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Prion protein prevents Bax‐mediated cell death in the absence of other Bcl‐2 family members in Saccharomyces cerevisiae
Author(s) -
Bounhar Younes,
Mann Koren K.,
Roucou Xavier,
LeBlanc Andréa C.
Publication year - 2006
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2006.00122.x
Subject(s) - saccharomyces cerevisiae , biology , programmed cell death , microbiology and biotechnology , apoptosis , yeast , population , cell , function (biology) , genetics , demography , sociology
Although there is no consensus regarding the normal function of the prion protein, increasing evidence points towards a role in cellular protection against cell death. We have previously shown that prion protein is a potent inhibitor of Bax‐induced apoptosis in human primary neurons and in the breast carcinoma MCF‐7 cells. Here, we used the yeast Saccharomyces cerevisiae to investigate if the neuroprotective function of prion protein requires other members of the Bcl‐2 family given that S. cerevisiae lacks Bcl‐2 genes but undergoes a mitochondrial‐dependent apoptotic cell death upon exogenous expression of Bax protein. We show that Bax induces cell death and growth inhibition in S. cerevisiae . Prion protein prevents Bax‐mediated cell death. Prion protein overcomes Bax‐mediated growth arrest in S phase but cannot overcome population growth inhibition because the cells then accumulate in G 2 /M phase. We conclude that prion protein does not require other Bcl‐2 family proteins to protect against Bax‐mediated cell death.

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