Evidence map›Paper›PMID 38894566›Full record

ArticleCell proliferation2024

MRE11 is essential for the long-term viability of undifferentiated spermatogonia.

Zhenghui Tang, Zhongyang Liang, Bin Zhang, Xiaohui Xu, Peng Li, Lejun Li, Lin-Yu Lu, Yidan Liu

Abstract read
In one paragraph

Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. 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

8 authors.

Zhenghui TangKey Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Zhongyang LiangKey Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Bin ZhangKey Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID https://orcid.org/0009-0003-6240-3446
Xiaohui XuZhejiang Provincial Key Laboratory of Precision Diagnosis and Therapy for Major Gynecological Diseases, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Peng LiKey Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID https://orcid.org/0000-0002-0667-0238
Lejun LiKey Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lin-Yu LuKey Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID https://orcid.org/0000-0002-7665-6650
Yidan LiuKey Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID https://orcid.org/0000-0002-6148-266X

Funding

National Natural Science Foundation of China 32070829National Natural Science Foundation of China 32100676National Natural Science Foundation of China 32370900Natural Science Foundation of Zhejiang Province LQ21C120001Natural Science Foundation of Zhejiang Province LZ21H040001
6 · The paper itself

Abstract

In the meiotic prophase, programmed SPO11-linked DNA double-strand breaks (DSBs) are repaired by homologous recombination (HR). The MRE11-RAD50-NBS1 (MRN) complex is essential for initiating DNA end resection, the first step of HR. However, residual DNA end resection still occurs in Nbs1 knockout (KO) spermatocytes for unknown reasons. Here, we show that DNA end resection is completely abolished in Mre11 KO spermatocytes. In addition, Mre11 KO, but not Nbs1 KO, undifferentiated spermatogonia are rapidly exhausted due to DSB accumulation, proliferation defects, and elevated apoptosis. Cellular studies reveal that a small amount of MRE11 retained in the nucleus of Nbs1 KO cells likely underlies the differences between Mre11 and Nbs1 KO cells. Taken together, our study not only demonstrates an irreplaceable role of the MRE11 in DNA end resection at SPO11-linked DSBs but also unveils a unique function of MRE11 in maintaining the long-term viability of undifferentiated spermatogonia.

Indexed as

Cell SurvivalDNA-Binding ProteinsDNA Breaks, Double-StrandedMRE11 Homologue ProteinSpermatogoniaAnimalsApoptosisCell Cycle ProteinsCell DifferentiationCell ProliferationEndodeoxyribonucleasesMaleMeiotic Recombination Protein SPO11MiceMice, KnockoutNuclear ProteinsCell Cycle ProteinsDNA-Binding ProteinsEndodeoxyribonucleasesMeiotic Recombination Protein SPO11Mre11a protein, mouseMRE11 Homologue ProteinNijmegen breakage syndrome 1 protein, mouseNuclear Proteins

Identifiers

PMID38894566
PMCPMC11503245

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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.