Cell fate choices in Drosophila tracheal morphogenesis (original) (raw)
Related papers
Elucidation of the role of breathless, a Drosophila FGF receptor homolog, in tracheal cell migration
Genes & Development, 1994
the posterior midline glial cells during embryonic development. To define the role of this receptor in cell migration, we have monitored the biological effects of a deregulated receptor containing the extracellular and transmembrane regions of the torso dominant allele and the cytoplasmic domain of DFGF-Rl. Ubiquitous expression of the chimeric receptor at the time of tracheal cell migration did not disrupt migration in wild-type embryos. However, induction of the chimeric receptor corrected the tracheal defects of breathless [btl] mutant embryos, allowing the tracheal cells to migrate along their normal tracts. This result indicates that the normal activity of DFGF-Rl in promoting cell migration does not require spatially restricted cues.
Genes & …, 1996
Receptor tyrosine kinases (RTKs) are members of a diverse class of signaling molecules well known for their roles in cell fate specification, cell differentiation, and oncogenic transformation. Recently several RTKs have been implicated in cell and axon motility, and RTKs are known to mediate chemotactic guidance of tissue culture cells. We have investigated whether the Drosophila FGF receptor homolog, Breathless (BTL), whose activity is necessary for each phase of branching morphogenesis in the embryonic tracheal system, might play a role in guiding the directed migration of tracheal cells. We found that expression of a constitutively active receptor during tracheal development interfered with directed tracheal cell migration and led to extra secondary and terminal branch-forming cells. Reduction in endogenous BTL signaling enhanced the cell migration defects while suppressing the ectopic branching defects. These results are consistent with a model for tracheal development in which spatially regulated BTL activity guides tracheal cell migration and quantitatively regulated BTL activity determines the patterns of secondary and terminal branching cell fates.
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.
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.
Regulation of cell migration during tracheal development in Drosophila melanogaster
2002
Most of the knowledge concerning the intracellular mechanisms involved in cell locomotion have been obtained from in vitro studies of cells in culture. Many of the concepts derived from these studies have been partially confirmed in in vivo systems but numerous questions regarding the developmental control of cell migration remain to be addressed. Tracheal morphogenesis in Drosophila melanogaster embryos represents an in vivo model system to study the genetic control of cell migration. We review what is known about tracheal development and regulation of tracheal cell migration. We try to link these in vivo studies and the movement of cells over two dimensional substrates and elaborate on important questions which remain to be addressed in the future.
Genes & Development, 1992
a Drosophila FGF receptor homolog (DFGF-Rl), was shown to be essential for the migration of the tracheal cells and the posterior midline glia cells. The temporal requirement for the activity of this receptor was dissected by a dominant-negative construct lacking a functional cytoplasmic tyrosine-kinase domain. Induction of the construct prior to the onset of tracheal or glial cell migration produced phenotypes that were similar to those observed in the corresponding tissues of breathless null mutant embryos. However, this effect is not detected if the dominant-negative receptor is induced after the initiation of tracheal cell migration, indicating that Breathless is required primarily at the onset of the migration process. Induction of the construct after the tracheal branches are completed, blocked the formation of tracheoles, i.e. extension of cellular processes by the terminal tracheal cells, demonstrating that Breathless plays an essential role in this process as well. The requirement for Breathless at the onset of migration and the diversity of processes in which it participates, suggest that the receptor is involved in triggering transcription factors, which may be distinct for each context.
Development (Cambridge, England), 1997
The formation of the tracheal network in Drosophila is driven by stereotyped migration of cells from the tracheal pits. No cell divisions take place during tracheal migration and the number of cells in each branch is fixed. This work examines the basis for the determination of tracheal branch fates, prior to the onset of migration. We show that the EGF receptor pathway is activated by localized processing of the ligand SPITZ in the tracheal placodes and is responsible for the capacity to form the dorsal trunk and visceral branch. The DPP pathway, on the contrary, is induced in the tracheal pit by local presentation of DPP from the adjacent dorsal and ventral ectodermal cells. This pathway patterns the dorsal and lateral branches. Elimination of both pathways blocks migration of all tracheal branches. Antagonistic interactions between the two pathways are demonstrated. The opposing activities of two pathways may refine the final determination of tracheal branch fates.
Mechanisms of Development, 2000
The Drosophila tracheal system arises from clusters of ectodermal cells that invaginate and migrate to originate a network of epithelial tubes. Genetic analyses have identi®ed several genes that are speci®cally expressed in the tracheal cells and are required for tracheal development. Among them, trachealess (trh) is able to induce ectopic tracheal pits and therefore it has been suggested that it would act as an inducer of tracheal cell fates; however, this capacity appears to be spatially restricted. Here we analyze the expression of the tracheal speci®c genes in the early steps of tracheal development and their cross-interactions. We ®nd that there is a set of primary genes including trh and ventral veinless (vvl) whose expression does not depend on any other tracheal gene and a set of downstream genes whose expression requires different combinations of the primary genes. We also ®nd that the combined expression of primary genes is suf®cient to induce some downstream genes but not others. These results indicate that there is not a single master gene responsible for the appropriate expression of the tracheal genes and support a model where tracheal cell fates are induced by the co-operation of several factors rather than by the activity of a single tracheal inducer. q