Evidence map›Paper›PMID 31315658›Full record

ArticleEpigenetics & chromatin2019

Leo1 is essential for the dynamic regulation of heterochromatin and gene expression during cellular quiescence.

Eriko Oya, Mickaël Durand-Dubief, Adiel Cohen, Vladimir Maksimov, Catherine Schurra, Jun-Ichi Nakayama, Ronit Weisman, Benoit Arcangioli, Karl Ekwall

Open access · goldAbstract read
In one paragraph

Article in Epigenetics & chromatin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  9. An essential role for the Ino80 chromatin remodeling complex in regulation of gene expression during cellular quiescence.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Article
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  16. Is There a Histone Code for Cellular Quiescence?Frontiers in cell and developmental biology · 2021
    Review
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  18. Article
  19. Review
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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

9 authors at 4 institutions in 4 countries.

Eriko OyaDepartment of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.
Mickaël Durand-DubiefDepartment of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.
Adiel CohenDepartment of Natural and Life Sciences, The Open University of Israel, Ra'anana, Israel.
Vladimir MaksimovDepartment of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden.
Catherine SchurraUnite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.
Jun-Ichi NakayamaDivision of Chromatin Regulation, National Institute for Basic Biology, Okazaki, Japan.
Ronit WeismanDepartment of Natural and Life Sciences, The Open University of Israel, Ra'anana, Israel.
Benoit ArcangioliUnite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.
Karl EkwallDepartment of Biosciences and Nutrition, Karolinska Institutet, NEO Building, 141 83, Huddinge, Sweden. karl.ekwall@ki.se.ORCID 0000-0002-3029-4041
Karolinska Institutet · SEInstitut Pasteur · FROpen University of Israel · ILNational Institute for Basic Biology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCellular quiescence is a reversible differentiation state during which cells modify their gene expression program to inhibit metabolic functions and adapt to a new cellular environment. The epigenetic changes accompanying these alterations are not well understood. We used fission yeast cells as a model to study the regulation of quiescence. When these cells are starved for nitrogen, the cell cycle is arrested in G1, and the cells enter quiescence (G0). A gene regulatory program is initiated, including downregulation of thousands of genes-for example, those related to cell proliferation-and upregulation of specific genes-for example, autophagy genes-needed to adapt to the physiological challenge. These changes in gene expression are accompanied by a marked alteration of nuclear organization and chromatin structure.

resultsHere, we investigated the role of Leo1, a subunit of the conserved RNA polymerase-associated factor 1 (Paf1) complex, in the quiescence process using fission yeast as the model organism. Heterochromatic regions became very dynamic in fission yeast in G0 during nitrogen starvation. The reduction of heterochromatin in early G0 was correlated with reduced target of rapamycin complex 2 (TORC2) signaling. We demonstrated that cells lacking Leo1 show reduced survival in G0. In these cells, heterochromatic regions, including subtelomeres, were stabilized, and the expression of many genes, including membrane transport genes, was abrogated. TOR inhibition mimics the effect of nitrogen starvation, leading to the expression of subtelomeric genes, and this effect was suppressed by genetic deletion of leo1.

conclusionsWe identified a protein, Leo1, necessary for survival during quiescence. Leo1 is part of a conserved protein complex, Paf1C, linked to RNA polymerase II. We showed that Leo1, acting downstream of TOR, is crucial for the dynamic reorganization of chromosomes and the regulation of gene expression during cellular quiescence. Genes encoding membrane transporters are not expressed in quiescent leo1 mutant cells, and cells die after 2 weeks of nitrogen starvation. Taken together, our results suggest that Leo1 is essential for the dynamic regulation of heterochromatin and gene expression during cellular quiescence.

Indexed as

Cell CycleEpigenesis, GeneticGene Expression Regulation, FungalHeterochromatinHistonesNuclear ProteinsResting Phase, Cell CycleRNA-Binding ProteinsRNA Polymerase IISchizosaccharomycesSchizosaccharomyces pombe ProteinsHeterochromatinHistonesNuclear ProteinsRNA-Binding ProteinsRNA Polymerase IISchizosaccharomyces pombe ProteinsCellular quiescenceFission yeastGene expressionHeterochromatinPaf1C

Identifiers

PMID31315658
PMCPMC6636030
OpenAlexW2961003475

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.