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Septin 9 exhibits polymorphic binding to F-actin and inhibits myosin and cofilin activity
Journal article   Open access   Peer reviewed

Septin 9 exhibits polymorphic binding to F-actin and inhibits myosin and cofilin activity

Clayton Smith, Lee Dolat, Dimitrios Angelis, Eva Forgacs, Elias T Spiliotis and Vitold E Galkin
Journal of molecular biology, v 427(20), pp 3273-3284
09 Oct 2015
PMID: 26297986
url
https://doi.org/10.1016/j.jmb.2015.07.026View
Published, Version of Record (VoR) Open

Abstract

Septins are a highly conserved family of proteins in eukaryotes that is recognized as a novel component of the cytoskeleton. Septin 9 (SEPT9) interacts directly with actin filaments and functions as an actin stress fiber cross-linking protein that promotes the maturation of nascent focal adhesions and cell migration. However, the molecular details of how SEPT9 interacts with F-actin remain unknown. Here, we use electron microscopy and image analysis to show that SEPT9 binds to F-actin in a highly polymorphic fashion. We demonstrate that the basic domain (B-domain) of the N-terminal tail of SEPT9 is responsible for actin cross-linking, while the GTP-binding domain (G-domain) does not bundle F-actin. We show that the B-domain of SEPT9 binds to three sites on F-actin, and the two of these sites overlap with the binding regions of myosin and cofilin. SEPT9 inhibits actin-dependent ATPase activity of myosin and competes with the weakly-bound state of myosin for binding to F-actin. At the same time, SEPT9 significantly reduces the extent of F-actin depolymerization by cofilin. Taken together, these data suggest that SEPT9 protects actin filaments from depolymerization by cofilin and myosin, and indicate a mechanism by which SEPT9 could maintain the integrity of growing and contracting actin filaments.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
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