Evidence map›Paper›PMID 28052247›Full record

ArticleCell reports2017

Sema-1a Reverse Signaling Promotes Midline Crossing in Response to Secreted Semaphorins.

Melissa Hernandez-Fleming, Ethan W Rohrbach, Greg J Bashaw

Abstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Semaphorin 1a-mediated dendritic wiring of theProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Article
  9. Article
  10. Identification ofMolecules and cells · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Varicose and cheerio collaborate with pebble to mediate semaphorin-1a reverse signaling inProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. 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

3 authors.

Melissa Hernandez-FlemingDepartment of Neuroscience, University of Pennsylvania Perelman School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA.
Ethan W RohrbachDepartment of Neuroscience, University of Pennsylvania Perelman School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA.
Greg J BashawDepartment of Neuroscience, University of Pennsylvania Perelman School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA. Electronic address: gbashaw@mail.med.upenn.edu.

Funding

SYSTEMS AND INTEGRATIVE BIOLOGYT32GM007517 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI GOLD, JOSHUA I · 1985 to 2017
$8.0M
Molecular mechanisms of axon guidance receptor regulation and signalingR35NS097340 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI BASHAW, GREG J. · 2017 to 2024
$5.8M
TRAINING PROGRAM IN DEVELOPMENTAL BIOLOGYT32HD007516 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI RAPER, JONATHAN A · 1998 to 2012
$5.6M
Robo receptor signaling and regulation during axon guidance in DrosophilaR01NS046333 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI BASHAW, GREG J. · 2003 to 2016
$3.9M
Transcriptional mechanisms coordinating midline and motor axon guidanceR01NS054739 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI BASHAW, GREG J. · 2008 to 2016
$2.4M
Mechanisms of Sema-1a dependent midline crossing in the Drosophila CNSF31NS086340 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HERNANDEZ, MELISSA COURTNEY · 2013 to 2015
$85k
NICHD NIH HHS T32 HD007516NIGMS NIH HHS T32 GM007517NINDS NIH HHS F31 NS086340NINDS NIH HHS R01 NS046333NINDS NIH HHS R01 NS054739NINDS NIH HHS R35 NS097340
6 · The paper itself

Abstract

Commissural axons must cross the midline to form functional midline circuits. In the invertebrate nerve cord and vertebrate spinal cord, midline crossing is mediated in part by Netrin-dependent chemoattraction. Loss of crossing, however, is incomplete in mutants for Netrin or its receptor Frazzled/DCC, suggesting the existence of additional pathways. We identified the transmembrane Semaphorin, Sema-1a, as an important regulator of midline crossing in the Drosophila CNS. We show that in response to the secreted Semaphorins Sema-2a and Sema-2b, Sema-1a functions as a receptor to promote crossing independently of Netrin. In contrast to other examples of reverse signaling where Sema1a triggers repulsion through activation of Rho in response to Plexin binding, in commissural neurons Sema-1a acts independently of Plexins to inhibit Rho to promote attraction to the midline. These findings suggest that Sema-1a reverse signaling can elicit distinct axonal responses depending on differential engagement of distinct ligands and signaling effectors.

Indexed as

Body PatterningSignal TransductionAnimalsAxonsCell Adhesion MoleculesChemotactic FactorsDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianGenetic TestingNerve Tissue ProteinsProtein DomainsSemaphorinsCell Adhesion MoleculesChemotactic FactorsDrosophila ProteinsNerve Tissue Proteinsplexinsemaphorin 1a, DrosophilaSemaphorinsaxon guidancechemoattractiondccDrosophilafrazzledgrowth conemidlinenetrinreverse signalingsemaphorin

Identifiers

PMID28052247
PMCPMC5253228

What OpenQuestion holds

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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.