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细胞色素b-细胞色素c氧化酶1基因盒中的两个I组线粒体内含子和细胞色素c氧化酶亚基I基因在剪接时需要相同的MRS1/PET157核基因产物。

Two group I mitochondrial introns in the cob-box and coxI genes require the same MRS1/PET157 nuclear gene product for splicing.

作者信息

Bousquet I, Dujardin G, Poyton R O, Slonimski P P

机构信息

Centre de Génétique Moléculaire, Laboratoire propre du CNRS associé à l'Université Pierre et Marie Curie, Gif-sur-Yvette, France.

出版信息

Curr Genet. 1990 Aug;18(2):117-24. doi: 10.1007/BF00312599.

Abstract

We have studied the role of the product of the nuclear gene PET157 in mitochondrial pre-mRNA splicing. Cytoduction experiments show that a mitochondrial genome deleted for the three introns bI3, aI5 and aI6 is able to suppress the pet157-1 mutation: the strain recovers respiratory competency indicating that the product of the PET157 gene is only required for mitochondrial pre-mRNA splicing. Characterization of the high molecular weight pre-mRNAs which accumulate in the pet157 mutant demonstrate that the product of the PET157 gene is required for the excision of two group I introns bI3 and aI6 (corresponding to aI5 beta) located in the cob-box and coxI genes respectively. Furthermore, the pet157 mutant strain accumulates the bI3 maturase in the form of a polypeptide of 50K (p50) previously observed in mitochondrial mutants defective in the excision of bI3. We have shown by restriction analysis and allelism tests that the pet157-1 mutation is allelic to the nuclear mrs1 mutation, previously described as specifically blocking the excision of bI3. Finally, revertants obtained by the deletion of bI3 or aI6 from the mitochondrial DNA were isolated from the MRS1 disrupted allele, confirming the involvement of the product of the MRS1/PET157 gene in the excision of the two introns bI3 and aI6.

摘要

我们研究了核基因PET157的产物在线粒体前体mRNA剪接中的作用。细胞融合实验表明,缺失三个内含子bI3、aI5和aI6的线粒体基因组能够抑制pet157-1突变:该菌株恢复了呼吸能力,这表明PET157基因的产物仅在线粒体前体mRNA剪接中发挥作用。对在pet157突变体中积累的高分子量前体mRNA的表征表明,PET157基因的产物对于分别位于cob-box和coxI基因中的两个I类内含子bI3和aI6(对应于aI5β)的切除是必需的。此外,pet157突变体菌株以50K多肽(p50)的形式积累bI3成熟酶,这种形式曾在线粒体bI3切除缺陷的突变体中观察到。我们通过限制性分析和等位性测试表明,pet157-1突变与核基因mrs1突变等位,mrs1突变先前被描述为特异性阻断bI3的切除。最后,从MRS1破坏等位基因中分离出通过从线粒体DNA中缺失bI3或aI6获得的回复突变体,证实了MRS1/PET157基因的产物参与了两个内含子bI3和aI6的切除。

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