Evidence map›Paper›PMID 15256498›Full record

ArticleGenes & development2004

Dm-myb mutant lethality in Drosophila is dependent upon mip130: positive and negative regulation of DNA replication.

Eileen L Beall, Maren Bell, Daphne Georlette, Michael R Botchan

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
–field-weighted citation impact
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

51 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Origins of DNA replication.PLoS genetics · 2019
    Review
  6. Article
  7. Review
  8. Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  9. Review
  10. Article
  11. A genetic interaction map of cell cycle regulators.Molecular biology of the cell · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Chromatin reader L(3)mbt requires the Myb-MuvB/DREAM transcriptional regulatory complex for chromosomal recruitment.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  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 1 institution in 1 country.

Eileen L BeallDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA.
Maren Bell
Daphne Georlette
Michael R Botchan
University of California, Berkeley · US

Funding

TRANSFORMATION OF CELLS BY SV-40 VIRUSR01CA030490 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI BERGER, JAMES M., BOTCHAN, MICHAEL R. · 1985 to 2020
$5.1M
REGULATORY INTERACTIONS BETWEEN TUMOR VIRUSES AND CELLSR37CA030490 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI BOTCHAN, MICHAEL R. · 1988 to 2014
$4.8M
REGULATORY BIOLOGY OF CANCER AND GROWTH CONTROLT32CA009041 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI FIRESTONE, GARY L · 1985 to 2011
$3.7M
NCI NIH HHS CA09041NCI NIH HHS CA-30490NCI NIH HHS R01 CA030490NCI NIH HHS R37 CA030490NCI NIH HHS T32 CA009041
6 · The paper itself

Abstract

Gene amplification at the chorion loci in Drosophila ovarian follicle cells is a model for the developmental regulation of DNA replication. Previously, we showed that the Drosophila homolog of the Myb oncoprotein family (DmMyb) is tightly associated with four additional proteins and that DmMyb is required for this replication-mediated amplification. Here we used targeted mutagenesis to generate a mutant in the largest subunit of the DmMyb complex, the Aly and Lin-9 family member, Myb-interacting protein 130 (Mip130). We found that mip130 mutant females are sterile and display inappropriate bromodeoxyuridine (BrdU) incorporation throughout the follicle cell nuclei at stages undergoing gene amplification. Whereas mutations in Dm-myb are lethal, mutations in mip130 are viable. Surprisingly, Dm-myb mip130 double mutants are also viable and display the same phenotypes as mip130 mutants alone. This suggests that Mip130 activity without DmMyb counteraction may be responsible for the Dm-myb mutant lethality. RNA interference (RNAi) to selectively remove each DmMyb complex member revealed that DmMyb protein levels are dependent upon the presence of several of the complex members. Together, these data support a model in which DmMyb activates a repressive complex containing Mip130 into a complex competent to support replication at specific loci in a temporally and developmentally proscribed manner.

Indexed as

AnimalsBromodeoxyuridineCarrier ProteinsCell Cycle ProteinsDNA PrimersDNA ReplicationDrosophilaDrosophila ProteinsFemaleGene AmplificationImmunoblottingMutagenesis, Site-DirectedMutationOvarian FolliclePlasmidsProto-Oncogene Proteins c-mybBromodeoxyuridineCarrier ProteinsCell Cycle ProteinsDNA PrimersDrosophila ProteinsMip130 protein, DrosophilaMyb protein, DrosophilaProto-Oncogene Proteins c-myb

Identifiers

PMID15256498
PMCPMC478189
OpenAlexW2146921384

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.