Evidence map›Paper›PMID 19657393›Full record

ArticlePloS one2009

Mad is required for wingless signaling in wing development and segment patterning in Drosophila.

Edward Eivers, Luis C Fuentealba, Veronika Sander, James C Clemens, Lori Hartnett, E M De Robertis

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. microPublication biology · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Mad dephosphorylation at the nuclear pore is essential for asymmetric stem cell division.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Temporal flexibility of gene regulatory network underlies a novel wing pattern in flies.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. TGF-β Family Signaling inCold Spring Harbor perspectives in biology · 2017
    Review
  12. Signaling Cross Talk between TGF-β/Smad and Other Signaling Pathways.Cold Spring Harbor perspectives in biology · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Brain tumor regulates neuromuscular synapse growth and endocytosis in Drosophila by suppressing mad expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    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.

Edward EiversDepartment of Biological Chemistry, Howard Hughes Medical Institute, University of California Los Angeles, Los Angeles, California, United States of America.
Luis C Fuentealba
Veronika Sander
James C Clemens
Lori Hartnett
E M De Robertis
Howard Hughes Medical Institute · USUniversity of California, Los Angeles · US

Funding

HOMEOBOX GENES AND THEIR TARGETS IN XENOPUS DEVELOPMENTR37HD021502 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DE ROBERTIS, EDWARD M · 1997 to 2006
$2.2M
HOMEOBOXES IN XENOPUS DEVELOPMENTR01HD021502 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DE ROBERTIS, EDWARD M · 1986 to 2011
$1.6M
Howard Hughes Medical InstituteNICHD NIH HHS HD21502-23NICHD NIH HHS R01 HD021502NICHD NIH HHS R37 HD021502
6 · The paper itself

Abstract

A key question in developmental biology is how growth factor signals are integrated to generate pattern. In this study we investigated the integration of the Drosophila BMP and Wingless/GSK3 signaling pathways via phosphorylations of the transcription factor Mad. Wingless was found to regulate the phosphorylation of Mad by GSK3 in vivo. In epistatic experiments, the effects of Wingless on wing disc molecular markers (senseless, distalless and vestigial) were suppressed by depletion of Mad with RNAi. Wingless overexpression phenotypes, such as formation of ectopic wing margins, were induced by Mad GSK3 phosphorylation-resistant mutant protein. Unexpectedly, we found that Mad phosphorylation by GSK3 and MAPK occurred in segmental patterns. Mad depletion or overexpression produced Wingless-like embryonic segmentation phenotypes. In Xenopus embryos, segmental border formation was disrupted by Smad8 depletion. The results show that Mad is required for Wingless signaling and for the integration of gradients of positional information.

Indexed as

Body PatterningAnimalsDNA-Binding ProteinsDrosophilaDrosophila ProteinsMutationPhenotypeRNA InterferenceSignal TransductionTranscription FactorsWings, AnimalWnt1 ProteinDNA-Binding ProteinsDrosophila ProteinsMAD protein, DrosophilaTranscription Factorswg protein, DrosophilaWnt1 Protein

Identifiers

PMID19657393
PMCPMC2717371
OpenAlexW1988587478

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.