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J. Biol. Chem., Vol. 275, Issue 51, 39846-39854, December 22, 2000
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and
Calmodulin via Interactions with N and C Termini of
1C*
,,
From the Department of Physiology and Pharmacology, Sackler School
of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel
Neuronal voltage-dependent Ca2+
channels of the N (
1B) and P/Q
(1A) type are inhibited by neurotransmitters that
activate Gi/o G proteins; a major part of the inhibition is
voltage-dependent, relieved by depolarization, and results from a
direct binding of G
subunit of G proteins to the channel.
Since cardiac and neuronal L-type (1C) voltage-dependent
Ca2+ channels are not modulated in this way, they are
presumed to lack interaction with G. However, here we demonstrate
that both G and calmodulin directly bind to cytosolic N and C
termini of the 1C subunit. Coexpression of G
reduces the current via the L-type channels. The inhibition depends on
the presence of calmodulin, occurs at basal cellular levels of
Ca2+, and is eliminated by EGTA. The N and C termini of
1C appear to serve as partially independent but
interacting inhibitory gates. Deletion of the N terminus or of the
distal half of the C terminus eliminates the inhibitory effect of
G. Deletion of the N terminus profoundly impairs the
Ca2+/calmodulin-dependent inactivation. We
propose that G and calmodulin regulate the L-type
Ca2+ channel in a concerted manner via a molecular
inhibitory scaffold formed by N and C termini of
1C.
Contributed equally to the results of this report.
§
To whom correspondence should be addressed. Tel:. 972-3-6409863;
Fax: 972-3-6409113; E-mail: dascaln@post.tau.ac.il.
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