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YkgM and YkgO maintain translation by replacing their paralogs, zinc-binding ribosomal proteins L31 and L36, with identical activities.
Genes to Cells ( IF 1.3 ) Pub Date : 2020-06-19 , DOI: 10.1111/gtc.12796 Masami Ueta 1 , Chieko Wada 1 , Akira Wada 1
Genes to Cells ( IF 1.3 ) Pub Date : 2020-06-19 , DOI: 10.1111/gtc.12796 Masami Ueta 1 , Chieko Wada 1 , Akira Wada 1
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When a cell is zinc‐deficient, ykgM and ykgO , which encode paralogs of the zinc‐binding ribosomal proteins L31 and L36, are expressed from the ykgM operon, which is ordinarily held inactive by the Zur repressor. In ribosomes lacking L31, ribosomal subunit association is weakened, resulting in reduced in vitro translation and the deletion mutants of rpmE , the gene encoding L31, forming small colonies. We isolated four suppressor mutants of ∆rpmE that formed normal colonies. All four mutation sites were located in zur , and ribosomes of zur mutant cells contained one copy of YkgM and had translational activities equivalent to those of ribosomes containing L31. L36 is highly conserved among bacteria, chloroplast and mitochondria. Analysis of a deletion mutant of rpmJ , which encodes L36, suggested that L36 is involved in late assembly of the 50S particle, in vitro translation and cell growth. In zur mutant cells lacking rpmJ , the paralog YkgO was expressed and took over the functions of L36. zur mutant cells contained four types of ribosomes containing combinations of L31 or YkgM, and L36 or YkgO. Copy numbers of L31 and YkgM, and L36 and YkgO, summed to 1, indicating that each paralog pair shares a binding site.
中文翻译：
YkgM和YkgO通过以相同的活性取代它们的旁系同源物，锌结合核糖体蛋白L31和L36来维持翻译。
当细胞缺锌时，ykgM操纵子会表达编码锌结合核糖体蛋白L31和L36旁系同源物的ykgM和ykgO，而ykgM操纵子通常被Zur阻遏物抑制。在缺少L31的核糖体中，核糖体亚基缔合被削弱，导致体外翻译减少以及rpmE（编码L31的基因）的缺失突变体，形成小菌落。我们分离了形成正常菌落的ΔrpmE的四个抑制突变体。所有四个突变位点都位于zur和zur的核糖体中突变细胞含有一个拷贝的YkgM，其翻译活性与含有L31的核糖体相同。L36在细菌，叶绿体和线粒体中高度保守。对编码L36的rpmJ缺失突变体的分析表明，L36参与了50S颗粒的后期组装，体外翻译和细胞生长。在缺少rpmJ的zur突变细胞中，旁系同源基因YkgO被表达并接管L36的功能。zur突变细胞包含四种类型的核糖体，包含L31或YkgM和L36或YkgO的组合。L31和YkgM以及L36和YkgO的拷贝数总计为1，表示每个旁系对共享一个结合位点。
更新日期：2020-08-11
中文翻译：
YkgM和YkgO通过以相同的活性取代它们的旁系同源物，锌结合核糖体蛋白L31和L36来维持翻译。
当细胞缺锌时，ykgM操纵子会表达编码锌结合核糖体蛋白L31和L36旁系同源物的ykgM和ykgO，而ykgM操纵子通常被Zur阻遏物抑制。在缺少L31的核糖体中，核糖体亚基缔合被削弱，导致体外翻译减少以及rpmE（编码L31的基因）的缺失突变体，形成小菌落。我们分离了形成正常菌落的ΔrpmE的四个抑制突变体。所有四个突变位点都位于zur和zur的核糖体中突变细胞含有一个拷贝的YkgM，其翻译活性与含有L31的核糖体相同。L36在细菌，叶绿体和线粒体中高度保守。对编码L36的rpmJ缺失突变体的分析表明，L36参与了50S颗粒的后期组装，体外翻译和细胞生长。在缺少rpmJ的zur突变细胞中，旁系同源基因YkgO被表达并接管L36的功能。zur突变细胞包含四种类型的核糖体，包含L31或YkgM和L36或YkgO的组合。L31和YkgM以及L36和YkgO的拷贝数总计为1，表示每个旁系对共享一个结合位点。
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