The antiapoptotic protein Bcl-x(L) prevents the cytotoxic effect of Bax, but not Bax-induced formation of reactive oxygen species, in Kluyveromyces lactis

The murine proapoptotic protein Bax was expressed in Kluyveromyces lactis to investigate its effect on cell survival and production of reactive oxygen species (ROS). Bax expression decreased the number of cells capable of growing and forming colonies, and it increased the number of cells producing R...

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Bibliographic Details
Published in:Microbiology (Society for General Microbiology) 2002-09, Vol.148 (Pt 9), p.2789-2795
Main Authors: Poliaková, Daniela, Sokolı Ková, Barbora, Kolarov, Jordan, Šabova, L'udmila
Format: Article
Language:English
Subjects:
Antioxidants - pharmacology
Apoptosis
bcl-2-Associated X Protein
bcl-X Protein
Blotting, Western
Kluyveromyces - cytology
Kluyveromyces - drug effects
Kluyveromyces - metabolism
Microscopy, Fluorescence
Mitochondria - metabolism
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - pharmacology
Proto-Oncogene Proteins c-bcl-2 - genetics
Proto-Oncogene Proteins c-bcl-2 - pharmacology
Reactive Oxygen Species - metabolism
Transfection
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Summary:The murine proapoptotic protein Bax was expressed in Kluyveromyces lactis to investigate its effect on cell survival and production of reactive oxygen species (ROS). Bax expression decreased the number of cells capable of growing and forming colonies, and it increased the number of cells producing ROS, as detected by both dihydrorhodamine 123 fluorescence and the intracellular content of SH groups. Mutation in the beta-subunit of F(1)-ATPase, or mitochondrial deficiency resulting from deletion of mtDNA (rho(0) mutant), increased the sensitivity to Bax, indicating that Bax cytotoxicity does not require mitochondrial respiratory-chain functions. The antiapoptotic protein Bcl-x(L), when co-expressed with Bax, localized to the mitochondria and prevented Bax cytotoxicity. However, this co-expression did not prevent the production of ROS. These data suggest that in K. lactis cells expressing Bax, ROS are not the sine qua non of cell death and that the antiapoptotic function of Bcl-x(L) is not limited to its antioxidant property.
ISSN:1350-0872
DOI:10.1099/00221287-148-9-2789