Evidence map›Paper›PMID 25010009›Full record

ArticlePLoS genetics2014

Hypersensitivity of primordial germ cells to compromised replication-associated DNA repair involves ATM-p53-p21 signaling.

Yunhai Luo, Suzanne A Hartford, Ruizhu Zeng, Teresa L Southard, Naoko Shima, John C Schimenti

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. HELQ Maintains Genome Stability of Primordial Germ Cells by Inhibiting LINE-1 Expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  6. Article
  7. Article
  8. [Homozygous Variant ofSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Cell genomics · 2023
    Article
  15. Article
  16. Transcription-replication conflicts in primordial germ cells necessitate the Fanconi anemia pathway to safeguard genome stability.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Yunhai LuoDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, United States of America.
Suzanne A HartfordDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, United States of America.
Ruizhu ZengDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, United States of America.
Teresa L SouthardDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, United States of America.
Naoko ShimaDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, United States of America.
John C SchimentiDepartment of Biomedical Sciences, Cornell University, Ithaca, New York, United States of America.
Cornell University · US

Funding

Genetics of recombination/genomic instability in miceR01GM045415 · NIGMS · JACKSON LABORATORY · PI SCHIMENTI, JOHN C · 1992 to 2016
$4.9M
Reproductive Sciences and Genomics Training ProgramT32HD052471 · NICHD · CORNELL UNIVERSITY · PI ROBERSON, MARK S · 2007 to 2016
$2.0M
NICHD NIH HHS T32 HD052471NICHD NIH HHS T32HD052471NIGMS NIH HHS R01 GM045415NIGMS NIH HHS R01GM45415
6 · The paper itself

Abstract

Genome maintenance in germ cells is critical for fertility and the stable propagation of species. While mechanisms of meiotic DNA repair and chromosome behavior are well-characterized, the same is not true for primordial germ cells (PGCs), which arise and propagate during very early stages of mammalian development. Fanconi anemia (FA), a genomic instability syndrome that includes hypogonadism and testicular failure phenotypes, is caused by mutations in genes encoding a complex of proteins involved in repair of DNA lesions associated with DNA replication. The signaling mechanisms underlying hypogonadism and testicular failure in FA patients or mouse models are unknown. We conducted genetic studies to show that hypogonadism of Fancm mutant mice is a result of reduced proliferation, but not apoptosis, of PGCs, resulting in reduced germ cells in neonates of both sexes. Progressive loss of germ cells in adult males also occurs, overlaid with an elevated level of meiotic DNA damage. Genetic studies indicated that ATM-p53-p21 signaling is partially responsible for the germ cell deficiency.

Indexed as

AnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsDNA RepairDNA ReplicationFanconi AnemiaGenomic InstabilityGerm CellsHumansHypogonadismMiceMutationrho GTP-Binding ProteinsSignal TransductionTumor Suppressor Protein p53Ataxia Telangiectasia Mutated ProteinsAtm protein, mouserho GTP-Binding ProteinsTumor Suppressor Protein p53

Identifiers

PMID25010009
PMCPMC4091704
OpenAlexW2054599502

What OpenQuestion holds

Textmetadata
LicenceCC0
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.