Evidence map›Paper›PMID 42173885›Full record

ArticleNature communications2026

Light- and chemical-induced ciliary signaling governs dorsal/ventral regionalization of human telencephalic organoids.

Issei S Shimada, Akari Goto, Yutaka Hashimoto, Hajime Inoue, Takuto Sugawara, Tomohiro Doura, Tsubasa Fujita, Toshiaki Iwata, Riko Shimmoto, Hiroshi Takase and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

13 authors.

Issei S Shimada *Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan. ishimada@med.nagoya-cu.ac.jp.ORCID http://orcid.org/0000-0002-8808-8419
Akari GotoDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Yutaka HashimotoDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Hajime InoueDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Aichi, Japan.
Takuto SugawaraDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Aichi, Japan.
Tomohiro DouraDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Aichi, Japan.ORCID http://orcid.org/0000-0003-1826-6010
Tsubasa FujitaDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Toshiaki IwataDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Riko ShimmotoDepartment of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Hiroshi TakaseCore Laboratory, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan.
Masayuki ItohDepartment of Biochemistry and Cellular Biology, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.ORCID http://orcid.org/0000-0001-7247-2259
Shigeki KiyonakaDepartment of Biomolecular Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Aichi, Japan.ORCID http://orcid.org/0000-0002-4100-6738
Yoichi Kato *Department of Cell Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Aichi, Japan. kato.41@med.nagoya-cu.ac.jp.ORCID http://orcid.org/0000-0002-2206-7279

Funding

Japan Agency for Medical Research and Development (AMED) 24zf0127012MEXT | Japan Society for the Promotion of Science (JSPS) 20K16157MEXT | Japan Society for the Promotion of Science (JSPS) 20K21584MEXT | Japan Society for the Promotion of Science (JSPS) 21K07803MEXT | Japan Society for the Promotion of Science (JSPS) 24H00492MEXT | Japan Society for the Promotion of Science (JSPS) 24H02265MEXT | Japan Society for the Promotion of Science (JSPS) 24K02425MEXT | Japan Society for the Promotion of Science (JSPS) 24K21823MEXT | NINS | National Institute for Basic Biology (NIBB) 24NIBB460Nagoya City University 2401101
6 · The paper itself

Abstract

Neural stem/progenitor cells (NPCs) have primary cilia, which are critical organelles for Sonic hedgehog signaling. However, little is known about the components of primary cilia in NPCs and whether manipulating signaling in the cilia is sufficient to alter dorsal/ventral regional identity. Using a human telencephalic organoid model, we perform comprehensive proteomic profiling of NPC cilia and find enrichment in GTPase signaling. Deletion of the ciliary GTPase ARL13B reduces ciliary localization of GPR161, an orphan G protein-coupled receptor 161 that negatively regulates Sonic hedgehog, resulting in ventralization of NPCs. GPR161 deletion also induces ventralization. To investigate whether manipulation of ciliary signaling is sufficient to restore dorsal identity in this context, we optogenetically elevate ciliary cAMP, rescuing dorsal fate in GPR161 KO organoids. Furthermore, chemogenetic induction of GPR161 removal from cilia is sufficient to increase ventral NPCs. These data indicate that ciliary signaling functions as a critical switch regulating dorsal/ventral fate decisions.

Indexed as

CiliaOrganoidsSignal TransductionTelencephalonADP-Ribosylation FactorsCyclic AMPHedgehog ProteinsHumansNeural Stem CellsReceptors, G-Protein-CoupledADP-Ribosylation FactorsARL13B protein, humanCyclic AMPGPR161 protein, humanHedgehog ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID42173885
PMCPMC13385379

What OpenQuestion holds

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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.