Evidence map›Paper›PMID 28057929›Full record

ArticleScientific reports2017

A novel role for the DNA repair gene Rad51 in Netrin-1 signalling.

K A Glendining, D Markie, R J M Gardner, E A Franz, S P Robertson, C L Jasoni

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. EFNB3 Frameshift Variant in Weimaraner Dogs with a Condition Resembling a Congenital Mirror Movement Disorder.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Maternal Obesity Modulates Expression ofLife (Basel, Switzerland) · 2020
    Article
  11. Article
  12. Revisiting Netrin-1: One Who Guides (Axons).Frontiers in cellular neuroscience · 2018
    Review
  13. Mutations in the netrin-1 gene cause congenital mirror movements.The Journal of clinical investigation · 2017
    Article
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

6 authors at 1 institution in 1 country.

K A GlendiningBrain Health Research Centre, Department of Anatomy, University of Otago, Dunedin, New Zealand.
D MarkieDepartment of Pathology, University of Otago, Dunedin, New Zealand.
R J M GardnerClinical Genetics Group, Department of Women's and Children's Health, University of Otago, Dunedin, New Zealand.
E A FranzDepartment of Psychology and fMRIOtago, University of Otago, Dunedin, New Zealand.
S P RobertsonClinical Genetics Group, Department of Women's and Children's Health, University of Otago, Dunedin, New Zealand.
C L JasoniBrain Health Research Centre, Department of Anatomy, University of Otago, Dunedin, New Zealand.
University of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in RAD51 have recently been linked to human Congenital Mirror Movements (CMM), a developmental disorder of the motor system. The only gene previously linked to CMM encodes the Netrin-1 receptor DCC, which is important for formation of corticospinal and callosal axon tracts. Thus, we hypothesised that Rad51 has a novel role in Netrin-1-mediated axon development. In mouse primary motor cortex neurons, Rad51 protein was redistributed distally down the axon in response to Netrin-1, further suggesting a functional link between the two. We next manipulated Rad51 expression, and assessed Netrin-1 responsiveness. Rad51 siRNA knockdown exaggerated Netrin-1-mediated neurite branching and filopodia formation. RAD51 overexpression inhibited these responses, whereas overexpression of the CMM-linked R250Q mutation, a predicted loss-of-function, had no effect. Thus, Rad51 appears to negatively regulate Netrin-1 signalling. Finally, we examined whether Rad51 might operate by modulating the expression of the Unc5 family, known negative regulators of Netrin-1-responsiveness. Unc5b and Unc5c transcripts were downregulated in response to Rad51 knockdown, and upregulated with RAD51 overexpression, but not R250Q. Thus, Rad51 negatively regulates Netrin-1 signalling, at least in part, by modulating the expression of Unc5s. Imbalance of positive and negative influences is likely to lead to aberrant motor system development resulting in CMMs.

Indexed as

AnimalsAxonsCells, CulturedMiceMice, Inbred C57BLMotor CortexMutationNetrin-1Netrin ReceptorsNeuronal OutgrowthRad51 RecombinaseSignal TransductionNetrin-1Netrin ReceptorsNtn1 protein, mouseRad51 protein, mouseRad51 Recombinase

Identifiers

PMID28057929
PMCPMC5216413
OpenAlexW2569982054

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.