Evidence map›Paper›PMID 20805556›Full record

ArticleGenetics2010

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

Gholamali Jafari, Jan Burghoorn, Takehiro Kawano, Manoj Mathew, Catarina Mörck, Claes Axäng, Michael Ailion, James H Thomas, Joseph G Culotti, Peter Swoboda and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.4field-weighted citation impact, top 45% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Border patrol: insights into the unique role of perlecan/heparan sulfate proteoglycan 2 at cell and tissue borders.Matrix biology : journal of the International Society for Matrix Biology · 2014
    Review
  13. Article
  14. Article
  15. Developmental genetics of the Caenorhabditis elegans pharynx.Wiley interdisciplinary reviews. Developmental biology
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 4 countries.

Gholamali JafariDepartment of Cell and Molecular Biology, University of Gothenburg, S-405 30 Gothenburg, Sweden.
Jan Burghoorn
Takehiro Kawano
Manoj Mathew
Catarina Mörck
Claes Axäng
Michael Ailion
James H Thomas
Joseph G Culotti
Peter Swoboda
Marc Pilon
University of Gothenburg · SEKarolinska Institutet · SEUniversity of Washington · USLunenfeld-Tanenbaum Research Institute · CAMount Sinai Hospital · CA

Funding

GENETIC ANALYSIS OF CHEMOSENSATION IN C ELEGANSR01GM048700 · NIGMS · UNIVERSITY OF WASHINGTON · PI THOMAS, JAMES H · 1993 to 2003
$1.2M
CIHR MOP-77722NIGMS NIH HHS R01 GM048700NIGMS NIH HHS R01 GM48700
6 · The paper itself

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.

Indexed as

Models, AnimalAllelesAnimalsBasement MembraneCaenorhabditis elegansCaenorhabditis elegans ProteinsChromosome MappingDisintegrinsExtracellular MatrixGene Knockdown TechniquesGenes, HelminthGenotypeMetalloendopeptidasesMutationOrgan SpecificityPharynxCaenorhabditis elegans ProteinsDisintegrinsMetalloendopeptidasesMIG-17 protein, C elegans

Identifiers

PMID20805556
PMCPMC2975278
OpenAlexW2137656433

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.