Evidence map›Paper›PMID 25959238›Full record

ArticleDevelopmental biology2015

MED GATA factors promote robust development of the C. elegans endoderm.

Morris F Maduro, Gina Broitman-Maduro, Hailey Choi, Francisco Carranza, Allison Chia-Yi Wu, Scott A Rifkin

Abstract read
In one paragraph

Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. A GATA factor radiation inbioRxiv : the preprint server for biology · 2025
    Article
  2. Review
  3. Article
  4. Review
  5. Evolutionary Change in Gut Specification inJournal of developmental biology · 2023
    Review
  6. The long isoform of themicroPublication biology · 2023
    Article
  7. Article
  8. Article
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  11. Review
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  13. Article
  14. A Strategy To Isolate Modifiers ofG3 (Bethesda, Md.) · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

6 authors at 2 institutions in 1 country.

Morris F MaduroBiology Department, University of California, Riverside, Riverside, CA 92521, United States. Electronic address: mmaduro@ucr.edu.
Gina Broitman-MaduroBiology Department, University of California, Riverside, Riverside, CA 92521, United States.
Hailey ChoiCell, Molecular and Developmental Biology Graduate Program, University of California, Riverside, Riverside, CA, United States.
Francisco CarranzaMARCU-STAR Program, University of California, Riverside, Riverside, CA, United States.
Allison Chia-Yi WuGraduate Program in Bioinformatics and Systems Biology, University of California, San Diego, La Jolla, CA, United States.
Scott A RifkinSection of Ecology, Behavior, and Evolution, Division of Biology, University of California, San Diego, La Jolla, CA, United States.
University of California, Riverside · USUniversity of California San Diego · US

Funding

UC Riverside MARC U* Star Undergraduate Research ProgramT34GM062756 · NIGMS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI MARTINEZ, ERNEST · 2001 to 2022
$8.7M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Dynamics and regulatory logic of the endodermal cell-fate decision in C. elegansR01GM103782 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RIFKIN, SCOTT · 2013 to 2017
$1.4M
NIGMS NIH HHS R01 GM103782NIGMS NIH HHS R01GM103782NIGMS NIH HHS T34 GM062756NIGMS NIH HHS T34GM062756NIH HHS P40 OD010440NIH HHS P40OD010440
6 · The paper itself

Abstract

The MED-1,2 GATA factors contribute to specification of E, the progenitor of the Caenorhabditis elegans endoderm, through the genes end-1 and end-3, and in parallel with the maternal factors SKN-1, POP-1 and PAL-1. END-1,3 activate elt-2 and elt-7 to initiate a program of intestinal development, which is maintained by positive autoregulation. Here, we advance the understanding of MED-1,2 in E specification. We find that expression of end-1 and end-3 is greatly reduced in med-1,2(-) embryos. We generated strains in which MED sites have been mutated in end-1 and end-3. Without MED input, gut specification relies primarily on POP-1 and PAL-1. 25% of embryos fail to make intestine, while those that do display abnormal numbers of gut cells due to a delayed and stochastic acquisition of intestine fate. Surviving adults exhibit phenotypes consistent with a primary defect in the intestine. Our results establish that MED-1,2 provide robustness to endoderm specification through end-1 and end-3, and reveal that gut differentiation may be more directly linked to specification than previously appreciated. The results argue against an "all-or-none" description of cell specification, and suggest that activation of tissue-specific master regulators, even when expression of these is maintained by positive autoregulation, does not guarantee proper function of differentiated cells.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsEndodermGATA Transcription FactorsIntestinal MucosaIntestinesTranscription FactorsCaenorhabditis elegans ProteinsEND-1 protein, C elegansEND-3 protein, C elegansGATA Transcription FactorsMED-1 protein, C elegansMED-2 protein, C elegansTranscription FactorsC. elegansCell specificationEndodermGATA factorsGene regulationGene regulatory networksRobustness

Identifiers

PMID25959238
PMCPMC4469534
OpenAlexW2137045074

What OpenQuestion holds

Textmetadata
LicenceTDM
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.