Evidence map›Paper›PMID 21820362›Full record

ArticleDevelopmental cell2011

Eliminating SF-1 (NR5A1) sumoylation in vivo results in ectopic hedgehog signaling and disruption of endocrine development.

Florence Y Lee, Emily J Faivre, Miyuki Suzawa, Erik Lontok, Daniel Ebert, Fang Cai, Denise D Belsham, Holly A Ingraham

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 85 citations in OpenAlex.

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  14. The role of SUMOylation during development.Biochemical Society transactions · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Florence Y LeeDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94143, USA.
Emily J Faivre
Miyuki Suzawa
Erik Lontok
Daniel Ebert
Fang Cai
Denise D Belsham
Holly A Ingraham
University of California, San Francisco · USUniversity Health Network · CA

Funding

DIABETES, ENDOCRINOLOGY &METABOLISM TRAINING PROGRAMT32DK007418 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EDWARD C HSIAO · 1986 to 2026
$14.3M
Modulating Orphan Receptor Activity via SumoylationR01DK070024 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI INGRAHAM, HOLLY A. · 2004 to 2011
$2.1M
Modifying SF-1 Transcriptional Programs by SumoylationF32DK082100 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FAIVRE, EMILY JEAN · 2008 to 2010
$149k
Neuroendocrine Pathways Governing Energy HomeostasisF32DK079499 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEE, FLORENCE YING · 2008 to 2010
$102k
CIHRNIDDK NIH HHS F32 DK079499NIDDK NIH HHS F32 DK082100NIDDK NIH HHS R01 DK070024NIDDK NIH HHS T32 DK007418NIDDK NIH HHS T32 DK07418
6 · The paper itself

Abstract

Sumoylation is generally considered a repressive mark for many transcription factors. However, the in vivo importance of sumoylation for any given substrate remains unclear and is questionable because the extent of sumoylation appears exceedingly low for most substrates. Here, we permanently eliminated SF-1/NR5A1 sumoylation in mice (Sf-1(K119R, K194R, or 2KR)) and found that Sf-1(2KR/2KR) mice failed to phenocopy a simple gain of SF-1 function or show elevated levels of well-established SF-1 target genes. Instead, mutant mice exhibited marked endocrine abnormalities and changes in cell fate that reflected an inappropriate activation of hedgehog signaling and other potential SUMO-sensitive targets. Furthermore, unsumoylatable SF-1 mutants activated Shh and exhibited preferential recruitment to Shh genomic elements in cells. We conclude that the sumoylation cycle greatly expands the functional capacity of transcription factors such as SF-1 and is leveraged during development to achieve cell-type-specific gene expression in multicellular organisms.

Indexed as

Adrenal GlandsAnimalsAnimals, NewbornAntigens, CDAntigens, Differentiation, B-LymphocyteCarrier ProteinsCells, CulturedCorticosteroneElectrophoretic Mobility Shift AssayEmbryo, MammalianEndocrine SystemFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalHedgehog ProteinsImmunoprecipitationAntigens, CDAntigens, Differentiation, B-LymphocyteCarrier ProteinsCorticosteroneGli1 protein, mouseHedgehog ProteinsKruppel-Like Transcription FactorsMembrane ProteinsPlatelet Endothelial Cell Adhesion Molecule-1Siglece protein, mouseSox9 protein, mouseSOX9 Transcription FactorSteroidogenic Factor 1steroidogenic factor 1, mouseTestosteroneZinc Finger Protein GLI1

Identifiers

PMID21820362
PMCPMC3157481
OpenAlexW2064686852

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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.