Abstract
The primary cilium, an antenna-like structure that protrudes out from the cell surface, is present in most cell types. It is a microtubule-based organelle that serves as a mega-signaling center and is important for sensing biochemical and mechanical signals to carry out various cellular processes such as proliferation, migration, differentiation, and many others. At any given time, cilia length is determined by a dynamic balance of cilia assembly and disassembly processes. Abnormally short or long cilia can cause a plethora of human diseases commonly referred to as ciliopathies, including, but not limited to, skeletal malformations, obesity, autosomal dominant polycystic kidney disease, retinal degeneration, and bardet-biedl syndrome. While the process of cilia assembly is studied extensively, the process of cilia disassembly and its biological role(s) are less well understood. This review discusses current knowledge on ciliary disassembly and how different cellular processes and molecular signals converge to carry out this process. This information will help us understand how the process of ciliary disassembly is regulated, identify the key steps that need further investigation, and possibly design therapeutic targets for a subset of ciliopathies that are causally linked to defective ciliary disassembly.
Highlights
Since NEK2 is expressed in the S and G2 phases of the cell cycle, it ensures that the Kinesin family member 24 (KIF24) dependent MT depolymerization and subsequent ciliary disassembly is conducted before cells enter into mitosis [94]
These dual roles of promoting cilia disassembly and inhibiting cilia assembly suggest that NEK2 and KIF24 ensure that the ciliary loss is irrevocable once the cells enter the cell cycle
These pathways collectively dampen the machinery required for cilia assembly and ensure that no ectopic ciliary assembly occurs during ciliary loss and entry into the cell cycle
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. MTs arises from mother centriole anchored to thetociliary membrane through transition fibers. Body entry andthe exit of signaling from the cilia from bodyThe andbasal transition and zone further supportdynamics the structural dynamics ofMTs the axonemal. TheAlong elongation of the axoneme, ciliary membrane extends and extends and sheaths the growing axoneme and harbors a wide variety of receptors and ion sheaths the growing axoneme and harbors a wide variety of receptors and ion channels channels that mediate multiple signaling pathways [3,9,10,11,12,13,14,15,29,30].
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