Ciliary shedding occurs from unicellular organisms to metazoans. Although required during the cell cycle and during neurogenesis, the process remains poorly understood. In all cellular models, this phenomenon occurs distal to the transition zone (TZ), suggesting conserved molecular mechanisms. The TZ module proteins (Meckel Gruber syndrome [MKS]/Nephronophtysis [NPHP]/Centrosomal protein of 290 kDa [CEP290]/Retinitis pigmentosa GTPase regulator-Interacting Protein 1-Like Protein [RPGRIP1L]) are known to cooperate to establish TZ formation and function. To determine whether they control deciliation, we studied the function of 5 of them (Transmembrane protein 107 [TMEM107], Transmembrane protein 216 [TMEM216], CEP290, RPGRIP1L, and NPHP4) in Paramecium. All proteins are recruited to the TZ of growing cilia and localize with 9-fold symmetry at the level of the most distal part of the TZ. We demonstrate that depletion of the MKS2/TMEM216 and TMEM107 proteins induces constant deciliation of some cilia, while depletion of either NPHP4, CEP290, or RPGRIP1L prevents Ca2+/EtOH deciliation. Our results constitute the first evidence for a role of conserved TZ proteins in deciliation and open new directions for understanding motile cilia physiology.

睫状体脱落从单细胞生物到后生动物。尽管在细胞周期和神经发生过程中是必需的，但该过程仍知之甚少。在所有细胞模型中，此现象都发生在过渡区（TZ）的远端，表明分子机制是保守的。已知TZ模块蛋白（Meckel Gruber综合征[MKS] /肾病[NPHP] / 290 kDa的中央体蛋白[CEP290] /色素性视网膜炎GTPase调节剂-相互作用蛋白1-Like蛋白[RPGRIP1L]）可协同建立TZ的形成并功能。以确定它们是否控制deciliation，我们在研究了它们（跨膜蛋白107 [TMEM107]，跨膜蛋白216 [TMEM216]，CEP290，RPGRIP1L，和NPHP4）的5的功能草履虫。所有蛋白都被募集到生长的纤毛的TZ中，并以9倍的对称性定位在TZ最远端的水平。我们证明，MKS2 / TMEM216和TMEM107蛋白质的消耗诱导某些纤毛的恒定递减，而NPHP4，CEP290或RPGRIP1L的消耗则阻止Ca2 + / EtOH递减。我们的结果构成了保守的TZ蛋白在脱纤中作用的第一个证据，并为理解运动性纤毛生理学开辟了新的方向。