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“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.

Swat Team (Drosophila as a Model of Wound Healing and Tissue Regeneration in Vertebrates by Yaiza Belacortu and Nuria Paricio, Dev Dyn 240:2379–2404) Most do not think twice about swatting a pesky fly. But here, Belacortu and Paricio detail the complex wound healing and regeneration processes that such a gesture launches into action. Although there are both similarities and differences between wound healing in mammals and flies, Drosophila have been valuable for discovering novel genes and pathways. Drosophila models of wound healing, embryonic dorsal closure, imaginal disc spreading, fusion, and closure have elucidated associated morphogenetic processes. The authors discuss these and other findings, as well as how the animal model may inform new therapeutic strategies. With an arsenal of special weapons and tactics at their disposal, any developmental biologist can join the Swat Team.

Must Be Fate (Axial Protocadherin [AXPC] Regulates Cell Fate During Notochordal Morphogenesis by Michael D. Yoder and Barry M. Gumbiner, Dev Dyn 240:2495–2504) Axial protocadherin (AXPC), of the δ-protocadherin subgroup of the cadherin family, had been swept under the rug. It was assumed that its previously discovered role in notochordal morphogenesis was caused by standard cadherin cell adhesion processes. Here, Yoder and Gumbiner draw attention to a second AXPC allele, the major allele expressed in early Xenopus, that behaves differently than expected. Morpholino (MO) experiments demonstrate that the newly identified allele is required for dorsal mesoderm to separate into axial (notochord) and paraxial (somite) tissues. Unexpectedly, in vitro cell dispersal and reaggregation assays suggest that the protocadherin does not do so by mediating changes in cell adhesion. Instead MO knockdown inhibits axial and paraxial markers, while early mesodermal markers are unaffected. Ruling out secondary effects due to altered morphogenesis, similar results are obtained in MO-treated animal caps treated with the mesoderm inducer, activin. It must be fate that caused the authors to stumble onto the alternative allele of AXPC and discover that, unlike its δ-protocadherin brethren, the gene may directly affect axial and paraxial specification.

Understanding Muenke Syndrome (The Muenke Syndrome Mutation [FgfR3P244R] Causes Cranial Base Shortening Associated with Growth Plate Dysfunction and Premature Perichondrial Ossification in Murine Basicranial Synchondroses by Jason Laurita, Eiki Koyama, Bianca Chin, Jesse A. Taylor, Gregory E. Lakin, Kurt D. Hankenson, Scott P. Bartlett, and Hyun-Duck Nah, Dev Dyn 240:2584–2596) At the molecular level, Muenke syndrome is caused by a P250R substitution mutation in fibroblast growth factor 3 (FGFR3), which enhances affinity for unnatural ligands. Patients exhibit craniosynostosis, an abnormal fusion between two or more cranial bones that is caused by premature ossification of coronal sutures. Yet this abnormal process fails to explain another characteristic phenotype, midface hypoplasia. Here, Laurita and colleagues conduct craniomorphometric measurements in FgfR3P244R mice and reveal an unreported shortening of the cranial base. The defect is caused by premature fusing of the basicranial synchondroses, the primary postnatal growth centers for the cranial base. A closer look shows that basicranial synchondroses display decreased chondrocyte proliferation and hypertrophy, and reduced expression of Indian hedgehog, a growth factor that regulates chondrocyte profileration. In addition, perichondrial ossification occurs prematurely, causing precocious formation of a bony bridge across the basicranial synchondroses. The possible mechanisms by which FGF/FGFR3 may stimulate perichondrial ossification are discussed.