Evidence map›Paper›PMID 39349721›Full record

ArticleScientific reports2024

The IgLON family of cell adhesion molecules expressed in developing neural circuits ensure the proper functioning of the sensory system in mice.

Katyayani Singh, Mohan Jayaram, Arpana Hanumantharaju, Tambet Tõnissoo, Toomas Jagomäe, Kaie Mikheim, Srirathi Muthuraman, Scott F Gilbert, Mario Plaas, Michael K E Schäfer and 4 more

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In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

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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

14 authors.

Katyayani SinghDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia. katyayani.micro@gmail.com.
Mohan JayaramDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.
Arpana HanumantharajuDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.
Tambet TõnissooInstitute of Molecular and Cell Biology, University of Tartu, Vanemuise 46-221, Ria 23-204, 51010, Tartu, Estonia.
Toomas JagomäeDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.
Kaie MikheimDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.
Srirathi MuthuramanDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.
Scott F GilbertDepartment of Biology, Swarthmore College, Swarthmore, PA, USA.
Mario PlaasLaboratory Animal Centre, Institute of Biomedicine and Translational Medicine, University of Tartu, 14B Ravila Street, 50411, Tartu, Estonia.
Michael K E SchäferDepartment of Anesthesiology, University Medical Center of the Johannes Gutenberg-University, 55131, Mainz, Germany.
Jürgen InnosDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.
Kersti LilleväliDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.
Mari-Anne PhilipsDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.
Eero VasarDepartment of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, 19 Ravila Street, 50411, Tartu, Estonia.

Funding

Estonian Research Foundation PRG 685European Regional Development Fund Project No. 2014-2020.4.01.15-0012
6 · The paper itself

Abstract

Deletions and malfunctions of the IgLON family of cell adhesion molecules are associated with anatomical, behavioral, and metabolic manifestations of neuropsychiatric disorders. We have previously shown that IgLON genes are expressed in sensory nuclei/pathways and that IgLON proteins modulate sensory processing. Here, we examined the expression of IgLON alternative promoter-specific isoforms during embryonic development and studied the sensory consequences of the anatomical changes when one of the IgLON genes, Negr1, is knocked out. At the embryonal age of E12.5 and E13.5, various IgLONs were distributed differentially and dynamically in the developing sensory areas within the central and peripheral nervous system, as well as in limbs and mammary glands. Sensory tests showed that Negr1 deficiency causes differences in vestibular function and temperature sensitivity in the knockout mice. Sex-specific differences were noted across olfaction, vestibular functioning, temperature regulation, and mechanical sensitivity. Our findings highlight the involvement of IgLON molecules during sensory circuit formation and suggest Negr1's critical role in somatosensory processing.

Indexed as

Mice, KnockoutAnimalsCell Adhesion MoleculesCell Adhesion Molecules, NeuronalFemaleGene Expression Regulation, DevelopmentalMaleMiceCell Adhesion MoleculesCell Adhesion Molecules, NeuronalDRGIgLONLSAMPNEGR1PNSSensory processing

Identifiers

PMID39349721
PMCPMC11442611

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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.