ZFIN ID: ZDB-PUB-090324-9
The characterization of a zebrafish mid-hindbrain mutant, mid-hindbrain gone (mgo)
Shima, T., Znosko, W., and Tsang, M.
Date: 2009
Source: Developmental dynamics : an official publication of the American Association of Anatomists   238(4): 899-907 (Journal)
Registered Authors: Shima, Takaki, Tsang, Michael, Znosko, Wade
Keywords: zebrafish, mutant, mid-hind brain boundary, pax2a
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Basic Helix-Loop-Helix Transcription Factors/genetics
  • Basic Helix-Loop-Helix Transcription Factors/metabolism
  • Embryo, Nonmammalian/embryology
  • Embryo, Nonmammalian/metabolism
  • Fibroblast Growth Factors/genetics
  • Fibroblast Growth Factors/metabolism
  • Gene Expression Regulation, Developmental
  • Mesencephalon/embryology*
  • Mesencephalon/metabolism*
  • Mutation/genetics
  • PAX2 Transcription Factor/genetics
  • PAX2 Transcription Factor/metabolism
  • Phenotype
  • RNA, Messenger/genetics
  • Rhombencephalon/embryology*
  • Rhombencephalon/metabolism*
  • Somites/embryology
  • Somites/metabolism
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 19301393 Full text @ Dev. Dyn.
FIGURES
ABSTRACT
The vertebrate mid-hindbrain boundary (MHB) is a crucial morphological structure required for patterning and neural differentiation of the midbrain and anterior hindbrain. We isolated a novel zebrafish mutant, MHB gone (mgo), that exhibited a defective MHB. Expression of engrailed3 in the prospective MHB was absent at the 1-somite stage, suggesting that initiation of the isthmic organizer was disrupted in mgo mutants. Complementation test with mgo and noi, in which the pax2a gene is mutated, infer that the mgo mutant may represent a novel noi allele. However, pronephric, otic vesicle, and commissural axonal defects described in noi mutants were not associated with mgo mutants. Genetic mapping revealed that the mgo mutation is linked to the Pax2a locus, but no mutation was detected in pax2a exons or within intron-exon boundaries. Based on these findings, we propose that the mgo mutation genetically interacts with pax2a required for the initiation of MHB formation.
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