Cytochrome c Oxidase Subunit III

You, Kyung-Ran; Wen, Jing; Lee, Soo-Taek; Kim, Dae‐Ghon

doi:10.1074/jbc.m109284200

Cited by 45 publications

(15 citation statements)

References 45 publications

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“…Inhibition of mitochondrial cytochrome c oxidase is known to trigger apoptosis in mammalian cells (38,39). In addition, apoptosis has been shown to be associated with reduction of MTCO3 (40). Similarly, Bax-induced apoptosis in yeast has been shown to result in reduction of cytochrome c oxidase (8,41).…”

Section: Inactivation Of Cdc13p Triggers Apoptotic Signals Inmentioning

confidence: 99%

Inactivation of Cdc13p TriggersMEC1-dependent Apoptotic Signals in Yeast

Qi¹,

Li²,

Kuo³

et al. 2003

Journal of Biological Chemistry

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Inactivation of the budding yeast telomere binding protein Cdc13 results in abnormal telomeres (exposed long G-strands) and activation of the DNA damage checkpoint. In the current study, we show that inactivation of Cdc13p induces apoptotic signals in yeast, as evidenced by caspase activation, increased reactive oxygen species production, and flipping of phosphatidylserine in the cytoplasmic membrane. These apoptotic signals were suppressed in a mitochondrial ( o ) mutant. Moreover, mitochondrial proteins (e.g. MTCO3) were identified as multicopy suppressors of cdc13-1, suggesting the involvement of mitochondrial functions in telomere-initiated apoptotic signaling. These telomereinitiated apoptotic signals were also shown to depend on MEC1, but not TEL1, and were antagonized by MRE11. Our results are consistent with a model in which single-stranded G-tails in the cdc13-1 mutant trigger MEC1-dependent apoptotic signaling in yeast.Cdc13p is a budding yeast telomere binding protein (1-3). Cdc13p appears to be a multifunctional protein involved in both telomere replication and protection (1-4). Its role in telomere replication has been suggested based on the findings that it interacts with the catalytic subunit of DNA polymerase ␣ and an essential subunit of telomerase, Est1p (4), and a mutation form of CDC13, cdc13-2, shows the telomerase negative phenotype (3). Its essential role in protecting yeast telomeres is presumably related to its binding to the exposed G-strand (1-3, 5). Cdc13-1p (P371S), a temperature-sensitive mutant form of Cdc13p, is unable to protect telomeres at the restrictive temperature (1). At the non-permissive temperature, cells with the cdc13-1 allele exhibit extensive degradation of telomeres from the 5Ј-ends, the C-rich strands (C-strands). The C-strand degradation results in long single-stranded Gtails (up to 20 kb) at the 3Ј-ends. The abnormal telomeres in cdc13-1 at the non-permissive temperature lead to RAD9-dependent cell cycle arrest at the G 2 /M phase, as well as cell death (1, 6). However, the mechanism of cell death triggered by Cdc13p inactivation is unclear. It was assumed that essential gene deletion because of the C-strand degradation is the cause of the cell death.Yeast apoptosis is not well understood. Bax, Bcl-2, and other established apoptotic proteins have not been found in yeast cells. However, expression of human BAX in yeast induces cell death (7,8), accompanied by mitochondrial alkalinization and cytosol acidification (9). This process can be blocked by coexpression of human anti-apoptosis protein Bcl-2 (8). Additionally, aged mother cells and H 2 O 2 -treated cells have shown apoptosis markers in yeast, including flipping of phosphatidylserine (PS) 1 from the inner leaflet to the outer leaflet of the cytoplasmic membrane, DNA damage (by TUNEL assay), and reactive oxygen species (ROS) induction (10, 11). More recently, a caspase-like protease Yca1p has been identified in yeast and was found to regulate yeast cell death induced by H 2 O 2 treatment (12). Moreover, a bro...

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Section: Inactivation Of Cdc13p Triggers Apoptotic Signals Inmentioning

confidence: 99%

Inactivation of Cdc13p TriggersMEC1-dependent Apoptotic Signals in Yeast

Qi¹,

Li²,

Kuo³

et al. 2003

Journal of Biological Chemistry

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“…Accordingly, CD437 permeabilizes proteoliposomes containing the purified PTPC or ANT (Belzacq et al, 2001), suggesting that (one of) its molecular target(s) is indeed ANT. Some investigators reported that 4-HPR-induced apoptosis (as tested on whole cells) would be inhibited by cyclosporin A and bongkrekic acid (Hail and Lotan, 2000), but others found that 4-HPR causes the downregulation of cyclophilin D (Hursting et al, 2002), the cyclosporin A target in mitochondria, and yet other groups reported that bongkrekic acid (You et al, 2002) and cyclosporin A actually enhanced 4-HPR-induced apoptosis (Lim et al, 2002).…”

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confidence: 99%

The chemopreventive agent N-(4-hydroxyphenyl)retinamide induces apoptosis through a mitochondrial pathway regulated by proteins from the Bcl-2 family

et al. 2003

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“…However, the underlying mechanism(s) by which 4HPR induces apoptosis remains unclear. Quite recently, we observed that 4HPR effectively induces apoptosis in Fas-defective hepatoma cells through caspase-8 activation (29), and 4HPR-induced apoptosis was effectively modulated by alteration of mitochondrial membrane potential (30). Thus, to elucidate the molecular and cellular mechanism(s) by which 4HPR induces apoptosis, we undertook to identify the gene(s) involved in this drug-induced apoptosis.…”

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confidence: 99%