首页> 外文OA文献 >Nonsense mutations in the \u3ci\u3eChlamydomonas\u3c/i\u3e chloroplast gene that codes for the large subunit of ribulosebisphosphate carboxylase/oxygenase
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Nonsense mutations in the \u3ci\u3eChlamydomonas\u3c/i\u3e chloroplast gene that codes for the large subunit of ribulosebisphosphate carboxylase/oxygenase

机译:叶绿体基因中的无义突变,其编码核酮糖二磷酸羧化酶/加氧酶的大亚基

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摘要

The Chlamydomonas reinhardtii chloroplast mutants 18-SB and 18-7G lack both the chloroplast-encoded large subunit and nuclear-encoded small subunit of the chloroplast enzyme ribulose-1,5-bisphosphate carboxylase/oxygenase (EC 4.1.1.39). A chloroplast intergenic-suppression model has been postulated to account for the genetic instability of 18-5B revertants. Here, we have determined the molecular basis of the 18-SB and 18-7G mutants. They contain nonsense mutations close to the 3\u27 and 5\u27 ends of their large-subunit genes, respectively. Puls-chase experiments revealed that the 18-SB mutant produces a truncated large subunit that is unstable. In connection with previous experiments, this work identifies nonsense suppression in the chloroplast. Small subunits are also synthesized but then degraded in the mutants. Thus, the coordinated absence of subunits is achieved through degradation of the small subunit in the specific absence of the large subunit.
机译:莱茵衣藻叶绿体突变体18-SB和18-7G缺少叶绿体酶核糖-1,5-双磷酸羧化酶/加氧酶(EC 4.1.1.39)的叶绿体编码的大亚基和核编码的小亚基。推测叶绿体基因间抑制模型可解释18-5B回复子的遗传不稳定性。在这里,我们确定了18-SB和18-7G突变体的分子基础。它们包含分别接近其大亚基基因3 \ u27和5 \ u27末端的无意义突变。脉冲追踪实验显示18-SB突变体产生不稳定的截短的大亚基。结合以前的实验,这项工作确定了叶绿体中的废话抑制。小亚基也被合成,但随后在突变体中降解。因此,在特定的大亚基不存在的情况下,通过降解小亚基可以实现亚基的协同缺失。

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