Evidence map›Paper›PMID 28207814›Full record

ArticlePLoS genetics2017

JMJD-5/KDM8 regulates H3K36me2 and is required for late steps of homologous recombination and genome integrity.

Pier Giorgio Amendola, Nico Zaghet, João J Ramalho, Jens Vilstrup Johansen, Mike Boxem, Anna Elisabetta Salcini

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

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  20. The small members of the JMJD protein family: Enzymatic jewels or jinxes?Biochimica et biophysica acta. Reviews on cancer · 2019
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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 2 institutions in 2 countries.

Pier Giorgio AmendolaBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-1476-1287
Nico ZaghetBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
João J RamalhoDevelopmental Biology, Department of Biology, Faculty of Science, Utrecht University, Padualaan 8, CH Utrecht, The Netherlands.
Jens Vilstrup JohansenBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Mike BoxemDevelopmental Biology, Department of Biology, Faculty of Science, Utrecht University, Padualaan 8, CH Utrecht, The Netherlands.ORCID 0000-0003-3966-4173
Anna Elisabetta SalciniBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
University of Copenhagen · DKUtrecht University · NL

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

The eukaryotic genome is organized in a three-dimensional structure called chromatin, constituted by DNA and associated proteins, the majority of which are histones. Post-translational modifications of histone proteins greatly influence chromatin structure and regulate many DNA-based biological processes. Methylation of lysine 36 of histone 3 (H3K36) is a post-translational modification functionally relevant during early steps of DNA damage repair. Here, we show that the JMJD-5 regulates H3K36 di-methylation and it is required at late stages of double strand break repair mediated by homologous recombination. Loss of jmjd-5 results in hypersensitivity to ionizing radiation and in meiotic defects, and it is associated with aberrant retention of RAD-51 at sites of double strand breaks. Analyses of jmjd-5 genetic interactions with genes required for resolving recombination intermediates (rtel-1) or promoting the resolution of RAD-51 double stranded DNA filaments (rfs-1 and helq-1) suggest that jmjd-5 prevents the formation of stalled postsynaptic recombination intermediates and favors RAD-51 removal. As these phenotypes are all recapitulated by a catalytically inactive jmjd-5 mutant, we propose a novel role for H3K36me2 regulation during late steps of homologous recombination critical to preserve genome integrity.

Indexed as

AnimalsApoptosisCaenorhabditis elegansCaenorhabditis elegans ProteinsChromatinDNA-Binding ProteinsDNA DamageDNA HelicasesDNA MethylationDNA RepairGenomic InstabilityGerm CellsHistone-Lysine N-MethyltransferaseHistonesHomologous RecombinationJumonji Domain-Containing Histone DemethylasesCaenorhabditis elegans ProteinsChromatinDNA-Binding ProteinsDNA HelicasesHELQ-1 protein, C elegansHistone-Lysine N-MethyltransferaseHistonesJumonji Domain-Containing Histone Demethylasesrad-51 protein, C elegansRad51 Recombinasercq-5 protein, C elegansRFS-1 protein, C elegans

Identifiers

PMID28207814
PMCPMC5336306
OpenAlexW2588601516

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.