ArticleDevelopment (Cambridge, England)2013
The secreted AdamTS-A metalloprotease is required for collective cell migration.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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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.
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Who cites it
40 citing papers in PubMed, 69 citations in OpenAlex.
- The extracellular protease AdamTS-B is a dosage-sensitive regulator of unicellular tracheal branch morphogenesis.Biology open · 2026Article
- Article
- Basement membrane patterning by spatial deployment of a secretion-regulating protease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role ofmicroPublication biology · 2025Article
- Adamts9 is required for the development of primary ovarian follicles and maintenance of female sex in zebrafish†.Biology of reproduction · 2024Article
- The journey of a generation: advances and promises in the study of primordial germ cell migration.Development (Cambridge, England) · 2024Article
- Article
- The RNF220 domain nuclear factor Teyrha-Meyrha (Tey) regulates the migration and differentiation of specific visceral and somatic muscles in Drosophila.Development (Cambridge, England) · 2023Article
- Caenorhabditis elegans for research on cancer hallmarks.Disease models & mechanisms · 2023Article
- The Role of the miR-548au-3p/CA12 Axis in Tracheal Chondrogenesis in Congenital Pulmonary Airway Malformations.Oxidative medicine and cellular longevity · 2023Article
- Identification of the extracellular metallo-endopeptidases ADAM and ADAMTS in the yellow fever mosquito Aedes aegypti.Insect biochemistry and molecular biology · 2022Article
- The Mechanism and Role of ADAMTS Protein Family in Osteoarthritis.Biomolecules · 2022Review
- Article
- Metalloproteases in gonad formation and ovulation.General and comparative endocrinology · 2021Review
- Crosstalk between basal extracellular matrix adhesion and building of apical architecture during morphogenesis.Biology open · 2021Review
- Delay in primordial germ cell migration in adamts9 knockout zebrafish.Scientific reports · 2021Article
- ADAMTS proteases in cardiovascular physiology and disease.Open biology · 2020Review
- Extracellular matrix dynamics in tubulogenesis.Cellular signalling · 2020Review
- Association of Polymorphism rs67920064 in ADAMTS9 Gene with Mandibular Retrognathism in a Chinese Population.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Collective Migrations ofGenetics · 2020Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Members of the ADAMTS family of secreted metalloproteases play crucial roles in modulating the extracellular matrix (ECM) in development and disease. Here, we show that ADAMTS-A, the Drosophila ortholog of human ADAMTS 9 and ADAMTS 20, and of C. elegans GON-1, is required for cell migration during embryogenesis. AdamTS-A is expressed in multiple migratory cell types, including hemocytes, caudal visceral mesoderm (CVM), the visceral branch of the trachea (VBs) and the secretory portion of the salivary gland (SG). Loss of AdamTS-A causes defects in germ cell, CVM and VB migration and, depending on the tissue, AdamTS-A functions both autonomously and non-autonomously. In the highly polarized collective of the SG epithelium, loss of AdamTS-A causes apical surface irregularities and cell elongation defects. We provide evidence that ADAMTS-A is secreted into the SG lumen where it functions to release cells from the apical ECM, consistent with the defects observed in AdamTS-A mutant SGs. We show that loss of the apically localized protocadherin Cad99C rescues the SG defects, suggesting that Cad99C serves as a link between the SG apical membrane and the secreted apical ECM component(s) cleaved by ADAMTS-A. Our analysis of AdamTS-A function in the SG suggests a novel role for ADAMTS proteins in detaching cells from the apical ECM, facilitating tube elongation during collective cell migration.
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Registered trials
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.