Evidence map›Paper›PMID 31839538›Full record

ArticleDevelopmental cell2020

GCNA Interacts with Spartan and Topoisomerase II to Regulate Genome Stability.

Gregoriy A Dokshin, Gregory M Davis, Ashley D Sawle, Matthew D Eldridge, Peter K Nicholls, Taylin E Gourley, Katherine A Romer, Luke W Molesworth, Hannah R Tatnell, Ahmet R Ozturk and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.9field-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

38 citing papers in PubMed, 58 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 4 countries.

Gregoriy A DokshinRNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Gregory M DavisSchool of Health and Life Sciences, Federation University, VIC 3841, Australia.
Ashley D SawleCancer Research UK Cambridge Institute, University of Cambridge, Cambridge CB2 0RE, UK.
Matthew D EldridgeCancer Research UK Cambridge Institute, University of Cambridge, Cambridge CB2 0RE, UK.
Peter K NichollsWhitehead Institute, 455 Main Street, Cambridge, MA 02142, USA.
Taylin E GourleySchool of Health and Life Sciences, Federation University, VIC 3841, Australia.
Katherine A RomerWhitehead Institute, 455 Main Street, Cambridge, MA 02142, USA; Computational and Systems Biology Program, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Luke W MolesworthSchool of Health and Life Sciences, Federation University, VIC 3841, Australia.
Hannah R TatnellSchool of Health and Life Sciences, Federation University, VIC 3841, Australia.
Ahmet R OzturkRNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Dirk G de RooijWhitehead Institute, 455 Main Street, Cambridge, MA 02142, USA; Reproductive Biology Group, Division of Developmental Biology, Department of Biology, Faculty of Science, Utrecht University, Utrecht 3584, the Netherlands; Center for Reproductive Medicine, Academic Medical Center, University of Amsterdam 1105, the Netherlands.
Gregory J HannonCancer Research UK Cambridge Institute, University of Cambridge, Cambridge CB2 0RE, UK; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
David C PageWhitehead Institute, 455 Main Street, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Whitehead Institute, Cambridge, MA 02142, USA.
Craig C MelloRNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA; Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: craig.mello@umassmed.edu.
Michelle A CarmellRNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA; Whitehead Institute, 455 Main Street, Cambridge, MA 02142, USA; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA. Electronic address: mcarmell@wellesley.edu.
Federation University · AUUniversity of Cambridge · GBUniversity of Massachusetts Chan Medical School · USHoward Hughes Medical Institute · USWhitehead Institute for Biomedical Research · USUtrecht University · NL

Funding

PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Understanding the architecture, regulation, and function of piRNA-producing genesP01HD078253 · NICHD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WENG, ZHIPING · 2015 to 2019
$6.5M
RNA MEDIATED GENETIC INTERFERENCE IN C ELEGANSR01GM058800 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MELLO, CRAIG C · 1999 to 2014
$4.6M
RNA Mediated Genetic Interference in C. elegansR37GM058800 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MELLO, CRAIG C · 2015 to 2024
$3.7M
CELL POLARITY SIGNALING IN C ELEGANS EMBRYOSR01HD036247 · NICHD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MELLO, CRAIG C · 1999 to 2008
$2.2M
Cancer Research UK 21143Howard Hughes Medical InstituteNICHD NIH HHS P01 HD078253NICHD NIH HHS R01 HD036247NIGMS NIH HHS R01 GM058800NIGMS NIH HHS R37 GM058800NIGMS NIH HHS T32 GM007287NIH HHS P40 OD010440
6 · The paper itself

Abstract

GCNA proteins are expressed across eukarya in pluripotent cells and have conserved functions in fertility. GCNA homologs Spartan (DVC-1) and Wss1 resolve DNA-protein crosslinks (DPCs), including Topoisomerase-DNA adducts, during DNA replication. Here, we show that GCNA mutants in mouse and C. elegans display defects in genome maintenance including DNA damage, aberrant chromosome condensation, and crossover defects in mouse spermatocytes and spontaneous genomic rearrangements in C. elegans. We show that GCNA and topoisomerase II (TOP2) physically interact in both mice and worms and colocalize on condensed chromosomes during mitosis in C. elegans embryos. Moreover, C. elegans gcna-1 mutants are hypersensitive to TOP2 poison. Together, our findings support a model in which GCNA provides genome maintenance functions in the germline and may do so, in part, by promoting the resolution of TOP2 DPCs.

Indexed as

DNA ReplicationGenomic InstabilityMitosisAnimalsCaenorhabditis elegansDNA-Binding ProteinsDNA DamageDNA RepairDNA Topoisomerases, Type IIGenomeGerm CellsMaleMiceMice, Inbred C57BLMutationNuclear ProteinsDNA-Binding ProteinsDNA Topoisomerases, Type IINuclear ProteinsSpartan protein, mouseDNA-protein crosslink (DPC) repairDVC-1GCNAgerm cellsSpartanSprTTop1Top2topoisomerase

Identifiers

PMID31839538
PMCPMC7227305
OpenAlexW2996384555

What OpenQuestion holds

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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.