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Investigating the Role of Calcium in BAX‐induced Cell Death in the Yeast, Saccharomyces cerevisiae
Author(s) -
Murphy Kevin,
Sullivan John,
Selinski Christian,
Swan Brendan,
Austriaco Nicanor
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.943.18
Subject(s) - aequorin , saccharomyces cerevisiae , programmed cell death , calcium , yeast , microbiology and biotechnology , apoptosis , mutant , biology , cell , mitochondrion , chemistry , biochemistry , gene , intracellular , organic chemistry
BAX is a proapoptotic member of the Bcl‐2 family of proteins. Upon activation, Bax binds to the outer mitochondrial membrane, which ultimately induces programmed cell death in mammalian cells. Naturally, the budding yeast, Saccharomyces cerevisiae, does not contain BAX. However, when mammalian BAX is over‐expressed in yeast, it induces programmed cell death. We are investigating the role of calcium in BAX‐induced cell death by overexpressing human BAX in a series of yeast mutants defective for calcium regulation. We have discovered that several of these mutants including strains lacking CCH1, CRZ1, PMC1, PMR1, and VCX1, are relatively sensitive to BAX‐induced toxicity. Using a calcium‐sensitive aequorin reporter, we are quantifying the calcium flux in cells overexpressing BAX to determine the relationship between calcium levels and programmed cell death. [Our laboratory is supported by the following grants: NIGMS R15 GM094712, NSF MRI‐R2 0959354, and NIH Grant 2 P20 RR016457 to the Rhode Island INBRE Program]