Premium
Biogenesis of mitochondrial metabolite carrier proteins in Trypanosoma brucei (574.1)
Author(s) -
Smith Joseph,
Chaudhuri Minu
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.574.1
Subject(s) - trypanosoma brucei , biogenesis , biology , mitochondrion , protein targeting , microbiology and biotechnology , mitochondrial carrier , inner mitochondrial membrane , translocase , metabolite , organelle , biochemistry , inner membrane , membrane protein , gene , bacterial outer membrane , chromosomal translocation , escherichia coli , membrane
Trypanosoma brucei, a parasitic protozoan and the causative agent of human African trypanosomiasis, possesses a single mitochondrion in which many essential metabolic processes occur. These biological processes require various metabolites to be fluxed in and out of the mitochondrial matrix by specialized transporters called metabolite carrier proteins (MCPs). Metabolite carriers are encoded in the nuclear genome and post‐translationally imported into mitochondria. In yeast and humans, there is a dedicated inner membrane protein translocase, TIM22, and soluble small Tim proteins of the intermembrane space, which are involved in MCP biogenesis. Trypanosoma brucei possesses a large family of MCPs; however, the parasite appears to lack the TIM22 translocase in its entirety. A few putative homologs of soluble Tims have been identified in this parasite, although functions of these proteins are not elucidated. Here, we begin to characterize the T. brucei homologs of the small Tim proteins (TbTim9, TbTim10, and TbTim13/8 that shows similarity to both Tim8 and Tim13 in higher eukaryotes) and their possible involvement in metabolite carrier import. We found that TbTim9, TbTim10, and TbTim13/8 are expressed and localized in mitochondria in T. brucei . Knockdown of TbTim9 and TbTim10 individually decreased cell growth, while knockdown of TbTim13/8 ceased cell growth within 5 days. Reducing the expression of these proteins also reduced the steady‐state levels of the metabolite carrier protein, TbMCP5, suggesting that these TbTims are likely involved in MCP biogenesis. Further experiments are now ongoing to understand the roles of TbTims in the import of TbMCP5 into the mitochondrial inner membrane and also to identify the inner membrane translocase involved in this process. Grant Funding Source : Supported by 2SC1GM081146 and 2R25GM059994