PUBLICATION

Characterization of genetic loss-of-function of Fus in zebrafish

Authors
Lebedeva, S., de Jesus Domingues, A.M., Butter, F., Ketting, R.F.
ID
ZDB-PUB-161130-2
Date
2017
Source
RNA Biology   14(1): 29-35 (Journal)
Registered Authors
Ketting, René
Keywords
CRISPR-Cas9, Danio rerio, Fus, genetic knockout, morpholino, zebrafish
Datasets
GEO:GSE85554
MeSH Terms
  • 3' Untranslated Regions
  • Alleles
  • Animals
  • Base Sequence
  • Binding Sites
  • Brain/metabolism
  • CRISPR-Cas Systems
  • Exons
  • Gene Knockout Techniques
  • Gene Targeting
  • Genetic Background
  • Genotype
  • Proteome
  • RNA, Guide
  • RNA-Binding Protein FUS/genetics*
  • RNA-Binding Protein FUS/metabolism
  • Transcriptome
  • Zebrafish/genetics*
  • Zebrafish/metabolism
PubMed
27898262 Full text @ RNA Biol.
Abstract
The RNA-binding protein FUS is implicated in transcription, alternative splicing of neuronal genes and DNA repair. Mutations in FUS have been linked to human neurodegenerative diseases such as ALS (amyotrophic lateral sclerosis). We genetically disrupted fus in zebrafish (Danio rerio) using the CRISPR-Cas9 system. The fus knockout animals are fertile and did not show any distinctive phenotype. Mutation of fus induces mild changes in gene expression on the transcriptome and proteome level in the adult brain. We observed a significant influence of genetic background on gene expression and 3'UTR usage, which could mask the effects of loss of Fus. Unlike published fus morphants, maternal zygotic fus mutants do not show motoneuronal degeneration and exhibit normal locomotor activity.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping