Evidence map›Paper›PMID 30940321›Full record

ArticleBMB reports2019

Ku complex suppresses recombination in the absence of MRX activity during budding yeast meiosis.

Hyeseon Yun, Keunpil Kim

Abstract read
In one paragraph

Article in BMB reports, 2019. 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

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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

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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
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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

2 authors.

Hyeseon YunDepartment of Life Science, Chung-Ang University, Seoul 06974, Korea.
Keunpil KimDepartment of Life Science, Chung-Ang University, Seoul 06974, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During meiosis, programmed double-strand breaks (DSBs) are repaired via recombination pathways that are required for faithful chromosomal segregation and genetic diversity. In meiotic progression, the non-homologous end joining (NHEJ) pathway is suppressed and instead meiotic recombination initiated by nucleolytic resection of DSB ends is the major pathway employed. This requires diverse recombinase proteins and regulatory factors involved in the formation of crossovers (COs) and non-crossovers (NCOs). In mitosis, spontaneous DSBs occurring at the G1 phase are predominantly repaired via NHEJ, mediating the joining of DNA ends. The Ku complex binds to these DSB ends, inhibiting additional DSB resection and mediating end joining with Dnl4, Lif1, and Nej1, which join the Ku complex and DSB ends. Here, we report the role of the Ku complex in DSB repair using a physical analysis of recombination in Saccharomyces cerevisiae during meiosis. We found that the Ku complex is not essential for meiotic progression, DSB formation, joint molecule formation, or CO/NCO formation during normal meiosis. Surprisingly, in the absence of the Ku complex and functional Mre11-Rad50-Xrs2 (MRX) complex, a large portion of meiotic DSBs was repaired via the recombination pathway to form COs and NCOs. Our data suggested that Ku complex prevents meiotic recombination in the elimination of MRX activity. [BMB Reports 2019; 52(10): 607-612].

Indexed as

Recombination, GeneticDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA End-Joining RepairEndodeoxyribonucleasesExodeoxyribonucleasesMeiosisSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpores, FungalDNA-Binding ProteinsEndodeoxyribonucleasesExodeoxyribonucleaseshigh affinity DNA-binding factor, S cerevisiaeMRE11 protein, S cerevisiaeRAD50 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsXRS2 protein, S cerevisiae

Identifiers

PMID30940321
PMCPMC6827578

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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.