Evidence map›Paper›PMID 30814509›Full record

ArticleNature communications2019

Persistent DNA-break potential near telomeres increases initiation of meiotic recombination on short chromosomes.

Vijayalakshmi V Subramanian, Xuan Zhu, Tovah E Markowitz, Luis A Vale-Silva, Pedro A San-Segundo, Nancy M Hollingsworth, Scott Keeney, Andreas Hochwagen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 70 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

8 authors at 7 institutions in 3 countries.

Vijayalakshmi V SubramanianDepartment of Biology, New York University, New York, NY, 10003, USA.ORCID http://orcid.org/0000-0003-4037-3832
Xuan ZhuMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.ORCID http://orcid.org/0000-0002-8422-2828
Tovah E MarkowitzDepartment of Biology, New York University, New York, NY, 10003, USA.
Luis A Vale-SilvaDepartment of Biology, New York University, New York, NY, 10003, USA.ORCID http://orcid.org/0000-0002-9658-5335
Pedro A San-SegundoInstituto de Biología Funcional y Genómica, Consejo Superior de Investigaciones Científicas, University of Salamanca, 37007, Salamanca, Spain.ORCID http://orcid.org/0000-0002-5616-574X
Nancy M HollingsworthDepartment of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, NY, 11794, USA.ORCID http://orcid.org/0000-0003-3300-6444
Scott KeeneyMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.ORCID http://orcid.org/0000-0002-1283-6417
Andreas HochwagenDepartment of Biology, New York University, New York, NY, 10003, USA. andi@nyu.edu.ORCID http://orcid.org/0000-0002-6184-443X
New York University · USAmazon (United States) · USConsejo Superior de Investigaciones Científicas · ESFrederick National Laboratory for Cancer Research · USHeidelberg University · DEMemorial Sloan Kettering Cancer Center · USStony Brook University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
ANALYSIS OF MEIOTIC CHROMOSOME SYNAPSIS IN YEASTR01GM050717 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI HOLLINGSWORTH, NANCY M. · 1995 to 2020
$8.0M
Mechanism and regulation of meiotic recombinationR35GM118092 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI Scott Keeney · 2016 to 2026
$7.0M
Mechanisms of Chromosome Scale Signal PropagationR01GM111715 · NIGMS · NEW YORK UNIVERSITY · PI HOCHWAGEN, ANDREAS · 2015 to 2022
$2.6M
NCI NIH HHS P30 CA008748NIGMS NIH HHS R01 GM050717NIGMS NIH HHS R01 GM111715NIGMS NIH HHS R35 GM118092
6 · The paper itself

Abstract

Faithful meiotic chromosome inheritance and fertility rely on the stimulation of meiotic crossover recombination by potentially genotoxic DNA double-strand breaks (DSBs). To avoid excessive damage, feedback mechanisms down-regulate DSBs, likely in response to initiation of crossover repair. In Saccharomyces cerevisiae, this regulation requires the removal of the conserved DSB-promoting protein Hop1/HORMAD during chromosome synapsis. Here, we identify privileged end-adjacent regions (EARs) spanning roughly 100 kb near all telomeres that escape DSB down-regulation. These regions retain Hop1 and continue to break in pachynema despite normal synaptonemal complex deposition. Differential retention of Hop1 requires the disassemblase Pch2/TRIP13, which preferentially removes Hop1 from telomere-distant sequences, and is modulated by the histone deacetylase Sir2 and the nucleoporin Nup2. Importantly, the uniform size of EARs among chromosomes contributes to disproportionately high DSB and repair signals on short chromosomes in pachynema, suggesting that EARs partially underlie the curiously high recombination rate of short chromosomes.

Indexed as

DNA Breaks, Double-StrandedChromosome PairingChromosomes, FungalDNA-Binding ProteinsMeiosisNuclear Pore Complex ProteinsNuclear ProteinsRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSirtuin 2TelomereDNA-Binding ProteinsHOP1 protein, S cerevisiaeNuclear Pore Complex ProteinsNuclear ProteinsNUP2 protein, S cerevisiaePch2 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR2 protein, S cerevisiaeSirtuin 2Zip1 protein, S cerevisiae

Identifiers

PMID30814509
PMCPMC6393486
OpenAlexW2952828531

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.