Evidence map›Paper›PMID 19063725›Full record

ArticleNeural development2008

Semaphorin-6A controls guidance of corticospinal tract axons at multiple choice points.

Annette E Rünker, Graham E Little, Fumikazu Suto, Hajime Fujisawa, Kevin J Mitchell

Open access · goldAbstract read
In one paragraph

Article in Neural development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
1.8field-weighted citation impact, top 18% 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

59 citing papers in PubMed, 102 citations in OpenAlex.

  1. Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026
    Review
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  10. Review
  11. Myelination defects in the medial prefrontal cortex of Fkbp5 knockout mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. Semaphorin-Mediated Corticospinal Axon Elimination Depends on the Activity-Induced Bax/Bak-Caspase Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  13. Article
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  15. Skilled Movements in Mice Require Inhibition of Corticospinal Axon Collateral Formation in the Spinal Cord by Semaphorin Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
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  18. The Spinal Transcriptome after Cortical Stroke: In Search of Molecular Factors Regulating Spontaneous Recovery in the Spinal Cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  19. Plexina2 and CRMP2 Signaling Complex Is Activated by Nogo-A-Liganded Ngr1 to Restrict Corticospinal Axon Sprouting after Trauma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  20. 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

5 authors at 3 institutions in 3 countries.

Annette E RünkerSmurfit Institute of Genetics, Trinity College Dublin, Dublin, Ireland. annette.ruenker@crt-dresden.de
Graham E Little
Fumikazu Suto
Hajime Fujisawa
Kevin J Mitchell
Trinity College Dublin · IENagoya University · JPNational Institute of Genetics · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe trajectory of corticospinal tract (CST) axons from cortex to spinal cord involves a succession of choice points, each of which is controlled by multiple guidance molecules. To assess the involvement of transmembrane semaphorins and their plexin receptors in the guidance of CST axons, we have examined this tract in mutants of Semaphorin-6A (Sema6A), Plexin-A2 (PlxnA2) and Plexin-A4 (PlxnA4).

resultsWe describe defects in CST guidance in Sema6A mutants at choice points at the mid-hindbrain boundary (MHB) and in navigation through the pons that dramatically affect how many axons arrive to the hindbrain and spinal cord and result in hypoplasia of the CST. We also observe defects in guidance within the hindbrain where a proportion of axons aberrantly adopt a ventrolateral position and fail to decussate. This function in the hindbrain seems to be mediated by the known Sema6A receptor PlxnA4, which is expressed by CST axons. Guidance at the MHB, however, appears independent of this and of the other known receptor, PlxnA2, and may depend instead on Sema6A expression on CST axons themselves at embryonic stages.

conclusionThese data identify Sema6A as a major contributor to the guidance of CST axons at multiple choice points. They highlight the active control of guidance at the MHB and also implicate the inferior olive as an important structure in the guidance of CST axons within the hindbrain. They also suggest that Sema6A, which is strongly expressed by oligodendrocytes, may affect CST regeneration in adults.

Indexed as

Signal TransductionAnimalsAxonsCerebral CortexImmunohistochemistryMiceMice, Inbred StrainsMice, TransgenicNerve Tissue ProteinsPyramidal TractsReceptors, Cell SurfaceRhombencephalonSemaphorinsSpinal CordNerve Tissue ProteinsPlxna2 protein, mousePlxna4 protein, mouseReceptors, Cell SurfaceSema6a protein, mouseSemaphorins

Identifiers

PMID19063725
PMCPMC2647909
OpenAlexW1976623789

What OpenQuestion holds

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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.