This proposal seeks to competitively renew funding for infrastructure, personnel, and resources in support of the MMRRC at the University of California (UC) Davis (UCD-MMRRC). The UCD-MMRRC, alongside 2 centers at the University of Missouri-Columbia and University of North Carolina-Chapel Hill, and an Informatics, Coordination, and Service Center (ICSC) at The Jackson Laboratory, serves as the distribution archives and data center for the MMRRC National Program. Since its inception 10 years ago, the UCD- MMRRC has been one of the primary mutant mouse archive and distribution repositories in the world. We are the largest archive of three centers, with an inventory of over 28,500 mutant mouse lines representing ~98% of all live colonies, germplasm, and/or embryonic stem (ES) cells in the system. The UCD-MMRRC has fulfilled nearly 6000 orders from more than 2000 investigators at 500 institutions in 30 countries. We have also been a leader in innovation and resource development for the system, introducing new products (e.g., gene trap ES cells) and initiating new services (e.g., blastocyst injection, ICSI) that have added scientific value to mouse models and enhanced utilization of the MMRRC by researchers. UCD-MMRRC has leveraged its infrastructure and expertise to extend its service role by contracting with NIH institutes, biotechnology companies, and several organizations to archive, distribute, custom breed, genotype, and phenotype 1000's of additional ES cell mutants, BAC-transgenic, CRE, ENU-induced, and other mutant mouse collections. In addition, we have worked with the Centers and NIH program staff and developed and implemented advertising and marketing strategies, database management and informatics applications, website and online resources, customer and user services, operating procedures and policies, and shared governance of the national program.
The UCD-MMRRC serves a primary role in ensuring that valuable mouse models of human disease, development, and behavioral abnormalities created in research laboratories are shared broadly among the biomedical scientific community. As a regionally-distributed repository and distribution archive, the UCD- MMRRC provides expertise, infrastructure, resources and services to preserve mouse strains in perpetuity, protect them from catastrophic loss, avoid genetic and phenotypic drift, and prevent pathogenic contamination and disease. By enabling availability and access of such valuable mouse models to the entire research community, the UCD-MMRRC fosters and promotes the discovery of new diagnostics, treatments, and prevention strategies against human diseases.
|Meehan, Terrence F; Conte, Nathalie; West, David B et al. (2017) Disease model discovery from 3,328 gene knockouts by The International Mouse Phenotyping Consortium. Nat Genet 49:1231-1238|
|Fidler, Trevor P; Middleton, Elizabeth A; Rowley, Jesse W et al. (2017) Glucose Transporter 3 Potentiates Degranulation and Is Required for Platelet Activation. Arterioscler Thromb Vasc Biol 37:1628-1639|
|Jung, Chris J; Zhang, Junli; Trenchard, Elizabeth et al. (2017) Efficient gene targeting in mouse zygotes mediated by CRISPR/Cas9-protein. Transgenic Res 26:263-277|
|Green, Adrian J; Graham, James L; Gonzalez, Eduardo A et al. (2017) Perinatal triphenyl phosphate exposure accelerates type 2 diabetes onset and increases adipose accumulation in UCD-type 2 diabetes mellitus rats. Reprod Toxicol 68:119-129|
|Vogel Ciernia, Annie; Pride, Michael C; Durbin-Johnson, Blythe et al. (2017) Early motor phenotype detection in a female mouse model of Rett syndrome is improved by cross-fostering. Hum Mol Genet 26:1839-1854|
|Moshiri, Ala; Humpal, Devin; Leonard, Brian C et al. (2017) Arap1 Deficiency Causes Photoreceptor Degeneration in Mice. Invest Ophthalmol Vis Sci 58:1709-1718|
|Fidler, Trevor P; Campbell, Robert A; Funari, Trevor et al. (2017) Deletion of GLUT1 and GLUT3 Reveals Multiple Roles for Glucose Metabolism in Platelet and Megakaryocyte Function. Cell Rep 20:881-894|
|Trindade-da-Silva, Carlos Antonio; Bettaieb, Ahmed; Napimoga, Marcelo Henrique et al. (2017) Soluble Epoxide Hydrolase Pharmacological Inhibition Decreases Alveolar Bone Loss by Modulating Host Inflammatory Response, RANK-Related Signaling, Endoplasmic Reticulum Stress, and Apoptosis. J Pharmacol Exp Ther 361:408-416|
|Lee, Linda L; Aung, Hnin H; Wilson, Dennis W et al. (2017) Triglyceride-rich lipoprotein lipolysis products increase blood-brain barrier transfer coefficient and induce astrocyte lipid droplets and cell stress. Am J Physiol Cell Physiol 312:C500-C516|
|Roberts, Megan N; Wallace, Marita A; Tomilov, Alexey A et al. (2017) A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice. Cell Metab 26:539-546.e5|
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