Evidence map›Paper›PMID 23042297›Full record

ArticleThe Journal of comparative neurology2013

Loss of Gsx1 and Gsx2 function rescues distinct phenotypes in Dlx1/2 mutants.

Bei Wang, Jason E Long, Pierre Flandin, Ramon Pla, Ronald R Waclaw, Kenneth Campbell, John L R Rubenstein

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of comparative neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing 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

56 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development.Advances in experimental medicine and biology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. DLX genes and proteins in mammalian forebrain development.Development (Cambridge, England) · 2024
    Review
  10. Erratum.The Journal of comparative neurology · 2024
    Article
  11. Gsx2, but not Gsx1, is necessary for early forebrain patterning and long-term survival in zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2023
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Bei WangDepartment of Psychiatry and the Nina Ireland Laboratory of Developmental Neurobiology, University of California San Francisco, San Francisco, California 94158-2324, USA.
Jason E Long
Pierre Flandin
Ramon Pla
Ronald R Waclaw
Kenneth Campbell
John L R Rubenstein
University of California, San Francisco · USCincinnati Children's Hospital Medical Center · US

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GERMAN, MICHAEL S · 2003 to 2019
$21.8M
Genetic Control of Basal Telencephalic DevelopmentR01MH081880 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 2009 to 2023
$8.1M
Roles of Gsx factors in telencephalic neurogenesisR01NS044080 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI CAMPBELL, KENNETH J, GEBELEIN, BRIAN · 2002 to 2018
$5.9M
Genetic Regulation of Telencephalon DevelopmentR37MH049428 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 2008 to 2017
$5.9M
NIDDK NIH HHS P30 DK063720NIMH NIH HHS R01 MH081880NIMH NIH HHS R37 MH049428NINDS NIH HHS R01 NS044080NINDS NIH HHS R01NS044080
6 · The paper itself

Abstract

Mice lacking the Dlx1 and Dlx2 homeobox genes (Dlx1/2 mutants) have severe deficits in subpallial differentiation, including overexpression of the Gsx1 and Gsx2 homeobox genes. To investigate whether Gsx overexpression contributes to the Dlx1/2 mutant phenotypes, we made compound loss-of-function mutants. Eliminating Gsx2 function from the Dlx1/2 mutants rescued the increased expression of Ascl1 and Hes5 (Notch signaling mediators) and Olig2 (oligodendrogenesis mediator). In addition, Dlx1/2;Gsx2 mutants, like Dlx1/2;Ascl1 mutants, exacerbated the Gsx2 and Dlx1/2 patterning and differentiation phenotypes, particularly in the lateral ganglionic eminence (LGE) caudal ganglionic eminence (CGE), and septum, including loss of GAD1 expression. On the other hand, eliminating Gsx1 function from the Dlx1/2 mutants (Dlx1/2;Gsx1 mutants) did not severely exacerbate their phenotype; on the contrary, it resulted in a partial rescue of medial ganglionic eminence (MGE) properties, including interneuron migration to the cortex. Thus, despite their redundant properties, Gsx1 and -2 have distinct interactions with Dlx1 and -2. Gsx2 interaction is strongest in the LGE, CGE, and septum, whereas the Gsx1 interaction is strongest in the MGE. From these studies, and earlier studies, we present a model of the transcriptional network that regulates early steps of subcortical development.

Indexed as

AnimalsBrainEmbryo, MammalianFluorescent Antibody TechniqueHomeodomain ProteinsIn Situ HybridizationMiceMice, Mutant StrainsNeurogenesisPhenotypeTranscription FactorsDistal-less homeobox proteinsGsh1 protein, mouseGsh2 protein, mouseHomeodomain ProteinsTranscription Factors

Identifiers

PMID23042297
PMCPMC3615175
OpenAlexW2008992192

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.