Patterning of connective tissues in the head: discussion report

The three papers presented by Noden, Thorogood and Lumsden in this session encompassed the connective tissues as broadly defined, i.e. soft (fibrous) connective tissue, cartilage, bone, muscle and the dental tissues, enamel and dentine, and utilized a variety of experimental techniques on both avian and mammalian embryos to explore specificity and patterning of the vertebrate head. Whether similar developmental processes pattern homologous structures in different Vertebrate classes (Amphibia, Aves, Mammalia) was discussed with reference to patterning of the cranial musculature, chondrocranium and dental tissues. A number of challenging ideas emerged during this session. Does the premigratory neural crest consist of a homogenous population of totipotent cells or of subpopulations of bi- or tripotential cells? Is fundamental patterning of the head an early embryonic event, perhaps specified during primary embryonic induction or the consequence of neuroepithelial folding, brain growth, inductive interactions and/or spatially and temporally distributed extracellular matrix products? Can the fact that mesoderm and angioblasts do not display distinctive patterning that relates to their particular embryologic origins be extrapolated to patterning in general? How does the documentation of an ondontogenic trunk neural crest in mammals affect our theories of how patterning mechanisms arose or were modified during vertebrate evolution?

Changes in lectin-mediated agglutinability during primary embryonic induction in the amphibian embryo

The present study was undertaken to investigate structural alterations at the surfaceof presumptive neural cells after primary embryonic induction. For this purpose, plant lectinmediated agglutinability of dissociated cells from the epiblast of Bufo arenarum gastrulae was tested. Two fragments of epiblast were excised from the same mid-gastrula: one from the dorsal side of the egg, making contact with the invaginating chordamesoblast and assumed to be composed of determined cells and the other from the ventral region of the egg, facing the blastocoele cavity and assumed to be composed of undetermined cells. Cells of the pooled fragments were dissociated in calcium-free Holtfreter's solution with potassium oxalate and incubated in the presence of different concentrations of phytohemagglutinin and concanavalin A. Epiblast cells overlying the archenteron roof are less agglutinated with both lectins than undetermined cells. On the other hand, when egg fragments were removed from the dorsal and ventral regions of early gastrulae before the archenteron was formed, no significant difference in lectin-mediated agglutinability was observed, even after having been cultured in vitro in absence of inducing tissue. These results suggest that the target of the inducing signal generated in the mesoblast is likely to be located on the surface of epiblast cells. Additional experiments showed that cells pretreated with colchicine, cytochalasin B or colchicine and cytochalasin B simultaneously exhibit no significant variation in agglutinability, suggesting that the cytoskeleton was not be involved in the cell surface alteration here described. Treatment of whole embryos or sandwich explants with concanavalin A or phytohemagglutinin has no effect on neural tube formation, suggesting that the carbohydratecontaining binding sites for these lectins are not involved in primary embryonic induction. Changes in cell agglutinability described in this paper are to be interpreted thus as a secondary expression of structural alterations in the cell surface concomitant with neural determination.