کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2035804 1072225 2011 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Centriolar Kinesin Kif24 Interacts with CP110 to Remodel Microtubules and Regulate Ciliogenesis
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیوشیمی، ژنتیک و زیست شناسی مولکولی (عمومی)
پیش نمایش صفحه اول مقاله
Centriolar Kinesin Kif24 Interacts with CP110 to Remodel Microtubules and Regulate Ciliogenesis
چکیده انگلیسی

SummaryWe have identified a protein, Kif24, that shares homology with the kinesin-13 subfamily of motor proteins and specifically interacts with CP110 and Cep97, centrosomal proteins that play a role in regulating centriolar length and ciliogenesis. Kif24 preferentially localizes to mother centrioles. Loss of Kif24 from cycling cells resulted in aberrant cilia assembly but did not promote growth of abnormally long centrioles, unlike CP110 and Cep97 depletion. We found that loss of Kif24 leads to the disappearance of CP110 from mother centrioles, specifically in cycling cells able to form cilia. Kif24 is able to bind and depolymerize microtubules in vitro. Remarkably, ectopically expressed Kif24 specifically remodels centriolar microtubules without significantly altering cytoplasmic microtubules. Thus, our studies have identified a centriolar kinesin that specifically remodels a subset of microtubules, thereby regulating cilia assembly. These studies also suggest mechanistic differences between the regulation of microtubule elongation associated with centrioles and cilia.

Graphical AbstractFigure optionsDownload high-quality image (154 K)Download as PowerPoint slideHighlights
► Centriolar kinesin Kif24 interacts with centrosome proteins CP110 and Cep97
► Loss of Kif24 in cycling cells induces primary cilia formation
► Kif24 binds microtubules and depolymerizes them in vitro
► Ectopic expression of Kif24 leads to remodeling of centriolar microtubules

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 145, Issue 6, 10 June 2011, Pages 914–925
نویسندگان
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