MRE11 is essential for the long-term viability of undifferentiated spermatogonia.
Journal
Cell proliferation
ISSN: 1365-2184
Titre abrégé: Cell Prolif
Pays: England
ID NLM: 9105195
Informations de publication
Date de publication:
18 Jun 2024
18 Jun 2024
Historique:
revised:
16
05
2024
received:
24
11
2023
accepted:
21
05
2024
medline:
19
6
2024
pubmed:
19
6
2024
entrez:
19
6
2024
Statut:
aheadofprint
Résumé
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.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13685Subventions
Organisme : Natural Science Foundation of Zhejiang Province
ID : LQ21C120001
Organisme : Natural Science Foundation of Zhejiang Province
ID : LZ21H040001
Organisme : National Natural Science Foundation of China
ID : 32070829
Organisme : National Natural Science Foundation of China
ID : 32100676
Organisme : National Natural Science Foundation of China
ID : 32370900
Informations de copyright
© 2024 The Author(s). Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.
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