Evidence map›Paper›PMID 24431450›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Shp2-dependent ERK signaling is essential for induction of Bergmann glia and foliation of the cerebellum.

Kairong Li, Alan W Leung, Qiuxia Guo, Wentian Yang, James Y H Li

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The anatomy of neuroepithelial tumours.Brain : a journal of neurology · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Transcriptional Regulator ZEB2 Is Essential for Bergmann Glia Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  18. Review
  19. Neuronal Migration During Development of the Cerebellum.Frontiers in cellular neuroscience · 2018
    Review
  20. Embryology.Handbook of clinical neurology · 2018
    Review
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

5 authors at 2 institutions in 1 country.

Kairong LiDepartment of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut 06030-6403 and Department of Orthopedics, Brown University, Providence, Rhode Island 0912.
Alan W Leung
Qiuxia Guo
Wentian Yang
James Y H Li
UConn Health · USBrown University · US

Funding

COBRE for Skeletal Health and RepairP20GM104937 · NIGMS · RHODE ISLAND HOSPITAL · PI CHEN, QIAN · 2012 to 2016
$10.8M
Molecular mechanisms of differentiation of habenular and thalamic neuronsR01MH094914 · NIMH · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI LI, JAMES Y.H · 2012 to 2016
$1.9M
NIGMS NIH HHS P20 GM104937NIMH NIH HHS R01 MH094914
6 · The paper itself

Abstract

Folding of the cortex and the persistence of radial glia (RG)-like cells called Bergmann glia (BG) are hallmarks of the mammalian cerebellum. Similar to basal RG in the embryonic neocortex, BG maintain only basal processes and continuously express neural stem cell markers. Past studies had focused on the function of BG in granule cell migration and how granule cell progenitors (GCP) regulate cerebellar foliation. The molecular control of BG generation and its role in cerebellar foliation are less understood. Here, we have analyzed the function of the protein tyrosine phosphatase Shp2 in mice by deleting its gene Ptpn11 in the entire cerebellum or selectively in the GCP lineage. Deleting Ptpn11 in the entire cerebellum by En1-cre blocks transformation of RG into BG but preserves other major cerebellar cell types. In the absence of BG, inward invagination of GCP persists but is uncoupled from the folding of the Purkinje cell layer and the basement membrane, leading to disorganized lamination and an absence of cerebellar folia. In contrast, removing Ptpn11 in the GCP lineage by Atoh1-cre has no effect on cerebellar development, indicating that Shp2 is not cell autonomously required in GCP. Furthermore, we demonstrate that Ptpn11 interacts with Fgf8 and is essential for ERK activation in RG and nascent BG. Finally, expressing constitutively active MEK1 rescues BG formation and cerebellar foliation in Shp2-deficient cerebella. Our results demonstrate an essential role of Shp2 in BG specification via fibroblast growth factor/extracellular signal-regulated protein kinase signaling, and reveal a crucial function of BG in organizing cerebellar foliation.

Indexed as

AnimalsCerebellumEpendymoglial CellsFemaleMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeurogliaProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 11Ptpn11 protein, mouseBergmann gliacerebellumextracellular signal-regulated kinasesmouseradial gliastem cell

Identifiers

PMID24431450
PMCPMC3891967
OpenAlexW2058693679

What OpenQuestion holds

Textmetadata
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.