ArticleGenetics2007
A genetic mosaic analysis with a repressible cell marker screen to identify genes involved in tracheal cell migration during Drosophila air sac morphogenesis.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 24 citations in OpenAlex.
- An endosome-associated actin network involved in directed apical plasma membrane growth.The Journal of cell biology · 2022Article
- Vps28 Is Involved in the Intracellular Trafficking of Awd, theFrontiers in physiology · 2019Article
- Modeling congenital disease and inborn errors of development in Drosophila melanogaster.Disease models & mechanisms · 2016Review
- ESCRT-0 is not required for ectopic Notch activation and tumor suppression in Drosophila.PloS one · 2014Article
- Functions and Mechanisms of Fibroblast Growth Factor (FGF) Signalling in Drosophila melanogaster.International journal of molecular sciences · 2013Article
- Power tools for gene expression and clonal analysis in Drosophila.Nature methods · 2011Review
- A systematic screen for tube morphogenesis and branching genes in the Drosophila tracheal system.PLoS genetics · 2011Article
- The Hrs/Stam complex acts as a positive and negative regulator of RTK signaling during Drosophila development.PloS one · 2010Article
- Genetic screen in Drosophila melanogaster uncovers a novel set of genes required for embryonic epithelial repair.Genetics · 2010Article
- Branching morphogenesis.Circulation research · 2009Article
- A clonal genetic screen for mutants causing defects in larval tracheal morphogenesis in Drosophila.Genetics · 2007Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Branching morphogenesis of the Drosophila tracheal system relies on the fibroblast growth factor receptor (FGFR) signaling pathway. The Drosophila FGF ligand Branchless (Bnl) and the FGFR Breathless (Btl/FGFR) are required for cell migration during the establishment of the interconnected network of tracheal tubes. However, due to an important maternal contribution of members of the FGFR pathway in the oocyte, a thorough genetic dissection of the role of components of the FGFR signaling cascade in tracheal cell migration is impossible in the embryo. To bypass this shortcoming, we studied tracheal cell migration in the dorsal air sac primordium, a structure that forms during late larval development. Using a mosaic analysis with a repressible cell marker (MARCM) clone approach in mosaic animals, combined with an ethyl methanesulfonate (EMS)-mutagenesis screen of the left arm of the second chromosome, we identified novel genes implicated in cell migration. We screened 1123 mutagenized lines and identified 47 lines displaying tracheal cell migration defects in the air sac primordium. Using complementation analyses based on lethality, mutations in 20 of these lines were genetically mapped to specific genomic areas. Three of the mutants were mapped to either the Mhc or the stam complementation groups. Further experiments confirmed that these genes are required for cell migration in the tracheal air sac primordium.
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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.