Evidence map›Paper›PMID 21085703›Full record

ArticlePloS one2010

The roles of the Saccharomyces cerevisiae RecQ helicase SGS1 in meiotic genome surveillance.

Amit Dipak Amin, Alexandre B H Chaix, Robert P Mason, Richard M Badge, Rhona H Borts

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Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

5 authors.

Amit Dipak AminDepartment of Genetics, University of Leicester, Leicester, United Kingdom.
Alexandre B H Chaix
Robert P Mason
Richard M Badge
Rhona H Borts

Funding

Cancer Research UK
6 · The paper itself

Abstract

backgroundThe Saccharomyces cerevisiae RecQ helicase Sgs1 is essential for mitotic and meiotic genome stability. The stage at which Sgs1 acts during meiosis is subject to debate. Cytological experiments showed that a deletion of SGS1 leads to an increase in synapsis initiation complexes and axial associations leading to the proposal that it has an early role in unwinding surplus strand invasion events. Physical studies of recombination intermediates implicate it in the dissolution of double Holliday junctions between sister chromatids. METHODOLOGY/PRINCIPAL

findingsIn this work, we observed an increase in meiotic recombination between diverged sequences (homeologous recombination) and an increase in unequal sister chromatid events when SGS1 is deleted. The first of these observations is most consistent with an early role of Sgs1 in unwinding inappropriate strand invasion events while the second is consistent with unwinding or dissolution of recombination intermediates in an Mlh1- and Top3-dependent manner. We also provide data that suggest that Sgs1 is involved in the rejection of 'second strand capture' when sequence divergence is present. Finally, we have identified a novel class of tetrads where non-sister spores (pairs of spores where each contains a centromere marker from a different parent) are inviable. We propose a model for this unusual pattern of viability based on the inability of sgs1 mutants to untangle intertwined chromosomes. Our data suggest that this role of Sgs1 is not dependent on its interaction with Top3. We propose that in the absence of SGS1 chromosomes may sometimes remain entangled at the end of pre-meiotic replication. This, combined with reciprocal crossing over, could lead to physical destruction of the recombined and entangled chromosomes. We hypothesise that Sgs1, acting in concert with the topoisomerase Top2, resolves these structures.

conclusionsThis work provides evidence that Sgs1 interacts with various partner proteins to maintain genome stability throughout meiosis.

Indexed as

Recombination, GeneticChromosomes, FungalDiploidyDNA Topoisomerases, Type IIGene DeletionGenome, FungalMeiosisModels, GeneticProtein BindingRecQ HelicasesSaccharomyces cerevisiae ProteinsSister Chromatid ExchangeSpores, FungalDNA Topoisomerases, Type IIRecQ HelicasesSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiaeTOP3 protein, S cerevisiae

Identifiers

PMID21085703
PMCPMC2976770

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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.