Evidence map›Paper›PMID 36241664›Full record

ArticleNature communications2022

Solving the MCM paradox by visualizing the scaffold of CMG helicase at active replisomes.

Hana Polasek-Sedlackova, Thomas C R Miller, Jana Krejci, Maj-Britt Rask, Jiri Lukas

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A Meier-Gorlin syndrome mutation impairs the loading of the MCM2-7 complex during DNA replication initiation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
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  7. Compact Origins and Where to Find Them: ORC's Guide to Genome-Wide Licensing.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Stage-specific MCM protein expression inFrontiers in cellular and infection microbiology · 2025
    Article
  12. Review
  13. Review
  14. Review
  15. Article
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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

5 authors at 2 institutions in 2 countries.

Hana Polasek-SedlackovaProtein Signaling Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. polasek-sedlackova@ibp.cz.ORCID 0000-0001-8234-6176
Thomas C R MillerCenter for Chromosome Stability, Department of Cellular and Molecular Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-9749-1656
Jana KrejciDepartment of Cell Biology and Epigenetics, Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic.ORCID 0000-0001-5204-0723
Maj-Britt RaskProtein Signaling Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Jiri LukasProtein Signaling Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. jiri.lukas@cpr.ku.dk.ORCID 0000-0001-9087-506X
University of Copenhagen · DKCzech Academy of Sciences · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome duplication is safeguarded by constantly adjusting the activity of the replicative CMG (CDC45-MCM2-7-GINS) helicase. However, minichromosome maintenance proteins (MCMs)-the structural core of the CMG helicase-have never been visualized at sites of DNA synthesis inside a cell (the so-called MCM paradox). Here, we solve this conundrum by showing that anti-MCM antibodies primarily detect inactive MCMs. Upon conversion of inactive MCMs to CMGs, factors that are required for replisome activity bind to the MCM scaffold and block MCM antibody binding sites. Tagging of endogenous MCMs by CRISPR-Cas9 bypasses this steric hindrance and enables MCM visualization at active replisomes. Thus, by defining conditions for detecting the structural core of the replicative CMG helicase, our results explain the MCM paradox, provide visual proof that MCMs are an integral part of active replisomes in vivo, and enable the investigation of replication dynamics in living cells exposed to a constantly changing environment.

Indexed as

DNA ReplicationMinichromosome Maintenance ProteinsDNADNAMinichromosome Maintenance Proteins

Identifiers

PMID36241664
PMCPMC9568601
OpenAlexW4306179643

What OpenQuestion holds

Textmetadata
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.