首页> 美国卫生研究院文献>Genetics >A Dominant Mutation in the Chlamydomonas Reinhardtii Nuclear Gene Sim30 Suppresses Translational Defects Caused by Initiation Codon Mutations in Chloroplast Genes
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A Dominant Mutation in the Chlamydomonas Reinhardtii Nuclear Gene Sim30 Suppresses Translational Defects Caused by Initiation Codon Mutations in Chloroplast Genes

机译:莱茵衣藻核基因Sim30的显性突变抑制了叶绿体基因中起始密码子突变引起的翻译缺陷。

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摘要

A suppressor of a translation initiation defect caused by an AUG to AUU mutation in the Chlamydomonas reinhardtii chloroplast petD gene was isolated, defining a nuclear locus that we have named SIM30. A dominant mutant allele at this locus, sim30-1d, was found to increase the translation initiation rate of the mutant petD mRNA. sim30-1d was also able to suppress the translational defect caused by an AUG to AUC mutation in the petD gene, and an AUG to AUU mutation in the chloroplast petA gene. We therefore suggest that the SIM30 gene may encode a general chloroplast translation factor. The ability of sim30-1d to suppress the petD AUG to AUU mutation is diminished in the presence of one or more antibiotic resistance markers located within the 16S and 23S rRNAs, suggesting that the activity of the sim30-1d gene product in translation initiation may involve interaction with ribosomal subunits.
机译:分离了由莱茵衣藻叶绿体petD基因中的AUG突变为AUU突变引起的翻译起始缺陷的抑制剂,定义了我们已命名为SIM30的核基因座。发现该位点的一个显性突变等位基因sim30-1d增加了突变petD mRNA的翻译起始速率。 sim30-1d还能够抑制petD基因中AUG到AUC突变以及叶绿体petA基因中AUG到AUU突变引起的翻译缺陷。因此,我们建议SIM30基因可能编码一般的叶绿体翻译因子。在16S和23S rRNA中存在一种或多种抗生素抗性标记的情况下,sim30-1d抑制petD AUG突变为AUU的能力减弱,这表明sim30-1d基因产物在翻译起始中的活性可能涉及与核糖体亚基的相互作用。

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