Campylobacter jejuni is a bacterial pathogen that is generally acquired as a zoonotic infection from poultry and animals. Adhesion of C. jejuni to human colorectal epithelial cells is weakened after loss of its cj0588 gene. The Cj0588 protein belongs to the type I group of TlyA (TlyA^I) enzymes, which 2′‐O ‐methylate nucleotide C1920 in 23S rRNA. Slightly longer TlyA^II versions of the methyltransferase are found in actinobacterial species including Mycobacterium tuberculosis , and methylate not only C1920 but also nucleotide C1409 in 16S rRNA. Loss of TlyA function attenuates virulence of both M. tuberculosis and C. jejuni . We show here that the traits impaired in C. jejuni null strains can be rescued by complementation not only with the original cj0588 (tlyA ^I ) but also with a mycobacterial tlyA ^II gene. There are, however, significant differences in the recombinant phenotypes. While cj0588 restores motility, biofilm formation, adhesion to and invasion of human epithelial cells and stimulation of IL‐8 production in a C. jejuni null strain, several of these properties are further enhanced by the mycobacterial tlyA ^II gene, in some cases to twice the original wild‐type level. These findings strongly suggest that subtle changes in rRNA modification patterns can affect protein synthesis in a manner that has serious consequences for bacterial pathogenicity.

中文翻译：

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通过在其rRNA中显示分枝杆菌TlyA甲基化模式，可增强空肠弯曲菌的毒力特性。

空肠弯曲杆菌是一种细菌病原体，通常是从人和动物身上获得的人畜共患病感染。空肠梭菌对人结肠直肠上皮细胞的粘附力在其cj0588基因丢失后减弱。Cj0588蛋白属于TlyA（TlyA ^I）酶的^I型，在23S rRNA中是2'- O-甲基化核苷酸C1920。在包括结核分枝杆菌在内的放线菌物种中发现了稍长一些的TlyA ^II版本的甲基转移酶，不仅在16S rRNA中甲基化了C1920，而且对C1409核苷酸进行了甲基化。TlyA功能的丧失减弱了结核分枝杆菌和空肠弯曲杆菌的毒力。我们在这里显示，不仅可以与原始cj0588（tlyA ^I）互补，而且可以与分枝杆菌tlyA ^II基因互补，可以拯救空肠弯曲杆菌无效菌株中的性状。但是，重组表型有显着差异。尽管cj0588恢复空肠弯曲杆菌无效菌株的运动性，生物膜形成，对人上皮细胞的粘附和侵袭以及IL-8产生的刺激，但分枝杆菌tlyA ^II进一步增强了其中一些特性 基因，在某些情况下是原始野生型水平的两倍。这些发现强烈表明，rRNA修饰模式的细微变化会以严重影响细菌致病性的方式影响蛋白质合成。