Evidence map›Paper›PMID 24105599›Full record

ArticleChromosoma2014

Dynamics of DOT1L localization and H3K79 methylation during meiotic prophase I in mouse spermatocytes.

David Ontoso, Liisa Kauppi, Scott Keeney, Pedro A San-Segundo

Open access · greenAbstract read
In one paragraph

Article in Chromosoma, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Chromatin structure in totipotent mouse early preimplantation embryos.The Journal of reproduction and development · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Connecting the DOTs on Cell Identity.Frontiers in cell and developmental biology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  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 3 institutions in 3 countries.

David OntosoInstituto de Biología Funcional y Genómica, Consejo Superior de Investigaciones Científicas and University of Salamanca, 37007, Salamanca, Spain.
Liisa Kauppi
Scott Keeney
Pedro A San-Segundo
Consejo Superior de Investigaciones Científicas · ESMemorial Sloan Kettering Cancer Center · USUniversity of Helsinki · FI

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Role of Spo11 and recombination in mouse meiosisR01HD040916 · NICHD · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI JASIN, MARIA · 2001 to 2011
$5.4M
Role of Spo11 and recombination in mouse meiosisR01GM105421 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA, KEENEY, SCOTT · 2013 to 2016
$2.4M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA008748NICHD NIH HHS R01 HD040916NIGMS NIH HHS R01 GM105421
6 · The paper itself

Abstract

During meiotic prophase I, interactions between maternal and paternal chromosomes, under checkpoint surveillance, establish connections between homologs that promote their accurate distribution to meiotic progeny. In human, faulty meiosis causes aneuploidy resulting in miscarriages and genetic diseases. Meiotic processes occur in the context of chromatin; therefore, histone post-translational modifications are expected to play important roles. Here, we report the cytological distribution of the evolutionarily conserved DOT1L methyltransferase and the different H3K79 methylation states resulting from its activity (mono-, di- and tri-methylation; H3K79me1, me2 and me3, respectively) during meiotic prophase I in mouse spermatocytes. In the wild type, whereas low amounts of H3K79me1 are rather uniformly present throughout prophase I, levels of DOT1L, H3K79me2 and H3K79me3 exhibit a notable increase from pachynema onwards, but with differential subnuclear distribution patterns. The heterochromatic centromeric regions and the sex body are enriched for H3K79me3. In contrast, H3K79me2 is present all over the chromatin, but is largely excluded from the sex body despite the accumulation of DOT1L. In meiosis-defective mouse mutants, the increase of DOT1L and H3K79me is blocked at the same stage where meiosis is arrested. H3K79me patterns, combined with the cytological analysis of the H3.3, γH2AX, macroH2A and H2A.Z histone variants, are consistent with a differential role for these epigenetic marks in male mouse meiotic prophase I. We propose that H3K79me2 is related to transcriptional reactivation on autosomes during pachynema, whereas H3K79me3 may contribute to the maintenance of repressive chromatin at centromeric regions and the sex body.

Indexed as

Meiotic Prophase IAnimalsCell NucleusHistone-Lysine N-MethyltransferaseHistonesHumansLysineMaleMethylationMethyltransferasesMiceMice, Inbred C57BLModels, BiologicalMutationProtein TransportSex ChromosomesDot1l protein, mousegamma-H2AX protein, mouseHistone-Lysine N-MethyltransferaseHistonesLysineMethyltransferases

Identifiers

PMID24105599
PMCPMC3969405
OpenAlexW2049738249

What OpenQuestion holds

Textmetadata
LicenceTDM
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.