Mouse CLK-1 is imported into mitochondria by an unusual process that requires a leader sequence but no membrane potential

被引:32
作者
Jiang, N
Levavasseur, F
McCright, B
Shoubridge, EA
Hekimi, S
机构
[1] McGill Univ, Dept Biol, Montreal, PQ H3A 1B1, Canada
[2] Montreal Neurol Inst, Montreal, PQ H3A 2B4, Canada
[3] McGill Univ, Dept Human Genet, Montreal, PQ H3A 2B4, Canada
关键词
D O I
10.1074/jbc.M103686200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
clk-1 has been identified and characterized in the nematode Caenorhabditis elegans as a gene that affects the rates, regularity, and synchrony of physiological processes. The CLK-1 protein is mitochondrial and is required for ubiquinone biosynthesis in yeast and in worms, but its biochemical function remains unclear. We have studied the expression of murine mclk1 in a variety of tissues, and we find that the pattern of mclk1 m-RNA accumulation closely resembles that of mitochondrial genes involved in oxidative phosphorylation. The pattern of protein accumulation, however, is sharply distinct in some tissues; mCLK1 appears relatively enriched in the gut and depleted in the nervous tissue. We also show that mCLK1 is synthesized as a preprotein that is imported into the mitochondrial matrix, where a leader sequence is cleaved off and the protein becomes loosely associated with the inner membrane. However, in contrast to all known mitochondrial proteins that contain a cleavable pre-sequence, the import of mCLK1 does not require a mitochondrial membrane potential.
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页码:29218 / 29225
页数:8
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