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<p>The centriole duplication cycle must be tightly controlled and coordinated with the chromosome cycle. Aberrations in centriole biogenesis can cause developmental disorders, ciliopathies and cancer, yet the molecular determinants controlling centriole numbers and the link between the two cycles remain poorly characterized. Here, we demonstrate that McIdas, previously implicated in cell cycle regulation and multiciliogenesis, plays a critical role in maintaining proper centriole numbers. McIdas localizes to centrioles, where it exhibits dynamic localization throughout the cell cycle, dependent upon a nuclear export signal (NES) in its coiled-coil domain. Overexpression of McIdas induces centriole overduplication, whereas its depletion perturbs daughter centriole biogenesis and SAS6 recruitment. An NES mutant of McIdas that fails to localize to centrioles does not induce centriole amplification. Moreover, McIdas depletion reduces PLK4-induced centriole amplification. McIdas interacts with and is phosphorylated by PLK4, which is critical for its role in centriole number control. Overall, our results demonstrate that in addition to its known nuclear localization, McIdas also localizes to centrioles, affecting centriole duplication. This novel, direct role of McIdas in centriole duplication connects its functions in cell cycle regulation and multiciliogenesis.</p>

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McIdas localizes to centrioles and controls centriole numbers through PLK4-dependent phosphorylation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月5日

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  • Marina Arbi,
  • Margarita Skamnelou,
  • Lydia Koufoudaki,
  • Vasiliki Bakali,
  • Spyridoula Bournaka,
  • Sihem Zitouni,
  • Stavroula Tsaridou,
  • Ozge Karayel,
  • Catherine G Vasilopoulou,
  • Aikaterini C Tsika,
  • Nikolaos N Giakoumakis,
  • Ourania Preza,
  • Georgios A Spyroulias,
  • Matthias Mann,
  • Mónica Bettencourt-Dias,
  • Stavros Taraviras,
  • Zoi Lygerou

摘要

The centriole duplication cycle must be tightly controlled and coordinated with the chromosome cycle. Aberrations in centriole biogenesis can cause developmental disorders, ciliopathies and cancer, yet the molecular determinants controlling centriole numbers and the link between the two cycles remain poorly characterized. Here, we demonstrate that McIdas, previously implicated in cell cycle regulation and multiciliogenesis, plays a critical role in maintaining proper centriole numbers. McIdas localizes to centrioles, where it exhibits dynamic localization throughout the cell cycle, dependent upon a nuclear export signal (NES) in its coiled-coil domain. Overexpression of McIdas induces centriole overduplication, whereas its depletion perturbs daughter centriole biogenesis and SAS6 recruitment. An NES mutant of McIdas that fails to localize to centrioles does not induce centriole amplification. Moreover, McIdas depletion reduces PLK4-induced centriole amplification. McIdas interacts with and is phosphorylated by PLK4, which is critical for its role in centriole number control. Overall, our results demonstrate that in addition to its known nuclear localization, McIdas also localizes to centrioles, affecting centriole duplication. This novel, direct role of McIdas in centriole duplication connects its functions in cell cycle regulation and multiciliogenesis.