Evidence map›Paper›PMID 23271984›Full record

ArticlePLoS genetics2012

The chromosomal proteins JIL-1 and Z4/Putzig regulate the telomeric chromatin in Drosophila melanogaster.

Rute Silva-Sousa, Elisenda López-Panadès, David Piñeyro, Elena Casacuberta

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Lysine-36 ofbioRxiv : the preprint server for biology · 2023
    Article
  5. Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

4 authors at 1 institution in 1 country.

Rute Silva-SousaInstitute of Evolutionary Biology, Institut de Biologia Evolutiva (CSIC-UPF), Barcelona, Spain.
Elisenda López-Panadès
David Piñeyro
Elena Casacuberta
Institut de Biologia Evolutiva · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drosophila telomere maintenance depends on the transposition of the specialized retrotransposons HeT-A, TART, and TAHRE. Controlling the activation and silencing of these elements is crucial for a precise telomere function without compromising genomic integrity. Here we describe two chromosomal proteins, JIL-1 and Z4 (also known as Putzig), which are necessary for establishing a fine-tuned regulation of the transcription of the major component of Drosophila telomeres, the HeT-A retrotransposon, thus guaranteeing genome stability. We found that mutant alleles of JIL-1 have decreased HeT-A transcription, putting forward this kinase as the first positive regulator of telomere transcription in Drosophila described to date. We describe how the decrease in HeT-A transcription in JIL-1 alleles correlates with an increase in silencing chromatin marks such as H3K9me3 and HP1a at the HeT-A promoter. Moreover, we have detected that Z4 mutant alleles show moderate telomere instability, suggesting an important role of the JIL-1-Z4 complex in establishing and maintaining an appropriate chromatin environment at Drosophila telomeres. Interestingly, we have detected a biochemical interaction between Z4 and the HeT-A Gag protein, which could explain how the Z4-JIL-1 complex is targeted to the telomeres. Accordingly, we demonstrate that a phenotype of telomere instability similar to that observed for Z4 mutant alleles is found when the gene that encodes the HeT-A Gag protein is knocked down. We propose a model to explain the observed transcriptional and stability changes in relation to other heterochromatin components characteristic of Drosophila telomeres, such as HP1a.

Indexed as

Cell Cycle ProteinsChromatinDrosophila ProteinsProtein Serine-Threonine KinasesTelomereAnimalsChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDrosophila melanogasterGene Products, gagGenomic InstabilityHistone-Lysine N-MethyltransferaseMutationRetroelementsCell Cycle ProteinsChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDrosophila ProteinsGene Products, gagHeT-A-gag protein, DrosophilaHistone-Lysine N-MethyltransferaseJIL-1 protein, DrosophilaProtein Serine-Threonine Kinasespzg protein, DrosophilaRetroelementsTART-element-gag protein, Drosophila

Identifiers

PMID23271984
PMCPMC3521665
OpenAlexW2086074894

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.