F. Ono et al., Subfamily-specific posttranscriptional mechanism underlies K+ channel expression in a developing neuronal blastomere, J NEUROSC, 19(16), 1999, pp. 6874-6886
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.