A pathway for error-free non-homologous end joining of resected meiotic double-strand breaks.
Nucleic Acids Res
; 49(2): 879-890, 2021 01 25.
Article
in En
| MEDLINE
| ID: mdl-33406239
ABSTRACT
Programmed DNA double-strand breaks (DSBs) made during meiosis are repaired by recombination with the homologous chromosome to generate, at selected sites, reciprocal crossovers that are critical for the proper separation of homologs in the first meiotic division. Backup repair processes can compensate when the normal meiotic recombination processes are non-functional. We describe a novel backup repair mechanism that occurs when the homologous chromosome is not available in Drosophila melanogaster meiosis. In the presence of a previously described mutation (Mcm5A7) that disrupts chromosome pairing, DSB repair is initiated by homologous recombination but is completed by non-homologous end joining (NHEJ). Remarkably, this process yields precise repair products. Our results provide support for a recombination intermediate recently proposed in mouse meiosis, in which an oligonucleotide bound to the Spo11 protein that catalyzes DSB formation remains bound after resection. We propose that this oligonucleotide functions as a primer for fill-in synthesis to allow scarless repair by NHEJ. We argue that this is a conserved repair mechanism that is likely to be invoked to overcome occasional challenges in normal meiosis.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Oligonucleotides
/
Cell Cycle Proteins
/
Drosophila Proteins
/
Drosophila melanogaster
/
DNA Breaks, Double-Stranded
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DNA End-Joining Repair
/
Meiosis
Limits:
Animals
Language:
En
Journal:
Nucleic Acids Res
Year:
2021
Document type:
Article
Affiliation country:
United States