PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy
- Autores
- Gaurón, María Celeste; Newton, Alexandra C.; Colombo, Maria Isabel
- Año de publicación
- 2021
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Hijacking the autophagic machinery is a key mechanism through which invasive pathogens such as Staphylococcus aureus replicate in their host cells. We have previously demonstrated that the bacteria replicate in phagosomes labeled with the autophagic protein LC3, before escaping to the cytoplasm. Here, we show that the Ca2+-dependent PKCα binds to S. aureus-containing phagosomes and that α-hemolysin, secreted by S. aureus, promotes this recruitment of PKCα to phagosomal membranes. Interestingly, the presence of PKCα prevents the association of the autophagic protein LC3. Live cell imaging experiments using the PKC activity reporter CKAR reveal that treatment of cells with S. aureus culture supernatants containing staphylococcal secreted factors transiently activates PKC. Functional studies reveal that overexpression of PKCα causes a marked inhibition of bacterial replication. Taken together, our data identify enhancing PKCα activity as a potential approach to inhibit S. aureus replication in mammalian cells.
Fil: Gaurón, María Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina. University of California at San Diego; Estados Unidos
Fil: Newton, Alexandra C.. University of California at San Diego; Estados Unidos
Fil: Colombo, Maria Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina - Materia
-
AUTOPHAGY
LC3
PROTEIN KINASE C
STAPHYLOCOCCUS AUREUS
XENOPHAGY - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/174636
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CONICET Digital (CONICET) |
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PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagyGaurón, María CelesteNewton, Alexandra C.Colombo, Maria IsabelAUTOPHAGYLC3PROTEIN KINASE CSTAPHYLOCOCCUS AUREUSXENOPHAGYhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Hijacking the autophagic machinery is a key mechanism through which invasive pathogens such as Staphylococcus aureus replicate in their host cells. We have previously demonstrated that the bacteria replicate in phagosomes labeled with the autophagic protein LC3, before escaping to the cytoplasm. Here, we show that the Ca2+-dependent PKCα binds to S. aureus-containing phagosomes and that α-hemolysin, secreted by S. aureus, promotes this recruitment of PKCα to phagosomal membranes. Interestingly, the presence of PKCα prevents the association of the autophagic protein LC3. Live cell imaging experiments using the PKC activity reporter CKAR reveal that treatment of cells with S. aureus culture supernatants containing staphylococcal secreted factors transiently activates PKC. Functional studies reveal that overexpression of PKCα causes a marked inhibition of bacterial replication. Taken together, our data identify enhancing PKCα activity as a potential approach to inhibit S. aureus replication in mammalian cells.Fil: Gaurón, María Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina. University of California at San Diego; Estados UnidosFil: Newton, Alexandra C.. University of California at San Diego; Estados UnidosFil: Colombo, Maria Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFrontiers Media2021-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/174636Gaurón, María Celeste; Newton, Alexandra C.; Colombo, Maria Isabel; PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy; Frontiers Media; Frontiers in Immunology; 12; 3-2021; 1-131664-3224CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fimmu.2021.662987/fullinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fimmu.2021.662987info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:43:47Zoai:ri.conicet.gov.ar:11336/174636instacron: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 10:43:47.734CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy |
title |
PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy |
spellingShingle |
PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy Gaurón, María Celeste AUTOPHAGY LC3 PROTEIN KINASE C STAPHYLOCOCCUS AUREUS XENOPHAGY |
title_short |
PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy |
title_full |
PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy |
title_fullStr |
PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy |
title_full_unstemmed |
PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy |
title_sort |
PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy |
dc.creator.none.fl_str_mv |
Gaurón, María Celeste Newton, Alexandra C. Colombo, Maria Isabel |
author |
Gaurón, María Celeste |
author_facet |
Gaurón, María Celeste Newton, Alexandra C. Colombo, Maria Isabel |
author_role |
author |
author2 |
Newton, Alexandra C. Colombo, Maria Isabel |
author2_role |
author author |
dc.subject.none.fl_str_mv |
AUTOPHAGY LC3 PROTEIN KINASE C STAPHYLOCOCCUS AUREUS XENOPHAGY |
topic |
AUTOPHAGY LC3 PROTEIN KINASE C STAPHYLOCOCCUS AUREUS XENOPHAGY |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
Hijacking the autophagic machinery is a key mechanism through which invasive pathogens such as Staphylococcus aureus replicate in their host cells. We have previously demonstrated that the bacteria replicate in phagosomes labeled with the autophagic protein LC3, before escaping to the cytoplasm. Here, we show that the Ca2+-dependent PKCα binds to S. aureus-containing phagosomes and that α-hemolysin, secreted by S. aureus, promotes this recruitment of PKCα to phagosomal membranes. Interestingly, the presence of PKCα prevents the association of the autophagic protein LC3. Live cell imaging experiments using the PKC activity reporter CKAR reveal that treatment of cells with S. aureus culture supernatants containing staphylococcal secreted factors transiently activates PKC. Functional studies reveal that overexpression of PKCα causes a marked inhibition of bacterial replication. Taken together, our data identify enhancing PKCα activity as a potential approach to inhibit S. aureus replication in mammalian cells. Fil: Gaurón, María Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina. University of California at San Diego; Estados Unidos Fil: Newton, Alexandra C.. University of California at San Diego; Estados Unidos Fil: Colombo, Maria Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina |
description |
Hijacking the autophagic machinery is a key mechanism through which invasive pathogens such as Staphylococcus aureus replicate in their host cells. We have previously demonstrated that the bacteria replicate in phagosomes labeled with the autophagic protein LC3, before escaping to the cytoplasm. Here, we show that the Ca2+-dependent PKCα binds to S. aureus-containing phagosomes and that α-hemolysin, secreted by S. aureus, promotes this recruitment of PKCα to phagosomal membranes. Interestingly, the presence of PKCα prevents the association of the autophagic protein LC3. Live cell imaging experiments using the PKC activity reporter CKAR reveal that treatment of cells with S. aureus culture supernatants containing staphylococcal secreted factors transiently activates PKC. Functional studies reveal that overexpression of PKCα causes a marked inhibition of bacterial replication. Taken together, our data identify enhancing PKCα activity as a potential approach to inhibit S. aureus replication in mammalian cells. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-03 |
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/11336/174636 Gaurón, María Celeste; Newton, Alexandra C.; Colombo, Maria Isabel; PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy; Frontiers Media; Frontiers in Immunology; 12; 3-2021; 1-13 1664-3224 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/174636 |
identifier_str_mv |
Gaurón, María Celeste; Newton, Alexandra C.; Colombo, Maria Isabel; PKCα is recruited to staphylococcus aureus-containing phagosomes and impairs bacterial replication by inhibition of autophagy; Frontiers Media; Frontiers in Immunology; 12; 3-2021; 1-13 1664-3224 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fimmu.2021.662987/full info:eu-repo/semantics/altIdentifier/doi/10.3389/fimmu.2021.662987 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Frontiers Media |
publisher.none.fl_str_mv |
Frontiers Media |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
reponame_str |
CONICET Digital (CONICET) |
collection |
CONICET Digital (CONICET) |
instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.name.fl_str_mv |
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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1844614473563766784 |
score |
13.070432 |