High impact information on unc-87

• A genomic clone was isolated that alleviates the mutant phenotype when introduced into unc-87 mutants [1].
• Analysis of the genomic sequence and of various transcripts represented in a cDNA library suggest that unc-87 mRNAs are subject to alternative splicing [1].
• To address the possibility that this disorganization is due to deterioration of the muscle as a result of contraction, we introduced into the unc-87 mutant background a mutation that decreases myosin heavy chain activity but does not substantially affect muscle structure [2].
• Mutations in the unc-87 gene of Caenorhabditis elegans cause disorganization of the myofilament lattice in adult bodywall muscle [2].
• The improved muscle structure and motility of the double mutants are consistent with the hypothesis that at least part of the disorganization phenotype of unc-87 mutants is a consequence of the wild-type levels of force generated during muscle contraction [2].

Co-localisations of unc-87

• The Caenorhabditis elegans unc-87 gene product is essential for the maintenance of the nematode body wall muscle where it is found colocalized with actin in the I band [3].

Analytical, diagnostic and therapeutic context of unc-87

• Immunohistochemistry of wildtype and mutant animals with antibodies to an unc-87 fusion protein indicates that the gene product is localized to the I-band of bodywall muscle [1].
• Through SDS-PAGE, a stress-related protein UNC-87 was found in osmotically desiccated IJs exposed to 40 degrees C for 3, 6, and 8 h, whose survival rates were 98.9+/-1.43, 78.5+/-5.87 and 20.9+/-4.93%, respectively [4].

References