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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.

Stretch and grow (Slow Stretching That Mimics Embryonic Growth Rate Stimulates Structural and Mechanical Development of Tendon-Like Tissue In Vitro by Nicholas S. Kalson, David F. Holmes, Andreas Herchenhan, Yinhui Lu, Toby Starborg, and Karl E. Kadler, Dev Dyn240:2520–2528) As you might expect, embryonic tendons grow during embryonic and postembryonic development. An increase in diameter and in fibril volume fraction (FVF), the proportion of tissue that fibrils occupy, lead to greater mechanical strength. What's more difficult to assess are the separate impacts of various processes, including vascularization and mechanical stimulus, on tendon growth. To test the effects of steady strain rates, like those caused by growth-related elongation of bones, Kalson and colleagues built an apparatus that slowly stretches chick tendon-like constructs in culture. Subjected to these conditions for 4days, the constructs showed a significant increase in fibril diameter, fibril volume fraction FVF, and cell volume fraction (CVF, proportion of transverse area occupied by cells). Also similar to in vivo tendon, they increased in tensile strength and stiffness. Serial section three-dimensional reconstruction reveals that cells changed morphologically, becoming longer and thinner, creating nuclear distortion. The authors postulate that changes in gene expression wrought by altered transcription factor affinity, nuclear matrix organization, and other processes that have been shown to accompany nuclear distortion, may be important for tendon growth.

Dissecting 22q11.2DS (ARVCF Depletion Cooperates with Tbx1 Deficiency in the Development of 22q11.2DS-like Phenotypes in Xenopus by Hong Thi Tran, Mieke Delvaeye, Veerle Verschuere, Emilie Descamps, Ellen Crabbe, Luc Van Hoorebeke, Pierre McCrea, Dominique Adriaens, Frans Van Roy, and Kris Vleminckx, Dev Dyn240:2680–2687) 22q11.2 deletion syndrome (DS), encompassing Di George, conotruncal anomaly face, and velo-cardio facial syndrome (VCFS), results in characteristic heart and facial abnormalities, among other phenotypes. Although the syndrome results from deletion of 30–40 genes in chromosome 22, it is only understood how loss of just a few of these genes contribute toward disease phenotypes. Here, Tran et al. use Xenopus to investigate the role of ARVCF (armadillo repeat gene deleted in VCFS), a protein involved in cadherin stability. Injection of ARVCF morpholinos (MOs) closely mimics animals treated with MOs against TBX1, a known central player in 22q11.2DS. Both cause abnormalities in cranial cartilage and aortic arches, which presage later heart and facial abnormalities. Furthermore, cranial neural crest cells (CNCC) contribute to cartilaginous structures of the head, and although these cells are specified normally, their migration is delayed. These findings dovetail with another Dev Dyn article from the same issue demonstrating a requirement for ARVCF in craniofacial development (Dev Dyn240:2601–2612). When MOs against the two genes are co-injected, these developmental affects are exacerbated, suggesting cooperative effects between the two. The work presented here uncovers a potential role for ARVCF in 22q11.2DS, and cement Xenopus as a model for investigating the etiology of this disease.