nMAT1, a nuclear-encoded maturase involved in the trans-splicing of nad1 intron 1, is essential for mitochondrial complex I assembly and function
nMAT1, a nuclear-encoded maturase involved in the trans-splicing of nad1 intron 1, is essential for mitochondrial complex I assembly and function
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DOI：
10.1111/j.1365-313x.2012.04998.x
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发表时间：
2012-08-01
期刊：
影响因子：
7.2
通讯作者：
Ostersetzer-Biran, Oren
中科院分区：
文献类型：
--
作者：
Keren, Ido;Tal, Liat;Ostersetzer-Biran, Oren
被子植物线粒体基因组（mtDNA）中含有大量的II类内含子，主要存在于细胞器基因组表达和呼吸所需的蛋白质编码基因中。虽然在非植物系统中II组内含子的剪接是由内含子本身内编码的蛋白质（成熟酶）促进的，但植物中的线粒体内含子已经分化并丢失了绝大多数内含子编码的ORF。植物mtDNA中只保留了一个成熟酶基因（matR），但其在线粒体内含子剪接中的作用目前尚不清楚。除了matR之外，植物还具有四个核成熟酶基因（nMat 1至4），其编码线粒体蛋白，预期这些线粒体蛋白在II组内含子的剪接中起作用。最近，我们建立了这些蛋白质之一，nMAT 2，在拟南芥中的几个线粒体内含子的剪接的作用。在这里，我们表明，nMAT1是必需的nad1内含子1的反式剪接，也在顺式剪接的nad2内含子1和nad4内含子2的功能。纯合nMat1植物表现出生长发育迟缓的表型，改变呼吸活性和改变应激反应，与线粒体复合物I缺陷密切相关。
Mitochondrial genomes (mtDNAs) in angiosperms contain numerous group II-type introns that reside mainly within protein-coding genes that are required for organellar genome expression and respiration. While splicing of group II introns in non-plant systems is facilitated by proteins encoded within the introns themselves (maturases), the mitochondrial introns in plants have diverged and have lost the vast majority of their intron-encoded ORFs. Only a single maturase gene (matR) is retained in plant mtDNAs, but its role(s) in the splicing of mitochondrial introns is currently unknown. In addition to matR, plants also harbor four nuclear maturase genes (nMat 1 to 4) encoding mitochondrial proteins that are expected to act in the splicing of group II introns. Recently, we established the role of one of these proteins, nMAT2, in the splicing of several mitochondrial introns in Arabidopsis. Here, we show that nMAT1 is required for trans-splicing of nad1 intron 1 and also functions in cis-splicing of nad2 intron 1 and nad4 intron 2. Homozygous nMat1 plants show retarded growth and developmental phenotypes, modified respiration activities and altered stress responses that are tightly correlated with mitochondrial complex I defects.