Actin-dependent regulation of cilia length by the inverted formin FHDC1
| العنوان: | Actin-dependent regulation of cilia length by the inverted formin FHDC1 |
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| المؤلفون: | John W. Copeland, Andrea McRae, Giulia Guarguaglini, Laura Trinkle-Mulcahy, Sarah J. Copeland |
| المصدر: | Molecular biology of the cell 29 (2018): 1611–1627. doi:10.1091/mbc.E18-02-0088 info:cnr-pdr/source/autori:Copeland S.J.; McRae A.; Guarguaglini G.; Trinkle-Mulcahy L.; Copeland J.W./titolo:Actin-dependent regulation of cilia length by the inverted formin FHDC1/doi:10.1091%2Fmbc.E18-02-0088/rivista:Molecular biology of the cell/anno:2018/pagina_da:1611/pagina_a:1627/intervallo_pagine:1611–1627/volume:29 |
| بيانات النشر: | American Society for Cell Biology (ASCB), 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | Fetal Proteins, 0301 basic medicine, Formins, Golgi Apparatus, Cep170, Biology, Mice, 03 medical and health sciences, 0302 clinical medicine, citoscheletro, Microtubule, Ciliogenesis, Animals, Cilia, Cytoskeleton, Molecular Biology, Actin, Centrioles, formina FHDC1, Cilium, Microfilament Proteins, Nuclear Proteins, Cell Biology, respiratory system, CEP170, Actins, Cell biology, 030104 developmental biology, ciliogenesi, Cytoplasm, NIH 3T3 Cells, biology.protein, 030217 neurology & neurosurgery, Protein Binding |
| الوصف: | A primary cilium is found on most mammalian cells, where it acts as a cellular antenna for the reception of both mechanical and chemical signals. A variety of diseases are associated with defective ciliogenesis, reflecting the ubiquity of the function of cilia and the number of proteins required for their assembly. Proper cilia length is necessary for cilia signaling and is regulated through a poorly understood balance of assembly and disassembly rates. FHDC1 is a unique member of the formin family of cytoskeletal regulatory proteins. Overexpression of FHDC1 induces F-actin accumulation and microtubule stabilization and acetylation. We find that overexpression of FHDC1 also has profound effects on ciliogenesis; in most cells FHDC1 overexpression blocks cilia assembly, but the cilia that are present are immensely elongated. FHDC1-induced cilia growth requires the FHDC1 FH2 and microtubule-binding domain and results from F-actin–dependent inhibition of cilia disassembly. FHDC1 depletion, or treatment with a pan-formin inhibitor, inhibits cilia assembly and induces cilia resorption. Endogenous FHDC1 protein localizes to cytoplasmic microtubules converging on the base of the cilia, and we identify the subdistal appendage protein Cep170 as an FHDC1 interacting protein. Our results suggest that FHDC1 plays a role in coordinating cytoskeletal dynamics during normal cilia assembly. |
| تدمد: | 1939-4586 1059-1524 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::30ba9464f8cf83182923e1217ada876c https://doi.org/10.1091/mbc.e18-02-0088 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....30ba9464f8cf83182923e1217ada876c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19394586 10591524 |
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