PUBLICATION

Biallelic Variants in UBA5 Reveal that Disruption of the UFM1 Cascade Can Result in Early-Onset Encephalopathy

Authors
Colin, E., Daniel, J., Ziegler, A., Wakim, J., Scrivo, A., Haack, T.B., Khiati, S., Denommé, A.S., Amati-Bonneau, P., Charif, M., Procaccio, V., Reynier, P., Aleck, K.A., Botto, L.D., Herper, C.L., Kaiser, C.S., Nabbout, R., N'Guyen, S., Mora-Lorca, J.A., Assmann, B., Christ, S., Meitinger, T., Strom, T.M., Prokisch, H., Miranda-Vizuete, A., Hoffmann, G.F., Lenaers, G., Bomont, P., Liebau, E., Bonneau, D.
ID
ZDB-PUB-160823-7
Date
2016
Source
American journal of human genetics   99(3): 695-703 (Journal)
Registered Authors
Bomont, Pascale
Keywords
none
MeSH Terms
  • Proteins/genetics
  • Proteins/metabolism*
  • Ubiquitin/genetics
  • Ubiquitin/metabolism
  • Epilepsy/genetics
  • Microcephaly/genetics
  • Animals
  • Humans
  • Brain Diseases/genetics*
  • Endoplasmic Reticulum/metabolism
  • Endoplasmic Reticulum/pathology
  • Male
  • Genes, Recessive/genetics
  • Caenorhabditis elegans Proteins/genetics
  • Caenorhabditis elegans Proteins/metabolism
  • Zebrafish Proteins/deficiency
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Child, Preschool
  • Synaptic Transmission/genetics
  • Zebrafish/genetics
  • Intellectual Disability/genetics
  • Mutation/genetics*
  • Caenorhabditis elegans/genetics
  • Age of Onset
  • Female
  • Alleles*
  • Magnetic Resonance Imaging
  • Movement Disorders
  • Ubiquitins/genetics
  • Ubiquitins/metabolism
  • Brain Mapping
  • Exome/genetics
  • Ubiquitin-Activating Enzymes/deficiency
  • Ubiquitin-Activating Enzymes/genetics*
  • Ubiquitin-Activating Enzymes/metabolism
  • Child
  • Fibroblasts
  • Cholinergic Neurons/metabolism
PubMed
27545681 Full text @ Am. J. Hum. Genet.
Abstract
Via whole-exome sequencing, we identified rare autosomal-recessive variants in UBA5 in five children from four unrelated families affected with a similar pattern of severe intellectual deficiency, microcephaly, movement disorders, and/or early-onset intractable epilepsy. UBA5 encodes the E1-activating enzyme of ubiquitin-fold modifier 1 (UFM1), a recently identified ubiquitin-like protein. Biochemical studies of mutant UBA5 proteins and studies in fibroblasts from affected individuals revealed that UBA5 mutations impair the process of ufmylation, resulting in an abnormal endoplasmic reticulum structure. In Caenorhabditis elegans, knockout of uba-5 and of human orthologous genes in the UFM1 cascade alter cholinergic, but not glutamatergic, neurotransmission. In addition, uba5 silencing in zebrafish decreased motility while inducing abnormal movements suggestive of seizures. These clinical, biochemical, and experimental findings support our finding of UBA5 mutations as a pathophysiological cause for early-onset encephalopathies due to abnormal protein ufmylation.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping