Mitochondrial dysfunction associated with TANGO2 deficiency

Transport and Golgi Organization protein 2 Homolog ( TANGO2 )-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced episodic rhabdomyolysis, and cardiac arrhythmias, al...

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Published inScientific reports Vol. 12; no. 1; p. 3045
Main Authors Heiman, Paige, Mohsen, Al-Walid, Karunanidhi, Anuradha, St Croix, Claudette, Watkins, Simon, Koppes, Erik, Haas, Richard, Vockley, Jerry, Ghaloul-Gonzalez, Lina
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Published London Nature Publishing Group UK 23.02.2022
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Abstract Transport and Golgi Organization protein 2 Homolog ( TANGO2 )-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced episodic rhabdomyolysis, and cardiac arrhythmias, along with severe metabolic crises including hypoglycemia, lactic acidosis, and hyperammonemia. Severity varies among and within families. Previous studies have reported contradictory evidence of mitochondrial dysfunction. Since the clinical symptoms and metabolic abnormalities are suggestive of a broad dysfunction of mitochondrial energy metabolism, we undertook a broad examination of mitochondrial bioenergetics in TANGO2 deficient patients utilizing skin fibroblasts derived from three patients exhibiting TANGO2 -related disease. Functional studies revealed that TANGO2 protein was present in mitochondrial extracts of control cells but not patient cells. Superoxide production was increased in patient cells, while oxygen consumption rate, particularly under stress, along with relative ATP levels and β-oxidation of oleate were reduced. Our findings suggest that mitochondrial function should be assessed and monitored in all patients with TANGO2 mutation as targeted treatment of the energy dysfunction could improve outcome in this condition.
AbstractList Transport and Golgi Organization protein 2 Homolog (TANGO2)-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced episodic rhabdomyolysis, and cardiac arrhythmias, along with severe metabolic crises including hypoglycemia, lactic acidosis, and hyperammonemia. Severity varies among and within families. Previous studies have reported contradictory evidence of mitochondrial dysfunction. Since the clinical symptoms and metabolic abnormalities are suggestive of a broad dysfunction of mitochondrial energy metabolism, we undertook a broad examination of mitochondrial bioenergetics in TANGO2 deficient patients utilizing skin fibroblasts derived from three patients exhibiting TANGO2-related disease. Functional studies revealed that TANGO2 protein was present in mitochondrial extracts of control cells but not patient cells. Superoxide production was increased in patient cells, while oxygen consumption rate, particularly under stress, along with relative ATP levels and β-oxidation of oleate were reduced. Our findings suggest that mitochondrial function should be assessed and monitored in all patients with TANGO2 mutation as targeted treatment of the energy dysfunction could improve outcome in this condition.
Transport and Golgi Organization protein 2 Homolog ( TANGO2 )-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced episodic rhabdomyolysis, and cardiac arrhythmias, along with severe metabolic crises including hypoglycemia, lactic acidosis, and hyperammonemia. Severity varies among and within families. Previous studies have reported contradictory evidence of mitochondrial dysfunction. Since the clinical symptoms and metabolic abnormalities are suggestive of a broad dysfunction of mitochondrial energy metabolism, we undertook a broad examination of mitochondrial bioenergetics in TANGO2 deficient patients utilizing skin fibroblasts derived from three patients exhibiting TANGO2 -related disease. Functional studies revealed that TANGO2 protein was present in mitochondrial extracts of control cells but not patient cells. Superoxide production was increased in patient cells, while oxygen consumption rate, particularly under stress, along with relative ATP levels and β-oxidation of oleate were reduced. Our findings suggest that mitochondrial function should be assessed and monitored in all patients with TANGO2 mutation as targeted treatment of the energy dysfunction could improve outcome in this condition.
Abstract Transport and Golgi Organization protein 2 Homolog (TANGO2)-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms typically manifest in early childhood and include developmental delay, stress-induced episodic rhabdomyolysis, and cardiac arrhythmias, along with severe metabolic crises including hypoglycemia, lactic acidosis, and hyperammonemia. Severity varies among and within families. Previous studies have reported contradictory evidence of mitochondrial dysfunction. Since the clinical symptoms and metabolic abnormalities are suggestive of a broad dysfunction of mitochondrial energy metabolism, we undertook a broad examination of mitochondrial bioenergetics in TANGO2 deficient patients utilizing skin fibroblasts derived from three patients exhibiting TANGO2-related disease. Functional studies revealed that TANGO2 protein was present in mitochondrial extracts of control cells but not patient cells. Superoxide production was increased in patient cells, while oxygen consumption rate, particularly under stress, along with relative ATP levels and β-oxidation of oleate were reduced. Our findings suggest that mitochondrial function should be assessed and monitored in all patients with TANGO2 mutation as targeted treatment of the energy dysfunction could improve outcome in this condition.
ArticleNumber 3045
Author Heiman, Paige
Karunanidhi, Anuradha
Ghaloul-Gonzalez, Lina
Mohsen, Al-Walid
Koppes, Erik
Watkins, Simon
St Croix, Claudette
Haas, Richard
Vockley, Jerry
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Snippet Transport and Golgi Organization protein 2 Homolog ( TANGO2 )-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene....
Transport and Golgi Organization protein 2 Homolog (TANGO2)-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene. Symptoms...
Abstract Transport and Golgi Organization protein 2 Homolog (TANGO2)-related disease is an autosomal recessive disorder caused by mutations in the TANGO2 gene....
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SubjectTerms 631/208
692/308
692/699
Acidosis
Adolescent
Adult
Aryl Hydrocarbon Receptor Nuclear Translocator - deficiency
Aryl Hydrocarbon Receptor Nuclear Translocator - genetics
Aryl Hydrocarbon Receptor Nuclear Translocator - metabolism
Bioenergetics
Cells, Cultured
Child
Children
Energy metabolism
Fatty Acids - metabolism
Female
Fibroblasts
Fibroblasts - metabolism
Golgi apparatus
Hereditary diseases
Humanities and Social Sciences
Humans
Hyperammonemia
Hypoglycemia
Lactic acidosis
Male
Metabolism
Mitochondria
Mitochondria - genetics
Mitochondria - metabolism
Mitochondria - ultrastructure
Mitochondrial Dynamics
Mitochondrial Proteins - metabolism
multidisciplinary
Mutation
Oxidation
Oxygen consumption
Patients
Protein transport
Rhabdomyolysis
Science
Science (multidisciplinary)
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Title Mitochondrial dysfunction associated with TANGO2 deficiency
URI https://link.springer.com/article/10.1038/s41598-022-07076-9
https://www.ncbi.nlm.nih.gov/pubmed/35197517
https://www.proquest.com/docview/2632035763
https://search.proquest.com/docview/2632801101
https://pubmed.ncbi.nlm.nih.gov/PMC8866466
https://doaj.org/article/bbd84a9f628544dc9e3cb0595985fc6f
Volume 12
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