Evidence map›Paper›PMID 40240347›Full record

ArticleNature communications2025

Mouse MRE11-RAD50-NBS1 is needed to start and extend meiotic DNA end resection.

Soonjoung Kim, Shintaro Yamada, Tao Li, Claudia Canasto-Chibuque, Jun Hyun Kim, Marina Marcet-Ortega, Jiaqi Xu, Diana Y Eng, Laura Feeney, John H J Petrini and 1 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Soonjoung KimMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. soonjk@yuhs.ac.ORCID http://orcid.org/0009-0003-0029-4715
Shintaro YamadaMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-4882-0871
Tao LiMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-5728-3721
Claudia Canasto-ChibuqueMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-0787-5892
Jun Hyun KimMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Marina Marcet-OrtegaMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Jiaqi XuMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Diana Y EngMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Laura FeeneyMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
John H J PetriniMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0001-5102-5679
Scott KeeneyMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. s-keeney@ski.mskcc.org.ORCID http://orcid.org/0000-0002-1283-6417

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Mechanism and regulation of meiotic recombinationR35GM118092 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI Scott Keeney · 2016 to 2026
$7.0M
DNA Damage & DNA Replication: a Complex RelationshipR35GM136278 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI John HJ Petrini · 2020 to 2026
$5.5M
The Mre11 complex: linking recombination to checkpointsR01GM059413 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1999 to 2011
$5.2M
Howard Hughes Medical Institute (HHMI) NANCI NIH HHS P30 CA008748NIGMS NIH HHS R01 GM059413NIGMS NIH HHS R35 GM118092NIGMS NIH HHS R35 GM136278U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R01 GM59413
6 · The paper itself

Abstract

Nucleolytic resection of DNA ends is critical for homologous recombination, but its mechanism is not fully understood, particularly in mammalian meiosis. Here we examine roles of the conserved MRN complex (MRE11, RAD50, and NBS1) through genome-wide analysis of meiotic resection during spermatogenesis in mice with various MRN mutations, including several that cause chromosomal instability in humans. Meiotic DSBs form at elevated levels but remain unresected if Mre11 is conditionally deleted, thus MRN is required for both resection initiation and regulation of DSB numbers. Resection lengths are reduced to varying degrees in MRN hypomorphs or if MRE11 nuclease activity is attenuated in a conditional nuclease-dead Mre11 model. These findings unexpectedly establish that MRN is needed for longer-range extension of resection beyond that carried out by the orthologous proteins in budding yeast meiosis. Finally, resection defects are additively worsened by combining MRN and Exo1 mutations, and mice that are unable to initiate resection or have greatly curtailed resection lengths experience catastrophic spermatogenic failure. Our results elucidate MRN roles in meiotic DSB end processing and establish the importance of resection for mammalian meiosis.

Indexed as

Cell Cycle ProteinsDNA-Binding ProteinsDNA Repair EnzymesMeiosisMRE11 Homologue ProteinNuclear ProteinsAcid Anhydride HydrolasesAnimalsDNA Breaks, Double-StrandedDNA RepairExodeoxyribonucleasesMaleMiceMice, KnockoutMutationSpermatogenesisAcid Anhydride HydrolasesCell Cycle ProteinsDNA-Binding ProteinsDNA Repair EnzymesExo1 protein, mouseExodeoxyribonucleasesMre11a protein, mouseMRE11 Homologue ProteinNijmegen breakage syndrome 1 protein, mouseNuclear ProteinsRad50 protein, mouse

Identifiers

PMID40240347
PMCPMC12003770

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Registered trials

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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.