Abstract

The long term goal of this project is to understand how skeletal muscle differentiation is regulated.
The specific aims are to determine how certain growth factors repress muscle differentiation, how proliferating myoblasts become """"""""committed"""""""" to a post-mitotic state when specific mitogens are withdrawn, and how the M- and B-creatine kinase genes are regulated during terminal muscle differentiation. Major methodologies used in this project are: cell culture, growth factor receptor analysis, mutant selection, somatic genetics, gene cloning, gene sequencing, gene structural analysis, fusion and mutant gene construction, introduction of genes into cells, and analysis of endogenous and exogenous gene expression. Health-related aspects of the project are its contribution toward the understanding of normal development and gene expression. Possible medical applications are to developmental disorders, to genetic diseases, to degenerative muscle diseases, to normal and neoplastic growth regulation and to general clinical diagnostic procedures involving M- and B-creatine kinase.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases (NIADDK)
Type
Research Project (R01)
Project #
2R01AM018860-09
Application #
3151167
Study Section
Molecular Cytology Study Section (CTY)
Project Start
1976-05-01
Project End
1987-11-30
Budget Start
1984-12-01
Budget End
1985-11-30
Support Year
9
Fiscal Year
1985
Total Cost
Indirect Cost

  Institution

Name
University of Washington
Department
Type
Schools of Medicine
DUNS #
135646524
City
Seattle
State
WA
Country
United States
Zip Code
98195

  Publications

Buskin, J N; Gregory, D L; La-Framboise, W A et al. (1996) Harvest protocol to reduce variability of soluble enzyme yield from cultured cells. Biotechniques 20:92-4, 96-8, 100
Apone, S; Hauschka, S D (1995) Muscle gene E-box control elements. Evidence for quantitatively different transcriptional activities and the binding of distinct regulatory factors. J Biol Chem 270:21420-7
Olwin, B B; Hauschka, S D (1990) Fibroblast growth factor receptor levels decrease during chick embryogenesis. J Cell Biol 110:503-9
Johnson, J E; Gartside, C L; Jaynes, J B et al. (1989) Expression of a transfected mouse muscle-creatine kinase gene is induced upon growth factor deprivation of myogenic but not of nonmyogenic cells. Dev Biol 134:258-62
Buskin, J N; Hauschka, S D (1989) Identification of a myocyte nuclear factor that binds to the muscle-specific enhancer of the mouse muscle creatine kinase gene. Mol Cell Biol 9:2627-40
Jaynes, J B; Johnson, J E; Buskin, J N et al. (1988) The muscle creatine kinase gene is regulated by multiple upstream elements, including a muscle-specific enhancer. Mol Cell Biol 8:62-70
Olwin, B B; Hauschka, S D (1988) Cell surface fibroblast growth factor and epidermal growth factor receptors are permanently lost during skeletal muscle terminal differentiation in culture. J Cell Biol 107:761-9
Seed, J; Olwin, B B; Hauschka, S D (1988) Fibroblast growth factor levels in the whole embryo and limb bud during chick development. Dev Biol 128:50-7
Seed, J; Hauschka, S D (1988) Clonal analysis of vertebrate myogenesis. VIII. Fibroblasts growth factor (FGF)-dependent and FGF-independent muscle colony types during chick wing development. Dev Biol 128:40-9
Clegg, C H; Hauschka, S D (1987) Heterokaryon analysis of muscle differentiation: regulation of the postmitotic state. J Cell Biol 105:937-47

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