Evidence map›Paper›PMID 21041451›Full record

ArticleThe Journal of cell biology2010

The Cdc42-selective GAP rich regulates postsynaptic development and retrograde BMP transsynaptic signaling.

Minyeop Nahm, A Ashleigh Long, Sang Kyoo Paik, Sungdae Kim, Yong Chul Bae, Kendal Broadie, Seungbok Lee

Abstract read
In one paragraph

Article in The Journal of cell biology, 2010. 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. Article
  2. The NDR family of kinases: essential regulators of aging.Frontiers in molecular neuroscience · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. TGF-β Family Signaling inCold Spring Harbor perspectives in biology · 2017
    Review
  10. Article
  11. Pathogenic Huntington Alters BMP Signaling and Synaptic Growth through Local Disruptions of Endosomal Compartments.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Two protein N-acetylgalactosaminyl transferases regulate synaptic plasticity by activity-dependent regulation of integrin signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  18. Article
  19. 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

7 authors.

Minyeop NahmInterdisplinary Program in Brain Science, Seoul National University, Seoul, Republic of Korea.
A Ashleigh Long
Sang Kyoo Paik
Sungdae Kim
Yong Chul Bae
Kendal Broadie
Seungbok Lee

Funding

GENETIC ANALYSIS OF SYNAPSE FORMATION AND FUNCTIONR01GM054544 · NIGMS · VANDERBILT UNIVERSITY · PI BROADIE, KENDAL · 1997 to 2010
$2.9M
NIGMS NIH HHS R01 GM054544NIGMS NIH HHS R01 GM54544
6 · The paper itself

Abstract

Retrograde bone morphogenetic protein signaling mediated by the Glass bottom boat (Gbb) ligand modulates structural and functional synaptogenesis at the Drosophila melanogaster neuromuscular junction. However, the molecular mechanisms regulating postsynaptic Gbb release are poorly understood. In this study, we show that Drosophila Rich (dRich), a conserved Cdc42-selective guanosine triphosphatase-activating protein (GAP), inhibits the Cdc42-Wsp pathway to stimulate postsynaptic Gbb release. Loss of dRich causes synaptic undergrowth and strongly impairs neurotransmitter release. These presynaptic defects are rescued by targeted postsynaptic expression of wild-type dRich but not a GAP-deficient mutant. dRich inhibits the postsynaptic localization of the Cdc42 effector Wsp (Drosophila orthologue of mammalian Wiskott-Aldrich syndrome protein, WASp), and manifestation of synaptogenesis defects in drich mutants requires Wsp signaling. In addition, dRich regulates postsynaptic organization independently of Cdc42. Importantly, dRich increases Gbb release and elevates presynaptic phosphorylated Mad levels. We propose that dRich coordinates the Gbb-dependent modulation of synaptic growth and function with postsynaptic development.

Indexed as

AnimalsBone Morphogenetic Proteinscdc42 GTP-Binding ProteinDrosophila melanogasterDrosophila ProteinsGTPase-Activating ProteinsSignal TransductionSynapsesTransforming Growth Factor betaWiskott-Aldrich Syndrome ProteinBone Morphogenetic Proteinscdc42 GTP-Binding ProteinDrosophila Proteinsgbb protein, DrosophilaGTPase-Activating ProteinsTransforming Growth Factor betaWASp protein, DrosophilaWiskott-Aldrich Syndrome Protein

Identifiers

PMID21041451
PMCPMC3003324

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.