TY - JOUR
T1 - Genetic analysis of a synaptic calcium channel in Drosophila
T2 - Intragenic modifiers of a temperature-sensitive paralytic mutant of cacophony
AU - Brooks, I. M.
AU - Felling, R.
AU - Kawasaki, F.
AU - Ordway, R. W.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2003/5/1
Y1 - 2003/5/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0037517041&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037517041&partnerID=8YFLogxK
M3 - Article
C2 - 12750329
AN - SCOPUS:0037517041
SN - 0016-6731
VL - 164
SP - 163
EP - 171
JO - Genetics
JF - Genetics
IS - 1
ER -