ZFIN ID: ZDB-PUB-040611-8
Zinc finger gene fez-like functions in the formation of subplate neurons and thalamocortical axons
Hirata, T., Suda, Y., Nakao, K., Narimatsu, M., Hirano, T., and Hibi, M.
Date: 2004
Source: Developmental dynamics : an official publication of the American Association of Anatomists   230(3): 546-556 (Journal)
Registered Authors: Hibi, Masahiko, Hirata, Tsutomu
Keywords: fez-like, mouse, forebrain, thalamocortical tract, subplate, hyperactive behavior
MeSH Terms:
  • Animals
  • Axons/physiology*
  • Behavior, Animal
  • Carrier Proteins/metabolism*
  • Mice
  • Mice, Knockout
  • Mutation
  • Neurons/cytology
  • Neurons/metabolism*
  • Recombination, Genetic
  • Thalamus/embryology*
  • Zebrafish Proteins/deficiency*
  • Zebrafish Proteins/metabolism*
  • Zinc Fingers/genetics*
PubMed: 15188439 Full text @ Dev. Dyn.
ABSTRACT
fez-like (fezl) is a forebrain-expressed zinc finger gene required for the formation of the hypothalamic dopaminergic and serotonergic (monoaminergic) neurons in zebrafish. To reveal its function in mammals, we analyzed the expression of the mouse orthologue of fezl and generated fezl-deficient mice by homologous recombination. Mouse fezl was expressed specifically in the forebrain from embryonic day 8.5. At mid-gestation, fezl expression was detected in subdomains of the forebrain, including the dorsal telencephalon and ventral diencephalon. Unlike the zebrafish fezl mutant too few, the fezl-deficient mice displayed normal development of hypothalamic monoaminergic neurons, but showed abnormal "hyperactive" behavior. In fezl(-/-) mice, the thalamocortical axons (TCA) were reduced in number and aberrantly projected to the cortex. These mutants had a reduced number of subplate neurons, which are involved in guiding the TCA from the dorsal thalamus, although the subplate neurons were born normally. These results suggest that fezl is required for differentiation or survival of the subplate neurons, and reduction of the subplate neurons in fezl-deficient mice leads to abnormal development of the TCA, providing a possible link between the transcriptional regulation of forebrain development and hyperactive behavior. Developmental Dynamics 230:546-556, 2004. Copyright 2004 Wiley-Liss, Inc.
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