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Genetics of extracellular matrix remodeling during organ growth using the Caenorhabditis elegans pharynx model.

Journal article
Authors Gholamali Jafari
Jan Burghoorn
Takehiro Kawano
Manoj Mathew
Catarina Mörck
Claes Axäng
Michael Ailion
James H Thomas
Joseph G Culotti
Peter Swoboda
Marc Pilon
Published in Genetics
Volume 186
Issue 3
Pages 969-82
ISSN 1943-2631
Publication year 2010
Published at Department of Cell and Molecular Biology
Pages 969-82
Language en
Links dx.doi.org/10.1534/genetics.110.120...
Subject categories Biological Sciences, Cell and molecular biology, Molecular biology, Morphology, Genetics, Developmental Biology, Neurobiology

Abstract

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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