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Characterizing the function of MCUb as an inducible activator of mitochondrial oxidative phosphorylation

ABSTRACT: Characterizing the function of MCUb as an inducible activator of mitochondrial oxidative phosphorylation

PROVIDER: PRJNA844074 | ENA |

REPOSITORIES: ENA

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Characterizing the function of MCUb as an inducible activator of mitochondrial oxidative phosphorylation

Project description:Influx of Ca2+ across the inner mitochondrial membrane via the mitochondrial Ca2+ uniporter (MCU) enhances the activity of several electron transport chain dehydrogenases and the F1F0 ATP synthase. In this study, we investigated the role of MCUb, an MCU complex gene product that is a direct inhibitor of MCU mediated Ca2+ influx. We find MCUb expression to be induced by caloric restriction in heart, skeletal muscle, liver and kidney where it functions as a metabolic activator of mitochondrial fatty acid utilization. Mice selectively deficient for Mcub in skeletal muscle showed a metabolic signature of deficient fatty acid utilization in muscle, associated with progressive age-related obesity, glucose intolerance and metabolic syndrome. To define transcriptional changes underlying, and potentially contributing to this regulation of Ca2+-dependent mitochondrial fatty acid utilization, microarray analyses of tibialis anterior (TA) muscle from control and knockout mice was carried out. We used microarrays to elucidate effects of MCU and MCUb ablation on transcriptional profiles of TA muscle

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Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis

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Oxidative phosphorylation promotes primary melanoma invasion

Project description:Dermal invasion is a hallmark of malignant melanoma. The molecular alterations driving the progression of primary melanoma to metastatic disease have been studied extensively, whereas the early progression of non-invasive primary melanoma to an invasive state is not well understood. To elucidate the mechanisms underlying the transition from radial to vertical growth, the first step in melanoma invasion, we developed a zebrafish melanoma model in which constitutive activation of ribosomal protein S6 kinase 1 (RSK1) drives tumor invasion. Transcriptomic analysis of RSK1-activated tumors identified metabolic changes, including upregulation of genes associated with oxidative phosphorylation. Vertical growth phase human melanoma cells show higher oxygen consumption and preferential utilization of glutamine compared to radial growth phase melanoma cells. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1a has been proposed as a master regulator of tumor oxidative phosphorylation. In human primary melanoma specimens we show that PGC1a protein expression is positively associated with increased tumor thickness and expression of the proliferative marker Ki-67 and the reactive oxygen species (ROS) scavenger SCARA3. PGC1a depletion modulates cellular processes associated with primary melanoma growth and invasion, including oxidative stress. Our results support a role for PGC1a in mediating glutamine-driven OXPHOS to facilitate the invasive growth of primary melanoma.

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