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Before radial symmetry-breaking of the blastoderm, the chick embryo is distinctly divided into a central area pellucida and a surrounding region, the area opaca. In this review, we focus on the area opaca and its functions. First, we survey current knowledge about how the area opaca is formed during the intrauterine period and how it sets up its initial tissue structure. With the formation of a vascularized mesoderm layer, the area opaca becomes subdivided into an inner area vasculosa and an outer area vitellina, which contribute to the development of extraembryonic membranes: the yolk sac and chorion. Second, we review the various functions of the area opaca during development including supplying nutrients, driving the expansion of the embryo by a specialized population of edge cells, and active, instructive signaling that plays a role in the establishment of embryonic polarity and orchestrates the formation of another extraembryonic tissue, the marginal zone, essential for positioning the first midline structure, the primitive streak, at the beginning of gastrulation. [Display omitted] • The chick embryo is divided into a central area pellucida and a peripheral area opaca. Here we focus on the latter. • We review current knowledge about how the area opaca is formed. • The area opaca then vascularizes, becoming subdivided into an inner area vasculosa and an outer area vitellina. • The area opaca contributes to the development of extraembryonic membranes: the yolk sac and chorion. • We review the functions of the area opaca during development including: o supplying nutrients, o driving the expansion of the embryo by a specialized population of edge cells, o active, instructive signaling that plays a role in the establishment of embryonic polarity and orchestrates the formation of another extraembryonic tissue, the marginal zone, essential for positioning the first midline structure, the primitive streak, at the beginning of gastrulation. • We present a list of molecular markers that characterize the area opaca. [ABSTRACT FROM AUTHOR]

Defects in choroid fissure (CF) formation and closure lead to coloboma, a major cause of childhood blindness. Despite genetic advances, the cellular defects underlying coloboma remain poorly elucidated due to our limited understanding of normal CF morphogenesis. We address this deficit by conducting high-resolution spatio-temporal analyses of CF formation and closure in the chick, mouse and fish. We show that a small ventral midline invagination initiates CF formation in the medial-proximal optic cup, subsequently extending it dorsally toward the lens, and proximally into the optic stalk. Unlike previously supposed, the optic disc does not form solely as a result of this invagination. Morphogenetic events that alter the shape of the proximal optic cup also direct clusters of outer layer and optic stalk cells to form dorsal optic disc. A cross-species comparison suggests that CF closure can be accomplished by breaking down basement membranes (BM) along the CF margins, and by establishing BM continuity along the dorsal and ventral surfaces of the CF. CF closure is subsequently accomplished via two distinct mechanisms: tissue fusion or the intercalation of various tissues into the inter-CF space. We identify several novel cell behaviors that underlie CF fusion, many of which involve remodeling of the retinal epithelium. In addition to BM disruption, these include NCAD downregulation along the SOX2 + retinal CF margin, and the protrusion or movement of partially polarized retinal cells into the inter-CF space to mediate fusion. Proximally, the inter-CF space does not fuse or narrow and is instead loosely packed with migrating SOX2 + /PAX2 + /Vimentin + astrocytes until it is closed by the outgoing optic nerve. Taken together, our results highlight distinct proximal-distal differences in CF morphogenesis and closure and establish detailed cellular models that can be utilized for understanding the genetic bases of coloboma. [ABSTRACT FROM AUTHOR]

Tissue closure involves the coordinated unidirectional movement of a group of cells without loss of cell–cell contact. However, the molecular mechanisms controlling the tissue closure are not fully understood. Here, we demonstrate that Lamin C, the sole A-type lamin in Drosophila , contributes to the process of thorax closure in pupa. High expression of Lamin C was observed at the leading front of the migrating wing imaginal discs. Live imaging analysis revealed that knockdown of Lamin C in the thorax region affected the coordinated movement of the leading front, resulting in incomplete tissue fusion required for formation of the adult thorax. The closure defect due to knockdown of Lamin C correlated with insufficient accumulation of F-actin at the front. Our study indicates a link between A-type lamin and the cell migration behavior during tissue closure. [ABSTRACT FROM AUTHOR]

The actual role of programmed cell death (PCD) in embryonic processes and the extrinsic signals that define the death fate in developing cells are still poorly understood. Here, we show that during secondary palate shelf fusion in the mouse, PCD appeared in the medial edge epithelia (MEE) of the anterior region only after shelf contact. Contact was necessary for efficient cell death activation in the MEE. However, exogenous all-trans-retinoic acid (RA) increased cell death independently of contact. Competence to induce cell death by contact or by RA exposure was obtained when the MEE were close to touch. Endogenous RA is a relevant regulator of the secondary palate PCD since this was reduced by a retinol dehydrogenase inhibitor and an RAR specific antagonist. Bmp-7 expression was positively regulated by RA. However, BMP-7 was unable to activate cell death within the palate tissue and NOGGIN, a natural BMP antagonist, did not block PCD. Reduction of PCD at the MEE directly with a caspase inhibitor or by inhibiting retinol dehydrogenase resulted in unfused palate shelves, but adhesion was not affected. In contrast, exogenous RA also blocked fusion, but in this situation the increased cell death within the MEE appeared to affect adhesion, thereby causing cleft palate in vivo. [Copyright &y& Elsevier]