Ostler, Nicole, Britzen-Laurent, Nathalie ORCID: 0000-0002-0494-7117, Liebl, Andrea, Naschberger, Elisabeth ORCID: 0000-0003-1291-622X, Lochnit, Guenter, Ostler, Markus, Forster, Florian, Kunzelmann, Peter, Ince, Semra, Supper, Verena, Praefcke, Gerrit J. K., Schubert, Dirk W., Stockinger, Hannes ORCID: 0000-0001-6404-4430, Herrmann, Christian and Stuerzl, Michael (2014). Gamma Interferon-Induced Guanylate Binding Protein 1 Is a Novel Actin Cytoskeleton Remodeling Factor. Mol. Cell. Biol., 34 (2). S. 196 - 210. WASHINGTON: AMER SOC MICROBIOLOGY. ISSN 1098-5549

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Abstract

Gamma interferon (IFN-gamma) regulates immune defenses against viruses, intracellular pathogens, and tumors by modulating cell proliferation, migration, invasion, and vesicle trafficking processes. The large GTPase guanylate binding protein 1 (GBP-1) is among the cellular proteins that is the most abundantly induced by IFN-gamma and mediates its cell biologic effects. As yet, the molecular mechanisms of action of GBP-1 remain unknown. Applying an interaction proteomics approach, we identified actin as a strong and specific binding partner of GBP-1. Furthermore, GBP-1 colocalized with actin at the subcellular level and was both necessary and sufficient for the extensive remodeling of the fibrous actin structure observed in IFN-gamma -exposed cells. These effects were dependent on the oligomerization and the GTPase activity of GBP-1. Purified GBP-1 and actin bound to each other, and this interaction was sufficient to impair the formation of actin filaments in vitro, as demonstrated by atomic force microscopy, dynamic light scattering, and fluorescence-monitored polymerization. Cosedimentation and band shift analyses demonstrated that GBP-1 binds robustly to globular actin and slightly to filamentous actin. This indicated that GBP-1 may induce actin remodeling via globular actin sequestering and/or filament capping. These results establish GBP-1 as a novel member within the family of actin-remodeling proteins specifically mediating IFN-gamma -dependent defense strategies.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Ostler, NicoleUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Britzen-Laurent, NathalieUNSPECIFIEDorcid.org/0000-0002-0494-7117UNSPECIFIED
Liebl, AndreaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Naschberger, ElisabethUNSPECIFIEDorcid.org/0000-0003-1291-622XUNSPECIFIED
Lochnit, GuenterUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ostler, MarkusUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Forster, FlorianUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Kunzelmann, PeterUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ince, SemraUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Supper, VerenaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Praefcke, Gerrit J. K.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schubert, Dirk W.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Stockinger, HannesUNSPECIFIEDorcid.org/0000-0001-6404-4430UNSPECIFIED
Herrmann, ChristianUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Stuerzl, MichaelUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-450954
DOI: 10.1128/MCB.00664-13
Journal or Publication Title: Mol. Cell. Biol.
Volume: 34
Number: 2
Page Range: S. 196 - 210
Date: 2014
Publisher: AMER SOC MICROBIOLOGY
Place of Publication: WASHINGTON
ISSN: 1098-5549
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
IFN-GAMMA; ENDOTHELIAL-CELLS; BARRIER FUNCTION; INFLAMMATORY CYTOKINES; NUCLEOTIDE-BINDING; TUMOR-DEVELOPMENT; RHO GTPASES; F-ACTIN; ACTIVATION; GROWTHMultiple languages
Biochemistry & Molecular Biology; Cell BiologyMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/45095

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