4.4 Article

Genetics of Extracellular Matrix Remodeling During Organ Growth Using the Caenorhabditis elegans Pharynx Model

Journal

GENETICS
Volume 186, Issue 3, Pages 969-U328

Publisher

GENETICS SOCIETY AMERICA
DOI: 10.1534/genetics.110.120519

Keywords

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Funding

  1. Vetenskapsradet
  2. Cancerfonden
  3. Ahlen Stiftelse
  4. Magnus Bergvalls Stiftelse
  5. Carl Tryggers Stiftelse
  6. Erik Philip-Sorensens Stiftelse
  7. Canadian Institutes of Health Research [MOP-77722]
  8. Canada Research Chair [950-202224]
  9. Howard Hughes Medical Institute
  10. Public Health Service Grant [R01 GM48700]
  11. Generalitat de Catalunya, Spain
  12. Sven and Lilly Lawski Foundation
  13. National Insitutes of Health National Center for Research Resources

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The organs of animal embryos are typically covered with an extracellular matrix (ECM) that must be carefully remodeled as these organs enlarge during post-embryonic growth; otherwise, their shape and functions may be compromised. We previously described the twisting of the Caenorhabditis elegans pharynx (here called the Twp phenotype) as a quantitative mutant phenotype that worsens as that organ enlarges during growth. Mutations previously known to cause pharyngeal twist affect membrane proteins with large extracellular domains (DIG-1 and SAX-7), as well as a C. elegans septin (UNC-61). Here we show that two novel alleles of the C. elegans papilin gene, mig-6(et4) and mig-6(sa580), can also cause the Twp phenotype. We also show that overexpression of the ADAMTS protease gene mig-17 can suppress the pharyngeal twist in mig-6 mutants and identify several alleles of other ECM-related genes that can cause or influence the Twp phenotype, including alleles of fibulin (fbl-1), perlecan (unc-52), collagens (cle-1, dpy-7), laminins (lam-1, lam-3), one ADAM protease (sup-17), and one ADAMTS protease (adt-1). The Twp phenotype in C. elegans is easily monitored using light microscopy, is quantitative via measurements of the torsion angle, and reveals that ECM components, metalloproteinases, and ECM attachment molecules are important for this organ to retain its correct shape during post-embryonic growth. The Twp phenotype is therefore a promising experimental system to study ECM remodeling and diseases.

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