RNF170-Related Hereditary Spastic Paraplegia: Confirmation by a Novel Mutation.


Journal

Movement disorders : official journal of the Movement Disorder Society
ISSN: 1531-8257
Titre abrégé: Mov Disord
Pays: United States
ID NLM: 8610688

Informations de publication

Date de publication:
03 2021
Historique:
revised: 09 09 2020
received: 03 07 2020
accepted: 16 10 2020
pubmed: 10 11 2020
medline: 28 4 2021
entrez: 9 11 2020
Statut: ppublish

Résumé

Spastic paraparesis and biallelic variants functionally characterized as deleterious in the RNF170 gene have recently been reported by Wagner et al. 2019, strongly supporting the involvement of this gene in hereditary spastic paraplegia. Exome sequencing was performed on 6 hereditary spastic paraplegia families previously tested on an hereditary spastic paraplegia-specific panel. We describe here a novel hereditary spastic paraplegia family with 4 affected members carrying a homozygous p.(Tyr114*) stop gain variant in RNF170. We confirm the involvement of biallelic truncating variants in RNF170 in a novel form of hereditary spastic paraplegia. © 2020 International Parkinson and Movement Disorder Society.

Sections du résumé

BACKGROUND
Spastic paraparesis and biallelic variants functionally characterized as deleterious in the RNF170 gene have recently been reported by Wagner et al. 2019, strongly supporting the involvement of this gene in hereditary spastic paraplegia.
METHODS
Exome sequencing was performed on 6 hereditary spastic paraplegia families previously tested on an hereditary spastic paraplegia-specific panel.
RESULTS
We describe here a novel hereditary spastic paraplegia family with 4 affected members carrying a homozygous p.(Tyr114*) stop gain variant in RNF170.
CONCLUSIONS
We confirm the involvement of biallelic truncating variants in RNF170 in a novel form of hereditary spastic paraplegia. © 2020 International Parkinson and Movement Disorder Society.

Identifiants

pubmed: 33165979
doi: 10.1002/mds.28371
doi:

Substances chimiques

RNF170 protein, human EC 2.3.2.27
Ubiquitin-Protein Ligases EC 2.3.2.27

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

771-774

Informations de copyright

© 2020 International Parkinson and Movement Disorder Society.

Références

Lu JP, Wang Y, Sliter DA, Pearce MMP, Wojcikiewicz RJH. RNF170 protein, an endoplasmic reticulum membrane ubiquitin ligase, mediates inositol 1,4,5-Trisphosphate receptor ubiquitination and degradation. J Biol Chem 2011;286:24426-24433.
Alazami AM, Adly N, Al Dhalaan H, Alkuraya FS. A nullimorphic ERLIN2 mutation defines a complicated hereditary spastic paraplegia locus (SPG18). Neurogenetics 2011;12:333-336.
Novarino G, Fenstermaker AG, Zaki MS, et al. Exome sequencing links corticospinal motor neuron disease to common neurodegenerative disorders. Science 2014;343:506-511.
Wagner M, Osborn DP, Gehweiler I, et al. Bi-allelic variants in RNF170 are associated with hereditary spastic paraplegia. Nat Commun 2019;10:4790.
Valdmanis PN, Dupre N, Lachance M, et al. A mutation in the RNF170 gene causes autosomal dominant sensory ataxia. Brain 2011;134:602-607.
Morais S, Raymond L, Mairey M, et al. Massive sequencing of 70 genes reveals a myriad of missing genes or mechanisms to be uncovered in hereditary spastic paraplegias. Eur J Hum Genet 2017;25:1217-1228.
Larcher L, Norris JW, Lejeune E, et al. The complete loss of function of the SMS gene results in a severe form of Snyder-Robinson syndrome. Eur J Med Genet 2020;63(4):103777.
Nagy E, Maquat LE. A rule for termination-codon position within intron-containing genes: when nonsense affects RNA abundance. Trends Biochem Sci 1998;23:198-199.

Auteurs

Jean-Madeleine de Sainte Agathe (JM)

Assistance Publique - Hôpitaux de Paris, GH Sorbonne Université, Département de Génétique, Hôpital Pitié-Salpêtrière, Paris, France.

Sandra Mercier (S)

Service de Génétique Médicale, CHU Nantes, Nantes, France.
Centre de Référence des Maladies Neuromusculaires, AOC, Hôtel-Dieu, Nantes, France.

Jean-Yves Mahé (JY)

Centre de Référence des Maladies Neuromusculaires, AOC, Hôtel-Dieu, Nantes, France.
Établissement de Santé pour Enfants et Adolescents de la région Nantaise, Nantes, France.

Yann Péréon (Y)

Centre de Référence des Maladies Neuromusculaires, AOC, Hôtel-Dieu, Nantes, France.
Laboratoire d'Explorations Fonctionnelles, CHU de Nantes, Nantes, France.

Julien Buratti (J)

Assistance Publique - Hôpitaux de Paris, GH Sorbonne Université, Département de Génétique, Hôpital Pitié-Salpêtrière, Paris, France.

Laurène Tissier (L)

Assistance Publique - Hôpitaux de Paris, GH Sorbonne Université, Département de Génétique, Hôpital Pitié-Salpêtrière, Paris, France.

Bophara Kol (B)

Assistance Publique - Hôpitaux de Paris, GH Sorbonne Université, Département de Génétique, Hôpital Pitié-Salpêtrière, Paris, France.

Samia Ait Said (SA)

Assistance Publique - Hôpitaux de Paris, GH Sorbonne Université, Département de Génétique, Hôpital Pitié-Salpêtrière, Paris, France.

Éric Leguern (É)

Assistance Publique - Hôpitaux de Paris, GH Sorbonne Université, Département de Génétique, Hôpital Pitié-Salpêtrière, Paris, France.
Institut du Cerveau, Sorbonne Université (INSERM 1127, CNRS 7225), Paris, France.

Guillaume Banneau (G)

Assistance Publique - Hôpitaux de Paris, GH Sorbonne Université, Département de Génétique, Hôpital Pitié-Salpêtrière, Paris, France.

Giovanni Stévanin (G)

Institut du Cerveau, Sorbonne Université (INSERM 1127, CNRS 7225), Paris, France.
Équipe de Neurogénétique, École Pratique des Hautes Etudes (EPHE), PSL Research University, Paris, France.

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Classifications MeSH