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A more recent version of this article appeared on March 1, 2004
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Submitted on February 26, 2003
Revised on November 13, 2003
Accepted on November 13, 2003
1 Department of Cell and Molecular Biology/Microbiology, Göteborg University, Box 465, SE-40530 Göteborg, Sweden
2 Institute of Physiological Chemistry, University of Tübingen, Hoppe-Seyler Strasse 4, 720 76 Tübingen Germany
* Corresponding author. E-mail address: Lennart.Adler{at}gmm.gu.se.
Yeast cells deleted for the SRO7/SOP1 encoded tumor suppressor homologue show increased sensitivity to NaCl stress. On exposure to growth-inhibiting NaCl concentrations sro7
mutants display a rapid loss in viability that is associated with markers of apoptosis: accumulation of reactive oxygen species, DNA breakage and nuclear fragmentation. Additional deletion of the yeast metacaspase gene YCA1 prevents the primary fast drop in viability and diminishes nuclear fragmentation and DNA breakage. We also observed that NaCl induced loss in viability of wild-type cells is Yca1p dependent. However, a yeast strain deleted for both SRO7 and its homologue SRO77 exhibits NaCl induced cell death that is independent on YCA1. Likewise, sro77 single mutants do not survive better after additional deletion of the YCA1 gene, and both sro77 and sro77yca1 mutants display apoptotic characteristics when exposed to growth inhibiting salinity, suggesting that yeast possesses Yca1p independent pathway(s) for apoptosis-like cell death. The activity of Yca1p increases with increasing NaCl stress and sro7 mutants achieve levels that are higher than in wild-type cells. However, mutants lacking SRO77 do not enhance caspase activity when subject to NaCl stress, suggesting that Sro7p and Sro77p exert opposing effects on the cellular activity of Yca1p.
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