Literature DB >> 7151169

Mutations in the unc-54 myosin heavy chain gene of Caenorhabditis elegans that alter contractility but not muscle structure.

D G Moerman, S Plurad, R H Waterston, D L Baillie.   

Abstract

Reversion analysis of mutants of unc-22 IV, a gene affecting muscle structure and function in Caenorhabditis elegans, led to the isolation of six extragenic dominant suppressors of the "twitching" phenotype of unc-22 mutants. All six suppressors are new alleles of unc-54 I, the major body wall myosin heavy chain gene. Homozygous suppressor strains are slow, stiff and have normal muscle structure, whereas previously identified unc-54 alleles confer flaccid paralysis and drastic reduction in thick filament number and organization. Placement of the three suppressor mutations s74, s77 and s95 on the genetic fine structure map of unc-54 demonstrates that they are clustered near the right end of the map. Since this end of the gene corresponds to the 5' end of the coding sequence, these suppressor mutations probably result in amino acid substitutions in the globular head of the myosin molecule, and should be of value in studies of myosin force generation.

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Year:  1982        PMID: 7151169     DOI: 10.1016/0092-8674(82)90439-1

Source DB:  PubMed          Journal:  Cell        ISSN: 0092-8674            Impact factor:   41.582


  48 in total

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4.  Suppressors of the organ-specific differentiation gene pha-1 of Caenorhabditis elegans.

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Review 7.  The behavioral genetics of Caenorhabditis elegans.

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8.  Troponin I controls ovulatory contraction of non-striated actomyosin networks in the C. elegans somatic gonad.

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9.  Caenorhabditis elegans unc-82 encodes a serine/threonine kinase important for myosin filament organization in muscle during growth.

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10.  Myosin isozymes in avian skeletal muscles. I. Sequential expression of myosin isozymes in developing chicken pectoralis muscles.

Authors:  S Lowey; P A Benfield; D D LeBlanc; G S Waller
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