PUBLICATION

Dynamics of Sonic hedgehog signaling in the ventral spinal cord are controlled by intrinsic changes in source cells requiring Sulfatase 1

Authors
Al Oustah, A., Danesin, C., Khouri-Farah, N., Farreny, M.A., Escalas, N., Cochard, P., Glise, B., and Soula, C.
ID
ZDB-PUB-140403-4
Date
2014
Source
Development (Cambridge, England)   141(6): 1392-1403 (Journal)
Registered Authors
Al Oustah, Amir, Danesin, Cathy, Glise, Bruno, Soula, Cathy
Keywords
Floor plate, Neural cell fate, Shh, Spinal cord, Sulfatase1, Zebrafish
MeSH Terms
  • Animals, Genetically Modified
  • Mice
  • Signal Transduction
  • Gene Knockdown Techniques
  • Neural Stem Cells/classification
  • Neural Stem Cells/metabolism
  • Spinal Cord/cytology
  • Spinal Cord/embryology*
  • Spinal Cord/metabolism*
  • Animals
  • Hedgehog Proteins/deficiency
  • Hedgehog Proteins/genetics
  • Hedgehog Proteins/metabolism*
  • Gene Expression Regulation, Developmental
  • Sulfotransferases/genetics
  • Sulfotransferases/metabolism
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Sulfatases/genetics
  • Sulfatases/metabolism*
  • Body Patterning/genetics
  • Body Patterning/physiology
  • Neurogenesis/genetics
  • Neurogenesis/physiology
  • Zebrafish Proteins/deficiency
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Gene Expression Regulation, Enzymologic
(all 29)
PubMed
24595292 Full text @ Development
Abstract

In the ventral spinal cord, generation of neuronal and glial cell subtypes is controlled by Sonic hedgehog (Shh). This morphogen contributes to cell diversity by regulating spatial and temporal sequences of gene expression during development. Here, we report that establishing Shh source cells is not sufficient to induce the high-threshold response required to specify sequential generation of ventral interneurons and oligodendroglial cells at the right time and place in zebrafish. Instead, we show that Shh-producing cells must repeatedly upregulate the secreted enzyme Sulfatase1 (Sulf1) at two critical time points of development to reach their full inductive capacity. We provide evidence that Sulf1 triggers Shh signaling activity to establish and, later on, modify the spatial arrangement of gene expression in ventral neural progenitors. We further present arguments in favor of Sulf1 controlling Shh temporal activity by stimulating production of active forms of Shh from its source. Our work, by pointing out the key role of Sulf1 in regulating Shh-dependent neural cell diversity, highlights a novel level of regulation, which involves temporal evolution of Shh source properties.

Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
sa199
    Point Mutation
    sb15TgTransgenic Insertion
      vu12TgTransgenic Insertion
        vu17TgTransgenic Insertion
          vu19TgTransgenic Insertion
            1 - 5 of 5
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            Human Disease / Model
            No data available
            Sequence Targeting Reagents
            Target Reagent Reagent Type
            sulf1MO5-sulf1MRPHLNO
            sulf1MO6-sulf1MRPHLNO
            1 - 2 of 2
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            Fish
            Antibodies
            No data available
            Orthology
            No data available
            Engineered Foreign Genes
            Marker Marker Type Name
            DsRed2EFGDsRed2
            EGFPEFGEGFP
            GFPEFGGFP
            1 - 3 of 3
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            Mapping
            No data available