The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility
- Autores
- Alvarez, Diego Ezequiel; Agaisse, Herve
- Año de publicación
- 2013
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Vaccinia virus dissemination relies on the N-WASP– ARP2/3 pathway, which mediates actin tail formation underneath cell-associated extracellular viruses (CEVs). Here, we uncover a previously unappreciated role for the formin FHOD1 and the small GTPase Rac1 in vaccinia actin tail formation. FHOD1 depletion decreased the number of CEVs forming actin tails and impaired the elongation rate of the formed actin tails. Recruitment of FHOD1 to actin tails relied on its GTPase binding domain in addition to its FH2 domain. In agreement with previous studies showing that FHOD1 is activated by the small GTPase Rac1, Rac1 was enriched and activated at the membrane surrounding actin tails. Rac1 depletion or expression of dominant-negative Rac1 phenocopied the effects of FHOD1 depletion and impaired the recruitment of FHOD1 to actin tails. FHOD1 overexpression rescued the actin tail formation defects observed in cells overexpressing dominant-negative Rac1. Altogether, our results indicate that, to display robust actin-based motility, vaccinia virus integrates the activity of the N-WASP– ARP2/3 and Rac1–FHOD1 pathways.
Fil: Alvarez, Diego Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Yale. School of Medicine; Estados Unidos
Fil: Agaisse, Herve. University of Yale. School of Medicine; Estados Unidos - Materia
-
VACCINIA VIRUS
FORMIN
ACTIN
RAC1
FHOD1 - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/24356
Ver los metadatos del registro completo
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The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motilityAlvarez, Diego EzequielAgaisse, HerveVACCINIA VIRUSFORMINACTINRAC1FHOD1https://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Vaccinia virus dissemination relies on the N-WASP– ARP2/3 pathway, which mediates actin tail formation underneath cell-associated extracellular viruses (CEVs). Here, we uncover a previously unappreciated role for the formin FHOD1 and the small GTPase Rac1 in vaccinia actin tail formation. FHOD1 depletion decreased the number of CEVs forming actin tails and impaired the elongation rate of the formed actin tails. Recruitment of FHOD1 to actin tails relied on its GTPase binding domain in addition to its FH2 domain. In agreement with previous studies showing that FHOD1 is activated by the small GTPase Rac1, Rac1 was enriched and activated at the membrane surrounding actin tails. Rac1 depletion or expression of dominant-negative Rac1 phenocopied the effects of FHOD1 depletion and impaired the recruitment of FHOD1 to actin tails. FHOD1 overexpression rescued the actin tail formation defects observed in cells overexpressing dominant-negative Rac1. Altogether, our results indicate that, to display robust actin-based motility, vaccinia virus integrates the activity of the N-WASP– ARP2/3 and Rac1–FHOD1 pathways.Fil: Alvarez, Diego Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Yale. School of Medicine; Estados UnidosFil: Agaisse, Herve. University of Yale. School of Medicine; Estados UnidosRockefeller Univ Press2013-09-23info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/24356Alvarez, Diego Ezequiel; Agaisse, Herve; The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility; Rockefeller Univ Press; Journal Of Cell Biology; 202; 7; 23-9-2013; 1075-10900021-9525CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://jcb.rupress.org/content/202/7/1075info:eu-repo/semantics/altIdentifier/doi/10.1083/jcb.201303055info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:40:46Zoai:ri.conicet.gov.ar:11336/24356instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:40:46.878CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility |
title |
The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility |
spellingShingle |
The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility Alvarez, Diego Ezequiel VACCINIA VIRUS FORMIN ACTIN RAC1 FHOD1 |
title_short |
The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility |
title_full |
The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility |
title_fullStr |
The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility |
title_full_unstemmed |
The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility |
title_sort |
The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility |
dc.creator.none.fl_str_mv |
Alvarez, Diego Ezequiel Agaisse, Herve |
author |
Alvarez, Diego Ezequiel |
author_facet |
Alvarez, Diego Ezequiel Agaisse, Herve |
author_role |
author |
author2 |
Agaisse, Herve |
author2_role |
author |
dc.subject.none.fl_str_mv |
VACCINIA VIRUS FORMIN ACTIN RAC1 FHOD1 |
topic |
VACCINIA VIRUS FORMIN ACTIN RAC1 FHOD1 |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
Vaccinia virus dissemination relies on the N-WASP– ARP2/3 pathway, which mediates actin tail formation underneath cell-associated extracellular viruses (CEVs). Here, we uncover a previously unappreciated role for the formin FHOD1 and the small GTPase Rac1 in vaccinia actin tail formation. FHOD1 depletion decreased the number of CEVs forming actin tails and impaired the elongation rate of the formed actin tails. Recruitment of FHOD1 to actin tails relied on its GTPase binding domain in addition to its FH2 domain. In agreement with previous studies showing that FHOD1 is activated by the small GTPase Rac1, Rac1 was enriched and activated at the membrane surrounding actin tails. Rac1 depletion or expression of dominant-negative Rac1 phenocopied the effects of FHOD1 depletion and impaired the recruitment of FHOD1 to actin tails. FHOD1 overexpression rescued the actin tail formation defects observed in cells overexpressing dominant-negative Rac1. Altogether, our results indicate that, to display robust actin-based motility, vaccinia virus integrates the activity of the N-WASP– ARP2/3 and Rac1–FHOD1 pathways. Fil: Alvarez, Diego Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Yale. School of Medicine; Estados Unidos Fil: Agaisse, Herve. University of Yale. School of Medicine; Estados Unidos |
description |
Vaccinia virus dissemination relies on the N-WASP– ARP2/3 pathway, which mediates actin tail formation underneath cell-associated extracellular viruses (CEVs). Here, we uncover a previously unappreciated role for the formin FHOD1 and the small GTPase Rac1 in vaccinia actin tail formation. FHOD1 depletion decreased the number of CEVs forming actin tails and impaired the elongation rate of the formed actin tails. Recruitment of FHOD1 to actin tails relied on its GTPase binding domain in addition to its FH2 domain. In agreement with previous studies showing that FHOD1 is activated by the small GTPase Rac1, Rac1 was enriched and activated at the membrane surrounding actin tails. Rac1 depletion or expression of dominant-negative Rac1 phenocopied the effects of FHOD1 depletion and impaired the recruitment of FHOD1 to actin tails. FHOD1 overexpression rescued the actin tail formation defects observed in cells overexpressing dominant-negative Rac1. Altogether, our results indicate that, to display robust actin-based motility, vaccinia virus integrates the activity of the N-WASP– ARP2/3 and Rac1–FHOD1 pathways. |
publishDate |
2013 |
dc.date.none.fl_str_mv |
2013-09-23 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/24356 Alvarez, Diego Ezequiel; Agaisse, Herve; The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility; Rockefeller Univ Press; Journal Of Cell Biology; 202; 7; 23-9-2013; 1075-1090 0021-9525 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/24356 |
identifier_str_mv |
Alvarez, Diego Ezequiel; Agaisse, Herve; The formin FHOD1 and the small GTPase Rac1 promote vaccinia virus actin-based motility; Rockefeller Univ Press; Journal Of Cell Biology; 202; 7; 23-9-2013; 1075-1090 0021-9525 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/http://jcb.rupress.org/content/202/7/1075 info:eu-repo/semantics/altIdentifier/doi/10.1083/jcb.201303055 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Rockefeller Univ Press |
publisher.none.fl_str_mv |
Rockefeller Univ Press |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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