Elongation of axolot1 tailbud embryos requires GPI-linked proteins and organizer-induced, active, ventral trunk endoderm cell rearrangements

Application of phosphatidylinositol-specific phospholipase C to early tailb ud stage axolotl embryos reveals that a specific subset of morphogenetic mo vements requires glycosylphosphatidylinositol (GPI)-linked cell-surface pro teins. These include pronephric duct extension, "gill bulge" formation, and embryonic elongation along the anteroposterior axis. The work of Kitchin ( 1949, T. Exp. Zool. 112, 393-416) led to the conclusion that extension of t he notochord provided the motive force driving anteroposterior stretching i n axolotl embryos, elongation of other tissues being a passive response. We therefore conjectured that axial mesoderm cells might display the GPI-link ed proteins required for elongation of the embryo. However, we show here th at removal of most of the neural plate and axial and paraxial mesoderm prio r to neural tube closure does not prevent elongation of ventrolateral tissu es. Tissue-extirpation and tissue-marking experiments indicate that elongat ion of the ventral trunk occurs via active, directed tissue rearrangements within the endoderm, directed by signals emanating from the blastopore regi on. Extension of both dorsal and ventral tissues requires GPI-linked protei ns. We conclude that elongation of axolotl embryos requires active cell rea rrangements within ventral as well as axial tissues. The fact that both typ es of elongation are prevented by removal of GPI-linked proteins implies th at they share a common molecular mechanism. (C) 2000 Academic Press.