Evidence map›Paper›PMID 22095083›Full record

ArticleGenetics2012

A screen for X-linked mutations affecting Drosophila photoreceptor differentiation identifies Casein kinase 1α as an essential negative regulator of wingless signaling.

Kevin Legent, Josefa Steinhauer, Magali Richard, Jessica E Treisman

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. TheJournal of cell science · 2018
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Endocytosis of Wingless via a dynamin-independent pathway is necessary for signaling inProceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  10. Regulatory mechanisms of EGFR signalling during Drosophila eye development.Cellular and molecular life sciences : CMLS · 2016
    Review
  11. RZZ and Mad1 dynamics in Drosophila mitosis.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Myc function in Drosophila.Cold Spring Harbor perspectives in medicine · 2013
    Review
  16. Article
  17. 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

4 authors at 1 institution in 1 country.

Kevin LegentKimmel Center for Biology and Medicine of the Skirball Institute and Department of Cell Biology, New York University School of Medicine, New York, New York 10016, USA.
Josefa Steinhauer
Magali Richard
Jessica E Treisman
New York University · US

Funding

Pattern formation in the eye discR01EY013777 · NEI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TREISMAN, JESSICA E · 2002 to 2017
$5.8M
NEI NIH HHS EY013777NEI NIH HHS R01 EY013777
6 · The paper itself

Abstract

The Wnt and Hedgehog signaling pathways are essential for normal development and are misregulated in cancer. The casein kinase family of serine/threonine kinases regulates both pathways at multiple levels. However, it has been difficult to determine whether individual members of this family have distinct functions in vivo, due to their overlapping substrate specificities. In Drosophila melanogaster, photoreceptor differentiation is induced by Hedgehog and inhibited by Wingless, providing a sensitive system in which to identify regulators of each pathway. We used a mosaic genetic screen in the Drosophila eye to identify mutations in genes on the X chromosome required for signal transduction. We recovered mutations affecting the transcriptional regulator CREB binding protein, the small GTPase dynamin, the cytoskeletal regulator Actin-related protein 2, and the protein kinase Casein kinase 1α. Consistent with its reported function in the β-Catenin degradation complex, Casein Kinase 1α mutant cells accumulate β-Catenin and ectopically induce Wingless target genes. In contrast to previous studies based on RNA interference, we could not detect any effect of the same Casein Kinase 1α mutation on Hedgehog signaling. We thus propose that Casein kinase 1α is essential to allow β-Catenin degradation and prevent inappropriate Wingless signaling, but its effects on the Hedgehog pathway are redundant with other Casein kinase 1 family members.

Indexed as

MutationSignal TransductionActin-Related Protein 2AnimalsCasein Kinase IalphaCell DifferentiationCREB-Binding ProteinDrosophilaDrosophila ProteinsDynaminsErbB ReceptorsFemaleGenes, X-LinkedHedgehog ProteinsMalePhotoreceptor Cells, InvertebrateActin-Related Protein 2Casein Kinase IalphaCREB-Binding ProteinDrosophila ProteinsDynaminsErbB ReceptorsHedgehog ProteinsProto-Oncogene Proteins c-mycReceptors, Notchwg protein, DrosophilaWnt1 Protein

Identifiers

PMID22095083
PMCPMC3276650
OpenAlexW2012418269

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.