Editorial highlights

Abstract

Every organism is a model organism for understanding development, evolution, disease, and regeneration, and we have only begun to scratch the surface of the interdisciplinary genetic, molecular, cellular, and developmental mechanisms that regulate these biological processes. These “Highlights” denote exciting advances recently reported in Developmental Dynamics that illustrate the complex dynamics of developmental biology.

Embryology “Embryology of the fat-tailed dunnart (Sminthopsis crassicaudata): A marsupial model for comparative mammalian developmental and evolutionary biology” by Axel Newton, Jennifer Hutchison, Ella Farley, Emily Scicluna, Neil Youngson, Jun Liu, Brandon Menzies, Thomas Hildebrandt, Ben Lawrence, Angus Sutherland, David Potter, Gerard Tarulli, Lynne Selwood, Stephen Frankenberg, Sara Ord, and Andrew Pask. Dev Dyn. 254.2, pp. 142–157. https://doi.org/10.1002/dvdy.711. Welcome to the fat-tailed dunnart that is making a name for itself as a marsupial model for developmental, evolutionary, and ecological studies. Marsupials currently remain underutilized in developmental biology studies, which limits our understanding of mammalian diversity. Mammals are a highly diverse lineage of vertebrates, comprising nearly 6500 extant species, classified into three clades: Prototheria, Metatheria, and Eutheria, also known as monotreme, marsupial, and placental mammals, respectively. The fat-tailed dunnart is an emerging laboratory animal, and in this study, the authors stablished methods to confirm pregnancy and generate timed embryos. This facilitated the collection and description of dunnart embryo development from cleavage to birth. Furthermore, detailed descriptions of dunnart organogenesis and heterochronic growth patterns, especially in comparisons with other species, highlight the dunnart's accelerated craniofacial and limb development, which are characteristic of marsupials. This makes the dunnart a valuable model system for investigating the molecular and cellular mechanisms’ underlying heterochrony.

In an accompanying study, “Breeding fat-tailed dunnarts (Sminthopsis crassicaudata) in captivity: revised practices to minimise stress whilst maintaining considerations of wild biology” by Emily Scicluna, Axel Newton, Jennifer Hutchison, Alicia Dimovski, Kerry Fanson, Gail D'Souza, Shiralee Whitehead and Andrew Pask (need to add in doi number and make sure its linked to web), the authors re-examine current captive management techniques for dunnarts, which rely on scent marking for their social communication and interactions. Although dunnarts have been successfully bred in captivity for decades, there are conflicting reports about best practices for the long-term maintenance of this species. The results of this study provide evidence for preferred cage base substrate types and establish and validate methodology for quantifying stress using fecal glucocorticoid metabolite levels as an indicator. Recapitulating as many aspects of the natural environment of dunnarts as possible, significantly reduces their stress and improves the overall reproductive fitness of captive-bred dunnart colonies. The study also emphasizes the importance of population management in captive breeding programs, and the value of maintaining genetic diversity and meticulous record keeping. Collectively, all of this helps to ensure the dunnart can serve as a valuable marsupial research model while also aiding in the conservation of related endangered species.

Body Wall Development and Closure “Ventral body wall closure: Mechanistic insights from mouse models and translation to human pathology” by Caroline Formstone, Bashar Aldeiri, Mark Davenport, and Philippa Francis-West. Dev Dyn. 254.2, pp. 102–141. https://doi.org/10.1002/dvdy.735. The ventral body wall encloses the thoracic and abdominal cavities. It consists of the skin, dermis, sternum, ribs, intercostal, and abdominal musculature, and forms during embryogenesis in two key steps. Initially the primary body wall, which consists of mesoderm and ectoderm layers, undergoes extensive migration and growth to cover most of the ventral region of the embryo, except the umbilicus. Next, the secondary body wall, which is derived from lateral plate and paraxial mesoderm, invades the primary body wall from the lateral edges, and extends toward the midline where it fuses, thus completing body wall closure. Anomalies in ventral body wall development or closure include thoracoabdominoschisis, ectopia cordis, exomphalos, and bladder exstrophy, which can accompany pelvic and genital defects. The etiology of ventral body wall anomalies is considered sporadic and multifactorial in origin. This review describes ventral body wall development and discusses insights obtained from animal models into human pathogenic and clinical defects, including the genetic and cellular mechanisms underpinning various ventral body wall developmental anomalies.

Eye Development “Increased Netrin downstream of overactive Hedgehog signaling disrupts optic fissure formation” by Sarah Lusk, Sarah LaPotin, Jason Presnell, and Kristen Kwan. Dev Dyn. 254.2, pp. 158–173. https://doi.org/10.1002/dvdy.733. The eye is a fluid filled sphere, surrounded by three distinct tissue layers. Structural defects in the proper three-dimensional structure of the eye, which is critical for vision, can result in vision impairment. For example, uveal coloboma, which is a significant cause of pediatric blindness worldwide, is caused by failure of the development of the optic fissure that forms a conduit during embryogenesis for retinal ganglion cell axons to exit the eye and for vasculature to enter. Human genetic studies and research in animal models have revealed that the genetic causes of coloboma are heterogeneous. In contrast, our understanding of the cellular and molecular mechanisms that drive the pathogenesis of coloboma remain poorly understood. In this study, the authors focus on Hedgehog (Hh) signaling, which is central to proper optic fissure development, and more specifically, intercellular signaling molecules that are known transcriptional targets of Hh signaling and that are expressed at the appropriate time and place to influence optic fissure and stalk morphogenesis. Netrin is one such factor, known primarily for its role in axon guidance, and herein the authors use loss-of-function zebrafish models to characterize novel roles for Netrin during early eye development. Netrin is sufficient but not required to disrupt optic fissure formation downstream of overactive Hh signaling.

Heart Development and Disease “Hypoxia regulate developmental coronary angiogenesis potentially through VEGF-R2- and SOX17-mediated signaling” by Halie Vitali, Bryce Kuschel, Chhiring Sherpa, Brendan Jones, Nisha Jacob, and Syeda Madiha. Dev Dyn. 254.2, pp. 174–188. https://doi.org/10.1002/dvdy.750. The coronary arteries are large blood vessels that supply oxygen and nutrients to the heart muscles. They are involved in the pathogenesis of myocardial infarction, which can result in heart failure, and coronary artery-related diseases are among the leading causes of death worldwide. Currently there is no cure to repair damaged coronary arteries, but the authors hypothesize that a better understanding of the mechanisms and signals underpinning coronary vessel development in the embryo could be harnessed and potentially reactivated in adults to repair and regenerate damaged coronary arteries. Hypoxia is a well-known stimulator of blood vessel and cardiomyocyte growth and may also promote coronary angiogenesis. Similarly, SOX17 is important for arterial differentiation and promotes sprouting angiogenesis. In this study, the authors utilized both in vivo and in vitro models mimicking cellular responses to increased or decreased hypoxia conditions, to analyze the role of hypoxia/VEGF-A signaling in the myocardial growth of coronary vessels and also to determine whether SOX17 functions through a hypoxia-mediated signaling axis in the regulation of coronary vessel formation. The authors conclude that hypoxia does indeed regulates developmental coronary growth, potentially through VEGF-R2 and SOX17 pathways, shedding light on the mechanisms of coronary vessel development.