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The swimming larvae of the chordate ascidians possess a dorsal hollowed central nervous system ( CNS), which is homologous to that of vertebrates. Despite the homology, the ascidian CNS consists of a countable number of cells. The simple nervous system of ascidians provides an excellent experimental system to study the developmental mechanisms of the chordate nervous system. The neural fate of the cells consisting of the ascidian CNS is determined in both autonomous and non-autonomous fashion during the cleavage stage. The ascidian neural plate performs the morphogenetic movement of neural tube closure that resembles that in vertebrate neural tube formation. Following neurulation, the CNS is separated into five distinct regions, whose homology with the regions of vertebrate CNS has been discussed. Following their larval stage, ascidians undergo a metamorphosis and become sessile adults. The metamorphosis is completed quickly, and therefore the metamorphosis of ascidians is a good experimental system to observe the reorganization of the CNS during metamorphosis. A recent study has shown that the major parts of the larval CNS remain after the metamorphosis to form the adult CNS. In contrast to such a conserved manner of CNS reorganization, most larval neurons disappear during metamorphosis. The larval glial cells in the CNS are the major source for the formation of the adult CNS, and some of the glial cells produce adult neurons. [ABSTRACT FROM AUTHOR]

Overexpression of a lefty orthologue, Ci-lefty, caused a failure of neural tube closure in the protochordate ascidian Ciona intestinalis. The body bent dorsally, and anterior–posterior elongation was inhibited. A similar phenotype was observed in embryos treated with SB431542, an inhibitor of Nodal receptors, suggesting that Ci-Lefty antagonized Nodal signaling as reported in other deuterostome species. Overexpression of Ci-nodal also resulted in a similar phenotype, suggesting that a correct quantity and/or a spatial restriction of Nodal signaling are important for the neural tube to form. In addition to known Ci-Nodal target genes, orthologues of Zic ( Ci-ZicL) and cdx ( Ci-cdx) were activated by Ci-Nodal. Expression of a dominant negative Ci-cdx caused defects in neural tube formation similar to those obtained on treatment with SB431542 or overexpression of Ci-lefty. A regulatory cascade composed of Ci-Nodal, Ci-ZicL, and Ci-Cdx may play an important role in neural tube formation in the Ciona embryo. [ABSTRACT FROM AUTHOR]