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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/153495
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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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13.070432 |