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Ca 2+  flux into mitochondria is an important regulator of cytoplasmic Ca 2+  signals, energy production and cell death pathways. Ca 2+  uptake can occur through the recently discovered mitochondrial uniporter channel (MCU) but whether the MCU is involved in shaping Ca 2+  signals and downstream responses to physiological levels of receptor stimulation is unknown. Here, we show that modest stimulation of leukotriene receptors with the pro-inflammatory signal LTC 4  evokes a series of cytoplasmic Ca 2+  oscillations that are rapidly and faithfully propagated into mitochondrial matrix. Knockdown of MCU or mitochondrial depolarisation, to reduce the driving force for Ca 2+  entry into the matrix, prevents the mitochondrial Ca 2+  rise and accelerates run down of the oscillations. The loss of cytoplasmic Ca 2+  oscillations appeared to be a consequence of enhanced Ca 2+ -dependent inactivation of InsP 3  receptors, which arose from the loss of mitochondrial Ca 2+  buffering. Ca 2+  dependent gene expression in response to leukotriene receptor activation was suppressed following knockdown of the MCU. In addition to buffering Ca 2+  release, mitochondria also sequestrated Ca 2+  entry through store-operated Ca 2+  channels and this too was prevented following loss of MCU. MCU is therefore an important regulator of physiological pulses of cytoplasmic Ca 2+ .

plos one

Mitochondrial Calcium Uniporter MCU Supports Cytoplasmic Ca2+ Oscillations, Store-Operated Ca2+ Entry and Ca2+-Dependent Gene Expression in Response to Receptor Stimulation