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Tufi 2019 Cell Rep

From Bioblast
Publications in the MiPMap
Tufi R, Gleeson TP, von Stockum S, Hewitt VL, Lee JJ, Terriente-Felix A, Sanchez-Martinez A, Ziviani E, Whitworth AJ (2019) Comprehensive genetic characterization of mitochondriaasl Ca2+ uniporter components reveals their different physiological requirements in vivo. https://doi.org/10.1016/j.celrep.2019.04.033

Β» Cell Rep 27:1541-50.e5. PMID: 31042479 Open Access

Tufi Roberta, Gleeson Thomas P, von Stockum Sophia, Hewitt Victoria L, Lee Juliette J, Terriente-Felix Ana, Sanchez-Martinez Alvaro, Ziviani Elena, Whitworth Alexander J (2019) Cell Rep

Abstract: Mitochondrial Ca2+ uptake is an important mediator of metabolism and cell death. Identification of components of the highly conserved mitochondrial Ca2+ uniporter has opened it up to genetic analysis in model organisms. Here, we report a comprehensive genetic characterization of all known uniporter components conserved in Drosophila. While loss of pore-forming MCU or EMRE abolishes fast mitochondrial Ca2+ uptake, this results in only mild phenotypes when young, despite shortened lifespans. In contrast, loss of the MICU1 gatekeeper is developmentally lethal, consistent with unregulated Ca2+ uptake. Mutants for the neuronally restricted regulator MICU3 are viable with mild neurological impairment. Genetic interaction analyses reveal that MICU1 and MICU3 are not functionally interchangeable. More surprisingly, loss of MCU or EMRE does not suppress MICU1 mutant lethality, suggesting that this results from uniporter-independent functions. Our data reveal the interplay among components of the mitochondrial Ca2+ uniporter and shed light on their physiological requirements in vivo. β€’ Keywords: Drosophila, EMRE, MCU, MICU1, MICU3, Calcium, Genetic interaction, Genetics, Mitochondria β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: UK Cambridge Whitworth A


Labels: MiParea: Respiration 


Organism: Drosophila 

Preparation: Homogenate 


Coupling state: OXPHOS  Pathway: N, S  HRR: Oxygraph-2k