ZFIN ID: ZDB-PUB-990607-11
alyron, an insertional mutation affecting early neural crest development in zebrafish
Cretekos, C.J. and Grunwald, D.J.
Date: 1999
Source: Developmental Biology   210(2): 322-338 (Journal)
Registered Authors: Cretekos, Chris, Grunwald, David
Keywords: zebrafish mutant; insertional mutagenesis; neural crest; pigmentation; heart
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Body Patterning
  • Cardiovascular Abnormalities/embryology
  • Cardiovascular Abnormalities/genetics
  • Cardiovascular System/embryology
  • Chromosome Mapping*
  • Embryo, Nonmammalian/physiology
  • Escherichia coli/genetics
  • Female
  • Genes, Lethal*
  • Genes, Recessive*
  • Genetic Linkage
  • Globins/genetics
  • Humans
  • Introns
  • Mice
  • Mice, Mutant Strains
  • Mosaicism
  • Mutagenesis, Insertional*
  • Neural Crest/physiology*
  • Oocytes/physiology
  • Phenotype
  • Restriction Mapping
  • Skin Pigmentation/genetics
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • beta-Galactosidase/genetics
PubMed: 10357894 Full text @ Dev. Biol.
FIGURES
ABSTRACT
alyronz12 (aln) is a recessive lethal mutation that affects early stages of neural crest development in the zebrafish. alyron appears to be an insertional mutation as the mutation was generated following microinjection of plasmid DNA into one-cell embryos and the stably integrated transgenic sequences are closely linked to the mutation. The insertion site harbors multiple copies of the plasmid sequence that have experienced complex rearrangements. Host-insert junction fragments have been molecularly cloned and host sequences adjacent to the transgene have been used to map the mutation to the distal arm of linkage group 15. alyron function is required cell-autonomously in the neural crest lineage. alyron mutants have a severe but not complete deficit of premigratory neural crest as judged by reduced expression of several markers associated with early stages of neural crest development. Lack of premigratory neural crest is likely to account for the two most conspicuous characteristics of alyron mutants: the absence of body pigmentation and the inability to affect blood circulation. The neural crest phenotype of alyron mutants resembles that observed in mouse mutants that lack Pax-3 or both Wnt-1 and Wnt-3a function, and expression of the zebrafish homologues of these genes is greatly reduced in the dorsal neural keels of alyron mutants. In contrast, ventral neural keel identity appears unaffected. Given our findings that the mutation is unlinked to pax or wnt genes that have been described in the zebrafish, we propose that alyron is a novel gene function required for the specification and/or proliferative expansion of neural crest progenitors.
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