Evidence map›Paper›PMID 26801178›Full record

ArticleGenetics2016

Hedgehog Signaling Strength Is Orchestrated by the mir-310 Cluster of MicroRNAs in Response to Diet.

Ibrahim Ömer Çiçek, Samir Karaca, Marko Brankatschk, Suzanne Eaton, Henning Urlaub, Halyna R Shcherbata

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2016. 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
3.3field-weighted citation impact, top 8% 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, 37 citations in OpenAlex.

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  9. Review
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  13. Dietary Modulation of the Epigenome.Physiological reviews · 2018
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. MicroRNAs and the metabolic hallmarks of aging.Molecular and cellular endocrinology · 2017
    Review
  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

6 authors at 2 institutions in 1 country.

Ibrahim Ömer ÇiçekMax Planck Research Group of Gene Expression and Signaling, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany.
Samir KaracaBioanalytical Mass Spectrometry Research Group, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany.
Marko BrankatschkMax Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.
Suzanne EatonMax Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.
Henning UrlaubBioanalytical Mass Spectrometry Research Group, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany.
Halyna R ShcherbataMax Planck Research Group of Gene Expression and Signaling, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany halyna.shcherbata@mpibpc.mpg.de.ORCID http://orcid.org/0000-0002-3855-0345
Max Planck Institute for Biophysical Chemistry · DEMax Planck Institute of Molecular Cell Biology and Genetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the discovery of microRNAs (miRNAs) only two decades ago, they have emerged as an essential component of the gene regulatory machinery. miRNAs have seemingly paradoxical features: a single miRNA is able to simultaneously target hundreds of genes, while its presence is mostly dispensable for animal viability under normal conditions. It is known that miRNAs act as stress response factors; however, it remains challenging to determine their relevant targets and the conditions under which they function. To address this challenge, we propose a new workflow for miRNA function analysis, by which we found that the evolutionarily young miRNA family, the mir-310s (mir-310/mir-311/mir-312/mir-313), are important regulators of Drosophila metabolic status. mir-310s-deficient animals have an abnormal diet-dependent expression profile for numerous diet-sensitive components, accumulate fats, and show various physiological defects. We found that the mir-310s simultaneously repress the production of several regulatory factors (Rab23, DHR96, and Ttk) of the evolutionarily conserved Hedgehog (Hh) pathway to sharpen dietary response. As the mir-310s expression is highly dynamic and nutrition sensitive, this signal relay model helps to explain the molecular mechanism governing quick and robust Hh signaling responses to nutritional changes. Additionally, we discovered a new component of the Hh signaling pathway in Drosophila, Rab23, which cell autonomously regulates Hh ligand trafficking in the germline stem cell niche. How organisms adjust to dietary fluctuations to sustain healthy homeostasis is an intriguing research topic. These data are the first to report that miRNAs can act as executives that transduce nutritional signals to an essential signaling pathway. This suggests miRNAs as plausible therapeutic agents that can be used in combination with low calorie and cholesterol diets to manage quick and precise tissue-specific responses to nutritional changes.

Indexed as

DietSignal TransductionAnimalsDrosophila melanogasterDrosophila ProteinsEnergy MetabolismFemaleHedgehog ProteinsHomeostasisMicroRNAsOvaryStem Cell NicheVesicular Transport ProteinsDrosophila ProteinsHedgehog ProteinsMicroRNAsRab23 protein, DrosophilaVesicular Transport Proteinsdietary restrictionDrosophilafollicle stem cellHedgehog signalingHh ligandmetabolic stressmiRNAoogenesisRab23the mir-310s

Identifiers

PMID26801178
PMCPMC4788116
OpenAlexW2296222259

What OpenQuestion holds

Textmetadata
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Registered trials

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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.