Centriolar satellites expedite mother centriole remodeling to promote ciliogenesis
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Título
Centriolar satellites expedite mother centriole remodeling to promote ciliogenesisAutoría
Fecha de publicación
2023-02-15Editor
eLife Sciences PublicationsCita bibliográfica
Hall, E. A., Kumar, D., Prosser, S. L., Yeyati, P. L., Herranz-Pérez, V., García-Verdugo, J. M., ... & Mill, P. (2023). Centriolar satellites expedite mother centriole remodeling to promote ciliogenesis. Elife, 12, e79299.Tipo de documento
info:eu-repo/semantics/articleVersión
info:eu-repo/semantics/publishedVersionPalabras clave / Materias
Resumen
Centrosomes are orbited by centriolar satellites, dynamic multiprotein assemblies nucleated by Pericentriolar Material 1 (PCM1). To study the requirement for centriolar satellites, we generated mice lacking PCM1, a ... [+]
Centrosomes are orbited by centriolar satellites, dynamic multiprotein assemblies nucleated by Pericentriolar Material 1 (PCM1). To study the requirement for centriolar satellites, we generated mice lacking PCM1, a crucial component of satellites. Pcm1-/- mice display partially penetrant perinatal lethality with survivors exhibiting hydrocephalus, oligospermia and cerebellar hypoplasia, and variably expressive phenotypes such as hydronephrosis. As many of these phenotypes have been observed in human ciliopathies and satellites are implicated in cilia biology, we investigated whether cilia were affected. PCM1 was dispensable for ciliogenesis in many cell types, whereas Pcm1-/- multiciliated ependymal cells and human PCM1-/- retinal pigmented epithelial 1 (RPE1) cells showed reduced ciliogenesis. PCM1-/- RPE1 cells displayed reduced docking of the mother centriole to the ciliary vesicle and removal of CP110 and CEP97 from the distal mother centriole, indicating compromised early ciliogenesis. Similarly, Pcm1-/- ependymal cells exhibited reduced removal of CP110 from basal bodies in vivo. We propose that PCM1 and centriolar satellites facilitate efficient trafficking of proteins to and from centrioles, including the departure of CP110 and CEP97 to initiate ciliogenesis, and that the threshold to trigger ciliogenesis differs between cell types. © 2023, eLife Sciences Publications Ltd. All rights reserved. [-]
Entidad financiadora
Medical Research Council | European Commission | Canadian Institutes of Health Research | National Institutes of Health | Jane Coffin Childs Memorial Fund for Medical Research | Sandler Foundation | Krembil Foundation | European Commission
Código del proyecto o subvención
MR_UU_1201018/26 | 866355 | 167279 | R01GM095941 | 702601 | R01AR054396 | RO1HD089918 | 5K99GM140175
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info:eu-repo/semantics/openAccess
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- MED_Articles [662]