Evidence map›Paper›PMID 41746809›Full record

ArticleCell reports2026

Nonsense-mediated mRNA decay orchestrates neuronal migration and cortical lamination while modulating Reelin and ciliary gene regulatory networks.

Lin Lin, Naoto Kubota, Yi-Li Lam, Michelle Mingxue Song, Min Zhang, Sika Zheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2026. 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

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

2 citing papers in PubMed.

  1. Article
  2. Review
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

6 authors.

Lin LinDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA 92521, USA; Center for RNA Biology and Medicine, University of California, Riverside, Riverside, CA 92521, USA.
Naoto KubotaDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA 92521, USA; Center for RNA Biology and Medicine, University of California, Riverside, Riverside, CA 92521, USA.
Yi-Li LamDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA 92521, USA; Center for RNA Biology and Medicine, University of California, Riverside, Riverside, CA 92521, USA.
Michelle Mingxue SongCalifornia University of Science and Medicine, Colton, CA 92324, USA.
Min ZhangDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA 92521, USA; Center for RNA Biology and Medicine, University of California, Riverside, Riverside, CA 92521, USA.
Sika ZhengDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA 92521, USA; Center for RNA Biology and Medicine, University of California, Riverside, Riverside, CA 92521, USA. Electronic address: sikaz@ucr.edu.

Funding

The Role of NMD in Cortical Neural Progenitor CellsR01NS125276 · NINDS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI Sika Zheng · 2022 to 2026
$2.6M
Genetic control mechanisms of long-term neuronal survivalR01NS139485 · NINDS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI Sika Zheng · 2024 to 2026
$1.9M
NINDS NIH HHS R01 NS125276NINDS NIH HHS R01 NS139485
6 · The paper itself

Abstract

Nonsense-mediated mRNA decay (NMD) is associated with neurodevelopmental disorders, yet its role in cortical organization is unknown. We demonstrate that NMD mediated by UPF2 is indispensable for cortical organization. Conditional deletion of Upf2 in radial glial cells delays neuronal migration and disrupts cortical lamination. Trp53 knockout rescues microcephaly from Upf2 deficiency but cannot rescue lamination defects, showing that UPF2's role in neuronal migration is uncoupled from its regulation of cell cycle and independent of p53. UPF2 deficiency downregulates key neuronal migration genes in the Reelin signaling pathway and microtubule assembly (e.g., Dab1, Lrp8, Tubb2b, and Tuba1a), partly through upregulation of the transcriptional repressor Ino80. Additionally, NMD inhibition induces widespread upregulation of ciliary genes. Ectopic expression of Foxj1, a master regulator of ciliary genes and an NMD target, impedes neuronal migration, phenocopying Upf2 loss. Therefore, NMD is a central post-transcriptional mechanism coordinating migration and ciliary gene networks crucial for cortical structure development.

Indexed as

Cell Adhesion Molecules, NeuronalCell MovementCerebral CortexCiliaExtracellular Matrix ProteinsGene Regulatory NetworksNerve Tissue ProteinsNeuronsNonsense Mediated mRNA DecaySerine EndopeptidasesAnimalsForkhead Transcription FactorsHumansMiceReelin ProteinSignal TransductionCell Adhesion Molecules, NeuronalExtracellular Matrix ProteinsForkhead Transcription FactorsNerve Tissue ProteinsReelin ProteinReln protein, mouseSerine Endopeptidasesciliary pathwaycortical laminationCP: molecular biologyCP: neuroscienceFoxj1Ino80microtubuleneuronal migrationNMDReelinUPF2

Identifiers

PMID41746809
PMCPMC13042203

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Registered trials

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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.