Evidence map›Paper›PMID 27226320›Full record

ArticleDevelopment (Cambridge, England)2016

SOX2 is sequentially required for progenitor proliferation and lineage specification in the developing pituitary.

Sam Goldsmith, Robin Lovell-Badge, Karine Rizzoti

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. JCEM case reports · 2025
    Article
  4. SOX2 is required independently in both stem and differentiated cells for pituitary tumorigenesis inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Identification of SLC20A1 and SLC15A4 among other genes as potential risk factors for combined pituitary hormone deficiency.Genetics in medicine : official journal of the American College of Medical Genetics · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. 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

3 authors at 1 institution in 1 country.

Sam GoldsmithThe Francis Crick Institute, Mill Hill Laboratory, The Ridgeway, Mill Hill, London NW7 1AA, UK.
Robin Lovell-BadgeThe Francis Crick Institute, Mill Hill Laboratory, The Ridgeway, Mill Hill, London NW7 1AA, UK robin.lovell-badge@crick.ac.uk karine.rizzoti@crick.ac.uk.ORCID 0000-0001-9364-4179
Karine RizzotiThe Francis Crick Institute, Mill Hill Laboratory, The Ridgeway, Mill Hill, London NW7 1AA, UK robin.lovell-badge@crick.ac.uk karine.rizzoti@crick.ac.uk.ORCID 0000-0003-0711-5452
The Francis Crick Institute · GB

Funding

Neurovascular RegenerationR01EB016629 · NIBIB · YALE UNIVERSITY · PI HIRSCHI, KAREN KEMPER · 2014 to 2018
$4.8M
Medical Research Council MC_U117562207Medical Research Council U117512772NIBIB NIH HHS R01 EB016629Worldwide Cancer Research 13-1270
6 · The paper itself

Abstract

Sox2 mutations are associated with pituitary hormone deficiencies and the protein is required for pituitary progenitor proliferation, but its function has not been well characterized in this context. SOX2 is known to activate expression of Six6, encoding a homeodomain transcription factor, in the ventral diencephalon. Here, we find that the same relationship likely exists in the pituitary. Moreover, because Six6 deletion is associated with a similar phenotype as described here for loss of Sox2, Six6 appears to be an essential downstream target of SOX2 in the gland. We also uncover a second role for SOX2. Whereas cell differentiation is reduced in Sox2 mutants, some endocrine cells are generated, such as POMC-positive cells in the intermediate lobe. However, loss of SOX2 here results in complete downregulation of the melanotroph pioneer factor PAX7, and subsequently a switch of identity from melanotrophs to ectopic corticotrophs. Rescuing proliferation by ablating the cell cycle negative regulator p27 (also known as Cdkn1b) in Sox2 mutants does not restore melanotroph emergence. Therefore, SOX2 has two independent roles during pituitary morphogenesis; firstly, promotion of progenitor proliferation, and subsequently, acquisition of melanotroph identity.

Indexed as

Cell LineageAnimalsCell CountCell ProliferationCorticotrophsCyclin-Dependent Kinase Inhibitor p27Down-RegulationGene DeletionGene Expression Regulation, DevelopmentalHomeodomain ProteinsMelanotrophsMice, Inbred C57BLModels, BiologicalMorphogenesisPAX7 Transcription FactorPituitary GlandCyclin-Dependent Kinase Inhibitor p27Hesx1 protein, mouseHomeodomain ProteinsPAX7 Transcription FactorPro-OpiomelanocortinRepressor ProteinsRNA, MessengerSix6 protein, mouseSOXB1 Transcription FactorsTrans-ActivatorsCell fateMorphogenesisPituitaryProgenitorSOX

Identifiers

PMID27226320
PMCPMC4958329
OpenAlexW2401752215

What OpenQuestion 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 OpenQuestion graph.