Colin M, Dorthu M P, Duby F, Remacle C, Dinant M, Wolwertz M R, Duyckaerts C, Sluse F, Matagne R F
Departement de Botanique, Université de Liège, Belgium.
Mol Gen Genet. 1995 Nov 15;249(2):179-84. doi: 10.1007/BF00290364.
Mitochondrial mutants of the green alga Chlamydomonas reinhardtii that are inactivated in the cytochrome pathway of respiration have previously been isolated. Despite the fact that the alternative oxidase pathway is still active the mutants have lost the capacity to grow heterotrophically (dark + acetate) and display reduced growth under mixotrophic conditions (light + acetate). In crosses between wild-type and mutant cells, the meiotic progeny only inherit the character transmitted by the mt- parent, which indicates that the mutations are located in the 15.8 kb linear mitochondrial genome. Two new mutants (dum-18 and dum-19) have now been isolated and characterized genetically, biochemically and at the molecular level. In addition, two previously isolated mutants (dum-11 and dum-15) were characterized in more detail. dum-11 contains two types of deleted mitochondrial DNA molecules: 15.1 kb monomers lacking the subterminal part of the genome, downstream of codon 147 of the apocytochrome b (COB) gene, and dimers resulting from head-to-head fusion of asymmetrically deleted monomers (15.1 and 9.5 kb DNA molecules, respectively). As in the wild type, the three other mutants contain only 15.8 kb mitochondrial DNA molecules. dum-15 is mutated at codon 140 of the COB gene, a serine (TCT) being changed into a tyrosine (TAC). dum-18 and dum-19 both inactivate cytochrome c oxidase, as a result of frameshift mutations (addition or deletion of 1 bp) at codons 145 and 152, respectively, of the COX1 gene encoding subunit I of cytochrome c oxidase. In a total of ten respiratory deficient mitochondrial mutants characterized thus far, only mutations located in COB or COX1 have been isolated.(ABSTRACT TRUNCATED AT 250 WORDS)
先前已分离出莱茵衣藻的线粒体突变体,这些突变体在细胞色素呼吸途径中失活。尽管交替氧化酶途径仍然活跃,但这些突变体已失去异养生长(黑暗+乙酸盐)的能力,并且在混合营养条件下(光照+乙酸盐)生长减缓。在野生型和突变体细胞之间的杂交中,减数分裂后代只继承mt-亲本传递的性状,这表明突变位于15.8 kb的线性线粒体基因组中。现在已经分离出两个新的突变体(dum-18和dum-19),并在遗传、生化和分子水平上进行了表征。此外,对两个先前分离的突变体(dum-11和dum-15)进行了更详细的表征。dum-11包含两种类型的缺失线粒体DNA分子:15.1 kb的单体,缺少基因组的亚末端部分,位于脱辅基细胞色素b(COB)基因密码子147下游;以及由不对称缺失单体(分别为15.1和9.5 kb DNA分子)头对头融合产生的二聚体。与野生型一样,其他三个突变体只包含15.8 kb的线粒体DNA分子。dum-15在COB基因的密码子140处发生突变,丝氨酸(TCT)变为酪氨酸(TAC)。dum-18和dum-19均使细胞色素c氧化酶失活,这是由于细胞色素c氧化酶亚基I编码基因COX1的密码子145和152分别发生移码突变(插入或缺失1个碱基对)所致。在迄今为止表征的总共十个呼吸缺陷型线粒体突变体中,仅分离出位于COB或COX1中的突变。(摘要截短于250字)