|ZFIN ID: ZDB-PUB-201002-211|
Mitochondrial Calcium Uniporter (MCU) deficiency reveals an alternate path for Ca2+ uptake in photoreceptor mitochondria
Bisbach, C.M., Hutto, R.A., Poria, D., Cleghorn, W.M., Abbas, F., Vinberg, F., Kefalov, V.J., Hurley, J.B., Brockerhoff, S.E.
|Source:||Scientific Reports 10: 16041 (Journal)|
|Registered Authors:||Abbas, Fatima, Brockerhoff, Susan, Hurley, James B.|
|PubMed:||32994451 Full text @ Sci. Rep.|
Bisbach, C.M., Hutto, R.A., Poria, D., Cleghorn, W.M., Abbas, F., Vinberg, F., Kefalov, V.J., Hurley, J.B., Brockerhoff, S.E. (2020) Mitochondrial Calcium Uniporter (MCU) deficiency reveals an alternate path for Ca2+ uptake in photoreceptor mitochondria. Scientific Reports. 10:16041.
ABSTRACTRods and cones use intracellular Ca2+ to regulate many functions, including phototransduction and neurotransmission. The Mitochondrial Calcium Uniporter (MCU) complex is thought to be the primary pathway for Ca2+ entry into mitochondria in eukaryotes. We investigate the hypothesis that mitochondrial Ca2+ uptake via MCU influences phototransduction and energy metabolism in photoreceptors using a mcu-/- zebrafish and a rod photoreceptor-specific Mcu-/- mouse. Using genetically encoded Ca2+ sensors to directly examine Ca2+ uptake in zebrafish cone mitochondria, we found that loss of MCU reduces but does not eliminate mitochondrial Ca2+ uptake. Loss of MCU does not lead to photoreceptor degeneration, mildly affects mitochondrial metabolism, and does not alter physiological responses to light, even in the absence of the Na+/Ca2+, K+ exchanger. Our results reveal that MCU is dispensable for vertebrate photoreceptor function, consistent with its low expression and the presence of an alternative pathway for Ca2+ uptake into photoreceptor mitochondria.