Evidence map›Paper›PMID 30980466›Full record

ArticleGlia2019

Sulfatase 2 promotes generation of a spinal cord astrocyte subtype that stands out through the expression of Olig2.

David Ohayon, Nathalie Escalas, Philippe Cochard, Bruno Glise, Cathy Danesin, Cathy Soula

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Astrocyte development-More questions than answers.Frontiers in cell and developmental biology · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Sulfation Pathways During Neurodevelopment.Frontiers in molecular biosciences · 2022
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

David OhayonCentre de Biologie du Développement (CBD) CNRS/UPS, Centre de Biologie Intégrative (CBI), Université de Toulouse, Toulouse, France.
Nathalie EscalasCentre de Biologie du Développement (CBD) CNRS/UPS, Centre de Biologie Intégrative (CBI), Université de Toulouse, Toulouse, France.
Philippe CochardCentre de Biologie du Développement (CBD) CNRS/UPS, Centre de Biologie Intégrative (CBI), Université de Toulouse, Toulouse, France.
Bruno GliseCentre de Biologie du Développement (CBD) CNRS/UPS, Centre de Biologie Intégrative (CBI), Université de Toulouse, Toulouse, France.
Cathy DanesinCentre de Biologie du Développement (CBD) CNRS/UPS, Centre de Biologie Intégrative (CBI), Université de Toulouse, Toulouse, France.
Cathy SoulaCentre de Biologie du Développement (CBD) CNRS/UPS, Centre de Biologie Intégrative (CBI), Université de Toulouse, Toulouse, France.ORCID 0000-0002-9027-9994
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Generation of glial cell diversity in the developing spinal cord is known to depend on spatio-temporal patterning programs. In particular, expression of the transcription factor Olig2 in neural progenitors of the pMN domain is recognized as critical to their fate choice decision to form oligodendrocyte precursor cells (OPCs) instead of astrocyte precursors (APs). However, generating some confusion, lineage-tracing studies of Olig2 progenitors in the spinal cord provided evidence that these progenitors also generate some astrocytes. Here, we addressed the role of the heparan sulfate-editing enzyme Sulf2 in the control of gliogenesis and found an unanticipated function for this enzyme. At initiation of gliogenesis in mouse, Sulf2 is expressed in ventral neural progenitors of the embryonic spinal cord, including in Olig2-expressing cells of the pMN domain. We found that sulf2 deletion, while not affecting OPC production, impairs generation of a previously unknown Olig2-expressing pMN-derived cell subtype that, in contrast to OPCs, does not upregulate Sox10, PDGFRα or Olig1. Instead, these cells activate expression of AP identity genes, including aldh1L1 and fgfr3 and, of note, retain Olig2 expression as they populate the spinal parenchyma at embryonic stages but also as they differentiate into mature astrocytes at postnatal stages. Thus, our study, by revealing the existence of Olig2-expressing APs that segregate early from pMN cells under the influence of Sulf2, supports the existence of a common source of APs and OPCs in the ventral spinal cord and highlights divergent regulatory mechanism for the development of pMN-derived OPCs and APs.

Indexed as

AnimalsAstrocytesGray MatterMice, TransgenicNeural Stem CellsNeurogenesisOligodendrocyte Transcription Factor 2Receptor, Fibroblast Growth Factor, Type 3SOXE Transcription FactorsSpinal CordSulfatasesFgfr3 protein, mouseOlig2 protein, mouseOligodendrocyte Transcription Factor 2Receptor, Fibroblast Growth Factor, Type 3Sox10 protein, mouseSOXE Transcription FactorsSulf2 protein, mouseSulfatasesastrocytegliogenesisolig2oligodendrocytespinal cordsulfatase 2

Identifiers

PMID30980466
PMCPMC6617735
OpenAlexW2935947492

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.