ZFIN ID: ZDB-PUB-090828-23
Temporal Notch activation through Notch1a and Notch3 is required for maintaining zebrafish rhombomere boundaries
Qiu, X., Lim, C.H., Ho, S.H., Lee, K.H., and Jiang, Y.J.
Date: 2009
Source: Development genes and evolution   219(7): 339-351 (Journal)
Registered Authors: Ho, Steven, Jiang, Yun-Jin, Lim, Chiaw Hwee, Qiu, Xuehui
Keywords: Notch, Zebrafish, Hindbrain, Lateral inhibition, Neurogenesis
MeSH Terms:
  • Animals
  • Base Sequence
  • Cell Differentiation
  • Gene Knockdown Techniques
  • Histone Deacetylase 1
  • Histone Deacetylases/genetics
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism*
  • Mutation
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism*
  • Neural Tube/cytology
  • Neural Tube/embryology
  • Neural Tube/metabolism
  • Receptor, Notch1/genetics
  • Receptor, Notch1/metabolism*
  • Receptors, Notch/genetics
  • Receptors, Notch/metabolism*
  • Rhombencephalon/cytology
  • Rhombencephalon/embryology*
  • Rhombencephalon/metabolism
  • Signal Transduction
  • Ubiquitin-Protein Ligases/genetics
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 19705151 Full text @ Dev. Genes Evol.
In vertebrates, hindbrain is subdivided into seven segments termed rhombomeres and the interface between each rhombomere forms the boundary. Similar to the D/V boundary formation in Drosophila, Notch activation has been shown to regulate the segregation of rhombomere boundary cells. Here we further explored the function of Notch signaling in the formation of rhombomere boundaries. By using bodipy ceramide cell-labeling technique, we found that the hindbrain boundary is formed initially in mib mutants but lost after 24 hours post-fertilization (hpf). This phenotype was more severe in mib ( ta52b ) allele than in mib ( tfi91 ) allele. Similarly, injection of su(h)-MO led to boundary defects in a dosage-dependent manner. Boundary cells were recovered in mib ( ta52b ) mutants in the hdac1-deficient background, where neurogenesis is inhibited. Furthermore, boundary cells lost sensitivity to reduced Notch activation from 15 somite stage onwards. We also showed that knockdown of notch3 function in notch1a mutants leads to the loss of rhombomere boundary cells and causes neuronal hyperplasia, indicating that Notch1a and Notch3 play a redundant role in the maintenance of rhombomere boundary.