QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, January 2, 2008, 28(1):31-38; doi:10.1523/JNEUROSCI.4498-07.2008

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Dickman, D. K. Articles by Schwarz, T. L. Search for Related Content PubMed PubMed Citation Articles by Dickman, D. K. Articles by Schwarz, T. L. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Compound via MeSH Substance via MeSH Hazardous Substances DB CALCIUM COMPOUNDS CALCIUM, ELEMENTAL

 Previous Article  |  Next Article 

Cellular/Molecular
Mutations in a Drosophila ₂ Voltage-Gated Calcium Channel Subunit Reveal a Crucial Synaptic Function

Dion K. Dickman, ^* Peri T. Kurshan, ^* and Thomas L. Schwarz

F. M. Kirby Neurobiology Center, Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115

Correspondence should be addressed to Thomas L. Schwarz, Children's Hospital, F. M. Kirby Neurobiology Center, Enders 208, Boston, MA 02115. Email: thomas.schwarz{at}childrens.harvard.edu

Voltage-dependent calcium channels regulate many aspects of neuronal biology, including synaptic transmission. In addition to their ₁ subunit, which encodes the essential voltage gate and selective pore, calcium channels also contain auxiliary ₂, β, and subunits. Despite progress in understanding the biophysical properties of calcium channels, the in vivo functions of these auxiliary subunits remain unclear. We have isolated mutations in the gene encoding an ₂ calcium channel subunit (d₂-3) using a forward genetic screen in Drosophila. Null mutations in this gene are embryonic lethal and can be rescued by expression in the nervous system, demonstrating that the essential function of this subunit is neuronal. The photoreceptor phenotype of d₂-3 mutants resembles that of the calcium channel ₁ mutant cacophony (cac), suggesting shared functions. We have examined in detail genotypes that survive to the third-instar stage. Electrophysiological recordings demonstrate that synaptic transmission is severely impaired in these mutants. Thus the ₂ calcium channel subunit is critical for calcium-dependent synaptic function. As such, this Drosophila isoform is the likely partner to the presynaptic calcium channel ₁ subunit encoded by the cac locus. Consistent with this hypothesis, cacGFP fluorescence at the neuromuscular junction is reduced in d₂-3 mutants. This is the first characterization of an ₂-3 mutant in any organism and indicates a necessary role for ₂-3 in presynaptic vesicle release and calcium channel expression at active zones.

Key words: calcium channel; synaptic transmission; bouton; active zone; neuromuscular junction; Drosophila

---

Received June 19, 2007; revised Oct. 11, 2007; accepted Oct. 14, 2007.

Correspondence should be addressed to Thomas L. Schwarz, Children's Hospital, F. M. Kirby Neurobiology Center, Enders 208, Boston, MA 02115. Email: thomas.schwarz{at}childrens.harvard.edu

This article has been cited by other articles:

				J. W. Worrell and R. B. Levine Characterization of Voltage-Dependent Ca2+ Currents in Identified Drosophila Motoneurons In Situ J Neurophysiol, August 1, 2008; 100(2): 868 - 878. [Abstract] [Full Text] [PDF]

				C. V. Ly, C.-K. Yao, P. Verstreken, T. Ohyama, and H. J. Bellen straightjacket is required for the synaptic stabilization of cacophony, a voltage-gated calcium channel {alpha}1 subunit J. Cell Biol., April 3, 2008; 181(1): 157 - 170. [Abstract] [Full Text] [PDF]

				Y. P. Wairkar, L. G. Fradkin, J. N. Noordermeer, and A. DiAntonio Synaptic Defects in a Drosophila Model of Congenital Muscular Dystrophy J. Neurosci., April 2, 2008; 28(14): 3781 - 3789. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help