Neurogenic phenotype of mind bomb mutants leads to severe patterning defects in the zebrafish hindbrain

Neurogenic phenotype of mind bomb mutants leads to severe patterning defects in the zebrafish... Failure of Notch signaling in zebrafish mind bomb (mib) mutants results in a neurogenic phenotype where an overproduction of early differentiating neurons is accompanied by the loss of later‐differentiating cell types. We have characterized in detail the hindbrain phenotype of mib mutants. Hindbrain branchiomotor neurons (BMNs) are reduced in number but not missing in mib mutants. In addition, BMN clusters are frequently fused across the midline in mutants. Mosaic analysis indicates that the BMN patterning and fusion defects in the mib hindbrain arise non–cell autonomously. Ventral midline signaling is defective in the mutant hindbrain, in part due to the differentiation of some midline cells into neural cells. Interestingly, while early hindbrain patterning appears normal in mib mutants, subsequent rhombomere‐specific gene expression is completely lost. The defects in ventral midline signaling and rhombomere patterning are accompanied by an apparent loss of neuroepithelial cells in the mutant hindbrain. These observations suggest that, by regulating the differentiation of neuroepithelial cells into neurons, Notch signaling preserves a population of non‐neuronal cells that are essential for maintaining patterning mechanisms in the developing neural tube. Developmental Dynamics, 2003. © 2003 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Developmental Dynamics Wiley

Neurogenic phenotype of mind bomb mutants leads to severe patterning defects in the zebrafish hindbrain

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Publisher
Wiley
Copyright
Copyright © 2003 Wiley‐Liss, Inc.
ISSN
1058-8388
eISSN
1097-0177
DOI
10.1002/dvdy.10429
Publisher site
See Article on Publisher Site

Abstract

Failure of Notch signaling in zebrafish mind bomb (mib) mutants results in a neurogenic phenotype where an overproduction of early differentiating neurons is accompanied by the loss of later‐differentiating cell types. We have characterized in detail the hindbrain phenotype of mib mutants. Hindbrain branchiomotor neurons (BMNs) are reduced in number but not missing in mib mutants. In addition, BMN clusters are frequently fused across the midline in mutants. Mosaic analysis indicates that the BMN patterning and fusion defects in the mib hindbrain arise non–cell autonomously. Ventral midline signaling is defective in the mutant hindbrain, in part due to the differentiation of some midline cells into neural cells. Interestingly, while early hindbrain patterning appears normal in mib mutants, subsequent rhombomere‐specific gene expression is completely lost. The defects in ventral midline signaling and rhombomere patterning are accompanied by an apparent loss of neuroepithelial cells in the mutant hindbrain. These observations suggest that, by regulating the differentiation of neuroepithelial cells into neurons, Notch signaling preserves a population of non‐neuronal cells that are essential for maintaining patterning mechanisms in the developing neural tube. Developmental Dynamics, 2003. © 2003 Wiley‐Liss, Inc.

Journal

Developmental DynamicsWiley

Published: Nov 1, 2003

References

  • Delta‐mediated specification of midline cell fates in zebrafish embryos
    Appel, Appel; Fritz, Fritz; Westerfield, Westerfield; Grunwald, Grunwald; Eisen, Eisen; Riley, Riley
  • The zebrafish trilobite gene is essential for tangential migration of branchiomotor neurons
    Bingham, Bingham; Higashijima, Higashijima; Okamoto, Okamoto; Chandrasekhar, Chandrasekhar
  • Turning heads: development of vertebrate branchiomotor neurons
    Chandrasekhar, Chandrasekhar
  • Zebrafish deadly seven functions in neurogenesis
    Gray, Gray; Moens, Moens; Amacher, Amacher; Eisen, Eisen; Beattie, Beattie
  • Zebrafish elav /HuC homologue as a very early neuronal marker
    Kim, Kim; Ueshima, Ueshima; Muraoka, Muraoka; Tanaka, Tanaka; Yeo, Yeo; Huh, Huh; Miki, Miki
  • Stages of embryonic development of the zebrafish
    Kimmel, Kimmel; Ballard, Ballard; Kimmel, Kimmel; Ullmann, Ullmann; Schilling, Schilling
  • Constructing the hindbrain: insights from the zebrafish
    Moens, Moens; Prince, Prince
  • Mutation of the zebrafish glass onion locus causes early cell‐nonautonomous loss of neuroepithelial integrity followed by severe neuronal patterning defects in the retina
    Pujic, Pujic; Malicki, Malicki

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