Evidence map›Paper›PMID 34253720›Full record

ArticleNature communications2021

Distinct pathways of homologous recombination controlled by the SWS1-SWSAP1-SPIDR complex.

Rohit Prakash, Thomas Sandoval, Florian Morati, Jennifer A Zagelbaum, Pei-Xin Lim, Travis White, Brett Taylor, Raymond Wang, Emilie C B Desclos, Meghan R Sullivan and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
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

29 citing papers in PubMed, 49 citations in OpenAlex.

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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

17 authors at 5 institutions in 3 countries.

Rohit PrakashDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. rohitpraka@gmail.com.ORCID 0000-0001-5981-8980
Thomas SandovalDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Florian MoratiCancer Research Center of Marseille, CNRS, Inserm, Institut Paoli-Calmettes, Aix-Marseille Université, Marseille, France.ORCID 0000-0001-7512-9501
Jennifer A ZagelbaumDepartment of Genetics and Development and Institute for Cancer Genetics, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Pei-Xin LimDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0000-0001-5742-3539
Travis WhiteDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Brett TaylorDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0000-0003-3962-6134
Raymond WangDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Emilie C B DesclosDepartment of Medical Biology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Meghan R SullivanDepartment of Microbiology and Molecular Genetics, UPMC Hillman Cancer Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Hayley L ReinDepartment of Microbiology and Molecular Genetics, UPMC Hillman Cancer Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Kara A BernsteinDepartment of Microbiology and Molecular Genetics, UPMC Hillman Cancer Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.ORCID 0000-0003-2247-6459
Przemek M KrawczykDepartment of Medical Biology, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Jean GautierDepartment of Genetics and Development and Institute for Cancer Genetics, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Mauro ModestiCancer Research Center of Marseille, CNRS, Inserm, Institut Paoli-Calmettes, Aix-Marseille Université, Marseille, France.ORCID 0000-0002-4964-331X
Fabio VanoliDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0000-0002-1260-8078
Maria JasinDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. m-jasin@ski.mskcc.org.ORCID 0000-0002-7976-2379
Memorial Sloan Kettering Cancer Center · USUPMC Hillman Cancer Center · USAmsterdam University Medical Centers · NLCancer Genetics (United States) · USCentre National de la Recherche Scientifique · FR

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Homology-directed repair: BRCA2 and RAD51 paralogsR35CA253174 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Maria Jasin · 2020 to 2026
$6.7M
DNA Repair and Genomic Instability in Cancer Development and TherapyR35CA197606 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GAUTIER, JEAN · 2015 to 2021
$5.7M
Replication fork dynamics and repair by Rad51 paralogues after DNA alkylationR01ES030335 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Kara A Bernstein · 2019 to 2026
$2.9M
HOMOLOGY-DIRECTED DNA REPAIR PROTEINS BRCA2 AND RAD51 PARALOGS IN TUMOR-RELEVANT TISSUESR01CA185660 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA · 2014 to 2020
$2.7M
Homologous recombination mechanisms in mammalian cellsR35GM118175 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA · 2016 to 2020
$2.6M
Deciphering the epistatic relationships of RAD51 Paralogs in mammary epitheliumF32GM110978 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI PRAKASH, ROHIT · 2014 to 2015
$117k
The interplay between RAD51C sub-complexes during replication fork repairF31ES027321 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SULLIVAN, MEGHAN · 2017 to 2018
$71k
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA185660NCI NIH HHS R35 CA197606NCI NIH HHS R35 CA253174NIEHS NIH HHS F31 ES027321NIEHS NIH HHS R01 ES030335NIGMS NIH HHS F32 GM110978NIGMS NIH HHS R35 GM118175
6 · The paper itself

Abstract

Homology-directed repair (HDR), a critical DNA repair pathway in mammalian cells, is complex, leading to multiple outcomes with different impacts on genomic integrity. However, the factors that control these different outcomes are often not well understood. Here we show that SWS1-SWSAP1-SPIDR controls distinct types of HDR. Despite their requirement for stable assembly of RAD51 recombinase at DNA damage sites, these proteins are not essential for intra-chromosomal HDR, providing insight into why patients and mice with mutations are viable. However, SWS1-SWSAP1-SPIDR is critical for inter-homolog HDR, the first mitotic factor identified specifically for this function. Furthermore, SWS1-SWSAP1-SPIDR drives the high level of sister-chromatid exchange, promotes long-range loss of heterozygosity often involved with cancer initiation, and impels the poor growth of BLM helicase-deficient cells. The relevance of these genetic interactions is evident as SWSAP1 loss prolongs Blm-mutant embryo survival, suggesting a possible druggable target for the treatment of Bloom syndrome.

Indexed as

AnimalsBloom SyndromeCell ProliferationDNA-Binding ProteinsHEK293 CellsHomologous RecombinationHumansMeiosisMiceMitosisMouse Embryonic Stem CellsMultiprotein ComplexesMutationPhenotypeRad51 RecombinaseSister Chromatid ExchangeDNA-Binding ProteinsMultiprotein ComplexesRad51 RecombinaseSpidr protein, mouseSwsap1 protein, mouseZswim7 protein, mouse

Identifiers

PMID34253720
PMCPMC8275761
OpenAlexW3182042813

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.