scholarly journals Glucose deprivation induces primary cilium formation through mTORC1 inactivation

2017 ◽  
Vol 131 (1) ◽  
pp. jcs208769 ◽  
Author(s):  
Kengo Takahashi ◽  
Tomoaki Nagai ◽  
Shuhei Chiba ◽  
Keiko Nakayama ◽  
Kensaku Mizuno
Keyword(s):  
Primary Cilium ◽  
Glucose Deprivation ◽  
Cilium Formation

scholarly journals A Model for Primary Cilium Biogenesis by Polarized Epithelial Cells: Role of the Midbody Remnant and Associated Specialized Membranes

2021 ◽  
Vol 8 ◽  
Author(s):  
Leticia Labat-de-Hoz ◽  
Armando Rubio-Ramos ◽  
Javier Casares-Arias ◽  
Miguel Bernabé-Rubio ◽  
Isabel Correas ◽  
...  
Keyword(s):  
Cell Surface ◽  
Primary Cilium ◽  
Primary Cilia ◽  
Control Cell ◽  
Future Research ◽  
Alternative Route ◽  
Ciliary Membrane ◽  
Cilium Formation ◽  
Membrane Compartmentalization

Primary cilia are solitary, microtubule-based protrusions surrounded by a ciliary membrane equipped with selected receptors that orchestrate important signaling pathways that control cell growth, differentiation, development and homeostasis. Depending on the cell type, primary cilium assembly takes place intracellularly or at the cell surface. The intracellular route has been the focus of research on primary cilium biogenesis, whereas the route that occurs at the cell surface, which we call the “alternative” route, has been much less thoroughly characterized. In this review, based on recent experimental evidence, we present a model of primary ciliogenesis by the alternative route in which the remnant of the midbody generated upon cytokinesis acquires compact membranes, that are involved in compartmentalization of biological membranes. The midbody remnant delivers part of those membranes to the centrosome in order to assemble the ciliary membrane, thereby licensing primary cilium formation. The midbody remnant's involvement in primary cilium formation, the regulation of its inheritance by the ESCRT machinery, and the assembly of the ciliary membrane from the membranes originally associated with the remnant are discussed in the context of the literature concerning the ciliary membrane, the emerging roles of the midbody remnant, the regulation of cytokinesis, and the role of membrane compartmentalization. We also present a model of cilium emergence during evolution, and summarize the directions for future research.

Pharmacological Regulation of Primary Cilium Formation Affects the Mechanosensitivity of Osteocytes

2020 ◽  
Vol 107 (6) ◽  
pp. 625-635
Author(s):  
Dong Ding ◽  
Xiao Yang ◽  
Hui-qin Luan ◽  
Xin-tong Wu ◽  
Cai He ◽  
...  
Keyword(s):  
Primary Cilium ◽  
Cilium Formation ◽  
Pharmacological Regulation

scholarly journals The Meckel–Gruber Syndrome proteins MKS1 and meckelin interact and are required for primary cilium formation

2006 ◽  
Vol 16 (2) ◽  
pp. 173-186 ◽  
Author(s):  
Helen R. Dawe ◽  
Ursula M. Smith ◽  
Andrew R. Cullinane ◽  
Dianne Gerrelli ◽  
Phillip Cox ◽  
...  
Keyword(s):  
Primary Cilium ◽  
Cilium Formation

TACC3 promotes prostate cancer cell proliferation and restrains primary cilium formation

2020 ◽  
Vol 390 (2) ◽  
pp. 111952 ◽  
Author(s):  
Yunkai Qie ◽  
Lin Wang ◽  
E. Du ◽  
Shuaiqi Chen ◽  
Chao Lu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Primary Cilium ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Cilium Formation

scholarly journals Galectin 3 Deficiency Alters Chondrocyte Primary Cilium Formation and Exacerbates Cartilage Destruction via Mitochondrial Apoptosis

2020 ◽  
Vol 21 (4) ◽  
pp. 1486 ◽  
Author(s):  
Narjès Hafsia ◽  
Marine Forien ◽  
Félix Renaudin ◽  
Delphine Delacour ◽  
Pascal Reboul ◽  
...  
Keyword(s):  
Primary Cilium ◽  
Primary Cilia ◽  
Mitochondrial Pathway ◽  
Cartilage Destruction ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Chondrocyte Apoptosis ◽  
Cytochrome C Release ◽  
Cilium Formation ◽  
Galectin 3

Mechanical overload and aging are the main risk factors of osteoarthritis (OA). Galectin 3 (GAL3) is important in the formation of primary cilia, organelles that are able to sense mechanical stress. The objectives were to evaluate the role of GAL3 in chondrocyte primary cilium formation and in OA in mice. Chondrocyte primary cilium was detected in vitro by confocal microscopy. OA was induced by aging and partial meniscectomy of wild-type (WT) and Gal3-null 129SvEV mice (Gal3−/−). Primary chondrocytes were isolated from joints of new-born mice. Chondrocyte apoptosis was assessed by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), caspase 3 activity and cytochrome c release. Gene expression was assessed by qRT-PCR. GAL3 was localized at the basal body of the chondrocyte primary cilium. Primary cilia of Gal3−/− chondrocytes were frequently abnormal and misshapen. Deletion of Gal3 triggered premature OA during aging and exacerbated joint instability-induced OA. In both aging and surgery-induced OA cartilage, levels of chondrocyte catabolism and hypertrophy markers and apoptosis were more severe in Gal3−/− than WT samples. In vitro, Gal3 knockout favored chondrocyte apoptosis via the mitochondrial pathway. GAL3 is a key regulator of cartilage homeostasis and chondrocyte primary cilium formation in mice. Gal3 deletion promotes OA development.

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