PUBLICATION

The role of the SPT6 chromatin remodeling factor in zebrafish embryogenesis

Authors
Kok, F.O., Oster, E., Mentzer, L., Hsieh, J.C., Henry, C.A., and Sirotkin, H.I.
ID
ZDB-PUB-070629-6
Date
2007
Source
Developmental Biology   307(2): 214-226 (Journal)
Registered Authors
Henry, Clarissa A., Kok, Fatma, Oster, Emma, Sirotkin, Howard
Keywords
Somitogenesis, Spt6, Notch, Zebrafish
MeSH Terms
  • Animals
  • Base Sequence
  • Chromatin Assembly and Disassembly/genetics
  • Chromatin Assembly and Disassembly/physiology*
  • Chromosome Mapping
  • DNA/genetics
  • Epistasis, Genetic
  • Gene Expression Regulation, Developmental
  • In Situ Hybridization
  • Mutation
  • Receptors, Notch/genetics
  • Receptors, Notch/metabolism
  • Signal Transduction
  • Somites/cytology
  • Somites/metabolism
  • Transcription Factors/genetics
  • Transcription Factors/metabolism*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
(all 22)
PubMed
17570355 Full text @ Dev. Biol.
Abstract
Somitogenesis is a highly controlled process that results in segmentation of the paraxial mesoderm. Notch pathway activity in the presomitic mesoderm is fundamental for management of synchronized gene expression which is necessary for regulation of somitogenesis. We have isolated an embryonic lethal mutation, SBU2, that causes somite formation defects very similar to Notch pathway mutants. SBU2 mutants generate only 6-7 asymmetrically arranged somites. However, in contrast to Notch pathway mutants, these mutants do not maintain previously formed somite boundaries and by 24 hpf, almost no somite boundaries remain. Other developmental processes disrupted in SBU2 mutants include tail morphogenesis, muscle fiber elongation, pigmentation, circulatory system development and neural differentiation. We demonstrated that these defects are the result of a nonsense mutation within the spt6 gene. spt6 encodes a transcription elongation factor that genetically interacts with the Paf-1 chromatin remodeling complex. SBU2 mutant phenotypes could be rescued by microinjection of spt6 mRNA and microinjection of spt6 morpholinos phenocopied the mutation. Our real-time PCR analysis revealed that Spt6 is essential for the transcriptional response to activation of the Notch pathway. Analysis of sbu2;mib double mutants indicates that Spt6 deficiency suppresses the neurogenic effects of the mib. Altogether, these results demonstrate that Spt6 is critical for somite formation in zebrafish and suggest that some defects observed in spt6 mutants result from alterations in Notch signaling. However, additional Spt6 mutant phenotypes are likely caused by vital functions of Spt6 in other pathways.
Genes / Markers
Marker Marker Type Name
dldGENEdeltaD
efnb2aGENEephrin-B2a
egr2bGENEearly growth response 2b
elavl3GENEELAV like neuron-specific RNA binding protein 3
gata1aGENEGATA binding protein 1a
her1GENEhairy-related 1
her7GENEhairy and enhancer of split related-7
mib1GENEMIB E3 ubiquitin protein ligase 1
myod1GENEmyogenic differentiation 1
pax2aGENEpaired box 2a
1 - 10 of 17
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Figures
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
mib1_unspecified
    Unspecified
    sbu2
      Point Mutation
      1 - 2 of 2
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      Human Disease / Model
      No data available
      Sequence Targeting Reagents
      Target Reagent Reagent Type
      supt6hMO1-supt6hMRPHLNO
      1 - 1 of 1
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      Fish
      Antibodies
      No data available
      Orthology
      No data available
      Engineered Foreign Genes
      No data available
      Mapping