Zebrafish is a premiere organism to study vertebrate development, physiology, behavior, genetics and disease. Powerful techniques allow efficient generation and recovery of zebrafish mutations affecting genes that regulate developmental patterning, organogenesis, physiology and behavior. Recent advances make it easy to study gene function in transgenic zebrafish and with antisense oligonucleotides. The functions of many, if not most, of these genes are conserved among vertebrate groups. Thus, analysis of zebrafish mutations provides insights into gene function in other vertebrates, including humans. The Zebrafish International Resource Center has been established as a repository that provides animals, materials and services to the research community. This proposal seeks continued funding 1) to provide a centralized repository for zebrafish genetic stocks and research materials;2) to provide consultation and pathology services;and 3) to develop improved zebrafish husbandry methods. These materials, services and information will be made widely available to the research community.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Animal (Mammalian and Nonmammalian) Model, and Animal and Biological Material Resource Grants (P40)
Project #
5P40RR012546-13
Application #
7940957
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Program Officer
Chang, Michael
Project Start
1998-05-01
Project End
2013-04-30
Budget Start
2010-05-01
Budget End
2011-04-30
Support Year
13
Fiscal Year
2010
Total Cost
$1,845,054
Indirect Cost
Name
University of Oregon
Department
Neurosciences
Type
Schools of Arts and Sciences
DUNS #
948117312
City
Eugene
State
OR
Country
United States
Zip Code
97403
Burns, A R; Watral, V; Sichel, S et al. (2018) Transmission of a common intestinal neoplasm in zebrafish by cohabitation. J Fish Dis 41:569-579
Gistelinck, Charlotte; Kwon, Ronald Y; Malfait, Fransiska et al. (2018) Zebrafish type I collagen mutants faithfully recapitulate human type I collagenopathies. Proc Natl Acad Sci U S A 115:E8037-E8046
Louie, Ke'ale W; Saera-Vila, Alfonso; Kish, Phillip E et al. (2017) Temporally distinct transcriptional regulation of myocyte dedifferentiation and Myofiber growth during muscle regeneration. BMC Genomics 18:854
Hur, Matthew; Gistelinck, Charlotte A; Huber, Philippe et al. (2017) MicroCT-based phenomics in the zebrafish skeleton reveals virtues of deep phenotyping in a distributed organ system. Elife 6:
Varga, Zoltán M; Wilson, Carole; Alestrøm, Peter (2016) European Zebrafish Meeting 2015 Husbandry Session Report. Zebrafish 13:230-1
Sukeena, Joshua M; Galicia, Carlos A; Wilson, Jacob D et al. (2016) Characterization and Evolution of the Spotted Gar Retina. J Exp Zool B Mol Dev Evol 326:403-421
Gistelinck, Charlotte; Witten, Paul Eckhard; Huysseune, Ann et al. (2016) Loss of Type I Collagen Telopeptide Lysyl Hydroxylation Causes Musculoskeletal Abnormalities in a Zebrafish Model of Bruck Syndrome. J Bone Miner Res 31:1930-1942
Saera-Vila, Alfonso; Kish, Phillip E; Kahana, Alon (2016) Fgf regulates dedifferentiation during skeletal muscle regeneration in adult zebrafish. Cell Signal 28:1196-204
Hanovice, Nicholas J; McMains, Emily; Gross, Jeffrey M (2016) A GAL4-inducible transgenic tool kit for the in vivo modulation of Rho GTPase activity in zebrafish. Dev Dyn 245:844-53
Sinha, Raunak; Lee, Amy; Rieke, Fred et al. (2016) Lack of CaBP1/Caldendrin or CaBP2 Leads to Altered Ganglion Cell Responses. eNeuro 3:

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