title: Asymmetric Distribution of Primary Cilia Allocates Satellite Cells for Self-Renewal.
abstract: Regeneration of vertebrate skeletal muscles requires satellite cells, a population of stem cells that are quiescent in normal conditions and divide, differentiate, and self-renew upon activation triggered by exercise, injury, and degenerative diseases. Satellite cell self-renewal is essential for long-term tissue homeostasis, and previous work has identified a number of external cues that control this process. However, little is known of the possible intrinsic control mechanisms of satellite cell self-renewal. Here, we show that quiescent satellite cells harbor a primary cilium, which is rapidly disassembled upon entry into the cell cycle. Contrasting with a commonly accepted belief, cilia reassembly does not occur uniformly in cells exiting the cell cycle. We found that primary cilia reassemble preferentially in cells committed to self-renew, and disruption of cilia reassembly causes a specific deficit in self-renewing satellite cells. These observations indicate that primary cilia provide an intrinsic cue essential for satellite cell self-renewal.
authors.affiliation: Department of Biomedical Science, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, UK.
authors.forename: Nur Hayati
authors.initials: NH
authors.lastname: Jaafar Marican
authors.affiliation: Department of Biomedical Science, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, UK.
authors.forename: Sara B
authors.initials: SB
authors.lastname: Cruz-Migoni
authors.affiliation: Department of Biomedical Science, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, UK. Electronic address: a.g.borycki@sheffield.ac.uk.
authors.forename: Anne-Gaëlle
authors.initials: AG
authors.lastname: Borycki
mesh_terms: D020727:ADP-Ribosylation Factors / Q000235:genetics / Q000378:metabolism; D000818:Animals; D054715:Cardiotoxins / Q000633:toxicity; D051242:Caveolin 1 / Q000235:genetics / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002923:Cilia / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure*; D005786:Gene Expression Regulation; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D018482:Muscle, Skeletal / Q000187:drug effects / Q000293:injuries / Q000378:metabolism / Q000648:ultrastructure*; D009210:Myofibrils / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure*; D018008:Myogenin / Q000235:genetics / Q000378:metabolism; D015739:Nocodazole / Q000494:pharmacology; D051763:PAX7 Transcription Factor / Q000235:genetics / Q000378:metabolism; D017239:Paclitaxel / Q000494:pharmacology; D032496:Satellite Cells, Skeletal Muscle / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D015398:Signal Transduction
chemical_list: C560093:Arl13b protein, mouse; D054715:Cardiotoxins; C495541:Cav1 protein, mouse; D051242:Caveolin 1; C503801:Myog protein, mouse; D018008:Myogenin; D051763:PAX7 Transcription Factor; C497322:Pax7 protein, mouse; D020727:ADP-Ribosylation Factors; D017239:Paclitaxel; D015739:Nocodazole