“Highlights” calls attention to exciting advances in developmental biology that have recently been reported in Developmental Dynamics. Development is a broad field encompassing many important areas. To reflect this fact, the section spotlights significant discoveries that occur across the entire spectrum of developmental events and problems: from new experimental approaches, to novel interpretations of results, to noteworthy findings utilizing different developmental organisms.
Ambushed from all sides (Echinoid Regulates Tracheal Morphology and Fusion Cell Fate in Drosophila by Caroline Laplante, Sarah M. Paul, Greg J. Beitel, and Laura A. Nilson, Dev Dyn239:2509–2519). The developing Drosophila trachea, a model for studying morphogenesis of tubular networks, didn't stand a chance. Embryos lacking maternal and zygotic echinoid (edM/Z), which encodes an immunoglobulin domain-containing cell adhesion molecule, bear convoluted tracheal tubes, breaks in tracheal branches, and ectopic branch fusions. Here, the authors determine the mechanisms behind the novel combination of phenotypes. The convoluted tubes are an indirect consequence of wild-type length tubes being forced to fit into a shortened body length, the latter caused by decreased spacing between epidermal segments and deep segmental grooves. The newly documented phenotype phenocopies another convolution phenotype caused by longer tubes within a wild-type body length, and calls into question the etiology of convolution tube mutants where tube length has not been measured. Unlike the convolution phenotype, the branching phenotypes in edM/Z embryos can be rescued by tracheal ed expression, and are thus autonomous. The branching edM/Z phenotypes are caused in part by the presence of supernumerary fusion cells per branch tip, which account for ectopic branch events. Oddly, however, even some edM/Z tracheal branches with wild-type cell fusion patterns failed to fuse. The seemingly contradictory extra fusion and lack-of-fusion branching phenotypes suggest that Ed is required both for specifying cell fusion fate and executing fusion events. The authors discuss evidence that supports, or discounts, links between Ed with signaling pathways involved in important steps of tracheal morphogenesis.
A toehold on metamorphosis (Sox14 Is Required for Transcriptional and Developmental Responses to 20-Hydroxyecdysone at the Onset of Drosophila Metamorphosis by Amanda R. Ritter and Robert B. Beckstead, Dev Dyn239:2685–2694) 20E-hydroxy-ecdysone (20E), or biologically active ecdysone, signals through an Ecdysone receptor (EcR)/Ultraspiracle (Usp) heterodimer to trigger metamorphic changes during the life cycle of the fly. However, little is known about the molecular pathways that link 20E to downstream biological processes. Here, Ritter and Beckstead show that sox14, a member of the venerable Sox transcription factor family that regulates a number of developmental processes, mediates EcR signaling during and subsequent to metamorphosis onset. Supporting evidence includes the finding that a strong zygotic sox14 loss-of-function mutant exhibits defective 20E mediated metamorphic events such as wing and leg elongation and destruction of larval midgut and salivary glands. Further, northern blot analysis reveals alteration in the timing of expression of known 20E regulated genes. Finally, a comparison of microarray results between sox14 and EcR regulated genes shows overlapping genesets with similar changes in expression patterns. Sox14 regulated genes, many of which are independent of EcR signaling, fall into several categories, most prominently cell death, autophagy, immunity and muscle development. Determining the mechanisms that distinguish EcR-dependent sox14 targets from other sox14 targets will give a leg up to understanding how 20E elicits distinct biological processes at different stages of the Drosophila life cycle.
Filling out muscle's story (Developmental Fate of the Mammalian Myotome by Marianne Deries, Ronen Schweitzer, and Marilyn J. Duxson, Dev Dyn239:2898–2910). The well-researched story of how somite-derived epaxial muscle precursors develop into the myotome offers important lessons on mechanisms of cell fate induction and differentiation. Here, Deries and colleagues outline the much-anticipated sequel of how the myotomal myocytes subsequently mature into the four muscle masses of the deep back. During this transition, mononucleated myocytes become multinucleated, change their orientation, migrate, elongate, expand, and segregate into four discrete masses. Upon close examination of these events, the authors suggest that several different interspersed cell types are involved in the processes of myocyte expansion, multinucleation, and migration. The epaxial myotome is initially sprinkled with Pax3- and Pax7-positive muscle progenitors, but as the myotome nears the end of its life, these redistribute such that Pax3-positive cells lie in regions relatively devoid of differentiated cells while Pax7-positive cells remain dispersed throughout the growing muscle mass. Overlaying these patterns with those of newly differentiated muscle and of multinucleated myocytes suggests that Pax3-positive cells are a source of cells involved in the final phases of embryonic myogenesis, while Pax7-positive cells drive multinucleation and growth of muscle masses. What's more, Scleraxis (Scx)-positive connective tissue cells are tightly associated with the muscle groups, and are especially prominent around the migrating end of the myotomal myocytes. This combined with the finding that myocytes lack branching lamellipodia and filopodia that are characteristic of migrating cells leads the authors to propose that Scx-positive cells may be the motive force for myocyte migration. With lessons in transformation, migration, and growth, the completed sequel will almost certainly be as enlightening as its predecessor.