Johnson E M, Schnabelrauch L S, Sears B B
Department of Botany and Plant Pathology, Michigan State University, East Lansing 48824.
Mol Gen Genet. 1991 Jan;225(1):106-12. doi: 10.1007/BF00282648.
Immunoblotting of a chloroplast mutant (pm7) of Oenothera showed that three proteins, cytochrome f and the 23 kDa and 16 kDa subunits of the oxygen-evolving subcomplex of photosystem II, were larger than the corresponding mature proteins of the wild type and, thus, appear to be improperly processed in pm7. The mutant is also chlorotic and has little or no internal membrane development in the plastids. The improperly processed proteins, and other proteins that are completely missing, represent products of both the plastid and nuclear genomes. To test for linkage of these defects, a green revertant of pm7 was isolated from cultures in which the mutant plastids were maintained in a nuclear background homozygous for the plastome mutator (pm) gene. In this revertant, all proteins analyzed co-reverted to the wild-type condition, indicating that a single mutation in a plastome gene is responsible for the complex phenotype of pm7. These results suggest that the defect in pm7 lies in a gene that affects a processing protease encoded in the chloroplast genome.
对月见草的叶绿体突变体（pm7）进行免疫印迹分析表明，三种蛋白质，即细胞色素f以及光系统II放氧亚复合体的23 kDa和16 kDa亚基，比野生型相应的成熟蛋白质更大，因此在pm7中似乎加工不当。该突变体也是褪绿的，并且质体中几乎没有内膜发育。加工不当的蛋白质以及其他完全缺失的蛋白质，代表了质体和核基因组的产物。为了测试这些缺陷的连锁关系，从培养物中分离出pm7的绿色回复突变体，其中突变体质体保持在质体基因组突变体（pm）基因纯合的核背景中。在这个回复突变体中，所有分析的蛋白质都共同回复到野生型状态，表明质体基因组中的单个突变导致了pm7的复杂表型。这些结果表明，pm7中的缺陷在于一个影响叶绿体基因组中编码的加工蛋白酶的基因。
