| Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2019: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
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| Outline of Final Research Achievements |
Carnitine palmitoyltransferase 1 (CPT1) is indispensable to transport long-chain fatty acids into the mitochondria. CPT1 deficiency causes fatal metabolic disorders in humans and embryonic lethality in mice. We report that Drosophila melanogaster efficiently catabolize fatty acids in the absence of CPT1. Defective expression of CPT1 had no significant effect on the metabolic rates, body weight, or ATP concentration in Drosophila. Genetic screening using CPT1-suppressed flies revealed that the solute carrier 25a50 (SLC25a50), a Drosophila ortholog of mitochondrial carrier homolog (MTCH), acted as a surrogate for CPT1-mediated fatty acid transport. Our genetic and biochemical analyses demonstrate that SLC25a50 resides in the mitochondrial inner membrane and mediates the transport of fatty acids, notably including medium-chain fatty acid, in a mitochondrial proton gradient-dependent manner.
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