期刊
NEURON
卷 49, 期 2, 页码 229-241出版社
CELL PRESS
DOI: 10.1016/j.neuron.2005.12.011
关键词
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资金
- Biotechnology and Biological Sciences Research Council [BB/D007585/1] Funding Source: Medline
- NEI NIH HHS [R01 EY008768-18, R01 EY008768-11, R01 EY008768-09, P30 EY016665, R01 EY008768-14A1, R01 EY008768-16, R01 EY008768-13, R01 EY008768-09S1, R01 EY008768-12, R01 EY008768-13S1, R01 EY008768-10A1, R01 EY008768-16S1, R01 EY008768-15, R01 EY008768-17, R01 EY008768-15S1, R01 EY008768-17S1, EY08768, R01 EY008768-12S1, R01 EY008768] Funding Source: Medline
- Biotechnology and Biological Sciences Research Council [BB/D007585/1] Funding Source: researchfish
- BBSRC [BB/D007585/1] Funding Source: UKRI
In sensory neurons, successful maturation of signaling molecules and regulation of Ca2+ are essential for cell function and survival. Here, we demonstrate a multifunctional role for calnexin as both a molecular chaperone uniquely required for rhodopsin maturation and a regulator of Ca2+ that enters photoreceptor cells during light stimulation. Mutations in Drosophila calnexin lead to severe defects in rhodopsin (Rh1) expression, whereas other photoreceptor cell proteins are expressed normally. Mutations in calnexin also impair the ability of photoreceptor cells to control cytosolic Ca2+ levels following activation of the light-sensitive TRP channels. Finally, mutations in calnexin lead to retinal degeneration that is enhanced by light, suggesting that calnexin's function as a Ca2+ buffer is important for photoreceptor cell survival. Our results illustrate a critical role for calnexin in Rh1 maturation and Ca2+ regulation and provide genetic evidence that defects in calnexin lead to retinal degeneration.
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