Subfamily-specific posttranscriptional mechanism underlies K(+) channel expression in a developing neuronal blastomere.

Na(+) and K(+) channels are the two key proteins that shape the action potentials in neurons. However, little is known about how the expression of these two channels is coordinated. To address this issue, we cloned a Shab-related K(+) channel gene from ascidian Halocynthia roretzi (TuKv2). In this animal, a blastomere of neuronal lineage isolated from the 8-cell embryo expresses single Na(+) channel and K(+) channel genes after neural induction. Expression of a dominant negative form of TuKv2 eliminated the native delayed rectifier K(+) currents, indicating that the entire delayed rectifier K(+) current of the neuronal blastomere is exclusively encoded by TuKv2. TuKv2 transcripts are expressed more broadly than Na(+) channel transcripts, which are restricted to the neuronal lineages. There is also a temporal mismatch in the expression of TuKv2 transcript and the K(+) current; TuKv2 transcripts are present throughout development, whereas delayed rectifier K(+) currents only appear after the tailbud stage, suggesting that the functional expression of the TuKv2 transcript is suppressed during the early embryonic stages. To test if this suppression occurs by a mechanism specific to the TuKv2 channel protein, an ascidian Shaker-related gene, TuKv1, was misexpressed in neural blastomeres. A TuKv1-encoded current was expressed earlier than the TuKv2 current. Furthermore, the introduction of the TuKv2-expressing plasmid into noninduced cells did not lead to the current expression. These results raise the possibility that the expression of TuKv2 is post-transcriptionally controlled through a mechanism that is dependent on neural induction.