Regulation of voltage-gated ion channels during ascidian embryogenesis.

In the proto-chordate Halocynthia roretzi, a voltage-activated sodium current undergoes a change in kinetics within 48 h of fertilization. Molecular cloning and microinjection of antisense DNA into single cells suggest that the kinetic changes are due to the increased expression of a neural-specific sodium channel gene, TuNa I. TuNa I gene transcription is first induced in late-stage gastrulae, preceding the appearance of the rapidly inactivating sodium current unique to alpha 4-2 derived neural cells. In cleavage-arrested and intact embryos, cell interactions between specific animal and vegetal blastomeres are required for induction of TuNa I gene expression. By contrast, another sodium channel gene, TuNa II, is mainly expressed in neural cells of the alpha 4-1 lineage. In this lineage, cells of endoderm, notochord and muscle develop. TuNa II gene transcription occurs in isolated alpha 4-1 blastomeres without interacting with other lineage cells. Thus, there are two distinct neural cell lineages in the ascidian tadpole: one is similar to the ectoderm-derived neural tissue controlled by a mechanism reminiscent of the neural induction in the vertebrate, the other is the lineage of posterior neural tube in which motor neurons develop in close association with the notochord or muscle lineage.