Molecular Cloning and Characterization of a Putative Neural Calcium Channel α1-Subunit from Squid Optic Lobe

1997 ◽  
Vol 230 (1) ◽  
pp. 147-154 ◽  
Author(s):  
Tadashi Kimura ◽  
Osamu Shouno ◽  
Kiyonori Hirota ◽  
Takehiko Saito ◽  
Gen Matsumoto ◽  
...  
Genetics ◽  
1998 ◽  
Vol 148 (3) ◽  
pp. 1159-1169
Author(s):  
Daniel F Eberl ◽  
Dejian Ren ◽  
Guoping Feng ◽  
Lori J Lorenz ◽  
David Van Vactor ◽  
...  

Abstract To begin unraveling the functional significance of calcium channel diversity, we identified mutations in Dmca1D, a Drosophila calcium channel α1 subunit cDNA that we recently cloned. These mutations constitute the l(2)35Fa lethal locus, which we rename Dmca1D. A severe allele, Dmca1DX10, truncates the channel after the IV-S4 transmembrane domain. These mutants die as late embryos because they lack vigorous hatching movements. In the weaker allele, Dmca1DAR66, a cysteine in transmembrane domain I-S1 is changed to tyrosine. Dmca1DAR66 embryos hatch but pharate adults have difficulty eclosing. Those that do eclose have difficulty in fluid-filling of the wings. These studies show that this member of the calcium channel α1 subunit gene family plays a nonredundant, vital role in larvae and adults.


Neuron ◽  
1991 ◽  
Vol 7 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Anna Hui ◽  
Patrick T. Ellinor ◽  
Olga Krizanova ◽  
Jing-Ding Wang ◽  
Ronald J. Diebold ◽  
...  

1999 ◽  
Vol 14 (3) ◽  
pp. 386-395 ◽  
Author(s):  
Juan C. Loza ◽  
Lillian C. Carpio ◽  
Peter G. Bradford ◽  
Rosemary Dziak

2002 ◽  
Vol 62 (3) ◽  
pp. 485-496 ◽  
Author(s):  
Ning Qin ◽  
Susan Yagel ◽  
Mary-Lou Momplaisir ◽  
Ellen E. Codd ◽  
Michael R. D'Andrea

1996 ◽  
Vol 25 ◽  
pp. S22
Author(s):  
Tadashi Kimura ◽  
Osamu Shouno ◽  
Kiyonori Hirota ◽  
Chikara Sato ◽  
Takehiko Saito ◽  
...  

FEBS Letters ◽  
1994 ◽  
Vol 338 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Thierry Coppola ◽  
Rainer Waldmann ◽  
Marc Borsotto ◽  
Catherine Heurteaux ◽  
Georges Romey ◽  
...  

Genetics ◽  
2003 ◽  
Vol 164 (1) ◽  
pp. 163-171
Author(s):  
I M Brooks ◽  
R Felling ◽  
F Kawasaki ◽  
R W Ordway

Abstract Our previous genetic analysis of synaptic mechanisms in Drosophila identified a temperature-sensitive paralytic mutant of the voltage-gated calcium channel α1 subunit gene, cacophony (cac). Electrophysiological studies in this mutant, designated cacTS2, indicated cac encodes a primary calcium channel α1 subunit functioning in neurotransmitter release. To further examine the functions and interactions of cac-encoded calcium channels, a genetic screen was performed to isolate new mutations that modify the cacTS2 paralytic phenotype. The screen recovered 10 mutations that enhance or suppress cacTS2, including second-site mutations in cac (intragenic modifiers) as well as mutations mapping to other genes (extragenic modifiers). Here we report molecular characterization of three intragenic modifiers and examine the consequences of these mutations for temperature-sensitive behavior, synaptic function, and processing of cac pre-mRNAs. These mutations may further define the structural basis of calcium channel α1 subunit function in neurotransmitter release.


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