Evidence map›Paper›PMID 25024163›Full record

ArticleGenome research2014

Evolutionarily diverse determinants of meiotic DNA break and recombination landscapes across the genome.

Kyle R Fowler, Mariko Sasaki, Neta Milman, Scott Keeney, Gerald R Smith

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
–field-weighted citation impact
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

77 citing papers in PubMed, 102 citations in OpenAlex.

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17 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Kyle R FowlerDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA;
Mariko SasakiMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA; Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10065, USA;
Neta MilmanDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA;
Scott KeeneyMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA; Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10065, USA; Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA gsmith@fhcrc.org s-keeney@ski.mskcc.org.
Gerald R SmithDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA; gsmith@fhcrc.org s-keeney@ski.mskcc.org.
Fred Hutch Cancer Center · USMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
MOLECULAR ANALYSIS OF HOTSPOTS OF GENETIC RECOMBINATIONR01GM031693 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI SMITH, GERALD R · 1985 to 2015
$9.7M
MOLECULAR MECHANISMS OF GENETIC RECOMBINATIONR01GM032194 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI SMITH, GERALD R · 1985 to 2016
$6.2M
Mechanism of meiotic recombination in yeastR01GM058673 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI KEENEY, SCOTT · 1999 to 2015
$6.0M
Molecular Analysis of Hotspots of Genetic RecombinationR56GM031693 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI SMITH, GERALD R · 2007 to 2007
$586k
NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA015704NIGMS NIH HHS GM031693NIGMS NIH HHS GM032194NIGMS NIH HHS GM058673NIGMS NIH HHS R01 GM031693NIGMS NIH HHS R01 GM032194NIGMS NIH HHS R01 GM058673NIGMS NIH HHS R56 GM031693
6 · The paper itself

Abstract

Fission yeast Rec12 (Spo11 homolog) initiates meiotic recombination by forming developmentally programmed DNA double-strand breaks (DSBs). DSB distributions influence patterns of heredity and genome evolution, but the basis of the highly nonrandom choice of Rec12 cleavage sites is poorly understood, largely because available maps are of relatively low resolution and sensitivity. Here, we determined DSBs genome-wide at near-nucleotide resolution by sequencing the oligonucleotides attached to Rec12 following DNA cleavage. The single oligonucleotide size class allowed us to deeply sample all break events. We find strong evidence across the genome for differential DSB repair accounting for crossover invariance (constant cM/kb in spite of DSB hotspots). Surprisingly, about half of all crossovers occur in regions where DSBs occur at low frequency and are widely dispersed in location from cell to cell. These previously undetected, low-level DSBs thus play an outsized and crucial role in meiosis. We further find that the influence of underlying nucleotide sequence and chromosomal architecture differs in multiple ways from that in budding yeast. DSBs are not strongly restricted to nucleosome-depleted regions, as they are in budding yeast, but are nevertheless spatially influenced by chromatin structure. Our analyses demonstrate that evolutionarily fluid factors contribute to crossover initiation and regulation.

Indexed as

Crossing Over, GeneticDNA Breaks, Double-StrandedMeiosisChromatinEvolution, MolecularGenome, FungalModels, GeneticSchizosaccharomycesSchizosaccharomyces pombe ProteinsSequence Analysis, DNAChromatinSchizosaccharomyces pombe Proteins

Identifiers

PMID25024163
PMCPMC4199369
OpenAlexW2111756870

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.