Orai1 Ca²⁺ channel is involved in ciliogenesis and cooperates with Shh signaling during LR asymmetry and limb bud formation.
4 affiliations
- 1Department of Biomedical Engineering, College of Information-Bio Convergence Engineering, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
- 2Department of Biological Sciences, College of Information-Bio Convergence Engineering, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
- 3Department of Biological Sciences, College of Information-Bio Convergence Engineering, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea. [email protected].
- 4Department of Biomedical Engineering, College of Information-Bio Convergence Engineering, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea. [email protected].
Abstract
Cilia are present in most cells and are vital components in signal transduction and developmental control. Although Ca²⁺ signaling has been recognized as a key regulator of these ciliary functions, the potential contribution of Store-operated calcium entry (SOCE) to this regulation has not been investigated. In this study, we provide evidence that SOCE is required for ciliogenesis and cilia-dependent signaling. SOCE dysfunction results in a significant reduction in both the percentage of ciliated cells and the average length of cilia. Conversely, SOCE activation enhances the Sonic Hedgehog (Shh) pathway, a crucial cilia-dependent signaling pathway. Impaired SOCE disrupts both ciliogenesis and Shh signaling in Xenopus and mice, leading to abnormal embryonic development, including defective Left-Right (LR) asymmetry and limb bud formation. Our findings establish Orai1 as a key ciliary Ca²⁺ channel driving ciliogenesis and Shh signaling, uncovering a fundamental mechanism of developmental regulation and linking Ca²⁺ dysregulation to ciliopathies.
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BibTeX
@article{kweon2026orai1,
title = {{Orai1 Ca²⁺ channel is involved in ciliogenesis and cooperates with Shh signaling during LR asymmetry and limb bud formation.}},
author = {Yeong Cheon Kweon and Dong Gil Jang and Yoon Young Lee and Ah Reum Lee and Tae Joo Park and Chan Young Park},
journal = {Cell communication and signaling : CCS},
year = {2026},
month = aug,
doi = {10.1186/s12964-026-03065-x},
url = {https://europepmc.org/article/MED/42972548},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Orai1 Ca²⁺ channel is involved in ciliogenesis and cooperates with Shh signaling during LR asymmetry and limb bud formation.
AU - Yeong Cheon Kweon
AU - Dong Gil Jang
AU - Yoon Young Lee
AU - Ah Reum Lee
AU - Tae Joo Park
AU - Chan Young Park
PY - 2026
DA - 2026/08/06
JO - Cell communication and signaling : CCS
DO - 10.1186/s12964-026-03065-x
UR - https://europepmc.org/article/MED/42972548
AB - Cilia are present in most cells and are vital components in signal transduction and developmental control. Although Ca²⁺ signaling has been recognized as a key regulator of these ciliary functions, the potential contribution of Store-operated calcium entry (SOCE) to this regulation has not been investigated. In this study, we provide evidence that SOCE is required for ciliogenesis and cilia-dependent signaling. SOCE dysfunction results in a significant reduction in both the percentage of ciliated cells and the average length of cilia. Conversely, SOCE activation enhances the Sonic Hedgehog (Shh) pathway, a crucial cilia-dependent signaling pathway. Impaired SOCE disrupts both ciliogenesis and Shh signaling in Xenopus and mice, leading to abnormal embryonic development, including defective Left-Right (LR) asymmetry and limb bud formation. Our findings establish Orai1 as a key ciliary Ca²⁺ channel driving ciliogenesis and Shh signaling, uncovering a fundamental mechanism of developmental regulation and linking Ca²⁺ dysregulation to ciliopathies.
SN - 1478-811X
ER -