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Resources » Paper

Waddle JA et al. (1991) International C. elegans Meeting "MOLECULAR ANALYSIS OF THE GENES ENCODING AN ACTIN-CAPPING PROTEIN IN C. ELEGANS."

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  • Comments on Waddle JA et al. (1991) International C. elegans Meeting "MOLECULAR ANALYSIS OF THE GENES ENCODING AN ACTIN-CAPPING PROTEIN IN C. ELEGANS." (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00021014

    Waddle JA, Cooper JA, & Waterston RH (1991). MOLECULAR ANALYSIS OF THE GENES ENCODING AN ACTIN-CAPPING PROTEIN IN C. ELEGANS presented in International C. elegans Meeting. Unpublished information; cite only with author permission.

    Actin capplng protein regulates the assembly of actin filaments in vitro. This heterodimeric protein has been found in all eukaryotic cells thus far examined. The actin capping protein of vertebrate skeletal muscle (CapZ) ls found at the Z-line, where it probably binds to the barbed ends of filaments(1). In S. cerevisiae deletion of the subunit of capping protein disrupts the organization of the actln cytoskeleton(2). In order to understand the function of capping protein ln organizing the actin cytoskeleton in muscle and non-muscle cells, we have initiated a study of this protein ln C. elegans. The nematode capping protein genes were identifed using the PCR and oligonucleotides based on conserved protein sequences from other species. Genomic and cDNA clones for the alpha (cap-l) and (cap-2) subunit genes were sequenced. We have determined the physical and genetic map positions of these two genes. Cap-1 is located between deb- l and unc-24 on LGIV; the cap-2 interval is defined by the right breakpoint of mnDf66 and the left breakpoint of mnDf87 on LGII. A mixture of the nematode alpha and subunits, expressed as fusion proteins ln bacteria, have activity characteristlc of capping protein in actin polymerization assays. We are currently screening for recessive lethal mutations in cap-2 by ldentifying those mutations whlch fall to complement mnDf90 but are covered by mnDf66 and mnDf87. The interval defined by this deficiency complementation pattern is probably less than 0.1 m.u. Any mutations satisfying these criteria will be tested by transformation rescue with a wild type copy of the cap-2 gene.


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