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13 results on '"Papakyrikos, Amanda M."'

5. Biological clocks and incremental growth line formation in dentine

Author

Papakyrikos, Amanda M., primary, Arora, Manish, additional, Austin, Christine, additional, Boughner, Julia C., additional, Capellini, Terence D., additional, Dingwall, Heather L., additional, Greba, Quentin, additional, Howland, John G., additional, Kato, Akiko, additional, Wang, Xiu‐Ping, additional, and Smith, Tanya M., additional

Published
2020
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7. PINK1 Phosphorylates MIC60/Mitofilin to Control Structural Plasticity of Mitochondrial Crista Junctions

Author

Tsai, Pei-I, primary, Lin, Chin-Hsien, additional, Hsieh, Chung-Han, additional, Papakyrikos, Amanda M., additional, Kim, Min Joo, additional, Napolioni, Valerio, additional, Schoor, Carmen, additional, Couthouis, Julien, additional, Wu, Ruey-Meei, additional, Wszolek, Zbigniew K., additional, Winter, Dominic, additional, Greicius, Michael D., additional, Ross, Owen A., additional, and Wang, Xinnan, additional

Published
2018
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11. Phosphorylation of MCAD selectively rescues PINK1deficiencies in behavior and metabolism

Author

Course, Meredith M., Scott, Anna I., Schoor, Carmen, Hsieh, Chung-Han, Papakyrikos, Amanda M., Winter, Dominic, Cowan, Tina M., and Wang, Xinnan

Abstract

PINK1 is a mitochondria-targeted kinase whose mutations are a cause of Parkinson’s disease. We found that PINK1 mediates the phosphorylation of MCAD, a mitochondrial matrix protein critical to fatty acid metabolism. Mimicking phosphorylation of this protein restores PINK1 deficiencies in behavior and metabolism in Drosophila.

Published
2018
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12. DrosophilaMIC60/mitofilin conducts dual roles in mitochondrial motility and crista structure

Author

Tsai, Pei-I, Papakyrikos, Amanda M., Hsieh, Chung-Han, and Wang, Xinnan

Abstract

Mitochondria are crucial organelles for providing energy for a cell. It is known that MIC60/mitofilin is important for maintaining mitochondrial structure in dissociated cells; however, its physiological roles in an intact animal are less clear. In this study, we unravel the functional consequences of deleting MIC60/mitofilin in fruit flies.

Published
2017
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13. Phosphorylation of MCAD selectively rescues PINK1 deficiencies in behavior and metabolism.

Author

Course MM, Scott AI, Schoor C, Hsieh CH, Papakyrikos AM, Winter D, Cowan TM, and Wang X

Subjects
Acyl-CoA Dehydrogenase genetics, Adenosine Triphosphate metabolism, Amino Acid Sequence, Amino Acids deficiency, Amino Acids metabolism, Animals, Animals, Genetically Modified, Carnitine analogs & derivatives, Carnitine metabolism, Drosophila Proteins chemistry, Drosophila Proteins genetics, Oxidation-Reduction, Phenotype, Phosphorylation, Phosphoserine metabolism, Protein Serine-Threonine Kinases metabolism, Acyl-CoA Dehydrogenase metabolism, Drosophila Proteins metabolism, Drosophila melanogaster metabolism, Protein Serine-Threonine Kinases deficiency
Abstract

PTEN-induced putative kinase 1 (PINK1) is a mitochondria-targeted kinase whose mutations are a cause of Parkinson's disease. We set out to better understand PINK1's effects on mitochondrial proteins in vivo. Using an unbiased phosphoproteomic screen in Drosophila, we found that PINK1 mediates the phosphorylation of MCAD, a mitochondrial matrix protein critical to fatty acid metabolism. By mimicking phosphorylation of this protein in a PINK1 null background, we restored PINK1 null's climbing, flight, thorax, and wing deficiencies. Owing to MCAD's role in fatty acid metabolism, we examined the metabolic profile of PINK1 null flies, where we uncovered significant disruptions in both acylcarnitines and amino acids. Some of these disruptions were rescued by phosphorylation of MCAD, consistent with MCAD's rescue of PINK1 null's organismal phenotypes. Our work validates and extends the current knowledge of PINK1, identifies a novel function of MCAD, and illuminates the need for and effectiveness of metabolic profiling in models of neurodegenerative disease.

Published
2018
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