Evidence map›Paper›PMID 18006691›Full record

ArticleGenes & development2007

Neuronal signaling modulates protein homeostasis in Caenorhabditis elegans post-synaptic muscle cells.

Susana M Garcia, M Olivia Casanueva, M Catarina Silva, Margarida D Amaral, Richard I Morimoto

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 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing 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

60 citing papers in PubMed, 105 citations in OpenAlex.

  1. Caenorhabditis elegans small heat-shock protein HSP-12.6 has a highly specialized protective function towards muscle thick filaments in vivo.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Article
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  3. UNC-49 is a redox-sensitive GABAScience advances · 2023
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  11. Life (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cell-Nonautonomous Regulation of Proteostasis in Aging and Disease.Cold Spring Harbor perspectives in biology · 2020
    Review
  17. Article
  18. Article
  19. Cellular clearance of circulating transthyretin decreases cell-nonautonomous proteotoxicity inProceedings of the National Academy of Sciences of the United States of America · 2018
    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 2 countries.

Susana M GarciaDepartment of Biochemistry, Molecular Biology and Cell Biology, Rice Institute for Biomedical Research, Northwestern University, Evanston, Illinois 60208, USA.
M Olivia Casanueva
M Catarina Silva
Margarida D Amaral
Richard I Morimoto
Northwestern University · USRice Institute · USUniversity of Lisbon · PT

Funding

C. Elegans Model for Neurodegenerative Diseases of AgingR01AG026647 · NIA · NORTHWESTERN UNIVERSITY · PI MORIMOTO, RICHARD I · 2005 to 2009
$2.0M
NIA NIH HHS R01 AG026647
6 · The paper itself

Abstract

Protein homeostasis maintains proper intracellular balance by promoting protein folding and clearance mechanisms while minimizing the stress caused by the accumulation of misfolded and damaged proteins. Chronic expression of aggregation-prone proteins is deleterious to the cell and has been linked to a wide range of conformational disorders. The molecular response to misfolded proteins is highly conserved and generally studied as a cell-autonomous process. Here, we provide evidence that neuronal signaling is an important modulator of protein homeostasis in post-synaptic muscle cells. In a forward genetic screen in Caenorhabditis elegans for enhancers of polyglutamine aggregation in muscle cells, we identified unc-30, a neuron-specific transcription factor that regulates the synthesis of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). We used additional sensors of protein conformational states to show that defective GABA signaling or increased acetylcholine (ACh) signaling causes a general imbalance in protein homeostasis in post-synaptic muscle cells. Moreover, exposure to GABA antagonists or ACh agonists has a similar effect, which reveals that toxins that act at the neuromuscular junction are potent modifiers of protein conformational disorders. These results demonstrate the importance of intercellular communication in intracellular homeostasis.

Indexed as

HomeostasisSignal TransductionSynapsesAcetylcholineAllelesAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsEthyl MethanesulfonateFluorescein-5-isothiocyanateFluorescent Antibody Technique, IndirectFluorescent DyesGABA Antagonistsgamma-Aminobutyric AcidHomeodomain ProteinsAcetylcholineCaenorhabditis elegans ProteinsEthyl MethanesulfonateFluorescein-5-isothiocyanateFluorescent DyesGABA Antagonistsgamma-Aminobutyric AcidHomeodomain ProteinsMuscle ProteinsMutagensNuclear ProteinsProteinsunc-30 protein, C elegans

Identifiers

PMID18006691
PMCPMC2049200
OpenAlexW2153459905

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.