The Journal of Neuroscience, August 15, 1999, 19(16):6874-6886
Subfamily-Specific Posttranscriptional Mechanism Underlies
K+ Channel Expression in a Developing Neuronal
Blastomere
Fumihito
Ono1, 2,
You
Katsuyama1,
Kouichi
Nakajo3, and
Yasushi
Okamura1, 3, 4
1 Ion Channel Group, Biomolecular Engineering
Department, National Institute of Bioscience and Human Technology,
Tsukuba, Ibaraki 305-8566, Japan, 2 Department of Medical
Physiology, Meiji College of Pharmacy, Kiyose 204-8588, Tokyo, Japan,
3 Department of Life Sciences, Graduate School of Arts and
Sciences, University of Tokyo, Meguro-ku, Tokyo 153-0041, Japan, and
4 Intelligence and Synthesis, Precursory Research for
Embryonic Science and Technology, Japan Science and Technology
Corporation
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.
Key words:
potassium channel; ascidian; gene expression; dominant negative; sodium channel; neuronal differentiation; post-transcriptional regulation
Copyright © 1999 Society for Neuroscience 0270-6474/99/19166874-13$05.00/0
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