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      Cell shape and contractility regulate ciliogenesis in cell cycle–arrested cells

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          Adhesive micropatterns show the effect of spatial confinement and actin network architecture on basal body positioning and primary cilium formation.


          In most lineages, cell cycle exit is correlated with the growth of a primary cilium. We analyzed cell cycle exit and ciliogenesis in human retinal cells and found that, contrary to the classical view, not all cells exiting the cell division cycle generate a primary cilium. Using adhesive micropatterns to control individual cell spreading, we demonstrate that cell spatial confinement is a major regulator of ciliogenesis. When spatially confined, cells assemble a contractile actin network along their ventral surface and a protrusive network along their dorsal surface. The nucleus–centrosome axis in confined cells is oriented toward the dorsal surface where the primary cilium is formed. In contrast, highly spread cells assemble mostly contractile actin bundles. The nucleus–centrosome axis of spread cells is oriented toward the ventral surface, where contractility prevented primary cilium growth. These results indicate that cell geometrical confinement affects cell polarity via the modulation of actin network architecture and thereby regulates basal body positioning and primary cilium growth.

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          Most cited references 24

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          The vertebrate primary cilium in development, homeostasis, and disease.

          Cilia are complex structures that have garnered interest because of their roles in vertebrate development and their involvement in human genetic disorders. In contrast to multicellular invertebrates in which cilia are restricted to specific cell types, these organelles are found almost ubiquitously in vertebrate cells, where they serve a diverse set of signaling functions. Here, we highlight properties of vertebrate cilia, with particular emphasis on their relationship with other subcellular structures, and explore the physiological consequences of ciliary dysfunction.
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            Cep164, a novel centriole appendage protein required for primary cilium formation

            Primary cilia (PC) function as microtubule-based sensory antennae projecting from the surface of many eukaryotic cells. They play important roles in mechano- and chemosensory perception and their dysfunction is implicated in developmental disorders and severe diseases. The basal body that functions in PC assembly is derived from the mature centriole, a component of the centrosome. Through a small interfering RNA screen we found several centrosomal proteins (Ceps) to be involved in PC formation. One newly identified protein, Cep164, was indispensable for PC formation and hence characterized in detail. By immunogold electron microscopy, Cep164 could be localized to the distal appendages of mature centrioles. In contrast to ninein and Cep170, two components of subdistal appendages, Cep164 persisted at centrioles throughout mitosis. Moreover, the localizations of Cep164 and ninein/Cep170 were mutually independent during interphase. These data implicate distal appendages in PC formation and identify Cep164 as an excellent marker for these structures.
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              A restriction point for control of normal animal cell proliferation.

               Arthur Pardee (1974)
              This paper provides evidence that normal animal cells possess a unique regulatory mechanism to shift them between proliferative and quiescent states. Cells cease to increase in number under a diversity of suboptimal nutritional conditions, whereas a uniformity of metabolic changes follows these nutritional shifts. Evidence is given here that cells are put into the same quiescent state by each of these diverse blocks to proliferation and that cells escape at the same point in G(1) of the cell cycle when nutrition is restored. The name restriction point is proposed for the specific time in the cell cycle at which this critical release event occurs. The restriction point control is proposed to permit normal cells to retain viability by a shift to a minimal metabolism upon differentiation in vivo and in vitro when conditions are suboptimal for growth. Malignant cells are proposed to have lost their restriction point control. Hence, under very adverse conditions, as in the presence of antitumor agents, they stop randomly in their division cycle and die.

                Author and article information

                J Cell Biol
                J. Cell Biol
                The Journal of Cell Biology
                The Rockefeller University Press
                18 October 2010
                : 191
                : 2
                : 303-312
                [1 ]Laboratoire Biopuces, Institut de Recherche en Sciences et Technologies pour le Vivant, Direction des Sciences du Vivant, Commissariat à l’Energie Atomique et aux Energies Alternatives, 38054 Grenoble, Cedex 09, France
                [2 ]Laboratoire de Physiologie Cellulaire et Végétale, Institut de Recherche en Sciences et Technologies pour le Vivant, Commissariat à l’Energie Atomique et aux Energies Alternatives, Centre National de la Recherche Scientifique, Université Joseph Fourier, Institut National de la Recherche Agronomique, 38054 Grenoble, Cedex 09, France
                [3 ]Institut Curie, Unité Mixte de Recherche144, Centre National de la Recherche Scientifique, 75006 Paris, Cedex 05, France
                Author notes
                Correspondence to Manuel Théry: manuel.thery@
                © 2010 Pitaval et al.

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at

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