Evidence map›Paper›PMID 35115609›Full record

ArticleScientific reports2022

The transcription factor unc-130/FOXD3/4 contributes to the biphasic calcium response required to optimize avoidance behavior.

Sayaka Hori, Shohei Mitani

Abstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Sayaka HoriDepartment of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, 162-8666, Japan.
Shohei MitaniDepartment of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, 162-8666, Japan. mitani.shohei@twmu.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The central neural network optimizes avoidance behavior depending on the nociceptive stimulation intensity and is essential for survival. How the property of hub neurons that enables the selection of behaviors is genetically defined is not well understood. We show that the transcription factor unc-130, a human FOXD3/4 ortholog, is required to optimize avoidance behavior depending on stimulus strength in Caenorhabditis elegans. unc-130 is necessary for both ON responses (calcium decreases) and OFF responses (calcium increases) in AIBs, central neurons of avoidance optimization. Ablation of predicted upstream inhibitory neurons reduces the frequency of turn behavior, suggesting that optimization needs both calcium responses. At the molecular level, unc-130 upregulates the expression of at least three genes: nca-2, a homolog of the vertebrate cation leak channel NALCN; glr-1, an AMPA-type glutamate receptor; and eat-4, a hypothetical L-glutamate transmembrane transporter in the central neurons of optimization. unc-130 shows more limited regulation in optimizing behavior than an atonal homolog lin-32, and unc-130 and lin-32 appear to act in parallel molecular pathways. Our findings suggest that unc-130 is required for the establishment of some AIB identities to optimize avoidance behavior.

Indexed as

Avoidance LearningBehavior, AnimalCalcium SignalingAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsCalciumIon ChannelsNeuronsReceptors, AMPASynapsesTranscription FactorsVesicular Glutamate Transport ProteinsCaenorhabditis elegans ProteinsCalciumEat-4 protein, C elegansglr-1 protein, C elegansIon ChannelsNCA-2 protein, C elegansReceptors, AMPATranscription Factorsunc-130 protein, C elegansVesicular Glutamate Transport Proteins

Identifiers

PMID35115609
PMCPMC8814005

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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.