Evidence map›Paper›PMID 29401457›Full record

ArticlePLoS genetics2018

Ras/ERK-signalling promotes tRNA synthesis and growth via the RNA polymerase III repressor Maf1 in Drosophila.

Shrivani Sriskanthadevan-Pirahas, Rujuta Deshpande, Byoungchun Lee, Savraj S Grewal

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Trametinib ameliorates aging-associated gut pathology inProceedings of the National Academy of Sciences of the United States of America · 2024
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  11. Review
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  14. ERK signalling: a master regulator of cell behaviour, life and fate.Nature reviews. Molecular cell biology · 2020
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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.

Shrivani Sriskanthadevan-PirahasClark H Smith Brain Tumour Centre, Arnie Charbonneau Cancer Institute, Alberta Children's Hospital Research Institute, and Department of Biochemistry and Molecular Biology Calgary, University of Calgary, Calgary, Alberta, Canada.
Rujuta DeshpandeClark H Smith Brain Tumour Centre, Arnie Charbonneau Cancer Institute, Alberta Children's Hospital Research Institute, and Department of Biochemistry and Molecular Biology Calgary, University of Calgary, Calgary, Alberta, Canada.
Byoungchun LeeClark H Smith Brain Tumour Centre, Arnie Charbonneau Cancer Institute, Alberta Children's Hospital Research Institute, and Department of Biochemistry and Molecular Biology Calgary, University of Calgary, Calgary, Alberta, Canada.
Savraj S GrewalClark H Smith Brain Tumour Centre, Arnie Charbonneau Cancer Institute, Alberta Children's Hospital Research Institute, and Department of Biochemistry and Molecular Biology Calgary, University of Calgary, Calgary, Alberta, Canada.ORCID 0000-0002-1923-6270
University of Calgary · CA

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
NIH HHS P40 OD018537
6 · The paper itself

Abstract

The small G-protein Ras is a conserved regulator of cell and tissue growth. These effects of Ras are mediated largely through activation of a canonical RAF-MEK-ERK kinase cascade. An important challenge is to identify how this Ras/ERK pathway alters cellular metabolism to drive growth. Here we report on stimulation of RNA polymerase III (Pol III)-mediated tRNA synthesis as a growth effector of Ras/ERK signalling in Drosophila. We find that activation of Ras/ERK signalling promotes tRNA synthesis both in vivo and in cultured Drosophila S2 cells. We also show that Pol III function is required for Ras/ERK signalling to drive proliferation in both epithelial and stem cells in Drosophila tissues. We find that the transcription factor Myc is required but not sufficient for Ras-mediated stimulation of tRNA synthesis. Instead we show that Ras signalling promotes Pol III function and tRNA synthesis by phosphorylating, and inhibiting the nuclear localization and function of the Pol III repressor Maf1. We propose that inhibition of Maf1 and stimulation of tRNA synthesis is one way by which Ras signalling enhances protein synthesis to promote cell and tissue growth.

Indexed as

Transcription Elongation, GeneticAnimalsAnimals, Genetically ModifiedCell ProliferationCells, CulturedDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianMAP Kinase Signaling SystemProtein Biosynthesisras ProteinsRepressor ProteinsRNA Polymerase IIIRNA, TransferSignal TransductionTranscription Factor TFIIIBBrf protein, DrosophilaDrosophila ProteinsMaf1 protein, Drosophilaras ProteinsRepressor ProteinsRNA Polymerase IIIRNA, TransferTranscription Factor TFIIIB

Identifiers

PMID29401457
PMCPMC5814106
OpenAlexW2950800259

What OpenQuestion holds

Textmetadata
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.