Evidence map›Paper›PMID 30701204›Full record

ArticleCommunications biology2019

Changes in long-range rDNA-genomic interactions associate with altered RNA polymerase II gene programs during malignant transformation.

Jeannine Diesch, Megan J Bywater, Elaine Sanij, Donald P Cameron, William Schierding, Natalie Brajanovski, Jinbae Son, Jirawas Sornkom, Nadine Hein, Maurits Evers and 6 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 46 citations in OpenAlex.

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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

16 authors at 6 institutions in 3 countries.

Jeannine Diesch1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.
Megan J Bywater1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.
Elaine Sanij1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.
Donald P Cameron1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.
William Schierding5Liggins Institute, The University of Auckland, Auckland, 1023 New Zealand.
Natalie Brajanovski1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.
Jinbae Son1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.
Jirawas Sornkom1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.ORCID 0000-0002-8939-416X
Nadine Hein3ACRF Department of Cancer Biology and Therapeutics, John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601 Australia.
Maurits Evers3ACRF Department of Cancer Biology and Therapeutics, John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601 Australia.
Richard B Pearson1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.ORCID 0000-0001-5919-5090
Grant A McArthur1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.
Austen R D Ganley9School of Biological Sciences, The University of Auckland, Auckland, 1010 New Zealand.
Justin M O'Sullivan5Liggins Institute, The University of Auckland, Auckland, 1023 New Zealand.ORCID 0000-0003-2927-450X
Ross D Hannan1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.
Gretchen Poortinga1Cancer Research Division, Peter MacCallum Cancer Centre, Melbourne, VIC 3000 Australia.ORCID 0000-0001-5990-9559
Australian National University · AUPeter MacCallum Cancer Centre · AUThe University of Melbourne · AUUniversity of Auckland · NZAuckland Institute of Studies · NZQIMR Berghofer Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The three-dimensional organization of the genome contributes to its maintenance and regulation. While chromosomal regions associate with nucleolar ribosomal RNA genes (rDNA), the biological significance of rDNA-genome interactions and whether they are dynamically regulated during disease remain unclear. rDNA chromatin exists in multiple inactive and active states and their transition is regulated by the RNA polymerase I transcription factor UBTF. Here, using a MYC-driven lymphoma model, we demonstrate that during malignant progression the rDNA chromatin converts to the open state, which is required for tumor cell survival. Moreover, this rDNA transition co-occurs with a reorganization of rDNA-genome contacts which correlate with gene expression changes at associated loci, impacting gene ontologies including B-cell differentiation, cell growth and metabolism. We propose that UBTF-mediated conversion to open rDNA chromatin during malignant transformation contributes to the regulation of specific gene pathways that regulate growth and differentiation through reformed long-range physical interactions with the rDNA.

Indexed as

Genes, rRNAGenetic Predisposition to DiseaseGenomeCell Line, TumorCell Transformation, NeoplasticChromatinChromatin Assembly and DisassemblyDisease ProgressionDNA, RibosomalEpistasis, GeneticGene Expression ProfilingGene Expression RegulationHumansNeoplasmsRNA Polymerase IIChromatinDNA, RibosomalRNA Polymerase II

Identifiers

PMID30701204
PMCPMC6349880
OpenAlexW2921552970

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.