Evidence map›Paper›PMID 21987787›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Minichromosome maintenance helicase paralog MCM9 is dispensible for DNA replication but functions in germ-line stem cells and tumor suppression.

Suzanne A Hartford, Yunhai Luo, Teresa L Southard, Irene M Min, John T Lis, John C Schimenti

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
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  7. Genetic insights into the complexity of premature ovarian insufficiency.Reproductive biology and endocrinology : RB&E · 2024
    Review
  8. A Human HomozygousGenes · 2024
    Article
  9. In vivo versus in silico assessment of potentially pathogenic missense variants in human reproductive genes.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Review
  11. The Role ofJournal of clinical medicine · 2023
    Article
  12. Article
  13. Article
  14. Histone Chaperones as Cardinal Players in Development.Frontiers in cell and developmental biology · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Cell Fate Decisions in the Wake of Histone H3 Deposition.Frontiers in cell and developmental biology · 2021
    Review
  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

6 authors at 1 institution in 1 country.

Suzanne A HartfordDepartment of Biomedical Sciences and Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
Yunhai Luo
Teresa L Southard
Irene M Min
John T Lis
John C Schimenti
Cornell University · US

Funding

COORDINATE GENE REGULATION IN ANIMAL CELLSR01GM025232 · NIGMS · CORNELL UNIVERSITY ITHACA · PI LIS, JOHN T · 1985 to 2020
$8.4M
Reproductive Sciences and Genomics Training ProgramT32HD052471 · NICHD · CORNELL UNIVERSITY · PI ROBERSON, MARK S · 2007 to 2016
$2.0M
NICHD NIH HHS T32 HD052471NIGMS NIH HHS R01 GM025232
6 · The paper itself

Abstract

Effective DNA replication is critical to the health and reproductive success of organisms. The six MCM2-7 proteins, which form the replicative helicase, are essential for high-fidelity replication of the genome. Many eukaryotes have a divergent paralog, MCM9, that was reported to be essential for loading MCM2-7 onto replication origins in the Xenopus oocyte extract system. To address the in vivo role of mammalian MCM9, we created and analyzed the phenotypes of mice with various mutations in Mcm9 and an intronic DNA replication-related gene Asf1a. Ablation of Mcm9 was compatible with cell proliferation and mouse viability, showing that it is nonessential for MCM2-7 loading or DNA replication. Mcm9 mutants underwent p53-independent embryonic germ-cell depletion in both sexes, with males also exhibiting defective spermatogonial stem-cell renewal. MCM9-deficient cells had elevated genomic instability and defective cell cycle reentry following replication stress, and mutant animals were prone to sex-specific cancers, most notably hepatocellular carcinoma in males. The phenotypes of mutant mice and cells suggest that MCM9 evolved a specialized but nonessential role in DNA replication or replication-linked quality-control mechanisms that are especially important for germ-line stem cells, and also for tumor suppression and genome maintenance in the soma.

Indexed as

AnimalsCarcinoma, HepatocellularCell CycleCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsDNA ReplicationGametogenesisGene ComponentsGenomic InstabilityGerm CellsImmunohistochemistryLiver NeoplasmsMaleMiceMicronucleus TestsAsf1a protein, mouseCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsMcm9 protein, mouseMinichromosome Maintenance ProteinsMolecular Chaperones

Identifiers

PMID21987787
PMCPMC3203795
OpenAlexW2109165103

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.