PUBLICATION

TALEN-mediated mutagenesis in zebrafish reveals a role for r-spondin 2 in fin ray and vertebral development

Authors
Tatsumi, Y., Takeda, M., Matsuda, M., Suzuki, T., Yokoi, H.
ID
ZDB-PUB-141203-53
Date
2014
Source
FEBS letters   588(24): 4543-50 (Journal)
Registered Authors
Suzuki, Tohru, Yokoi, Hayato
Keywords
Fin ray, Mutagenesis, R-spondin2, Skeletogenesis, TALEN, Zebrafish
MeSH Terms
  • Amino Acid Sequence
  • Animals
  • DNA Restriction Enzymes/metabolism*
  • Gene Expression Regulation
  • Humans
  • Intercellular Signaling Peptides and Proteins/chemistry
  • Intercellular Signaling Peptides and Proteins/genetics*
  • Intercellular Signaling Peptides and Proteins/metabolism*
  • Molecular Sequence Data
  • Mutagenesis*
  • Mutation
  • Protein Structure, Tertiary
  • Skates, Fish/abnormalities
  • Skates, Fish/genetics*
  • Skates, Fish/growth & development*
  • Zebrafish/genetics*
  • Zebrafish Proteins/chemistry
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism*
PubMed
25448983 Full text @ FEBS Lett.
Abstract
R-spondin (Rspo) encodes a multi-domain protein that modulates the Wnt-signaling pathway. Two distinct rspo2 zebrafish mutants were generated by TALEN-mediated mutagenesis: a null mutant, rspo2(null), lacking all functional domains, and a hypomorphic mutant, rspo2(tsp), lacking the two N-terminal domains. Mutants were analyzed mainly for abnormalities in the skeletal system. Fin ray skeletons were formed normally in the rspo2(tsp) mutants, but were absent from the rspo2(null) mutants. Hypoplasia of the neural/hemal arches and ribs was observed in both mutants. Thus, the two rspo2 mutants help to identify the functions of Rspo2 in skeletogenesis, as well as functional differences among multiple Rspo2 domains.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping