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Author Notes:

Address correspondence to: Don Moerman (moerman@zoology.ubc.ca)

Some strains used in this work were provided by the Caenorhabditis Genetics Center, which is supported by the National Center for Research Resources of the National Institutes of Health. We thank the C. elegans Gene Knockout Consortium for providing the pxl-1 knockout strain VC1012. We also like thank Edward Hedgecock for use of the strain NJ0784 and David Hall and Zeynep Altun for analysis of pxl-1 expression in the pharynx.

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Research Funding:

This research was supported by grants from the Canadian Institute for Health Research and the National Science and Engineering Research Council of Canada to D.G.M. and Grant AR052133 from the National Institutes of Health to G.M.B. D.G.M. also received support from the Canadian Institute for Advanced Research.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Cell Biology
  • EXTRACELLULAR-MATRIX DEGRADATION
  • INTEGRIN ADHESION COMPLEXES
  • BODY-WALL MUSCLE
  • C-ELEGANS
  • FOCAL ADHESIONS
  • LIM DOMAIN
  • ATTACHMENT STRUCTURES
  • PROTEIN PAXILLIN
  • ADAPTER PROTEIN
  • THICK FILAMENTS

The Caenorhabditis elegans paxillin orthologue, PXL-1, is required for pharyngeal muscle contraction and for viability

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Journal Title:

Molecular Biology of the Cell

Volume:

Volume 22, Number 14

Publisher:

, Pages 2551-2563

Type of Work:

Article | Final Publisher PDF

Abstract:

We have identified the gene C28H8.6 (pxl-1) as the Caenorhabditis elegans orthologue of vertebrate paxillin. PXL-1 contains the four C-terminal LIM domains conserved in paxillin across all species and three of the five LD motifs found in the N-terminal half of most paxillins. In body wall muscle, PXL-1 antibodies and a full-length green fluorescent protein translational fusion localize to adhesion sites in the sarcomere, the functional repeat unit in muscle responsible for contraction. PXL-1 also localizes to ring-shaped structures near the sarcolemma in pharyngeal muscle corresponding to podosome-like sites of actin attachment. Our analysis of a loss-of-function allele of pxl-1, ok1483, shows that loss of paxillin leads to early larval arrested animals with paralyzed pharyngeal muscles and eventual lethality, presumably due to an inability to feed. We rescued the mutant phenotype by expressing paxillin solely in the pharynx and found that these animals survived and are essentially wild type in movement and body wall muscle structure. This indicates a differential requirement for paxillin in these two types of muscle. In pharyngeal muscle it is essential for contraction, whereas in body wall muscle it is dispensable for filament assembly, sarcomere stability, and ultimately movement.

Copyright information:

© 2011 Warner et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License (http://creativecommons.org/licenses/by-nc-sa/3.0/).

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