Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae

Autores
Lauff, Diana Beatriz; Santa Maria, Guillermo Esteban
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Cell culture in low potassium (K+) media has been associated to programmed cell death (PCD) in metazoans. In this study, deprivation of K + led Saccharomyces cerevisiae cells to a death process that involved phosphatidylserine externalization, changes in chromatin condensation, DNA and vacuole fragmentation as well as enhanced accumulation of reactive oxygen species. During the course of K+ starvation, plasma membrane hyperpolarization and increased accumulation of calcium (Ca2+) took place. The presence of rubidium (Rb+), a K+-analogue element, in the K+-deprived medium was accompanied by Rb+ accumulation but did not fully prevent the appearance of PCD markers. This argues for a specific effect of K+ on the course of cell death. While the absence of the YCA1 metacaspase did not have a major effect, the absence of TRK (transport of K+) K+-transporters led to changes in the pattern of annexin V/propidium iodide labeling. This change paralleled a fast accumulation of Ca2+. Addition of ethylene glycol tetraacetic acid improved growth and reduced cell death in trk1Δtrk2Δ cells. These findings reveal that K+ deprivation is sufficient to induce PCD in a cell-walled eukaryotic organism and suggest that the phenotype attributed to the lack of TRK genes is partially due to the effect of the encoded transporters on Ca2+ homeostasis.
Fil: Lauff, Diana Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; Argentina
Fil: Santa Maria, Guillermo Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; Argentina
Materia
APOPTOSIS
POTASSIUM TRANSPORT
PROGRAMMED CELL DEATH
SACCHAROMYCES CEREVISIAE
TRK
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/153495

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spelling Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiaeLauff, Diana BeatrizSanta Maria, Guillermo EstebanAPOPTOSISPOTASSIUM TRANSPORTPROGRAMMED CELL DEATHSACCHAROMYCES CEREVISIAETRKhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Cell culture in low potassium (K+) media has been associated to programmed cell death (PCD) in metazoans. In this study, deprivation of K + led Saccharomyces cerevisiae cells to a death process that involved phosphatidylserine externalization, changes in chromatin condensation, DNA and vacuole fragmentation as well as enhanced accumulation of reactive oxygen species. During the course of K+ starvation, plasma membrane hyperpolarization and increased accumulation of calcium (Ca2+) took place. The presence of rubidium (Rb+), a K+-analogue element, in the K+-deprived medium was accompanied by Rb+ accumulation but did not fully prevent the appearance of PCD markers. This argues for a specific effect of K+ on the course of cell death. While the absence of the YCA1 metacaspase did not have a major effect, the absence of TRK (transport of K+) K+-transporters led to changes in the pattern of annexin V/propidium iodide labeling. This change paralleled a fast accumulation of Ca2+. Addition of ethylene glycol tetraacetic acid improved growth and reduced cell death in trk1Δtrk2Δ cells. These findings reveal that K+ deprivation is sufficient to induce PCD in a cell-walled eukaryotic organism and suggest that the phenotype attributed to the lack of TRK genes is partially due to the effect of the encoded transporters on Ca2+ homeostasis.Fil: Lauff, Diana Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Santa Maria, Guillermo Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; ArgentinaWiley Blackwell Publishing, Inc2010-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/153495Lauff, Diana Beatriz; Santa Maria, Guillermo Esteban; Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae; Wiley Blackwell Publishing, Inc; Fems Yeast Research; 10; 5; 8-2010; 497-5071567-1356CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/femsyr/article/10/5/497/601735info:eu-repo/semantics/altIdentifier/doi/10.1111/j.1567-1364.2010.00628.xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:02:59Zoai:ri.conicet.gov.ar:11336/153495instacron: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 10:03:00.187CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
title Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
spellingShingle Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
Lauff, Diana Beatriz
APOPTOSIS
POTASSIUM TRANSPORT
PROGRAMMED CELL DEATH
SACCHAROMYCES CEREVISIAE
TRK
title_short Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
title_full Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
title_fullStr Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
title_full_unstemmed Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
title_sort Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
dc.creator.none.fl_str_mv Lauff, Diana Beatriz
Santa Maria, Guillermo Esteban
author Lauff, Diana Beatriz
author_facet Lauff, Diana Beatriz
Santa Maria, Guillermo Esteban
author_role author
author2 Santa Maria, Guillermo Esteban
author2_role author
dc.subject.none.fl_str_mv APOPTOSIS
POTASSIUM TRANSPORT
PROGRAMMED CELL DEATH
SACCHAROMYCES CEREVISIAE
TRK
topic APOPTOSIS
POTASSIUM TRANSPORT
PROGRAMMED CELL DEATH
SACCHAROMYCES CEREVISIAE
TRK
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Cell culture in low potassium (K+) media has been associated to programmed cell death (PCD) in metazoans. In this study, deprivation of K + led Saccharomyces cerevisiae cells to a death process that involved phosphatidylserine externalization, changes in chromatin condensation, DNA and vacuole fragmentation as well as enhanced accumulation of reactive oxygen species. During the course of K+ starvation, plasma membrane hyperpolarization and increased accumulation of calcium (Ca2+) took place. The presence of rubidium (Rb+), a K+-analogue element, in the K+-deprived medium was accompanied by Rb+ accumulation but did not fully prevent the appearance of PCD markers. This argues for a specific effect of K+ on the course of cell death. While the absence of the YCA1 metacaspase did not have a major effect, the absence of TRK (transport of K+) K+-transporters led to changes in the pattern of annexin V/propidium iodide labeling. This change paralleled a fast accumulation of Ca2+. Addition of ethylene glycol tetraacetic acid improved growth and reduced cell death in trk1Δtrk2Δ cells. These findings reveal that K+ deprivation is sufficient to induce PCD in a cell-walled eukaryotic organism and suggest that the phenotype attributed to the lack of TRK genes is partially due to the effect of the encoded transporters on Ca2+ homeostasis.
Fil: Lauff, Diana Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; Argentina
Fil: Santa Maria, Guillermo Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; Argentina
description Cell culture in low potassium (K+) media has been associated to programmed cell death (PCD) in metazoans. In this study, deprivation of K + led Saccharomyces cerevisiae cells to a death process that involved phosphatidylserine externalization, changes in chromatin condensation, DNA and vacuole fragmentation as well as enhanced accumulation of reactive oxygen species. During the course of K+ starvation, plasma membrane hyperpolarization and increased accumulation of calcium (Ca2+) took place. The presence of rubidium (Rb+), a K+-analogue element, in the K+-deprived medium was accompanied by Rb+ accumulation but did not fully prevent the appearance of PCD markers. This argues for a specific effect of K+ on the course of cell death. While the absence of the YCA1 metacaspase did not have a major effect, the absence of TRK (transport of K+) K+-transporters led to changes in the pattern of annexin V/propidium iodide labeling. This change paralleled a fast accumulation of Ca2+. Addition of ethylene glycol tetraacetic acid improved growth and reduced cell death in trk1Δtrk2Δ cells. These findings reveal that K+ deprivation is sufficient to induce PCD in a cell-walled eukaryotic organism and suggest that the phenotype attributed to the lack of TRK genes is partially due to the effect of the encoded transporters on Ca2+ homeostasis.
publishDate 2010
dc.date.none.fl_str_mv 2010-08
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/11336/153495
Lauff, Diana Beatriz; Santa Maria, Guillermo Esteban; Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae; Wiley Blackwell Publishing, Inc; Fems Yeast Research; 10; 5; 8-2010; 497-507
1567-1356
CONICET Digital
CONICET
url http://hdl.handle.net/11336/153495
identifier_str_mv Lauff, Diana Beatriz; Santa Maria, Guillermo Esteban; Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae; Wiley Blackwell Publishing, Inc; Fems Yeast Research; 10; 5; 8-2010; 497-507
1567-1356
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://academic.oup.com/femsyr/article/10/5/497/601735
info:eu-repo/semantics/altIdentifier/doi/10.1111/j.1567-1364.2010.00628.x
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
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
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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