Dual Origin of Tissue-Specific Progenitor Cells in Drosophila Tracheal Remodeling (original) (raw)
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Cell fate choices in Drosophila tracheal morphogenesis
BioEssays, 2000
The Drosophila tracheal system is a branched tubular structure that supplies air to target tissues. The elaborate tracheal morphology is shaped by two linked inductive processes, one involving the choice of cell fates, and the other a guided cell migration. We will describe the molecular basis for these processes, and the allocation of cell fate decisions to four temporal hierarchies. First, tracheal placodes are specified within the embryonic ectoderm. Subsequently, branch fates are allocated within the tracheal placodes, prior to migration. Localized presentation of the FGF ligand, Branchless, to tracheal cells that express the FGF receptor, Breathless, guides migration. Once cell migration is initiated, distinct cell fates are determined within each migrating branch. Finally, inhibitory feedback mechanisms ensure the correct assignment of these fates. Tracheal cell fate choices are determined by signaling cascades triggered by signals emanating from the tracheal cells, as well as by ligands produced by adjacent tissues.
Adult progenitor cells activation is a key event in the formation of adult organs during development. The initiation of proliferation of these progenitor cells requires specific temporal signals, mostly of them still unknown. In Drosophila, formation of adult tracheal system depends on the activation of tracheal adult progenitors (tracheoblasts) of Tr4 and Tr5 tracheal metamers specific spiracular branches (SB) during the last larval stage. The mitotic activity of these tracheoblasts generate a pool of tracheal differentiated cells that migrate during pupal development along the larval trachea by the activation of the Branchless (Bnl)/Fibroblast growth factor (FGF) signaling to form the abdominal adult tracheal system. In here, we found that, in addition to migration, Bnl/FGF signaling, mediated by the transcription factor Pointed, is also required for adult progenitor cell proliferation in the SBs. Moreover, we found that tracheoblast proliferation in Tr4 and Tr5 SBs relies on the ...
Developmental compartments in the larval trachea of Drosophila
eLife, 2015
The Drosophila tracheal system is a branched tubular network that forms in the embryo by a post-mitotic program of morphogenesis. In third instar larvae (L3), cells constituting the second tracheal metamere (Tr2) reenter the cell cycle. Clonal analysis of L3 Tr2 revealed that dividing cells in the dorsal trunk, dorsal branch and transverse connective branches respect lineage restriction boundaries near branch junctions. These boundaries corresponded to domains of gene expression, for example where cells expressing Spalt, Delta and Serrate in the dorsal trunk meet vein-expressing cells in the dorsal branch or transverse connective. Notch signaling was activated to one side of these borders and was required for the identity, specializations and segregation of border cells. These findings suggest that Tr2 is comprised of developmental compartments and that developmental compartments are an organizational feature relevant to branched tubular networks.
Genetic Control of Cell Intercalation during Tracheal Morphogenesis in Drosophila
Current Biology, 2004
Klingelbergstrasse 70 into a coordinated response [1]. Epithelial sheets are often remodeled into tubular net-CH-4056 Basel Switzerland works, allowing for an efficient exchange of fluids or gases with surrounding tissues [2, 3]. A particularly wellstudied example of such a remodeling process occurs during the development of the tracheal system in the Summary Drosophila embryo [4, 5]. The larval tracheal system consists of hundreds of interconnected tubes that trans-Background: Branching morphogenesis transforms an port oxygen and other gases throughout the body. Traepithelial sheet into a tubular network with distinct feacheal branches are simple tubes consisting of an epithetures regarding the length and diameter of individual lial monolayer wrapped around a central lumen. The tubes. Branching is controlled by several signaling pathdevelopment of the trachea is initiated in the early emways, but the molecular consequences of these pathbryo upon the determination of ten bilaterally symmetriways in the responding cells are poorly understood. cal clusters of approximately 80 tracheal precursor cells. Results: We have undertaken a detailed characteriza-Each cluster, called a tracheal placode, subsequently tion of cell rearrangements during tracheal branching undergoes a similar sequence of developmental events morphogenesis in Drosophila embryos with a GFP futo generate one segment of the network in the absence sion protein labeling the adherens junctions (AJs) and of further cell divisions.
A Clonal Genetic Screen for Mutants Causing Defects in Larval Tracheal Morphogenesis in Drosophila
Genetics, 2007
The initial establishment of the tracheal network in the Drosophila embryo is beginning to be understood in great detail, both in its genetic control cascades and in its cell biological events. By contrast, the vast expansion of the system during larval growth, with its extensive ramification of preexisting tracheal branches, has been analyzed less well. The mutant phenotypes of many genes involved in this process are probably not easy to reveal, as these genes may be required for other functions at earlier developmental stages. We therefore conducted a screen for defects in individual clonal homozygous mutant cells in the tracheal network of heterozygous larvae using the mosaic analysis with a repressible cell marker (MARCM) system to generate marked, recombinant mitotic clones. We describe the identification of a set of mutants with distinct phenotypic effects. In particular we found a range of defects in terminal cells, including failure in lumen formation and reduced or extensive branching. Other mutations affect cell growth, cell shape, and cell migration.
Compensatory branching morphogenesis in the Drosophila tracheal system
2015
Compensatory Branching Morphogenesis in the Drosophila Tracheal System Deanne Francis Amin Ghabrial Most organs and glands are composed of interconnected networks of tubes. Tubes carryout many important functions throughout the body, such as homeostasis, nutrient and oxygen transport. Surprisingly, given the importance of interconnected tubular networks, how connections between different tubes are maintained remains undetermined. To address this question we used the Drosophila tracheal system as a model to study tube connectivity. The Drosophila trachea is composed of multi-cellular, auto-cellular and seamless tubes. Multi-cellular tubes are composed of multiple interconnected cells, auto-cellular tubes form by wrapping and membrane self-adhesion, while seamless tubes form entirely intracellularly. In all epithelial tube types, the cell apical domain faces the lumen. In this work, I focused on the connection between the auto-cellular tube in the stalk cell and the seamless tube in t...
Genetics, 2007
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.