Evidence map›Paper›PMID 20351283›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Hrp48 attenuates Sxl expression to allow for proper notch expression and signaling in wing development.

Yaron Suissa, Yossi Kalifa, Tama Dinur, Patricia Graham, Girish Deshpande, Paul Schedl, Offer Gerlitz

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Auto-regulatory feedback by RNA-binding proteins.Journal of molecular cell biology · 2019
    Review
  5. Modulation of the Hippo pathway and organ growth by RNA processing proteins.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Sex-lethal enables germline stem cell differentiation by down-regulating Nanos protein levels during Drosophila oogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  13. Article
  14. Review
  15. 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

7 authors at 2 institutions in 2 countries.

Yaron SuissaDevelopmental Biology and Cancer Research, Institute for Medical Research Israel-Canada, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel.
Yossi Kalifa
Tama Dinur
Patricia Graham
Girish Deshpande
Paul Schedl
Offer Gerlitz
Princeton University · USWeizmann Institute of Science · IL

Funding

MOLECULAR AND GENETIC ANALYSIS OF CHROMATIN STRUCTURER01GM043432 · NIGMS · PRINCETON UNIVERSITY · PI SCHEDL, PAUL D · 1990 to 2017
$5.8M
NIGMS NIH HHS R01 GM043432
6 · The paper itself

Abstract

Different signaling pathways are deployed in specific developmental contexts to generate sexually dimorphic traits. Recently, Sex-lethal (Sxl), the female determinant in Drosophila melanogaster, was shown to down-regulate Notch (N) signaling to accomplish sex-specific patterning. Paradoxically, however, both Sxl and N are ubiquitously expressed in all of the female cells. This raises a key question as to how, during monomorphic female development, N signaling escapes the negative impact of Sxl. Here, we uncover a regulatory loop involving Hrp48, an abundant Drosophila hnRNP, Sxl and N. Phenotypic consequences of the partial loss of hrp48 resemble that of N but are more pronounced in females than in males. Likewise, N levels are drastically diminished only in females. Interestingly, monomorphic female tissues including wing, eye and antennal discs display considerable increase in Sxl amounts. Finally, female-specific attenuation of N signaling is rescued upon simultaneous removal of Sxl. Thus, our data demonstrate that in monomorphic contexts, Hrp48 functions as a moderator of Sxl expression to achieve adequate levels of N receptor production and signaling. We propose that it is critical to modulate the activities of the master determinant underling sexual dimorphism, to ensure that it does not function inappropriately in monomorphic tissues and disrupt their development.

Indexed as

Gene Expression Regulation, DevelopmentalAllelesAnimalsCrosses, GeneticDrosophila melanogasterDrosophila ProteinsFemaleHeterogeneous-Nuclear RibonucleoproteinsMaleMitosisModels, BiologicalReceptors, NotchRNA-Binding ProteinsSex FactorsSignal TransductionWings, AnimalDrosophila ProteinsHeterogeneous-Nuclear RibonucleoproteinsHrb27C protein, DrosophilaReceptors, NotchRNA-Binding ProteinsSxl protein, Drosophila

Identifiers

PMID20351283
PMCPMC2872424
OpenAlexW2084345817

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.