Ammons D, Rampersad J, Fox G E
Department of Biology and Biochemistry, University of Houston, Houston, TX 77204-5934, USA.
Nucleic Acids Res. 1999 Jan 15;27(2):637-42. doi: 10.1093/nar/27.2.637.
In Escherichia coli, ribosomal RNAs (16S, 23S and 5S) are co-transcribed in a highly regulated manner from seven genomically dispersed operons. Previous studies on the cellular effects of altered levels of two of these rRNAs (16S and 23S) have been useful in better understanding the regulation of rRNA expression. Furthering these studies, we have investigated the effect of 5S rRNA deficiencies on cell fitness through the sequential deletion of 5S rRNA genes. Our findings indicate that the loss of 5S rDNA from multiple genes decreases cell fitness more rapidly than loss of a similar number of 16S and 23S rRNA genes. These results suggest that the cell's innate ability to up-regulate rRNA operons does not compensate for 5S rRNA deficiencies, as was previously shown for 16S and 23S rRNAs. A plasmid-borne 5S rRNA gene is able to compensate for the deleted 5S rRNA genes.
在大肠杆菌中，核糖体RNA（16S、23S和5S）以高度调控的方式从七个基因组分散的操纵子中共同转录。先前关于其中两种rRNA（16S和23S）水平改变对细胞影响的研究，有助于更好地理解rRNA表达的调控。为进一步推进这些研究，我们通过依次缺失5S rRNA基因，研究了5S rRNA缺陷对细胞适应性的影响。我们的研究结果表明，多个基因中5S rDNA的缺失比相同数量的16S和23S rRNA基因的缺失更迅速地降低细胞适应性。这些结果表明，细胞上调rRNA操纵子的固有能力无法弥补5S rRNA的缺陷，正如先前对16S和23S rRNA所显示的那样。一个质粒携带的5S rRNA基因能够弥补缺失的5S rRNA基因。
