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BioMed Research International
Volume 2017 (2017), Article ID 4367019, 16 pages
Review Article

New Roles of the Primary Cilium in Autophagy

1Departamento de Fisiología, Facultad Ciencias Biológicas, Pontificia Universidad Católica de Chile, 7820436 Santiago, Chile
2Advanced Center for Chronic Diseases (ACCDiS), Facultad Ciencias Químicas y Farmacéuticas & Facultad de Medicina, 8380494 Santiago, Chile
3Center for Molecular Studies of the Cell (CEMC), Facultad de Medicina, 8380453 Santiago, Chile
4Instituto de Investigación en Ciencias Odontológicas (ICOD), Facultad de Odontología, 8380492 Santiago, Chile

Correspondence should be addressed to Eugenia Morselli and Alfredo Criollo

Received 31 March 2017; Accepted 3 July 2017; Published 23 August 2017

Academic Editor: Anton M. Jetten

Copyright © 2017 Yenniffer Ávalos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The primary cilium is a nonmotile organelle that emanates from the surface of multiple cell types and receives signals from the environment to regulate intracellular signaling pathways. The presence of cilia, as well as their length, is important for proper cell function; shortened, elongated, or absent cilia are associated with pathological conditions. Interestingly, it has recently been shown that the molecular machinery involved in autophagy, the process of recycling of intracellular material to maintain cellular and tissue homeostasis, participates in ciliogenesis. Cilium-dependent signaling is necessary for autophagosome formation and, conversely, autophagy regulates both ciliogenesis and cilium length by degrading specific ciliary proteins. Here, we will discuss the relationship that exists between the two processes at the cellular and molecular level, highlighting what is known about the effects of ciliary dysfunction in the control of energy homeostasis in some ciliopathies.