable attributes that are characteristics of biological entities, organisms, or parts of organisms. OBA has a modular design which provides several benefits for users and data integrators, including an automated and meaningful classification of trait terms computed on the basis of logical inferences drawn from domain-specific ontologies for cells, anatomical and other relevant entities. The logical axioms in OBA also provide a previously missing bridge that can computationally link Mendelian phenotypes with GWAS and quantitative traits. The term components in OBA provide semantic links and enable knowledge and data integration across specialised research community boundaries, thereby breaking silos.

Published
2023

5. An emerging multi-omic understanding of the genetics of opioid addiction

Author

Johnson, Eric O., Fisher, Heidi S., Sullivan, Kyle A., Corradin, Olivia, Sanchez-Roige, Sandra, Gaddis, Nathan C., Sami, Yasmine N., Townsend, Alice, Prates, Erica Teixeira, Pavicic, Mirko, Kruse, Peter, Chesler, Elissa J., Palmer, Abraham A., Troiani, Vanessa, Bubier, Jason A., Jacobson, Daniel A., and Maher, Brion S.

Subjects
Medical research, Medicine, Experimental
Abstract

Opioid misuse, addiction, and associated overdose deaths remain global public health crises. Despite the tremendous need for pharmacological treatments, current options are limited in number, use, and effectiveness. Fundamental leaps forward in our understanding of the biology driving opioid addiction are needed to guide development of more effective medication- assisted therapies. This Review focuses on the omics-identified biological features associated with opioid addiction. Recent GWAS have begun to identify robust genetic associations, including variants in OPRM1, FURIN, and the gene cluster SCAI/PPP6C/RABEPK. An increasing number of omics studies of postmortem human brain tissue examining biological features (e.g., histone modification and gene expression) across different brain regions have identified broad gene dysregulation associated with overdose death among opioid misusers. Drawn together by meta-analysis and multi- omic systems biology, and informed by model organism studies, key biological pathways enriched for opioid addiction- associated genes are emerging, which include specific receptors (e.g., GABAB receptors, GPCR, and Trk) linked to signaling pathways (e.g., Trk, ERK/MAPK, orexin) that are associated with synaptic plasticity and neuronal signaling. Studies leveraging the agnostic discovery power of omics and placing it within the context of functional neurobiology will propel us toward much- needed, field-changing breakthroughs, including identification of actionable targets for drug development to treat this devastating brain disease., Introduction Opioid misuse, addiction, and associated overdose deaths remain major public health crises. Worldwide, more than 60 million people currently misuse opioids (1), 21 million people have opioid use disorder [...]

Published
2024
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6. Mouse phenome database: curated data repository with interactive multi-population and multi-trait analyses

Author

Bogue, Molly A., Ball, Robyn L., Walton, David O., Dunn, Matthew H., Kolishovski, Georgi, Berger, Alexander, Lamoureux, Anna, Grubb, Stephen C., Gerring, Matthew, Kim, Matthew, Liang, Hongping, Emerson, Jake, Stearns, Timothy, He, Hao, Mukherjee, Gaurab, Bluis, John, Davis, Sara, Desai, Sejal, Sundberg, Beth, Kadakkuzha, Beena, Kunde-Ramamoorthy, Govindarajan, Philip, Vivek M., and Chesler, Elissa J.

Published
2023
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7. Identifying genetic determinants of inflammatory pain in mice using a large-scale gene-targeted screen

Author

Wotton, Janine M, Peterson, Emma, Flenniken, Ann M, Bains, Rasneer S, Veeraragavan, Surabi, Bower, Lynette R, Bubier, Jason A, Parisien, Marc, Bezginov, Alexandr, Haselimashhadi, Hamed, Mason, Jeremy, Moore, Michayla A, Stewart, Michelle E, Clary, Dave A, Delbarre, Daniel J, Anderson, Laura C, D'Souza, Abigail, Goodwin, Leslie O, Harrison, Mark E, Huang, Ziyue, Mckay, Matthew, Qu, Dawei, Santos, Luis, Srinivasan, Subhiksha, Urban, Rachel, Vukobradovic, Igor, Ward, Christopher S, Willett, Amelia M, Consortium, The International Mouse Phenotyping, Braun, Robert E, Brown, Steve DM, Dickinson, Mary E, Heaney, Jason D, Kumar, Vivek, Lloyd, KC Kent, Mallon, Ann-Marie, McKerlie, Colin, Murray, Stephen A, Nutter, Lauryl MJ, Parkinson, Helen, Seavitt, John R, Wells, Sara, Samaco, Rodney C, Chesler, Elissa J, Smedley, Damian, Diatchenko, Luda, Baumbauer, Kyle M, Young, Erin E, Bonin, Robert P, Mandillo, Silvia, and White, Jacqueline K

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Human Genome, Pain Research, Genetics, Biotechnology, Chronic Pain, 2.1 Biological and endogenous factors, Generic health relevance, Animals, Freund's Adjuvant, Mice, Mice, Knockout, Nociception, Pain, Pain Measurement, Nocifensive behavior, Sensitization, Formalin, Hargreaves, von Frey, Complete Freund's adjuvant, Single-gene knockout mouse, Screen, IMPC, Comorbidity, Autism, International Mouse Phenotyping Consortium, Medical and Health Sciences, Psychology and Cognitive Sciences, Anesthesiology, Biomedical and clinical sciences, Health sciences, Psychology
Abstract

AbstractIdentifying the genetic determinants of pain is a scientific imperative given the magnitude of the global health burden that pain causes. Here, we report a genetic screen for nociception, performed under the auspices of the International Mouse Phenotyping Consortium. A biased set of 110 single-gene knockout mouse strains was screened for 1 or more nociception and hypersensitivity assays, including chemical nociception (formalin) and mechanical and thermal nociception (von Frey filaments and Hargreaves tests, respectively), with or without an inflammatory agent (complete Freund's adjuvant). We identified 13 single-gene knockout strains with altered nocifensive behavior in 1 or more assays. All these novel mouse models are openly available to the scientific community to study gene function. Two of the 13 genes (Gria1 and Htr3a) have been previously reported with nociception-related phenotypes in genetically engineered mouse strains and represent useful benchmarking standards. One of the 13 genes (Cnrip1) is known from human studies to play a role in pain modulation and the knockout mouse reported herein can be used to explore this function further. The remaining 10 genes (Abhd13, Alg6, BC048562, Cgnl1, Cp, Mmp16, Oxa1l, Tecpr2, Trim14, and Trim2) reveal novel pathways involved in nociception and may provide new knowledge to better understand genetic mechanisms of inflammatory pain and to serve as models for therapeutic target validation and drug development.

Published
2022

10. Co-expression of prepulse inhibition and Schizophrenia genes in the mouse and human brain

Author

Aguilar-Pimental, Juan A., Amarie, Oana V., Becker, Lore, Calzada-Wack, Julia, Da Silva-Buttkus, Patricia, Dragano, Nathalia, Kraiger, Markus, Lengger, Christoph, Leuchtenberger, Stefanie, Marschall, Susan, Oestereicher, Manuela A., Rathkolb, Birgit, Sanz-Moreno, Adrián, Seisenberger, Claudia, Spielmann, Nadine, Stoeger, Claudia, Kumar, Vivek, Keskivali, Piia, King, Ruairidh, Haselimashhadi, Hamed, Bezginov, Alexandr, Norris, Clare, Taylor, Sarah, Pimm, Dale, Kelsey, Lois, Berberovic, Zorana, Qu, Dawei, D'Souza, Abigail, Bradaschia, Vivian, Eskandarian, Mohammed, Shang, Xueyuan, Duffin, Kyle, Roberton, Kyle, Xu, Catherine, Baguinat, Gloria, Laurin, Valerie, Lan, Qing, Sleep, Gillian, Lintott, Lauri, Gertsenstein, Marina, Tondat, Sandra, Cruz, Maribelle, Miller, David, Sorg, Tania, Riet, Fabrice, Tolentino, Heather, Tolentino, Todd, Schuchbauer, Mike, Hockenbury, Nichole, Beeman, Karrie, Pedroia, Sheryl, Salazar, Jason, Heffner, Mollie, Hsu, Joanne, Fletcher, Colin, Vanzanten, Maya, Golini, Elisabetta, Seavitt, John R., Lanza, Denise G., Lorenzo, Isabel, Gaspero, Angelina, Rios, Amanda, Garrett, Lillian, Trümbach, Dietrich, Lee, Donghyung, Mandillo, Silvia, Samaco, Rodney, Flenniken, Ann M., Stewart, Michelle, White, Jacqueline K., McKerlie, Colin, Nutter, Lauryl M.J., Vukobradovic, Igor, Veeraragavan, Surabi, Yuva, Lisa, Heaney, Jason D., Dickinson, Mary E., Meziane, Hamid, Hérault, Yann, Wells, Sara, Lloyd, K.C. Kent, Bower, Lynette, Lanoue, Louise, Clary, Dave, Zimprich, Annemarie, Gailus-Durner, Valerie, Fuchs, Helmut, Brown, Steve D.M., Chesler, Elissa J., Wurst, Wolfgang, Hrabě de Angelis, Martin, and Hölter, Sabine M.

Published
2024
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11. Integration of evidence across human and model organism studies: A meeting report

Author

Palmer, Rohan HC, Johnson, Emma C, Won, Hyejung, Polimanti, Renato, Kapoor, Manav, Chitre, Apurva, Bogue, Molly A, Benca‐Bachman, Chelsie E, Parker, Clarissa C, Verma, Anurag, Reynolds, Timothy, Ernst, Jason, Bray, Michael, Bin Kwon, Soo, Lai, Dongbing, Quach, Bryan C, Gaddis, Nathan C, Saba, Laura, Chen, Hao, Hawrylycz, Michael, Zhang, Shan, Zhou, Yuan, Mahaffey, Spencer, Fischer, Christian, Sanchez‐Roige, Sandra, Bandrowski, Anita, Lu, Qing, Shen, Li, Philip, Vivek, Gelernter, Joel, Bierut, Laura J, Hancock, Dana B, Edenberg, Howard J, Johnson, Eric O, Nestler, Eric J, Barr, Peter B, Prins, Pjotr, Smith, Desmond J, Akbarian, Schahram, Thorgeirsson, Thorgeir, Walton, Dave, Baker, Erich, Jacobson, Daniel, Palmer, Abraham A, Miles, Michael, Chesler, Elissa J, Emerson, Jake, Agrawal, Arpana, Martone, Maryann, and Williams, Robert W

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Brain Disorders, Substance Misuse, Human Genome, Networking and Information Technology R&D (NITRD), Drug Abuse (NIDA only), 1.5 Resources and infrastructure (underpinning), 2.6 Resources and infrastructure (aetiology), Good Health and Well Being, cross-species, data integration, drug abuse, genomics, GWAS, model organisms, multi-omic, substance use disorders, working group, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery, Neurosciences
Abstract

The National Institute on Drug Abuse and Joint Institute for Biological Sciences at the Oak Ridge National Laboratory hosted a meeting attended by a diverse group of scientists with expertise in substance use disorders (SUDs), computational biology, and FAIR (Findability, Accessibility, Interoperability, and Reusability) data sharing. The meeting's objective was to discuss and evaluate better strategies to integrate genetic, epigenetic, and 'omics data across human and model organisms to achieve deeper mechanistic insight into SUDs. Specific topics were to (a) evaluate the current state of substance use genetics and genomics research and fundamental gaps, (b) identify opportunities and challenges of integration and sharing across species and data types, (c) identify current tools and resources for integration of genetic, epigenetic, and phenotypic data, (d) discuss steps and impediment related to data integration, and (e) outline future steps to support more effective collaboration-particularly between animal model research communities and human genetics and clinical research teams. This review summarizes key facets of this catalytic discussion with a focus on new opportunities and gaps in resources and knowledge on SUDs.

Published
2021

15. Reproducibility and replicability of rodent phenotyping in preclinical studies

Author

Kafkafi, Neri, Agassi, Joseph, Chesler, Elissa J, Crabbe, John C, Crusio, Wim E, Eilam, David, Gerlai, Robert, Golani, Ilan, Gomez-Marin, Alex, Heller, Ruth, Iraqi, Fuad, Jaljuli, Iman, Karp, Natasha A, Morgan, Hugh, Nicholson, George, Pfaff, Donald W, Richter, S Helene, Stark, Philip B, Stiedl, Oliver, Stodden, Victoria, Tarantino, Lisa M, Tucci, Valter, Valdar, William, Williams, Robert W, Würbel, Hanno, and Benjamini, Yoav

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Behavioral and Social Science, Basic Behavioral and Social Science, Animal Experimentation, Animals, Behavior, Animal, Information Dissemination, Models, Animal, Phenotype, Reproducibility of Results, Research, Research Design, Rodentia, Reproducibility, Replicability, GxE interaction, Validity, Data sharing, False discoveries, Heterogenization, Medical and Health Sciences, Psychology and Cognitive Sciences, Behavioral Science & Comparative Psychology, Biomedical and clinical sciences, Health sciences
Abstract

The scientific community is increasingly concerned with the proportion of published "discoveries" that are not replicated in subsequent studies. The field of rodent behavioral phenotyping was one of the first to raise this concern, and to relate it to other methodological issues: the complex interaction between genotype and environment; the definitions of behavioral constructs; and the use of laboratory mice and rats as model species for investigating human health and disease mechanisms. In January 2015, researchers from various disciplines gathered at Tel Aviv University to discuss these issues. The general consensus was that the issue is prevalent and of concern, and should be addressed at the statistical, methodological and policy levels, but is not so severe as to call into question the validity and the usefulness of model organisms as a whole. Well-organized community efforts, coupled with improved data and metadata sharing, have a key role in identifying specific problems and promoting effective solutions. Replicability is closely related to validity, may affect generalizability and translation of findings, and has important ethical implications.

Published
2018

16. Sex Differences in the Brain Transcriptome Related to Alcohol Effects and Alcohol Use Disorder

Author

Hitzemann, Robert, Bergeson, Susan E., Berman, Ari E., Bubier, Jason A., Chesler, Elissa J., Finn, Deborah A., Hein, Matthew, Hoffman, Paula, Holmes, Andrew, Kisby, Brent R., Lockwood, Denesa, Lodowski, Kerrie H., McManus, Michelle, Owen, Julie A., Ozburn, Angela R., Panthagani, Praneetha, Ponomarev, Igor, Saba, Laura, Tabakoff, Boris, Walchale, Aashlesha, Williams, Robert W., and Phillips, Tamara J.

Published
2022
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17. Co-expression of prepulse inhibition and schizophrenia genes in the mouse and human brain

Author

Garrett, Lillian, primary, Trümbach, Dietrich, additional, Lee, Dongyhung, additional, Mandillo, Silvia, additional, Samaco, Rodney, additional, Flenniken, Ann M., additional, Stewart, Michelle, additional, Aguilar-Pimental, Juan A., additional, Amarie, Oana V., additional, Becker, Lore, additional, Calzada-Wack, Julia, additional, Da Silva-Buttkus, Patricia, additional, Dragano, Nathalia, additional, Kraiger, Markus, additional, Lengger, Christoph, additional, Leuchtenberger, Stefanie, additional, Marschall, Susan, additional, Oestereicher, Manuela A., additional, Rathkolb, Birgit, additional, Sanz-Moreno, Adrián, additional, Seisenberger, Claudia, additional, Spielmann, Nadine, additional, Stoeger, Claudia, additional, Kumar, Vivek, additional, Keskivali, Piia, additional, King, Ruairidh, additional, Haselimashhadi, Hamed, additional, Bezginov, Alexandr, additional, Norris, Clare, additional, Taylor, Sarah, additional, Pimm, Dale, additional, Kelsey, Lois, additional, Berberovic, Zorana, additional, Qu, Dawei, additional, D'Souza, Abigail, additional, Bradaschia, Vivian, additional, Eskandarian, Mohammed, additional, Shang, Xueyuan, additional, Duffin, Kyle, additional, Roberton, Kyle, additional, Xu, Catherine, additional, Baguinat, Gloria, additional, Laurin, Valerie, additional, Lan, Qing, additional, Sleep, Gillian, additional, Lintott, Lauri, additional, Gertsenstein, Marina, additional, Tondat, Sandra, additional, Cruz, Maribelle, additional, Miller, David, additional, Sorg, Tania, additional, Riet, Fabrice, additional, Tolentino, Heather, additional, Tolentino, Todd, additional, Schuchbauer, Mike, additional, Hockenbury, Nichole, additional, Beeman, Karrie, additional, Pedroia, Sheryl, additional, Salazar, Jason, additional, Heffner, Mollie, additional, Hsu, Joanne, additional, Fletcher, Colin, additional, Vanzanten, Maya, additional, Golini, Elisabetta, additional, Seavitt, John R., additional, Lanza, Denise G., additional, Lorenzo, Isabel, additional, Gaspero, Angelina, additional, Rios, Amanda, additional, White, Jacqueline K., additional, McKerlie, Colin, additional, Nutter, Lauryl M.J., additional, Vukobradovic, Igor, additional, Veeraragavan, Surabi, additional, Yuva, Lisa, additional, Heaney, Jason D., additional, Dickinson, Mary E., additional, Meziane, Hamid, additional, Hérault, Yann, additional, Wells, Sara, additional, Lloyd, K.C.Kent, additional, Bower, Lynette, additional, Lanoue, Louise, additional, Clary, Dave, additional, Zimprich, Annemarie, additional, Gailus-Durner, Valerie, additional, Fuchs, Helmut, additional, Brown, Steve D.M., additional, Chesler, Elissa J., additional, Wurst, Wolfgang, additional, Hrabě de Angelis, Martin, additional, and Hölter, Sabine M., additional

Published
2024
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19. Mechanistic Differences in Neuropathic Pain Modalities Revealed by Correlating Behavior with Global Expression Profiling.

Author

Cobos, Enrique J, Nickerson, Chelsea A, Gao, Fuying, Chandran, Vijayendran, Bravo-Caparrós, Inmaculada, González-Cano, Rafael, Riva, Priscilla, Andrews, Nick A, Latremoliere, Alban, Seehus, Corey R, Perazzoli, Gloria, Nieto, Francisco R, Joller, Nicole, Painter, Michio W, Ma, Chi Him Eddie, Omura, Takao, Chesler, Elissa J, Geschwind, Daniel H, Coppola, Giovanni, Rangachari, Manu, Woolf, Clifford J, and Costigan, Michael

Subjects
T-Lymphocytes, Macrophages, Animals, Mice, Inbred C57BL, Mice, Transgenic, Mice, Neuralgia, Hyperalgesia, Behavior, Animal, Touch, Male, TRPV Cation Channels, Cold Temperature, Sensory Receptor Cells, Transcriptome, T cells, TrpV1, WCGNA, cold allodynia, gene expression, immune system, macrophages, neuropathic pain, tactile allodynia, transcript profiling, Inbred C57BL, Transgenic, Behavior, Animal, Pain Research, Chronic Pain, Peripheral Neuropathy, Neurodegenerative, Neurosciences, Clinical Research, 2.1 Biological and endogenous factors, Neurological, Pain Conditions - Chronic, Biochemistry and Cell Biology, Medical Physiology
Abstract

Chronic neuropathic pain is a major morbidity of neural injury, yet its mechanisms are incompletely understood. Hypersensitivity to previously non-noxious stimuli (allodynia) is a common symptom. Here, we demonstrate that the onset of cold hypersensitivity precedes tactile allodynia in a model of partial nerve injury, and this temporal divergence was associated with major differences in global gene expression in innervating dorsal root ganglia. Transcripts whose expression change correlates with the onset of cold allodynia were nociceptor related, whereas those correlating with tactile hypersensitivity were immune cell centric. Ablation of TrpV1 lineage nociceptors resulted in mice that did not acquire cold allodynia but developed normal tactile hypersensitivity, whereas depletion of macrophages or T cells reduced neuropathic tactile allodynia but not cold hypersensitivity. We conclude that neuropathic pain incorporates reactive processes of sensory neurons and immune cells, each leading to distinct forms of hypersensitivity, potentially allowing drug development targeted to each pain type.

Published
2018

22. Prevalence of sexual dimorphism in mammalian phenotypic traits

Author

Karp, Natasha A, Mason, Jeremy, Beaudet, Arthur L, Benjamini, Yoav, Bower, Lynette, Braun, Robert E, Brown, Steve DM, Chesler, Elissa J, Dickinson, Mary E, Flenniken, Ann M, Fuchs, Helmut, Angelis, Martin Hrabe de, Gao, Xiang, Guo, Shiying, Greenaway, Simon, Heller, Ruth, Herault, Yann, Justice, Monica J, Kurbatova, Natalja, Lelliott, Christopher J, Lloyd, KC Kent, Mallon, Ann-Marie, Mank, Judith E, Masuya, Hiroshi, McKerlie, Colin, Meehan, Terrence F, Mott, Richard F, Murray, Stephen A, Parkinson, Helen, Ramirez-Solis, Ramiro, Santos, Luis, Seavitt, John R, Smedley, Damian, Sorg, Tania, Speak, Anneliese O, Steel, Karen P, Svenson, Karen L, Wakana, Shigeharu, West, David, Wells, Sara, Westerberg, Henrik, Yaacoby, Shay, and White, Jacqueline K

Subjects
Biological Psychology, Biological Sciences, Biomedical and Clinical Sciences, Psychology, Women's Health, Genetics, Estrogen, 2.1 Biological and endogenous factors, Infection, Generic health relevance, Animals, Body Weight, Female, Genes, Modifier, Genotype, Mammals, Mice, Phenotype, Quantitative Trait, Heritable, Sex Characteristics, International Mouse Phenotyping Consortium
Abstract

The role of sex in biomedical studies has often been overlooked, despite evidence of sexually dimorphic effects in some biological studies. Here, we used high-throughput phenotype data from 14,250 wildtype and 40,192 mutant mice (representing 2,186 knockout lines), analysed for up to 234 traits, and found a large proportion of mammalian traits both in wildtype and mutants are influenced by sex. This result has implications for interpreting disease phenotypes in animal models and humans.

Published
2017

26. Characterization of genetically complex Collaborative Cross mouse strains that model divergent locomotor activating and reinforcing properties of cocaine

Author

Schoenrock, Sarah A., Kumar, Padam, Gómez-A, Alexander, Dickson, Price E., Kim, Sam-Moon, Bailey, Lauren, Neira, Sofia, Riker, Kyle D., Farrington, Joseph, Gaines, Christiann H., Khan, Saad, Wilcox, Troy D., Roy, Tyler A., Leonardo, Michael R., Olson, Ashley A., Gagnon, Leona H., Philip, Vivek M., Valdar, William, de Villena, Fernando Pardo-Manuel, Jentsch, James D., Logan, Ryan W., McClung, Colleen A., Robinson, Donita L., Chesler, Elissa J., and Tarantino, Lisa M.

Published
2020
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27. Applying the ARRIVE Guidelines to an In Vivo Database.

Author

Karp, Natasha A, Meehan, Terry F, Morgan, Hugh, Mason, Jeremy C, Blake, Andrew, Kurbatova, Natalja, Smedley, Damian, Jacobsen, Julius, Mott, Richard F, Iyer, Vivek, Matthews, Peter, Melvin, David G, Wells, Sara, Flenniken, Ann M, Masuya, Hiroshi, Wakana, Shigeharu, White, Jacqueline K, Lloyd, KC Kent, Reynolds, Corey L, Paylor, Richard, West, David B, Svenson, Karen L, Chesler, Elissa J, de Angelis, Martin Hrabě, Tocchini-Valentini, Glauco P, Sorg, Tania, Herault, Yann, Parkinson, Helen, Mallon, Ann-Marie, and Brown, Steve DM

Subjects
Animals, Mice, Animal Experimentation, Phenotype, Guidelines as Topic, Databases as Topic, Developmental Biology, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences
Abstract

The Animal Research: Reporting of In Vivo Experiments (ARRIVE) guidelines were developed to address the lack of reproducibility in biomedical animal studies and improve the communication of research findings. While intended to guide the preparation of peer-reviewed manuscripts, the principles of transparent reporting are also fundamental for in vivo databases. Here, we describe the benefits and challenges of applying the guidelines for the International Mouse Phenotyping Consortium (IMPC), whose goal is to produce and phenotype 20,000 knockout mouse strains in a reproducible manner across ten research centres. In addition to ensuring the transparency and reproducibility of the IMPC, the solutions to the challenges of applying the ARRIVE guidelines in the context of IMPC will provide a resource to help guide similar initiatives in the future.

Published
2015

31. GenomeMUSter mouse genetic variation service enables multitrait, multipopulation data integration and analysis

Author

Ball, Robyn L., primary, Bogue, Molly A., additional, Liang, Hongping, additional, Srivastava, Anuj, additional, Ashbrook, David G., additional, Lamoureux, Anna, additional, Gerring, Matthew W., additional, Hatoum, Alexander S., additional, Kim, Matthew J., additional, He, Hao, additional, Emerson, Jake, additional, Berger, Alexander K., additional, Walton, David O., additional, Sheppard, Keith, additional, El Kassaby, Baha, additional, Castellanos, Francisco, additional, Kunde-Ramamoorthy, Govindarajan, additional, Lu, Lu, additional, Bluis, John, additional, Desai, Sejal, additional, Sundberg, Beth A., additional, Peltz, Gary, additional, Fang, Zhuoqing, additional, Churchill, Gary A., additional, Williams, Robert W., additional, Agrawal, Arpana, additional, Bult, Carol J., additional, Philip, Vivek M., additional, and Chesler, Elissa J., additional

Published
2024
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32. Discovery and validation of genes driving drug‐intake and related behavioral traits in mice

Author

Roy, Tyler A., primary, Bubier, Jason A., additional, Dickson, Price E., additional, Wilcox, Troy D., additional, Ndukum, Juliet, additional, Clark, James W., additional, Sukoff Rizzo, Stacey J., additional, Crabbe, John C., additional, Denegre, James M., additional, Svenson, Karen L., additional, Braun, Robert E., additional, Kumar, Vivek, additional, Murray, Stephen A., additional, White, Jacqueline K., additional, Philip, Vivek M., additional, and Chesler, Elissa J., additional

Published
2024
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33. High-Resolution Sex-Specific Linkage Maps of the Mouse Reveal Polarized Distribution of Crossovers in Male Germline

Author

Liu, Eric Yi, Morgan, Andrew P, Chesler, Elissa J, Wang, Wei, Churchill, Gary A, and de Villena, Fernando Pardo-Manuel

Subjects
Biotechnology, Contraception/Reproduction, Genetics, Human Genome, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Animals, Chromosome Mapping, Crossing Over, Genetic, Female, Genomics, Genotyping Techniques, Male, Mice, Pedigree, Sex Characteristics, Siblings, Species Specificity, Spermatozoa, recombination, linkage map, sex effects, cold regions, mouse CC, Developmental Biology
Abstract

Since the publication of the first comprehensive linkage map for the laboratory mouse, the architecture of recombination as a basic biological process has become amenable to investigation in mammalian model organisms. Here we take advantage of high-density genotyping and the unique pedigree structure of the incipient Collaborative Cross to investigate the roles of sex and genetic background in mammalian recombination. Our results confirm the observation that map length is longer when measured through female meiosis than through male meiosis, but we find that this difference is modified by genotype at loci on both the X chromosome and the autosomes. In addition, we report a striking concentration of crossovers in the distal ends of autosomes in male meiosis that is absent in female meiosis. The presence of this pattern in both single- and double-recombinant chromosomes, combined with the absence of a corresponding asymmetry in the distribution of double-strand breaks, indicates a regulated sequence of events specific to male meiosis that is anchored by chromosome ends. This pattern is consistent with the timing of chromosome pairing and evolutionary constraints on male recombination. Finally, we identify large regions of reduced crossover frequency that together encompass 5% of the genome. Many of these "cold regions" are enriched for segmental duplications, suggesting an inverse local correlation between recombination rate and mutation rate for large copy number variants.

Published
2014

34. Tmod2 Is a Regulator of Cocaine Responses through Control of Striatal and Cortical Excitability and Drug-Induced Plasticity.

Author

Mitra, Arojit, Deats, Sean P., Dickson, Price E., Jiuhe Zhu, Gardin, Justin, Nieman, Brian J., Henkelman, R. Mark, Nien-Pei Tsai, Chesler, Elissa J., Zhong-Wei Zhang, and Kumar, Vivek

Subjects
MEDIUM spiny neurons, NUCLEUS accumbens, DRUG side effects, KNOCKOUT mice, COCAINE, NEUROPLASTICITY, DOPAMINE receptors
Abstract

Drugs of abuse induce neuroadaptations, including synaptic plasticity, that are critical for transition to addiction, and genes and pathways that regulate these neuroadaptations are potential therapeutic targets. Tropomodulin 2 (Tmod2) is an actin-regulating gene that plays an important role in synapse maturation and dendritic arborization and has been implicated in substance abuse and intellectual disability in humans. Here, we mine the KOMP2 data and find that Tmod2 knock-out mice show emotionality phenotypes that are predictive of addiction vulnerability. Detailed addiction phenotyping shows that Tmod2 deletion does not affect the acute locomotor response to cocaine administration. However, sensitized locomotor responses are highly attenuated in these knock-outs, indicating perturbed drug-induced plasticity. In addition, Tmod2 mutant animals do not self-administer cocaine indicating lack of hedonic responses to cocaine. Whole-brain MR imaging shows differences in brain volume across multiple regions, although transcriptomic experiments did not reveal perturbations in gene coexpression networks. Detailed electrophysiological characterization of Tmod2 KO neurons showed increased spontaneous firing rate of early postnatal and adult cortical and striatal neurons. Cocaine-induced synaptic plasticity that is critical for sensitization is either missing or reciprocal in Tmod2 KO nucleus accumbens shell medium spiny neurons, providing a mechanistic explanation of the cocaine response phenotypes. Combined, these data, collected from both males and females, provide compelling evidence that Tmod2 is a major regulator of plasticity in the mesolimbic system and regulates the reinforcing and addictive properties of cocaine. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Variable Sensitivity to Noxious Heat Is Mediated by Differential Expression of the CGRP Gene

Author

Mogil, Jeffrey S., Miermeister, Frank, Seifert, Frank, Strasburg, Kate, Zimmermann, Katharina, Reinold, Heiko, Austin, Jean-Sebastien, Bernardini, Nadia, Chesler, Elissa J., Hofmann, Heiko A., Hordo, Christian, Messlinger, Karl, Rankin, Andrew L., Ritchie, Jennifer, Siegling, Angela, Smith, Shad B., Sotocinal, Susana, Vater, Axel, Lehto, Sonya G., Klussmann, Sven, Quirion, Remi, Michaelis, Martin, Devor, Marshall, Reeh, Peter W., and McEwen, Bruce S.

Published
2005

38. GenomeMUSter mouse genetic variation service enables multi-trait, multi-population data integration and analyses

Author

Ball, Robyn L., primary, Bogue, Molly A., additional, Liang, Hongping, additional, Srivastava, Anuj, additional, Ashbrook, David G., additional, Lamoureux, Anna, additional, Gerring, Matthew W., additional, Hatoum, Alexander S., additional, Kim, Matthew, additional, He, Hao, additional, Emerson, Jake, additional, Berger, Alexander K., additional, Walton, David O., additional, Sheppard, Keith, additional, Kassaby, Baha El, additional, Castellanos, Francisco, additional, Kunde-Ramamoorthy, Govind, additional, Lu, Lu, additional, Bluis, John, additional, Desai, Sejal, additional, Sundberg, Beth A., additional, Peltz, Gary, additional, Fang, Zhuoqing, additional, Churchill, Gary A., additional, Williams, Robert W., additional, Agrawal, Arpana, additional, Bult, Carol J., additional, Philip, Vivek M., additional, and Chesler, Elissa J., additional

Published
2023
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50. A Context-Driven Gene Prioritization Method for Web-Based Functional Genomics

Author

Jay, Jeremy J., Baker, Erich J., Chesler, Elissa J., Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Doug, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Istrail, Sorin, editor, Pevzner, Pavel, editor, Waterman, Michael S., editor, Cai, Zhipeng, editor, Eulenstein, Oliver, editor, Janies, Daniel, editor, and Schwartz, Daniel, editor

Published
2013
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