ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Sulfatase 1 promotes the motor neuron-to-oligodendrocyte fate switch by activating Shh signaling in Olig2 progenitors of the embryonic ventral spinal cord.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Article
- Functional synaptic connectivity of engrafted spinal cord neurons with hindlimb motor circuitry in the injured spinal cord.Nature communications · 2025Article
- Lateral Motor Column specific expression of Sonic Hedgehog contributes to maintenance and scaling of pMN progenitor cell populations during oligodendrogenesis.Research square · 2024Article
- High-throughput mRNA sequencing of human placenta shows sex differences across gestation.Placenta · 2024Article
- Characterisation of the consequences of maternal immune activation on distinct cell populations in the developing rat spinal cord.Journal of anatomy · 2022Article
- Physiology and Pathophysiology of Heparan Sulfate in Animal Models: Its Biosynthesis and Degradation.International journal of molecular sciences · 2022Review
- Oligodendrocyte precursor cell specification is regulated by bidirectional neural progenitor-endothelial cell crosstalk.Nature neuroscience · 2021Article
- Sulf2a controls Shh-dependent neural fate specification in the developing spinal cord.Scientific reports · 2021Article
- Expression of Heparan Sulfate Endosulfatases in the Adult Mouse Brain: Co-expression ofFrontiers in neuroanatomy · 2021Article
- Prdm8 regulates pMN progenitor specification for motor neuron and oligodendrocyte fates by modulating the Shh signaling response.Development (Cambridge, England) · 2020Article
- yippee like 3 (ypel3) is a novel gene required for myelinating and perineurial glia development.PLoS genetics · 2020Article
- Article
- Sequential specification of oligodendrocyte lineage cells by distinct levels of Hedgehog and Notch signaling.Developmental biology · 2018Article
- Myelination of Neuronal Cell Bodies when Myelin Supply Exceeds Axonal Demand.Current biology : CB · 2018Article
- FGF signaling controls Shh-dependent oligodendroglial fate specification in the ventral spinal cord.Neural development · 2018Article
- Developmental and Repairing Production of Myelin: The Role of Hedgehog Signaling.Frontiers in cellular neuroscience · 2018Article
- Epithelial heparan sulfate regulates Sonic Hedgehog signaling in lung development.PLoS genetics · 2017Article
- Moving the Shh Source over Time: What Impact on Neural Cell Diversification in the Developing Spinal Cord?Journal of developmental biology · 2017Review
- Hedgehog: A Key Signaling in the Development of the Oligodendrocyte Lineage.Journal of developmental biology · 2016Review
- Regulation of Hedgehog Signalling Inside and Outside the Cell.Journal of developmental biology · 2016Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the developing ventral spinal cord, motor neurons (MNs) and oligodendrocyte precursor cells (OPCs) are sequentially generated from a common pool of neural progenitors included in the so-called pMN domain characterized by Olig2 expression. Here, we establish that the secreted Sulfatase 1 (Sulf1) is a major component of the mechanism that causes these progenitors to stop producing MNs and change their fate to generate OPCs. We show that specification of OPCs is severely affected in sulf1-deficient mouse embryos. This defect does not rely on abnormal patterning of the spinal cord or failure in maintenance of pMN progenitors at the onset of OPC specification. Instead, the efficiency of OPC induction is reduced, only few Olig2 progenitors are recruited to generate OPCs, meanwhile they continue to produce MNs beyond the normal timing of the neuroglial switch. Using the chicken embryo, we show that Sulf1 activity is required precisely at the stage of the MN-to-OPC fate switch. Finally, we bring arguments supporting the view that Sulf1 controls the level of Sonic Hedgehog (Shh) signaling activity, behaving as an enhancer rather than an obligatory component in the Shh pathway. Our study provides additional insights into the temporal control of Olig2 progenitor cell fate change by the identification of Sulf1 as an extracellular timing signal in the ventral spinal cord.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.