Evidence map›Paper›PMID 18241851›Full record

ArticleDevelopmental biology2008

Drosophila growth and development in the absence of dMyc and dMnt.

Sarah B Pierce, Cynthia Yost, Sarah A R Anderson, Erin M Flynn, Jeffrey Delrow, Robert N Eisenman

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Heat tolerance inPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article
  4. Article
  5. The homeostatic regulation of ribosome biogenesis.Seminars in cell & developmental biology · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Interspecies analysis of MYC targets identifies tRNA synthetases as mediators of growth and survival in MYC-overexpressing cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. MYC and the control of DNA replication.Cold Spring Harbor perspectives in medicine · 2014
    Review
  17. Article
  18. Myc function in Drosophila.Cold Spring Harbor perspectives in medicine · 2013
    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 1 institution in 1 country.

Sarah B PierceDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, MS A2-025, POB 19024, Seattle, WA 98109-1024, USA.
Cynthia Yost
Sarah A R Anderson
Erin M Flynn
Jeffrey Delrow
Robert N Eisenman
Fred Hutch Cancer Center · US

Funding

MYC ONCOPROTEIN FUNCTIONR37CA057138 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 2003 to 2013
$8.0M
MYC ONCOPROTEIN FUNCTIONR01CA057138 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 1991 to 2018
$4.9M
NCI NIH HHS R01 CA057138NCI NIH HHS R37 CA057138NCI NIH HHS R37CA57138
6 · The paper itself

Abstract

Myc oncoproteins are essential regulators of the growth and proliferation of mammalian cells. In Drosophila the single ortholog of Myc (dMyc), encoded by the dm gene, influences organismal size and the growth of both mitotic and endoreplicating cells. A null mutation in dm results in attenuated endoreplication and growth arrest early in larval development. Drosophila also contains a single ortholog of the mammalian Mad/Mnt transcriptional repressor proteins (dMnt), which is thought to antagonize dMyc function. Here we show that animals lacking both dMyc and dMnt display increased viability and grow significantly larger and develop further than dMyc single mutants. We observe increased endoreplication and growth of larval tissues in these double mutants and disproportionate growth of the imaginal discs. Gene expression analysis indicates that loss of dMyc leads to decreased expression of genes required for ribosome biogenesis and protein synthesis. The additional loss of dMnt partially rescues expression of a small number of dMyc and dMnt genes that are primarily involved in rRNA synthesis and processing. Our results indicate that dMnt repression is normally overridden by dMyc activation during larval development. Therefore the severity of the dm null phenotype is likely due to unopposed repression by dMnt on a subset of genes critical for cell and organismal growth. Surprisingly, considerable growth and development can occur in the absence of both dMyc and dMnt.

Indexed as

Genes, InsectMutationAnimalsBase SequenceBasic Helix-Loop-Helix ProteinsDNA-Binding ProteinsDNA PrimersDrosophilaDrosophila ProteinsFemaleGene DeletionGene Expression ProfilingGene Expression Regulation, DevelopmentalLarvaMaleMetamorphosis, BiologicalBasic Helix-Loop-Helix ProteinsDNA-Binding ProteinsDNA PrimersDrosophila ProteinsMyc protein, DrosophilaRepressor ProteinsTranscription Factors

Identifiers

PMID18241851
PMCPMC2322934
OpenAlexW2031114253

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.