The genetic complexity of muscle structure and function will be investigated using the free-living nematode Caenorhabditis elegans. Mutants defective for muscle function will be isolated and analyzed genetically, biochemically, and anatomically. Such mutants identify genes required for development of a functional muscle cell. The genes encoding paramyosin and myosin light chain proteins will be investigated directly using recombinant DNA techniques. The molecular interactions responsible for the heterozygous mutant phenotype of dominant mutations affecting a myosin heavy chain gene will be identified. The long range goals are to identify genes and proteins required for muscle function, and to understand how these components function during sarcomere assembly and contraction. Genetic properties of the nematode transposable element Tcl will be investigated. The nucleotide sequences of Tcl insertions and excisions will be determined. The genetic basis for strain-specific and tissue-specific activity of Tcl will be studied. The long range goals are to understand the biological roles for transposable elements, and to use Tcl as an investigative tool to study the differences between basic genetic mechanisms of germ cells and somatic cells. This work contributes to the national health by describing the molecular mechanisms that underlie fundamental cellular and genetic phenomena.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM030132-05
Application #
3277735
Study Section
Genetics Study Section (GEN)
Project Start
1982-02-01
Project End
1988-08-31
Budget Start
1986-09-01
Budget End
1987-08-31
Support Year
5
Fiscal Year
1986
Total Cost
Indirect Cost
Name
University of Wisconsin Madison
Department
Type
Earth Sciences/Resources
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715
Rushforth, A M; White, C C; Anderson, P (1998) Functions of the Caenorhabditis elegans regulatory myosin light chain genes mlc-1 and mlc-2. Genetics 150:1067-77
Maryon, E B; Saari, B; Anderson, P (1998) Muscle-specific functions of ryanodine receptor channels in Caenorhabditis elegans. J Cell Sci 111 ( Pt 19):2885-95
Rushforth, A M; Anderson, P (1996) Splicing removes the Caenorhabditis elegans transposon Tc1 from most mutant pre-mRNAs. Mol Cell Biol 16:422-9
Maryon, E B; Coronado, R; Anderson, P (1996) unc-68 encodes a ryanodine receptor involved in regulating C. elegans body-wall muscle contraction. J Cell Biol 134:885-93
Rushforth, A M; Saari, B; Anderson, P (1993) Site-selected insertion of the transposon Tc1 into a Caenorhabditis elegans myosin light chain gene. Mol Cell Biol 13:902-10
Kim, Y K; Valdivia, H H; Maryon, E B et al. (1992) High molecular weight proteins in the nematode C. elegans bind [3H]ryanodine and form a large conductance channel. Biophys J 63:1379-84
Bejsovec, A; Anderson, P (1990) Functions of the myosin ATP and actin binding sites are required for C. elegans thick filament assembly. Cell 60:133-40
Collins, J; Forbes, E; Anderson, P (1989) The Tc3 family of transposable genetic elements in Caenorhabditis elegans. Genetics 121:47-55
Eide, D; Anderson, P (1988) Insertion and excision of Caenorhabditis elegans transposable element Tc1. Mol Cell Biol 8:737-46
Pulak, R A; Anderson, P (1988) Structures of spontaneous deletions in Caenorhabditis elegans. Mol Cell Biol 8:3748-54

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