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Calcium influx via TRP channels is required to maintain PIP2 levels in Drosophila photoreceptors

被引：167
作者：
Hardie, RC
Raghu, P
Moore, S
Juusola, M
Baines, RA
Sweeney, ST
机构：
[1] Univ Cambridge, Dept Anat, Cambridge, England
[2] Univ Cambridge, Dept Physiol, Cambridge, England
[3] Univ Cambridge, Dept Zool, Cambridge, England
[4] Univ Cambridge, Dept Genet, Cambridge CB2 3EH, England
来源：
NEURON | 2001年 / 30卷 / 01期
基金：
英国惠康基金; 英国生物技术与生命科学研究理事会;
关键词：
D O I：
10.1016/S0896-6273(01)00269-0
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
The trp (transient receptor potential) gene encodes a Ca2+ channel responsible for the major component of the phospholipase C (PLC) mediated light response in Drosophila. In trp mutants, maintained light leads to response decay and temporary total loss of sensitivity (inactivation). Using genetically targeted PIP2-sensitive inward rectifier channels (Kir2.1) as biosensors, we provide evidence that trp decay reflects depletion of PIP2 Two independent mutations in the PIP2 recycling pathway (rdgB and cds) prevented recovery from inactivation. Abolishing Ca2+ influx in wild-type photoreceptors mimicked inactivation, while raising Ca2+ by blocking Na+/Ca2+ exchange prevented inactivation in trp. The results suggest that Ca2+ influx prevents PIP, depletion by inhibiting PLC activity and facilitating PIP2 recycling. Without this feedback one photon appears sufficient to deplete the phosphoinositide pool of similar to4 microvilli.
引用
收藏
页码：149 / 159
页数：11
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