Abstract
To gain insight into the origin of the molecular diversity of voltage-gated sodium channels (NaVs), a putative sodium channel gene (TuNa2) was cloned from the protochordate ascidian. TuNa2 showed two unusual features in its primary structure; (1) lysine in the P-region of the third repeat, a critical site determining ion selectivity, was changed to glutamic acid, predicting that the ionic permeability would not be rigidly sodium-selective (2) the III-IV linker, determinant of fast inactivation, was only weakly conserved. In contrast with a pan-neuronally expressed NaV (TuNa1), expression of TuNa2 was confined to subsets of neurons including motor neurons, suggesting that TuNa2 plays specialized roles in electrical activities unique to these neurons. Basic FGF, a neural inducer in the ascidian embryo, induces TuNa2 RNA expression in the ectodermal cells at lower doses than that required for TuNa1 gene expression. Thus, two types of NaV may play distinct roles and their gene expressions are controlled by distinct mechanisms.
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