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首页> 外文期刊>Journal of bacteriology >Inactivation of the RluD Pseudouridine Synthase Has Minimal Effects on Growth and Ribosome Function in Wild-Type Escherichia coli and Salmonella enterica
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Inactivation of the RluD Pseudouridine Synthase Has Minimal Effects on Growth and Ribosome Function in Wild-Type Escherichia coli and Salmonella enterica

机译：RluD伪尿苷合酶的灭活对野生型大肠杆菌和肠沙门氏菌的生长和核糖体功能的影响最小。

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The Escherichia coli rluD gene encodes a pseudouridine synthase responsible for the pseudouridine (Ψ) modifications at positions 1911, 1915, and 1917 in helix 69 of 23S rRNA. It has been reported that deletion of rluD in K-12 strains of E. coli is associated with extremely slow growth, increased readthrough of stop codons, and defects in 50S ribosomal subunit assembly and 30S-50S subunit association. Suppressor mutations in the prfB and prfC genes encoding release factor 2 (RF2) and RF3 that restore the wild type-growth rate and also correct the ribosomal defects have now been isolated. These suppressors link helix 69 Ψ residues with the termination phase of protein synthesis. However, further genetic analysis reported here also reveals that the slow growth and other defects associated with inactivation of rluD in E. coli K-12 strains are due to a defective RF2 protein, with a threonine at position 246, which is present in all K-12 strains. This is in contrast to the more typical alanine found at this position in most bacterial RF2s, including those of other E. coli strains. Inactivation of rluD in E. coli strains containing the prfB allele from E. coli B or in Salmonella enterica, both carrying an RF2 with Ala246, has negligible effects on growth, termination, or ribosome function. The results indicate that, in contrast to those in wild bacteria, termination functions in E. coli K-12 strains carrying a partially defective RF2 protein are especially susceptible to perturbation of ribosome-RF interactions, such as that caused by loss of h69 Ψ modifications.
机译：大肠杆菌rluD 基因编码一个伪尿苷合酶，该酶负责23S rRNA螺旋69的1911、1915和1917位的伪尿苷（modifications）修饰。据报道，在 E的K-12株中 rluD 的缺失。大肠杆菌与极慢的生长，终止密码子的通读增加以及50S核糖体亚基组装体和30S-50S亚基缔合的缺陷有关。现在已经分离出编码释放因子2（RF2）和RF3的 prfB 和 prfC 基因中的抑制子突变，这些突变恢复了野生型的生长速率并纠正了核糖体缺陷。这些抑制剂将螺旋69Ψ残基与蛋白质合成的终止阶段联系起来。但是，这里报道的进一步的遗传分析也显示， E中 rluD 的失活与缓慢的生长和其他缺陷有关。大肠杆菌K-12菌株归因于RF2蛋白缺陷，苏氨酸位于246位，在所有K-12菌株中都存在苏氨酸。这与大多数细菌RF2（包括其他 E的那些）在此位置发现的更典型的丙氨酸形成对比。大肠杆菌菌株。 E中 rluD 的灭活。包含来自 E的 prfB 等位基因的大肠杆菌菌株。带有Ala246的RF2的大肠埃希菌B或小肠沙门氏菌对生长，终止或核糖体功能的影响微不足道。结果表明，与野生细菌相比， E具有终止功能。携带部分有缺陷的RF2蛋白的大肠杆菌K-12菌株尤其容易受到核糖体-RF相互作用的干扰，例如由h69 loss修饰缺失引起的相互作用。

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