Evidence map›Paper›PMID 17219175›Full record

ArticleChromosoma2007

Developmentally regulated histone modifications in Drosophila follicle cells: initiation of gene amplification is associated with histone H3 and H4 hyperacetylation and H1 phosphorylation.

Tom Hartl, Carl Boswell, Terry L Orr-Weaver, Giovanni Bosco

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Chromosoma, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 48 citations in OpenAlex.

  1. Finishing the egg.Genetics · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. The ecdysone receptor (ScEcR-A) binds DNA puffs at the start of DNA amplification in Sciara coprophila.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Regulation of DNA replication during development.Development (Cambridge, England) · 2012
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Defining the replication program through the chromatin landscape.Critical reviews in biochemistry and molecular biology · 2011
    Review
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 2 institutions in 1 country.

Tom HartlDepartment of Molecular and Cellular Biology, Arizona Cancer Center, University of Arizona, Tucson, AZ 85724, USA.
Carl Boswell
Terry L Orr-Weaver
Giovanni Bosco
University of Arizona · USWhitehead Institute for Biomedical Research · US

Funding

GRADUATE TRAINING IN BIOCHEMISTRY AND MOLECULAR BIOLOGYT32GM008659 · NIGMS · UNIVERSITY OF ARIZONA · PI CAPALDI, ANDREW PAUL, WEINERT, TED A. · 1997 to 2019
$5.3M
Developmental control of replication by Drosophila RBR01GM069462 · NIGMS · UNIVERSITY OF ARIZONA · PI BOSCO, GIOVANNI · 2004 to 2012
$2.5M
NIGMS NIH HHS 5T32GM008659NIGMS NIH HHS R01 GM069462-01NIGMS NIH HHS R01 GM57451
6 · The paper itself

Abstract

We have used gene amplification in Drosophila follicle cells as a model of metazoan DNA replication to address whether changes in histone modifications are associated with replication origin activation. We observe that replication initiation is associated with distinct histone modifications. Acetylated lysines K5, K8, and K12 on histone H4 and K14 on histone H3 are specifically enriched during replication initiation at the amplification origins. Strikingly, H4 acetylation persists at an amplification origin well after replication forks have progressed significantly outward from the origin, indicating that H4 acetylation is associated with origin regulation and not histone deposition at the replication forks. Origin recognition complex subunit 2 (orc2) mutants with severe amplification defects do not abolish H4 acetylation, whereas the dup/cdt1 mutant delays the appearance of acetylation foci, and mutants in rbf result in temporal persistence. These data indicate that core histone acetylation is associated with origin activity. Furthermore, follicle cells undergoing gene amplification exhibit high levels of histone H1 phosphorylation. The patterns of H1 phosphorylation provide insights into cell cycle states during amplification, as H1 kinase activity in follicle cells is responsive to high Cyclin E activity, and it can be abolished by overexpressing the retinoblastoma homolog, Rbf, that represses Cyclin E. These data suggest that amplification origins are able to initiate when the cells are in a late S-phase, when the genome is normally not licensed for replication.

Indexed as

AcetylationAnimalsBromodeoxyuridineCell CycleChromatin ImmunoprecipitationCyclin EDNA ReplicationDrosophilaDrosophila ProteinsFemaleFluorescent Antibody TechniqueGene AmplificationHistonesNucleic Acid Amplification TechniquesOrigin Recognition ComplexOvarian FollicleBromodeoxyuridineCyclin EDrosophila ProteinsHistonesOrigin Recognition ComplexRbf protein, DrosophilaRetinoblastoma ProteinTranscription Factors

Identifiers

PMID17219175
OpenAlexW2023594640

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.