Hallier U W, Schmitt J R, Heber U, Chaianova S V, Volodarsky A D
Biochim Biophys Acta. 1978 Oct 11;504(1):67-83. doi: 10.1016/0005-2728(78)90007-5.
In spite of only slightly subnormal pigment contents, two plastome mutants of Oenothera (Valpha, Isigma) were practically incapable of photosynthetic CO2 fixation and another one exhibited considerably reduced photosynthesis (IVbeta). While other photosynthetic enzymes were present as far as investigated, ribulose-1,5-bisphosphate carboxylase (EC 4.1.1.39) activity was very low or missing altogether. As shown by gel electrophoresis, mutant IVbeta contained some, though little, fraction I protein. In the other two mutants fraction I protein could not be detected. Also, neither the small nor the large subunit of ribulose-1,5-biphosphate carboxylase could be found in these mutants. In immunodiffusion experiments with a monospecific antiserum against rye ribulose-1,5-bisphosphate carboxylase, only extracts from wild-type Oenothera produced visible precipitation lines. Still, the presence of very low levels of immunochemically reactive antigen was indicated for all three mutants. The highest level was observed in mutant IVbeta. The behaviour of the mutant extracts suggested that the antigens of mutant and wild type leaves reacting with the antiserum were not identical. All mutants appeared to have a coupled electron transport system as shown by ATP measurements, light scattering and 515 nm absorption changes. Linear electron transport was possible in the mutants. Still, the photoresponse of cytochrome f and fluorescence measurements suggested altered electron transport properties in the mutants. These are interpreted to be secondary lesions of the photosynthetic apparatus caused by primary deficiency in ribulose-1,5-bisphosphate carboxylase activity. From the absence in two mutants (Valpha, Isigna) of the small subunit of ribulose-1,5-bisphosphate carboxylase, which is known to be coded for by nuclear DNA and to be synthesized on cytoplasmic ribosomes, it appears that the genetic system of the plastids is capable of interfering with the genome-controlled synthesis of plastid components.
尽管色素含量仅略低于正常水平,但月见草的两个质体基因组突变体(Valpha、Isigma)几乎无法进行光合二氧化碳固定,另一个突变体(IVbeta)的光合作用则显著降低。就所研究的情况而言,虽然存在其他光合酶,但1,5-二磷酸核酮糖羧化酶(EC 4.1.1.39)的活性非常低或完全缺失。凝胶电泳显示,突变体IVbeta含有一些(尽管很少)I类蛋白。在另外两个突变体中未检测到I类蛋白。此外,在这些突变体中也未发现1,5-二磷酸核酮糖羧化酶的小亚基和大亚基。在用针对黑麦1,5-二磷酸核酮糖羧化酶的单特异性抗血清进行的免疫扩散实验中,只有野生型月见草的提取物产生可见的沉淀线。不过,所有三个突变体都显示存在极低水平的免疫化学反应性抗原。在突变体IVbeta中观察到的水平最高。突变体提取物的行为表明,与抗血清反应的突变体和野生型叶片的抗原并不相同。如ATP测量、光散射和515nm吸收变化所示,所有突变体似乎都具有偶联电子传递系统。突变体中线性电子传递是可能的。然而,细胞色素f的光响应和荧光测量表明突变体中的电子传递特性发生了改变。这些被解释为由1,5-二磷酸核酮糖羧化酶活性的原发性缺陷导致的光合装置的继发性损伤。从两个突变体(Valpha、Isigna)中不存在1,5-二磷酸核酮糖羧化酶的小亚基来看,已知该小亚基由核DNA编码并在细胞质核糖体上合成,这似乎表明质体的遗传系统能够干扰基因组控制的质体成分合成。