ZFIN ID: ZDB-PUB-090527-7
Sublineage-specific cues required for early and later neural crest development in the zebrafish, Danio Rerio
Arduini, B.L.
Date: 2005
Source: Ph.D. Thesis : (Thesis)
Registered Authors: Arduini, Brigitte
Keywords: none
MeSH Terms: none
PubMed: none
The neural crest (NC) of vertebrate animals gives rise to many derivatives, including pigment cells, peripheral neurons, glia and elements of the craniofacial skeleton. The generation of NC-derived cells has been studied extensively to elucidate mechanisms involved in cell fate specification, differentiation, migration and survival. Zebrafish trpm7/touchtone, endzone, and foxd3/sympathetic mutation1 are discrete loci required by subsets of neural crest derivatives. Severe mutant alleles of the divalent cation channel gene trpm7 are lethal and cell-autonomously cause reductions in the number and size of crest-derived melanophores, while sparing other NC lineages. The deficit in cell numbers can be accounted for at least in part by cell death of melanophore precursors. Pleiotropic effects in non-crest derived tissues, including altered order of bone ossification and kidney dysfunction, are observed in homozygotes for semi-viable alleles. Mutations in endzone affect all three pigment cell lineages found in zebrafish. Normally large and stellate, melanophores and xanthophores take on a rounded, punctate appearance in these mutants. Iridiphores are also reduced in size. These three cell types appear to be similarly reduced in numbers in endzone mutant embryos. While neuronal, glial and ectomesenchymal derivatives of the NC appear to be normal in endzone homozygotes, the non-crest-derived pigmented retinal epithelium is developmentally delayed, pointing to pleiotropism for these mutations, as well. Both trpm7 and endzone act relatively late during chromatophore development; accordingly molecular analyses reveal no defects in the early NC cell populations of these mutants. foxd3sym1 affects multiple derivatives within the NC. FoxD3 is required for sympathetic and sensory neuron development, but appears to be dispensable for chromatophore lineages. Anterior elements of the craniofacial skeleton are reduced, and posterior elements are missing, indicating a role for foxd3 in axial patterning of the pharyngeal arches. Expression of critical transcription factors in early crest cells and crest migration are both abrogated, although the premigratory NC population appears to be induced normally. Simultaneous abrogation of Foxd3 and Tfap2a function leads to loss of all chromatophores and most craniofacial cartilages. Collectively, these data suggest that subpopulations with distinct genetic requirements exist within the early neural crest and its later sublineages.
Ph.D. Thesis, Ohio State University