Evidence map›Paper›PMID 10097116›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Morphogenetic movements at gastrulation require the SH2 tyrosine phosphatase Shp2.

T M Saxton, T Pawson

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 89 citations in OpenAlex.

  1. From Stem to Sternum: The Role of Shp2 in the Skeleton.Calcified tissue international · 2023
    Review
  2. Review
  3. Genes · 2022
    Article
  4. Review
  5. Review
  6. Article
  7. The Q510E mutation in Shp2 perturbs heart valve development by increasing cell migration.Journal of applied physiology (Bethesda, Md. : 1985) · 2015
    Article
  8. Article
  9. Traffic jam in the primitive streak: the role of defective mesoderm migration in birth defects.Birth defects research. Part A, Clinical and molecular teratology · 2014
    Review
  10. SHP-2 deletion in postmigratory neural crest cells results in impaired cardiac sympathetic innervation.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  11. Article
  12. Review
  13. Review
  14. Shp2 plays a crucial role in cell structural orientation and force polarity in response to matrix rigidity.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  15. Article
  16. Xenopus: An emerging model for studying congenital heart disease.Birth defects research. Part A, Clinical and molecular teratology · 2011
    Review
  17. Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

T M SaxtonProgramme in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G-1X5 Canada.
T Pawson
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SH2 domain-containing tyrosine phosphatase Shp2 plays a pivotal role during the gastrulation of vertebrate embryos. However, because of the complex phenotype observed in mouse mutant embryos, the precise role of Shp2 during development is unclear. To define the specific functions of this phosphatase, Shp2 homozygous mutant embryonic stem cells bearing the Rosa-26 LacZ transgene were isolated and used to perform a chimeric analysis. Here, we show that Shp2 mutant cells amass in the tail bud of embryonic day 10.5 chimeric mouse embryos and that this accumulation begins at the onset of gastrulation. At this early stage, Shp2 mutant cells collect in the primitive streak of the epiblast and thus show deficiencies in their contribution to the mesoderm lineage. In high-contribution chimeras, we show that overaccumulation of Shp2 mutant cells at the posterior end of the embryo results in two abnormal phenotypes: spina bifida and secondary neural tubes. Consistent with a failure to undergo morphogenic movements at gastrulation, Shp2 is required for embryo fibroblast cells to mount a positive chemotactic response to acidic fibroblast growth factor in vitro. Our results demonstrate that Shp2 is required at the initial steps of gastrulation, as nascent mesodermal cells form and migrate away from the primitive streak. The aberrant behavior of Shp2 mutant cells at gastrulation may result from their inability to properly respond to signals initiated by fibroblast growth factors.

Indexed as

Animalsbeta-GalactosidaseCell MovementChimeraEmbryonic and Fetal DevelopmentGastrulaHomozygoteIntracellular Signaling Peptides and ProteinsMiceMice, TransgenicMicroscopy, Electron, ScanningMorphogenesisProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesSH2 Domain-Containing Protein Tyrosine Phosphatasesbeta-GalactosidaseIntracellular Signaling Peptides and ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesPtpn11 protein, mousePtpn6 protein, mouseSH2 Domain-Containing Protein Tyrosine Phosphatases

Identifiers

PMID10097116
PMCPMC22373
OpenAlexW2125512314

What OpenQuestion holds

Texttitle and abstract
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.