| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2001: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Research Abstract |
Mitochondria play pivotal roles in iron metabolism in cells as the biosynthesis of heme and iron-sulfur cluster, the prosthetic groups of iron proteins, take place. In Sacckromyces cerevisiae, we found the activity of Aftl transcriptional activator, the major regulator of cellular iron metabolism, was affected by the aberration of mitochondrial iron metabolism. Based on this finding, we analyzed the mechanisms for regulating the activity of Aftl and its connection to the iron metabolism in mitochondria. Moreover, we cloned a battery of genes in chicken cells which are homologous to the ones expected to be involved in mitochondrial iron metabolism and established the cell line which is deficient in the relevant gene in chicken B cell line, DT40 to see how the deficiency of the relevant gene affects iron metabolism in mitochondria. We found that the NifS gene that is important for the formation of iron-sulfur cluster is essential for cell viability. In addition, we also established the mitochondrial thioredoxio, Trx-2 deficient cell line and found that loss of Trx-2 leads to apoptosis of cells partly due to the accumulation of reactive oxygen species (ROS) generated in Trx-2 deficient mitochondria
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