Fig. 6

Cap1 is required for adaxial cells to form apical constrictions, intercalate, and broaden. Cells from embryos co-injected with rhodamine-dextran and translation blocking or mismatch control morpholinos were transplanted into presumptive mesodermal precursor regions of wild type embryos at the late blastula stage. Confocal images of adaxial cells at the mid-notochord level of fixed 8–10 somite stage embryos labeled with phalloidin (green) and DAPI (blue). Rhodamine-dextran labels transplanted cells (red). Dorsal view with anterior to the left in all panels. (A, B) Injection of Cap1 morpholino does not cause defects in non-adaxial mesoderm cell behaviors. (A) Cap1 morpholino-containing notochord cells undergo normal intercalation behaviors and are otherwise indistinguishable from wild-type neighbors. (B) Cap1 morpholino-containing cells in the more lateral somite display the same shapes and distributions as their wild type neighbors. (C) Adaxial cells containing mismatch control morpholinos are able to complete the typical array of cell behaviors, becoming broadened and making somite attachments (arrow) in a manner indistinguishable from their wild-type neighbors. (D) Cap1-deficient adaxial cells display the normal cuboidal and columnar cell shapes in presomitic mesoderm (arrows). (E, F) Cap1-deficient adaxial cells fail to make apical constrictions, to intercalate normally, or to broaden and make bipolar somite boundary attachments. Instead they display an isolated rounded appearance (arrows in panels E, F) among neighboring wild-type adaxial cells that have broadened (arrowheads in panels E, F).