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 potentia ls in neurons. However, little is known about how the expression of these t wo 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 rectifi er 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 restrict ed to the neuronal lineages. There is also a temporal mismatch in the expre ssion 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 T uKv2 transcript is suppressed during the early embryonic stages. To test if this suppression occurs by a mechanism specific to the TuKv2 cha nnel protein, an ascidian Shaker-related gene, TuKv1, was misexpressed in n eural blastomeres. A TuKv1-encoded current was expressed earlier than the T uKv2 current. Furthermore, the introduction of the TuKv2-expressing plasmid into noninduced cells did not lead to the current expression. These result s raise the possibility that the expression of TuKv2 is post-transcriptiona lly controlled through a mechanism that is dependent on neural induction.