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Rods and cones use intracellular Ca
2+
to regulate many functions, including phototransduction and neurotransmission. The Mitochondrial Calcium Uniporter (MCU) complex is thought to be the primary pathway for Ca
2+
entry into mitochondria in eukaryotes. We investigate the hypothesis that mitochondrial Ca
2+
uptake via MCU influences phototransduction and energy metabolism in photoreceptors using a
mcu
-/-
zebrafish and a rod photoreceptor-specific
Mcu
-/-
mouse. Using genetically encoded Ca
2+
sensors to directly examine Ca
2+
uptake in zebrafish cone mitochondria, we found that loss of MCU reduces but does not eliminate mitochondrial Ca
2+
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
+
/Ca
2+
, 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 Ca
2+
uptake into photoreceptor mitochondria.