{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rao VG"],"funding":["HHS | National Institutes of Health","HHS | National Institutes of Health (NIH)","HHS | NIH | National Institute of General Medical Sciences","NCRR NIH HHS","NHLBI NIH HHS","HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)","HHS | NIH | National Heart, Lung, and Blood Institute","NIH HHS","HHS | NIH | National Institute of General Medical Sciences (NIGMS)","NIGMS NIH HHS"],"pagination":["2192-2220"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12019409"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(8)"],"pubmed_abstract":["Cilia regeneration is a physiological event, and while studied extensively in unicellular organisms, it remains poorly understood in vertebrates. In this study, using Xenopus multiciliated cells (MCCs), we demonstrate that, unlike unicellular organisms, deciliation removes the transition zone (TZ) and the ciliary axoneme. While MCCs immediately begin regenerating the axoneme, surprisingly, the TZ assembly is delayed. However, ciliary tip proteins, Sentan and Clamp, localize to regenerating cilia without delay. Using cycloheximide (CHX) to block protein synthesis, we show that the TZ protein B9d1 is not present in the cilia precursor pool and requires new transcription/translation, providing insights into the delayed repair of TZ. Moreover, MCCs in CHX treatment assemble fewer but near wild-type length cilia by gradually concentrating ciliogenesis proteins like IFTs at a few basal bodies. Using mathematical modeling, we show that cilia length, compared to cilia number, has a larger influence on the force generated by MCCs. Our results question the requirement of TZ in motile cilia assembly and provide insights into the fundamental question of how cells determine organelle size and number."],"journal":["EMBO reports"],"pubmed_title":["Mechanisms of cilia regeneration in Xenopus multiciliated epithelium in vivo."],"pmcid":["PMC12019409"],"funding_grant_id":["R00 HL133606","R01 GM144668","K99HL133606","S10 OD011966","K99 HL133606","R35 GM146856","G20-RR31199","1S10OD011966-01A1","R00HL13360","1R01GM144668-01","G20 RR031199"],"pubmed_authors":["Redemann S","Subramanianbalachandar VA","Magaj MM","Rao VG","Kulkarni SS"],"additional_accession":[]},"is_claimable":false,"name":"Mechanisms of cilia regeneration in Xenopus multiciliated epithelium in vivo.","description":"Cilia regeneration is a physiological event, and while studied extensively in unicellular organisms, it remains poorly understood in vertebrates. In this study, using Xenopus multiciliated cells (MCCs), we demonstrate that, unlike unicellular organisms, deciliation removes the transition zone (TZ) and the ciliary axoneme. While MCCs immediately begin regenerating the axoneme, surprisingly, the TZ assembly is delayed. However, ciliary tip proteins, Sentan and Clamp, localize to regenerating cilia without delay. Using cycloheximide (CHX) to block protein synthesis, we show that the TZ protein B9d1 is not present in the cilia precursor pool and requires new transcription/translation, providing insights into the delayed repair of TZ. Moreover, MCCs in CHX treatment assemble fewer but near wild-type length cilia by gradually concentrating ciliogenesis proteins like IFTs at a few basal bodies. Using mathematical modeling, we show that cilia length, compared to cilia number, has a larger influence on the force generated by MCCs. Our results question the requirement of TZ in motile cilia assembly and provide insights into the fundamental question of how cells determine organelle size and number.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-06-02T20:38:55.075Z","creation":"2025-07-01T03:05:18.589Z"},"accession":"S-EPMC12019409","cross_references":{"pubmed":["40087471"],"doi":["10.1038/s44319-025-00414-8"]}}