期刊
MOLECULAR AND BIOCHEMICAL PARASITOLOGY
卷 159, 期 1, 页码 30-43出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.molbiopara.2008.01.003
关键词
trypanosoma brucei; Tim17; membrane potential; mitochondrial protein import; the bloodstream and procyclic forms
资金
- NCI NIH HHS [U54 CA091408, U54CA91408] Funding Source: Medline
- NCRR NIH HHS [U54 RR019192, U54RR019192-04, G12 RR003032, RR03032-19] Funding Source: Medline
- NHLBI NIH HHS [K01 HL003839-04, K01 HL003839-05, K01 HL003839-03, K01 HL003839-02] Funding Source: Medline
- NIGMS NIH HHS [3S06GM08037-30S1, S06 GM008037-320066, SC1 GM081146, S06 GM008037-300066, S06 GM008037-30S10066, S06 GM008037-30S20066, S06 GM008037-290066, SC1 GM081146-01, S06 GM008037-280066, S06 GM008037-310066, S06 GM008037, S06 GM008037-31S10066, S06 GM008037-30S30066] Funding Source: Medline
- NINDS NIH HHS [U54NS041071-06, U54 NS041071] Funding Source: Medline
Mitochondrial protein translocation machinery in the kinetoplastid parasites, like Trypanosoma brucei, has been characterized poorly. In T brucei genome database, one homolog for a protein translocator of mitochondrial inner membrane (Tim) has been found, which is closely related to Tim17 from other species. The T brucei Tim17 (TbTim17) has a molecular mass 16.2kDa and it possesses four characteristic transmembrane domains. The protein is localized in the mitochondrial inner membrane. The level of TbTim 17 protein is 6-7-fold higher in the procyclic form that has a fully active mitochondrion, than in the mammalian bloodstream form of T brucei, where many of the mitochondrial activities are suppressed. Knockdown of TbTim17 expression by RNAi caused a cessation of cell growth in the procyclic form and reduced growth rate in the bloodstream form. Depletion of TbTim17 decreased mitochondrial membrane potential more in the procyclic than bloodstream form. However, TbTim17 knockdown reduced the expression level of several nuclear encoded mitochondrial proteins in both the forms. Furthermore, import of presequence containing nuclear encoded mitochondrial proteins was significantly reduced in TbTim17 depleted mitochondria of the procyclic as well as the bloodstream form, confirming that TbTim17 is critical for mitochondrial protein import in both developmental forms. Together, these show that TbTim17 is the translocator of nuclear encoded mitochondrial proteins and its expression is regulated according to mitochondrial activities in T brucei. (C) 2008 Elsevier B.V. All rights reserved.
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