PUBLICATION

Mutations in CAPN1 Cause Autosomal-Recessive Hereditary Spastic Paraplegia

Authors
Gan-Or, Z., Bouslam, N., Birouk, N., Lissouba, A., Chambers, D.B., Vérièpe, J., Androschuck, A., Laurent, S.B., Rochefort, D., Spiegelman, D., Dionne-Laporte, A., Szuto, A., Liao, M., Figlewicz, D.A., Bouhouche, A., Benomar, A., Yahyaoui, M., Ouazzani, R., Yoon, G., Dupré, N., Suchowersky, O., Bolduc, F.V., Parker, J.A., Dion, P.A., Drapeau, P., Rouleau, G.A., Bencheikh, B.O.
ID
ZDB-PUB-160507-4
Date
2016
Source
American journal of human genetics   98: 1038-1046 (Journal)
Registered Authors
Drapeau, Pierre
Keywords
none
MeSH Terms
  • Adult
  • Animals
  • Axons/pathology*
  • Brain/physiology
  • Caenorhabditis elegans/genetics
  • Calpain/genetics*
  • Cell Movement/genetics
  • Disease Models, Animal
  • Drosophila melanogaster/genetics
  • Female
  • Genetic Predisposition to Disease/genetics*
  • Humans
  • Male
  • Motor Neurons/cytology
  • Motor Neurons/pathology*
  • Spastic Paraplegia, Hereditary/genetics*
  • Young Adult
  • Zebrafish/genetics
PubMed
27153400 Full text @ Am. J. Hum. Genet.
Abstract
Hereditary spastic paraplegia (HSP) is a genetically and clinically heterogeneous disease characterized by spasticity and weakness of the lower limbs with or without additional neurological symptoms. Although more than 70 genes and genetic loci have been implicated in HSP, many families remain genetically undiagnosed, suggesting that other genetic causes of HSP are still to be identified. HSP can be inherited in an autosomal-dominant, autosomal-recessive, or X-linked manner. In the current study, we performed whole-exome sequencing to analyze a total of nine affected individuals in three families with autosomal-recessive HSP. Rare homozygous and compound-heterozygous nonsense, missense, frameshift, and splice-site mutations in CAPN1 were identified in all affected individuals, and sequencing in additional family members confirmed the segregation of these mutations with the disease (spastic paraplegia 76 [SPG76]). CAPN1 encodes calpain 1, a protease that is widely present in the CNS. Calpain 1 is involved in synaptic plasticity, synaptic restructuring, and axon maturation and maintenance. Three models of calpain 1 deficiency were further studied. In Caenorhabditis elegans, loss of calpain 1 function resulted in neuronal and axonal dysfunction and degeneration. Similarly, loss-of-function of the Drosophila melanogaster ortholog calpain B caused locomotor defects and axonal anomalies. Knockdown of calpain 1a, a CAPN1 ortholog in Danio rerio, resulted in abnormal branchiomotor neuron migration and disorganized acetylated-tubulin axonal networks in the brain. The identification of mutations in CAPN1 in HSP expands our understanding of the disease causes and potential mechanisms.
Errata / Notes
This article is corrected by ZDB-PUB-220906-44.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping