Evidence map›Paper›PMID 17901218›Full record

ArticleGenes & development2007

The requirement for Phr1 in CNS axon tract formation reveals the corticostriatal boundary as a choice point for cortical axons.

A Joseph Bloom, Bradley R Miller, Joshua R Sanes, Aaron DiAntonio

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing 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

92 citing papers in PubMed, 144 citations in OpenAlex.

  1. Article
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  8. NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023
    Review
  9. Review
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  12. The Ubiquitinated Axon: Local Control of Axon Development and Function by Ubiquitin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  13. Experimental Model Systems for Understanding Human Axonal Injury Responses.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
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  17. Review
  18. Review
  19. Article
  20. Article

32 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

A Joseph BloomDepartment of Molecular Biology and Pharmacology, Washington University, Saint Louis, Missouri 63110, USA.
Bradley R Miller
Joshua R Sanes
Aaron DiAntonio
Washington University in St. Louis · USHarvard University · US

Funding

MOLECULAR PATHWAYS REGULATING SYNAPTIC GROWTHR01DA020812 · NIDA · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON · 2007 to 2016
$3.3M
NIDA NIH HHS R01 DA020812
6 · The paper itself

Abstract

Phr1 is the single well-conserved murine ortholog of the invertebrate ubiquitin ligase genes highwire (in Drosophila) and rpm-1 (in Caenorhabditis elegans). The function and mechanism of action of highwire and rpm-1 are similar--both cell-autonomously regulate synaptogenesis by down-regulating the ortholog of the mitogen-activated protein kinase kinase kinase dual leucine zipper kinase (MAPKKK DLK). Here, using a targeted conditional mutant, we demonstrate that Phr1 also plays essential roles in mammalian neural development. As in invertebrates, Phr1 functions cell-autonomously to sculpt motor nerve terminals. In addition, Phr1 plays essential roles in the formation of major CNS axon tracts including those of the internal capsule, in part via cell-nonautonomous mechanisms, and these results reveal a choice point for cortical axons at the corticostriatal boundary. Furthermore, whereas the neurite morphology phenotypes of highwire and rpm-1 are suppressed by loss of DLK in flies and worms, Phr1-dependent CNS defects persist in Phr1, DLK double mutants. Thus, in the mammalian nervous system Phr1 is required for formation of major CNS axon tracts via a mechanism that is both cell-nonautonomous and independent of DLK.

Indexed as

Agenesis of Corpus CallosumAnimalsAxonsBase SequenceCentral Nervous SystemCerebral CortexCorpus CallosumCorpus StriatumDNA PrimersDown-RegulationEvolution, MolecularFemaleMaleMAP Kinase Kinase KinasesMembrane ProteinsMiceDNA PrimersMAP Kinase Kinase KinasesMembrane ProteinsPlekhb1 protein, mouse

Identifiers

PMID17901218
PMCPMC2000324
OpenAlexW2099421316

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.