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MBC in Press, published online ahead of print July 5, 2007
Mol. Biol. Cell 10.1091/mbc.E07-02-0118

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Submitted on February 12, 2007
Revised on June 22, 2007
Accepted on June 25, 2007

Yeast Cells Lacking the CIT1-encoded Mitochondrial Citrate Synthase Are Hypersusceptible to Heat- or Aging-induced Apoptosis

Yong Joo Lee,* Kwang Lae Hoe,{dagger} and Pil Jae Maeng*

*Department of Microbiology, School of Bioscience and Biotechnology, Chungnam National University, 305-764 Daejeon Korea; and {dagger}Functional Genomics Research Center, Korea Research Institute of Bioscience and Biotechnology, 305-806 Daejeon, Korea

Monitoring Editor: Peter Walter

In S. cerevisiae, the initial reaction of the tricarboxylic acid cycle is catalyzed by the mitochondrial citrate synthase Cit1. The function of Cit1 has previously been studied mainly in terms of acetate utilization and metabolon construction. Here, we report the relationship between the function of Cit1 and apoptosis. Yeast cells with cit1 deletion showed a temperature-sensitive growth phenotype, and displayed a rapid loss in viability associated with typical apoptotic hallmarks, i.e., ROS accumulation, nuclear fragmentation, DNA breakage, and phosphatidylserine translocation, when exposed to heat stress. On long-term cultivation, cit1 null strains showed increased potentials for both aging-induced apoptosis and adaptive regrowth. Activation of the metacaspase Yca1 was detected during heat- or aging-induced apoptosis in cit1 null strains, and accordingly, deletion of YCA1 suppressed the apoptotic phenotype caused by cit1 null mutation. Cells with cit1 deletion showed higher tendency toward glutathione (GSH) depletion and subsequent ROS accumulation than the wild-type, which was rescued by exogenous GSH, glutamate, or glutathione disulfide (GSSG). These results led us to conclude that GSH deficiency in cit1 null cells is caused by an insufficient supply of glutamate necessary for biosynthesis of GSH rather than the depletion of reducing power required for reduction of GSSG to GSH.

Address correspondence to: Pil Jae Maeng (pjmaeng{at}cnu.ac.kr)






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