Evidence map›Paper›PMID 30329080›Full record

ArticleNucleic acids research2019

Resting cells rely on the DNA helicase component MCM2 to build cilia.

Teresa Casar Tena, Lars D Maerz, Karol Szafranski, Marco Groth, Tamara J Blätte, Cornelia Donow, Sabrina Matysik, Paul Walther, Penelope A Jeggo, Martin D Burkhalter and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. A CThe New phytologist · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Cholesterol and Phosphoinositides in Cilia Biology.Advances in experimental medicine and biology · 2023
    Review
  8. Article
  9. Homozygous mutation inJournal of medical genetics · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. 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

11 authors at 3 institutions in 2 countries.

Teresa Casar TenaInstitute of Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.
Lars D MaerzInstitute of Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.
Karol SzafranskiLeibniz Institute on Aging, Fritz Lipmann Institute, 07745 Jena, Germany.
Marco GrothLeibniz Institute on Aging, Fritz Lipmann Institute, 07745 Jena, Germany.
Tamara J BlätteInstitute of Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.
Cornelia DonowInstitute of Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.
Sabrina MatysikInstitute of Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.
Paul WaltherCentral Facility for Electron Microscopy, Ulm University, 89081 Ulm, Germany.
Penelope A JeggoGenome Damage and Stability Centre, University of Sussex, Brighton BN1 9RQ, UK.
Martin D BurkhalterInstitute of Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.
Melanie PhilippInstitute of Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.
Universität Ulm · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEUniversity of Sussex · GB

Funding

Medical Research Council G0500897
6 · The paper itself

Abstract

Minichromosome maintenance (MCM) proteins facilitate replication by licensing origins and unwinding the DNA double strand. Interestingly, the number of MCM hexamers greatly exceeds the number of firing origins suggesting additional roles of MCMs. Here we show a hitherto unanticipated function of MCM2 in cilia formation in human cells and zebrafish that is uncoupled from replication. Zebrafish depleted of MCM2 develop ciliopathy-phenotypes including microcephaly and aberrant heart looping due to malformed cilia. In non-cycling human fibroblasts, loss of MCM2 promotes transcription of a subset of genes, which cause cilia shortening and centriole overduplication. Chromatin immunoprecipitation experiments show that MCM2 binds to transcription start sites of cilia inhibiting genes. We propose that such binding may block RNA polymerase II-mediated transcription. Depletion of a second MCM (MCM7), which functions in complex with MCM2 during its canonical functions, reveals an overlapping cilia-deficiency phenotype likely unconnected to replication, although MCM7 appears to regulate a distinct subset of genes and pathways. Our data suggests that MCM2 and 7 exert a role in ciliogenesis in post-mitotic tissues.

Indexed as

Transcription, GeneticAnimalsCiliaCiliopathiesDNA HelicasesHumansMinichromosome Maintenance Complex Component 2Minichromosome Maintenance Complex Component 7MitosisTranscription Initiation SiteZebrafishDNA HelicasesMCM2 protein, humanMCM7 protein, humanMinichromosome Maintenance Complex Component 2Minichromosome Maintenance Complex Component 7

Identifiers

PMID30329080
PMCPMC6326816
OpenAlexW2897573317

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.