Evidence map›Paper›PMID 17507674›Full record

ArticleGenetics2007

Defective decapentaplegic signaling results in heart overgrowth and reduced cardiac output in Drosophila.

Aaron N Johnson, Lindsey A Burnett, Julia Sellin, Achim Paululat, Stuart J Newfeld

Open access · greenAbstract read
In one paragraph

Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. TGF-β Family Signaling inCold Spring Harbor perspectives in biology · 2017
    Review
  3. On the Morphology of the Drosophila Heart.Journal of cardiovascular development and disease · 2016
    Review
  4. SPARC-Dependent Cardiomyopathy in Drosophila.Circulation. Cardiovascular genetics · 2016
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Salmonella pathogenesis reveals that BMP signaling regulates blood cell homeostasis and immune responses in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  14. 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

5 authors at 2 institutions in 2 countries.

Aaron N JohnsonSchool of Life Sciences, Arizona State University, Tempe, Arizona 85287-4501, USA.
Lindsey A Burnett
Julia Sellin
Achim Paululat
Stuart J Newfeld
Osnabrück University · DEArizona State University · US

Funding

Transgenic analysis of Smad tumor suppressor genesR01CA095875 · NCI · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI NEWFELD, STUART J · 2002 to 2006
$1.5M
NCI NIH HHS CA095857NCI NIH HHS R01 CA095875
6 · The paper itself

Abstract

During germ-band extension, Decapentaplegic (Dpp) signals from the dorsal ectoderm to maintain Tinman (Tin) expression in the underlying mesoderm. This signal specifies the cardiac field, and homologous genes (BMP2/4 and Nkx2.5) perform this function in mammals. We showed previously that a second Dpp signal from the dorsal ectoderm restricts the number of pericardial cells expressing the transcription factor Zfh1. Here we report that, via Zfh1, the second Dpp signal restricts the number of Odd-skipped-expressing and the number of Tin-expressing pericardial cells. Dpp also represses Tin expression independently of Zfh1, implicating a feed-forward mechanism in the regulation of Tin pericardial cell number. In the adjacent dorsal muscles, Dpp has the opposite effect. Dpp maintains Krüppel and Even-skipped expression required for muscle development. Our data show that Dpp refines the cardiac field by limiting the number of pericardial cells. This maintains the boundary between pericardial and dorsal muscle cells and defines the size of the heart. In the absence of the second Dpp signal, pericardial cells overgrow and this significantly reduces larval cardiac output. Our study suggests the existence of a second round of BMP signaling in mammalian heart development and that perhaps defects in this signal play a role in congenital heart defects.

Indexed as

Cardiac OutputSignal TransductionAnimalsBone Morphogenetic ProteinsCell ProliferationDNA-Binding ProteinsDrosophilaDrosophila ProteinsHeartPericardiumRepressor ProteinsTranscription FactorsBone Morphogenetic ProteinsDNA-Binding Proteinsdpp protein, DrosophilaDrosophila Proteinsodd protein, DrosophilaRepressor ProteinsTranscription Factorszfh1 protein, Drosophila

Identifiers

PMID17507674
PMCPMC1931542
OpenAlexW2064180160

What OpenQuestion holds

Textmetadata
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.