Rödel G, Körte A, Kaudewitz F
Institut für Genetik und Mikrobiologie, Ludwig-Maximilians-Universität, München, Federal Republic of Germany.
Curr Genet. 1985;9(8):641-8. doi: 10.1007/BF00449816.
We describe a mitochondrial suppressor mutation, which restores respiratory competence to the nuclear pet- -mutant MK2. This mutant lacks the message of the mitochondrial cob-gene and instead accumulates a partially spliced pre-mRNA which is not translated. Complete processing and translation of the cob-RNA is restored by a rearrangement of the mitochondrial DNA, leading to a fusion of the cob-coding sequences with the leader of oli1, the mitochondrial gene coding for subunit IX of the ATPase. We conclude that the nuclear gene affected in MK2 is essential to allow translation of transcripts which contain the cob-leader sequence.
我们描述了一种线粒体抑制突变,它恢复了核pet-突变体MK2的呼吸能力。该突变体缺乏线粒体cob基因的信息,而是积累了一种未翻译的部分剪接前体mRNA。线粒体DNA的重排恢复了cob-RNA的完全加工和翻译,导致cob编码序列与oli1的前导序列融合,oli1是编码ATPase亚基IX的线粒体基因。我们得出结论,MK2中受影响的核基因对于允许包含cob前导序列的转录本的翻译至关重要。