TY - JOUR
T1 - Light activation, adaptation, and cell survival functions of the Na +/Ca2+ exchanger CalX
AU - Wang, Tao
AU - Xu, Hong
AU - Oberwinkler, Johannes
AU - Gu, Yuchun
AU - Hardie, Roger C.
AU - Montell, Craig
PY - 2005/2/3
Y1 - 2005/2/3
N2 - In sensory neurons, Ca2+ entry is crucial for both activation and subsequent attenuation of signaling. Influx of Ca2+ is counterbalanced by Ca2+ extrusion, and Na+/Ca2+ exchange is the primary mode for rapid Ca2+ removal during and after sensory stimulation. However, the consequences on sensory signaling resulting from mutations in Na+/Ca2+ exchangers have not been described. Here, we report that mutations in the Drosophila Na +/Ca2+ exchanger calx have a profound effect on activity-dependent survival of photoreceptor cells. Loss of CalX activity resulted in a transient response to light, a dramatic decrease in signal amplification, and unusually rapid adaptation. Conversely, overexpression of CalX had reciprocal effects and greatly suppressed the retinal degeneration caused by constitutive activity of the TRP channel. These results illustrate the critical role of Ca2+ for proper signaling and provide genetic evidence that Ca2+ overload is responsible for a form of retinal degeneration resulting from defects in the TRP channel.
AB - In sensory neurons, Ca2+ entry is crucial for both activation and subsequent attenuation of signaling. Influx of Ca2+ is counterbalanced by Ca2+ extrusion, and Na+/Ca2+ exchange is the primary mode for rapid Ca2+ removal during and after sensory stimulation. However, the consequences on sensory signaling resulting from mutations in Na+/Ca2+ exchangers have not been described. Here, we report that mutations in the Drosophila Na +/Ca2+ exchanger calx have a profound effect on activity-dependent survival of photoreceptor cells. Loss of CalX activity resulted in a transient response to light, a dramatic decrease in signal amplification, and unusually rapid adaptation. Conversely, overexpression of CalX had reciprocal effects and greatly suppressed the retinal degeneration caused by constitutive activity of the TRP channel. These results illustrate the critical role of Ca2+ for proper signaling and provide genetic evidence that Ca2+ overload is responsible for a form of retinal degeneration resulting from defects in the TRP channel.
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U2 - 10.1016/j.neuron.2004.12.046
DO - 10.1016/j.neuron.2004.12.046
M3 - Article
C2 - 15694324
AN - SCOPUS:13244298286
SN - 0896-6273
VL - 45
SP - 367
EP - 378
JO - Neuron
JF - Neuron
IS - 3
ER -