Mechanistic understanding of mesendoderm formation in reptiles is scanty, and relies heavily on a handful of descriptive studies of histological sections. The few exceptions are studies by two authors, Pasteels (1937) and Nayar (1959, 1966), who applied dye on the epiblast of Chelonia embryos and registered the position of the marker after a short period of time. The results of these histological and labeling studies pointed to a mechanism based mainly on involution as the mode of mesendoderm internalization at the site of gastrulation. While involution of epiblast cells through the blastopore lip is clear, ingression also appears to play a role. These two modes combined would more satisfactorily account for the presence of the mass of cells positioned in the anterior/lateral and posterior regions of the gastrulating reptile embryo (Coolen et al. 2008; Bachvarova et al. 2009) (Fig. 4A). Characterization of the lower layers in reptiles (the hypoblast or extra-embryonic endoderm and the definitive endoderm) is far from being accomplished. In chick embryos the hypoblast forms a flat layer of cells underlying the pre-gastrulating epiblast. The canonical view of hypoblast formation in amniotes (mostly derived from chick studies) is based upon delamination of cells from the epiblast and their aggregation into groups called the island of the hypoblast, followed by coalescence and spreading over the lower surface of the epiblast (Stern & Downs 2012). In reptiles, the germ cell marker Dazl is expressed in cells embedded in the lower layer of an early gastrulaing embryo (Bachvarova et al. 2009), suggesting the presence of a chick-like hypoblast layer. Histologically, the development of the lower layer in gastrulating reptile embryos has been analyzed and debated by a number of researchers including Will, Kupffer, Mitsukuri, Schauinsland, Ballowitz, Peter and Pasteels. Peter, for example, argued that the first endodermal layer forms under the embryonic shield in loco from the “deeper blastomeres” (Peter 1934), while Pasteels proposed that in turtles and lizards the hypoblast (endophylle) forms by delamination from the upper epiblast (ectoblast) (Pasteels 1937, 1957a), like in chick. With regard to the definitive endoderm (the entoblast), Pasteels (1957a), summarizing his own work on turtles and that of others before him, suggested that these cells involute at the blastopore lip and account for the formation of a thin layer of endoderm cells covering the ventral surface of the epiblast. In the midline, the axial mesendoderm called chorda-hypoblast is continuous with this thin layer of cells (Mitsukuri 1891; Pasteels 1957a). The hypoblast is then pushed into extra-embryonic areas by the endoderm. The idea of endoderm pushing the pre-existing lower layer had been the accepted view in the amniote experimental models, chick and mouse. However, recent experiments suggested a certain degree of intercalation between the hypoblast and the forming endoderm, with hypoblast cells contributing to definitive endoderm (Bertocchini & Stern 2008; Kwon et al. 2008; Burtscher & Lickert 2009). A possible partial contribution of the hypoblast to the definitive gut epithelium in reptiles was brought up in the old literature (Mehnert 1892; Will 1892), but it is still unclear whether and to what extent this hypoblast/endoderm mixing occurs in reptiles. In addition to the hypoblast and the involuting endoderm, a third population of lower layer cells is recognized in the primitive plate. These endoderm cells ingress from the epiblast, and, together with mesoderm cells (see below), form a uniform mass of not yet characterized tissue. The lack of lower-layer molecular markers, together with the paucity of information from histological sections, makes it difficult to speculate on the positioning and movements of the different dorsal and ventral components of the endoderm.