Evidence map›Paper›PMID 16267219›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Molecular control of spinal accessory motor neuron/axon development in the mouse spinal cord.

Allison K Dillon, Shinobu C Fujita, Michael P Matise, Andrew A Jarjour, Timothy E Kennedy, Heike Kollmus, Hans-Henning Arnold, Joshua A Weiner, Joshua R Sanes, Zaven Kaprielian

Abstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Transcriptional Control of Axon Guidance at Midline Structures.Frontiers in cell and developmental biology · 2022
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Phenotypic analysis of mice completely lacking netrin 1.Development (Cambridge, England) · 2015
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Transcriptional regulation of guidance at the midline and in motor circuits.Cellular and molecular life sciences : CMLS · 2014
    Review
  19. Review
  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

10 authors.

Allison K DillonDepartment of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Shinobu C Fujita
Michael P Matise
Andrew A Jarjour
Timothy E Kennedy
Heike Kollmus
Hans-Henning Arnold
Joshua A Weiner
Joshua R Sanes
Zaven Kaprielian

Funding

Spinal Accessory Motor Neuron Development in MammalsF31NS043852 · NINDS · YESHIVA UNIVERSITY · PI DILLON, ALLISON K · 2003 to 2005
$150k
NINDS NIH HHS F31 NS043852NINDS NIH HHS F31 NS43852-03
6 · The paper itself

Abstract

Within the developing vertebrate spinal cord, motor neuron subtypes are distinguished by the settling positions of their cell bodies, patterns of gene expression, and the paths their axons follow to exit the CNS. The inclusive set of cues required to guide a given motor axon subtype from cell body to target has yet to be identified, in any species. This is attributable, in part, to the unavailability of markers that demarcate the complete trajectory followed by a specific class of spinal motor axons. Most spinal motor neurons extend axons out of the CNS through ventral exit points. In contrast, spinal accessory motor neurons (SACMNs) project dorsally directed axons through lateral exit points (LEPs), and these axons assemble into the spinal accessory nerve (SAN). Here we show that an antibody against BEN/ALCAM/SC1/DM-GRASP/MuSC selectively labels mouse SACMNs and can be used to trace the pathfinding of SACMN axons. We use this marker, together with a battery of transcription factor-deficient or guidance cue/receptor-deficient mice to identify molecules required for distinct stages of SACMN development. Specifically, we find that Gli2 is required for the initial extension of axons from SACMN cell bodies, and that netrin-1 and its receptor Dcc are required for the proper dorsal migration of these cells and the dorsally directed extension of SACMN axons toward the LEPs. Furthermore, in the absence of the transcription factor Nkx2.9, SACMN axons fail to exit the CNS. Together, these findings suggest molecular mechanisms that are likely to regulate key steps in SACMN development.

Indexed as

Accessory NerveAnimalsAxonsCell DifferentiationFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMotor NeuronsMuscle ProteinsNuclear ProteinsPregnancySpinal CordTrans-ActivatorsGtf2ird1 protein, mouseMuscle ProteinsNuclear ProteinsTrans-Activators

Identifiers

PMID16267219
PMCPMC6725793

What OpenQuestion holds

Textmetadata
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.