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Role of Ca2+ signaling for Oscillation of Circadian Transcriptional Circuits

https://repo.qst.go.jp/records/2002201
https://repo.qst.go.jp/records/2002201
b4d8aa76-5eec-4f30-86c4-8e855f647570
アイテムタイプ 会議発表用資料 / Presentation(1)
公開日 2025-06-17
タイトル
タイトル Role of Ca2+ signaling for Oscillation of Circadian Transcriptional Circuits
言語 en
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言語 eng
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資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference presentation
著者 Kon Naohiro

× Kon Naohiro

Kon Naohiro

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内容記述 Our group is focusing on roles of Ca2+ signaling in circadian clock system. In mammals, circadian Ca2+ signaling is transduced by CaMKII that phosphorylates CLOCK to promote E-box-dependent gene expression (Kon et al., Genes and Development, 2014). Recently, we found that Na+/Ca2+ exchanger (NCX) mediates cold Ca2+ signaling for temperature compensation, and the role of NCX is conserved among mammals, insects, plants and cyanobacteria (Kon et al., Science Advances, 2021). The study suggests that Ca2+ signaling was involved in ancestral clock system. In order to investigate a hierarchical structure in the clock system, we developed mammalian cellular and fruit fly models that lost transcriptional rhythms without disrupting genes encoding the clock-related transcriptional factors. In the mammalian cells, expression of known clock genes was not sufficient to generate autonomous transcriptional rhythms of Per2 and Bmal1. Importantly, their anti-phasic expression rhythms were sustained by once-daily activation of Ca2+ signaling. The forced oscillation of transcriptional circuits was also observed in Drosophila mutant of Ca2+ signaling. Importantly, we found that circadian Ca2+ rhythms were present in mammalian cells lacking Bmal1. These results lead a novel clock model that the circadian transcriptional circuits are sustained by Ca2+ oscillation.
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内容記述 EBRS2025
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日付 2025-08-24
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