Evidence map›Paper›PMID 28406902›Full record

ArticlePLoS genetics2017

Bicaudal C mutation causes myc and TOR pathway up-regulation and polycystic kidney disease-like phenotypes in Drosophila.

Chiara Gamberi, David R Hipfner, Marie Trudel, William D Lubell

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. mRNA (New York, N.Y.) · 2025
    Article
  4. Review
  5. Medical science pulse · 2025
    Article
  6. Review
  7. Review
  8. Bicaudal-C Post-transcriptional regulator of cell fates and functions.Frontiers in cell and developmental biology · 2022
    Review
  9. Article
  10. Empowering Melatonin Therapeutics withDiseases (Basel, Switzerland) · 2021
    Review
  11. Review
  12. Review
  13. Article
  14. Cyst Reduction by Melatonin in a NovelMolecules (Basel, Switzerland) · 2020
    Article
  15. Review
  16. Review
  17. Drug screening in Drosophila; why, when, and when not?Wiley interdisciplinary reviews. Developmental biology · 2019
    Review
  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

4 authors at 3 institutions in 1 country.

Chiara GamberiDepartment of Biology, Concordia University, Montréal, QC, Canada.ORCID 0000-0002-7122-6491
David R HipfnerInstitut de recherches cliniques de Montréal, 110 Pine Avenue West, Montréal, QC, Canada.
Marie TrudelInstitut de recherches cliniques de Montréal, 110 Pine Avenue West, Montréal, QC, Canada.
William D LubellDépartement de chimie, Université de Montréal, Montréal, QC, Canada.
Montreal Clinical Research Institute · CAConcordia University · CAUniversité de Montréal · CA

Funding

Canadian Institute for Health Research 106426
6 · The paper itself

Abstract

Progressive cystic kidney degeneration underlies diverse renal diseases, including the most common cause of kidney failure, autosomal dominant Polycystic Kidney Disease (PKD). Genetic analyses of patients and animal models have identified several key drivers of this disease. The precise molecular and cellular changes underlying cystogenesis remain, however, elusive. Drosophila mutants lacking the translational regulator Bicaudal C (BicC, the fly ortholog of vertebrate BICC1 implicated in renal cystogenesis) exhibited progressive cystic degeneration of the renal tubules (so called "Malpighian" tubules) and reduced renal function. The BicC protein was shown to bind to Drosophila (d-) myc mRNA in tubules. Elevation of d-Myc protein levels was a cause of tubular degeneration in BicC mutants. Activation of the Target of Rapamycin (TOR) kinase pathway, another common feature of PKD, was found in BicC mutant flies. Rapamycin administration substantially reduced the cystic phenotype in flies. We present new mechanistic insight on BicC function and propose that Drosophila may serve as a genetically tractable model for dissecting the evolutionarily-conserved molecular mechanisms of renal cystogenesis.

Indexed as

AnimalsAnimals, Genetically ModifiedCystsDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsFemaleGene Expression RegulationMalpighian TubulesMutationPolycystic Kidney DiseasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-mycRNA-Binding ProteinsUp-RegulationBicC protein, DrosophilaDrosophila ProteinsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-mycRNA-Binding Proteins

Identifiers

PMID28406902
PMCPMC5390980
OpenAlexW2605925078

What OpenQuestion holds

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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.