ATPase-deficient mitochondrial inner membrane protein ATAD3A disturbs mitochondrial dynamics in dominant hereditary spastic paraplegia

De novo mutations in ATAD3A (ATPase family AAA-domain containing protein 3A) were recently found to cause a neurological syndrome with developmental delay, hypotonia, spasticity, optic atrophy, axonal neuropathy, and hypertrophic cardiomyopathy. Using whole-exome sequencing, we identified a dominant...

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Vydané v:Human molecular genetics Ročník 26; číslo 8; s. 1432 - 1443
Hlavní autori: Cooper, Helen M, Yang, Yang, Ylikallio, Emil, Khairullin, Rafil, Woldegebriel, Rosa, Lin, Kai-Lan, Euro, Liliya, Palin, Eino, Wolf, Alexander, Trokovic, Ras, Isohanni, Pirjo, Kaakkola, Seppo, Auranen, Mari, Lönnqvist, Tuula, Wanrooij, Sjoerd, Tyynismaa, Henna
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Jazyk:English
Vydavateľské údaje: England 15.04.2017
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Abstract De novo mutations in ATAD3A (ATPase family AAA-domain containing protein 3A) were recently found to cause a neurological syndrome with developmental delay, hypotonia, spasticity, optic atrophy, axonal neuropathy, and hypertrophic cardiomyopathy. Using whole-exome sequencing, we identified a dominantly inherited heterozygous variant c.1064G > A (p.G355D) in ATAD3A in a mother presenting with hereditary spastic paraplegia (HSP) and axonal neuropathy and her son with dyskinetic cerebral palsy, both with disease onset in childhood. HSP is a clinically and genetically heterogeneous disorder of the upper motor neurons. Symptoms beginning in early childhood may resemble spastic cerebral palsy. The function of ATAD3A, a mitochondrial inner membrane AAA ATPase, is yet undefined. AAA ATPases form hexameric rings, which are catalytically dependent on the co-operation of the subunits. The dominant-negative patient mutation affects the Walker A motif, which is responsible for ATP binding in the AAA module of ATAD3A, and we show that the recombinant mutant ATAD3A protein has a markedly reduced ATPase activity. We further show that overexpression of the mutant ATAD3A fragments the mitochondrial network and induces lysosome mass. Similarly, we observed altered dynamics of the mitochondrial network and increased lysosomes in patient fibroblasts and neurons derived through differentiation of patient-specific induced pluripotent stem cells. These alterations were verified in patient fibroblasts to associate with upregulated basal autophagy through mTOR inactivation, resembling starvation. Mutations in ATAD3A can thus be dominantly inherited and underlie variable neurological phenotypes, including HSP, with intrafamiliar variability. This finding extends the group of mitochondrial inner membrane AAA proteins associated with spasticity.
AbstractList De novo mutations in ATAD3A (ATPase family AAA-domain containing protein 3A) were recently found to cause a neurological syndrome with developmental delay, hypotonia, spasticity, optic atrophy, axonal neuropathy, and hypertrophic cardiomyopathy. Using whole-exome sequencing, we identified a dominantly inherited heterozygous variant c.1064G > A (p.G355D) in ATAD3A in a mother presenting with hereditary spastic paraplegia (HSP) and axonal neuropathy and her son with dyskinetic cerebral palsy, both with disease onset in childhood. HSP is a clinically and genetically heterogeneous disorder of the upper motor neurons. Symptoms beginning in early childhood may resemble spastic cerebral palsy. The function of ATAD3A, a mitochondrial inner membrane AAA ATPase, is yet undefined. AAA ATPases form hexameric rings, which are catalytically dependent on the co-operation of the subunits. The dominant-negative patient mutation affects the Walker A motif, which is responsible for ATP binding in the AAA module of ATAD3A, and we show that the recombinant mutant ATAD3A protein has a markedly reduced ATPase activity. We further show that overexpression of the mutant ATAD3A fragments the mitochondrial network and induces lysosome mass. Similarly, we observed altered dynamics of the mitochondrial network and increased lysosomes in patient fibroblasts and neurons derived through differentiation of patient-specific induced pluripotent stem cells. These alterations were verified in patient fibroblasts to associate with upregulated basal autophagy through mTOR inactivation, resembling starvation. Mutations in ATAD3A can thus be dominantly inherited and underlie variable neurological phenotypes, including HSP, with intrafamiliar variability. This finding extends the group of mitochondrial inner membrane AAA proteins associated with spasticity.
Author Lin, Kai-Lan
Tyynismaa, Henna
Cooper, Helen M
Wanrooij, Sjoerd
Lönnqvist, Tuula
Khairullin, Rafil
Wolf, Alexander
Yang, Yang
Euro, Liliya
Ylikallio, Emil
Isohanni, Pirjo
Trokovic, Ras
Palin, Eino
Kaakkola, Seppo
Auranen, Mari
Woldegebriel, Rosa
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  givenname: Helen M
  surname: Cooper
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  organization: Åbo Akademi University, Faculty of Natural Sciences and Technology, Turku, Finland
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  surname: Yang
  fullname: Yang, Yang
  organization: Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, P.R. China
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  organization: Clinical Neurosciences, Neurology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
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  givenname: Rafil
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  fullname: Khairullin, Rafil
  organization: Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, Kazan, Russia
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  surname: Woldegebriel
  fullname: Woldegebriel, Rosa
  organization: Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland
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  fullname: Lin, Kai-Lan
  organization: Åbo Akademi University, Faculty of Natural Sciences and Technology, Turku, Finland
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  organization: Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland
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  organization: Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland
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  fullname: Wolf, Alexander
  organization: Institute of Molecular Toxicology and Pharmacology, Helmholtz-Zentrum Muenchen-German Research Center for Environmental Health, Neuherberg, Germany
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  surname: Trokovic
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  organization: Research Programs Unit, Molecular Neurology, University of Helsinki, Helsinki, Finland
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  organization: Clinical Neurosciences, Neurology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
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  organization: Clinical Neurosciences, Neurology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
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  organization: Department of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden
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  organization: Department of Medical and Clinical Genetics, University of Helsinki, Helsinki, Finland
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Snippet De novo mutations in ATAD3A (ATPase family AAA-domain containing protein 3A) were recently found to cause a neurological syndrome with developmental delay,...
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StartPage 1432
SubjectTerms Adenosine Triphosphatases - biosynthesis
Adenosine Triphosphatases - genetics
Adolescent
Adult
ATPases Associated with Diverse Cellular Activities
Axons - metabolism
Axons - pathology
Cerebral Palsy - genetics
Cerebral Palsy - pathology
Child, Preschool
Female
Gene Expression Regulation
Humans
Male
Membrane Proteins - biosynthesis
Membrane Proteins - genetics
Mitochondria - metabolism
Mitochondria - pathology
Mitochondrial Dynamics - genetics
Mitochondrial Membranes - metabolism
Mitochondrial Membranes - pathology
Mitochondrial Proteins - biosynthesis
Mitochondrial Proteins - genetics
Mutation
Spastic Paraplegia, Hereditary - genetics
Spastic Paraplegia, Hereditary - pathology
TOR Serine-Threonine Kinases - genetics
Title ATPase-deficient mitochondrial inner membrane protein ATAD3A disturbs mitochondrial dynamics in dominant hereditary spastic paraplegia
URI https://www.ncbi.nlm.nih.gov/pubmed/28158749
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Volume 26
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