Premium
Thioredoxin‐2 ( TRX‐2 ) is an essential gene regulating mitochondria‐dependent apoptosis
Author(s) -
Tanaka Toru,
Hosoi Fumihito,
YamaguchiIwai Yuko,
Nakamura Hajime,
Masutani Hiroshi,
Ueda Shugo,
Nishiyama Akira,
Takeda Shunichi,
Wada Hiromi,
Spyrou Giannis,
Yodoi Junji
Publication year - 2002
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/21.7.1695
Subject(s) - biology , thioredoxin , mitochondrion , cytochrome c , microbiology and biotechnology , apoptosome , apoptosis , transgene , reactive oxygen species , signal transduction , intracellular , thioredoxin reductase , caspase , programmed cell death , gene , biochemistry
Thioredoxin‐2 (Trx‐2) is a mitochondria‐specific member of the thioredoxin superfamily. Mitochondria have a crucial role in the signal transduction for apoptosis. To investigate the biological significance of Trx‐2, we cloned chicken TRX‐2 cDNA and generated clones of the conditional Trx‐2‐deficient cells using chicken B‐cell line, DT40. Here we show that TRX‐2 is an essential gene and that Trx‐2‐deficient cells undergo apoptosis upon repression of the TRX‐2 transgene, showing an accumulation of intracellular reactive oxygen species (ROS). Cytochrome c is released from mitochondria, while caspase‐9 and caspase‐3, but not caspase‐8, are activated upon inhibition of the TRX‐2 transgene. In addition, Trx‐2 and cytochrome c are co‐immunoprecipitated in an in vitro assay. These results suggest that mitochondrial Trx‐2 is essential for cell viability, playing a crucial role in the scavenging ROS in mitochondria and regulating the mitochondrial apoptosis signaling pathway.