The cells of many embryonic tissues actively narrow in one dimension (convergence) and lengthen in the perpendicular dimension (extension). Convergence and extension are ubiquitous and important tissue movements in metazoan morphogenesis. In vertebrates, the dorsal axial and paraxial mesodermal tissues, the notochordal and somitic mesoderm, converge and extend. In amphibians as well as a number of other organisms where these movements appear, they occur by mediolateral cell intercalation, the rearrangement of cells along the mediolateral axis to produce an array that is narrower in this axis and longer in the anteroposterior axis. In amphibians, mesodermal cell intercalation is driven by bipolar, mediolaterally directed protrusive activity, which appears to exert traction on adjacent cells and pulls the cells between one another. In addition, the notochordal^somitic boundary functions in convergence and extension bỳ capturing' notochordal cells as they contact the boundary, thus elongating the boundary. The prospective neural tissue also actively converges and extends parallel with the mesoderm. In contrast to the mesoderm, cell intercalation in the neural plate normally occurs by monopolar protrusive activity directed medially, towards the midline notoplate^£oor-plate region. In contrast, the notoplate^£oor-plate region appears to converge and extend by adhering to and being towed by or perhaps migrating on the underlying notochord. Converging and extending mesoderm sti¡ens by a factor of three or four and exerts up to 0.6 m N force. Therefore, active, force-producing convergent extension, the mechanism of cell intercalation, requires a mechanism to actively pull cells between one another while maintaining a tissue sti¡ness su¤cient to push with a substantial force. Based on the evidence thus far, a cell^cell traction model of intercalation is described. The essential elements of such a morphogenic machine appear to be (i) bipolar, mediolaterally orientated or monopolar, medially directed protrusive activity; (ii) this protrusive activity results in mediolaterally orientated or medially directed traction of cells on one another; (iii) tractive protrusions are con¢ned to the ends of the cells; (iv) a mechanically stable cell cortex over the bulk of the cell body which serves as a movable substratum for the orientated or directed cell traction. The implications of this model for cell adhesion, regulation of cell motility and cell polarity, and cell and tissue biomechanics are discussed.

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Physical forces drive the movement of tissues within the early embryo. Classical and modern approaches have been used to infer and in rare cases measure mechanical properties and the location and magnitude of forces within embryos. Elongation of the dorsal axis is a critical event in early vertebrate development yet the mechanics of dorsal tissues in driving embryonic elongation that later support neural tube closure and formation of the central nervous system is not known. Among vertebrates, amphibian embryos allow complex physical manipulation of embryonic tissues that are required to measure the mechanical properties of tissues. In this paper we measure the stiffness of dorsal isolate explants of frog (Xenopus laevis) from gastrulation to neurulation and find dorsal tissues stiffen from less than 20 Pa to over 80 Pa. By iteratively removing tissues from these explants we find paraxial somitic mesoderm is nearly twice as stiff as either the notochord or neural plate and at least 20-fold stiffer than the endoderm. Stiffness measurements from explants with reduced fibronectin fibril assembly or disrupted actomyosin contractility suggest that it is the state of the actomyosin cell cortex rather than accumulating fibronectin that controls tissue stiffness in early amphibian embryos.

We describe mesendoderm morphogenesis during gastrulation in the frog Xenopus laevis and investigate the mechanics of these movements with tissue explants. When a dorsal marginal zone explant is plated onto fibronectin, the mesendoderm moves away from the dorsal axial tissues as an intact sheet. Mesendodermal cells within these explants display monopolar protrusive activity and radially intercalate during explant extension. Live time-lapse confocal sequences of actin dynamics at the margin of these extending explants prompt us to propose that integrin-mediated traction drives these movements. We demonstrate that integrin alpha(5)beta(1) recognition of the synergy site located within the type III(9) repeat of fibronectin is required for mesendoderm extension. Normal mesendoderm morphogenesis occurs with a unique "cup-shaped" geometry of the extending mesendodermal mantle and coincides with a higher rate of tissue extension than that seen in the simpler dorsal marginal zone explant. These higher rates can be reconstituted with "in-the-round" configurations of several explants. We propose several mechanically based hypotheses to explain both the initial fibronectin-dependent extension of the mesendoderm and additional requirement of tissue geometry during the high-velocity closure of the mesendodermal mantle.