Current biology, 2012-06, Vol.22 (12), p.1109-1115
2012
Volltextzugriff (PDF)
Details
- Autor(en) / Beteiligte
- Titel
- Septin-Driven Coordination of Actin and Microtubule Remodeling Regulates the Collateral Branching of Axons
- Ist Teil von
- Current biology, 2012-06, Vol.22 (12), p.1109-1115
- Ort / Verlag
- England: Elsevier Inc
- Erscheinungsjahr
- 2012
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Axon branching is fundamental to the development of the peripheral and central nervous system [1, 2]. Branches that sprout from the axon shaft are termed collateral or interstitial branches [3, 4]. Collateral branching of axons requires the formation of filopodia from actin microfilaments (F-actin) and their engorgement with microtubules (MTs) that splay from the axon shaft [4–6]. The mechanisms that drive and coordinate the remodeling of actin and MTs during branch morphogenesis are poorly understood. Septins comprise a family of GTP-binding proteins that oligomerize into higher-order structures, which associate with membranes and the actin and microtubule cytoskeleton [7, 8]. Here, we show that collateral branching of axons requires SEPT6 and SEPT7, two interacting septins [9]. In the axons of sensory neurons, both SEPT6 and SEPT7 accumulate at incipient sites of filopodia formation. We show that SEPT6 localizes to axonal patches of F-actin and increases the recruitment of cortactin, a regulator of Arp2/3-mediated actin polymerization, triggering the emergence of filopodia. Conversely, SEPT7 promotes the entry of axonal MTs into filopodia, enabling the formation of collateral branches. Surprisingly, septins provide a novel mechanism for the collateral branching of axons by coordinating the remodeling of the actin and microtubule cytoskeleton. [Display omitted] ► Collateral branching of axons is regulated by SEPT6 and SEPT7 ► SEPT6 and SEPT7 are recruited to nascent sites of filopodia formation ► SEPT6 recruits cortactin to patches of F-actin and triggers filopodia formation ► SEPT7 alters axonal MT organization, triggering MT entry into filopodia
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0960-9822eISSN: 1879-0445DOI: 10.1016/j.cub.2012.04.019Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3381998
- Format
- –
- Schlagworte
- actin, Actins - metabolism, Analysis of Variance, Animals, axons, Axons - physiology, Axons - ultrastructure, Blotting, Western, central nervous system, Chick Embryo, Cortactin - metabolism, DNA Primers - genetics, Electrophoresis, Polyacrylamide Gel, engorgement, G-proteins, Ganglia, Spinal - cytology, Green Fluorescent Proteins - metabolism, Growth Cones - physiology, Growth Cones - ultrastructure, Hippocampus - cytology, Image Processing, Computer-Assisted, Immunoprecipitation, microfilaments, Microscopy, Electron, Microscopy, Fluorescence, microtubules, Microtubules - metabolism, Models, Biological, morphogenesis, Morphogenesis - physiology, polymerization, pseudopodia, Pseudopodia - metabolism, Rats, RNA, Small Interfering - genetics, sensory neurons, Septins - metabolism, Septins - physiology, Time-Lapse Imaging