ZFIN ID: ZDB-PUB-060315-7
Identification of alternatively spliced dab1 isoforms in zebrafish
Costagli, A., Felice, B., Guffanti, A., Wilson, S.W., and Mione, M.
Date: 2006
Source: Development genes and evolution   216(6): 291-299 (Journal)
Registered Authors: Mione, Marina, Wilson, Steve
Keywords: Disabled1, Neuronal migration, Transcriptional variants, Reelin, Tyrosine phosphorylation
MeSH Terms:
  • Adaptor Proteins, Signal Transducing
  • Alternative Splicing*
  • Animals
  • Animals, Genetically Modified
  • Base Sequence
  • Codon, Initiator
  • Codon, Terminator
  • DNA, Complementary
  • Exons
  • Gene Expression Regulation
  • Humans
  • In Situ Hybridization
  • Introns
  • Mice
  • Molecular Sequence Data
  • Nerve Tissue Proteins/genetics*
  • Nerve Tissue Proteins/metabolism*
  • Neurons/physiology
  • Phylogeny
  • Protein Isoforms/genetics
  • Protein Isoforms/metabolism
  • Species Specificity
  • Tyrosine/genetics
  • Zebrafish/genetics*
PubMed: 16520940 Full text @ Dev. Genes Evol.
We have investigated the genomic organization, the occurrence of alternative splicing and the differential expression of the zebrafish disabled1 (dab1) gene. Dab1 is a key effector of the Reelin pathway, which regulates neuronal migration during brain development in vertebrates. The coding region of the zebrafish dab1 gene spans over 600 kb of genomic DNA and is composed of 15 exons. Alternative splicing in a region enriched for tyrosine residues generates at least three different isoforms. These isoforms are developmentally regulated and show differential tissue expression. Comparison with mouse and human data shows an overall conservation of the genomic organization with different alternative splicing events generating species-specific isoforms. Because these alternative splicing events give rise to isoforms with different numbers of phosphorylateable tyrosines, we speculate that alternative splicing of the dab1 gene in zebrafish and in other vertebrates regulates the nature of the cellular response to the Reelin signal.