Evidence map›Paper›PMID 21423663›Full record

ArticlePLoS genetics2011

Global analysis of the relationship between JIL-1 kinase and transcription.

Catherine Regnard, Tobias Straub, Angelika Mitterweger, Ina K Dahlsveen, Viola Fabian, Peter B Becker

Abstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed.

  1. Article
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  5. Review
  6. Drosophila P75 safeguards oogenesis by preventing H3K9me2 spreading.Journal of genetics and genomics = Yi chuan xue bao · 2020
    Article
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  15. Article
  16. Dosage compensation in Drosophila.Cold Spring Harbor perspectives in biology · 2015
    Review
  17. Article
  18. Review
  19. Review
  20. A new player in X identification: the CLAMP protein is a key factor in Drosophila dosage compensation.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2014
    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

6 authors.

Catherine RegnardAdolf-Butenandt-Institute and Centre for Integrated Protein Science (CiPSM), Ludwig-Maximilians-University, Munich, Germany.
Tobias Straub
Angelika Mitterweger
Ina K Dahlsveen
Viola Fabian
Peter B Becker

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ubiquitous tandem kinase JIL-1 is essential for Drosophila development. Its role in defining decondensed domains of larval polytene chromosomes is well established, but its involvement in transcription regulation has remained controversial. For a first comprehensive molecular characterisation of JIL-1, we generated a high-resolution, chromosome-wide interaction profile of the kinase in Drosophila cells and determined its role in transcription. JIL-1 binds active genes along their entire length. The presence of the kinase is not proportional to average transcription levels or polymerase density. Comparison of JIL-1 association with elongating RNA polymerase and a variety of histone modifications suggests two distinct targeting principles. A basal level of JIL-1 binding can be defined that correlates best with the methylation of histone H3 at lysine 36, a mark that is placed co-transcriptionally. The additional acetylation of H4K16 defines a second state characterised by approximately twofold elevated JIL-1 levels, which is particularly prominent on the dosage-compensated male X chromosome. Phosphorylation of the histone H3 N-terminus by JIL-1 in vitro is compatible with other tail modifications. In vivo, phosphorylation of H3 at serine 10, together with acetylation at lysine 14, creates a composite histone mark that is enriched at JIL-1 binding regions. Its depletion by RNA interference leads to a modest, but significant, decrease of transcription from the male X chromosome. Collectively, the results suggest that JIL-1 participates in a complex histone modification network that characterises active, decondensed chromatin. We hypothesise that one specific role of JIL-1 may be to reinforce, rather than to establish, the status of active chromatin through the phosphorylation of histone H3 at serine 10.

Indexed as

Transcriptional ActivationTranscription, GeneticAnimalsCell LineChromatinChromatin ImmunoprecipitationDosage Compensation, GeneticDrosophila melanogasterDrosophila ProteinsFemaleGenes, InsectGenes, ReporterGenes, X-LinkedGenetic LociHistonesMaleChromatinDrosophila ProteinsHistonesJIL-1 protein, DrosophilaProtein Serine-Threonine KinasesRNA Polymerase II

Identifiers

PMID21423663
PMCPMC3053325

What OpenQuestion holds

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Registered trials

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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.