Department of Microbiology and Immunology, Kirksville College of Osteopathic Medicine, A.T. Still University, Kirksville, MO, 63501, USA.
Sci Rep. 2021 Sep 15;11(1):18372. doi: 10.1038/s41598-021-97736-z.
Enterohaemorrhagic Escherichia coli (EHEC) comprise a group of intestinal pathogens responsible for a range of illnesses, including kidney failure and neurological compromise. EHEC produce critical virulence factors, Shiga toxin (Stx) 1 or 2, and the synthesis of Stx2 is associated with worse disease manifestations. Infected patients only receive supportive treatment because some conventional antibiotics enable toxin production. Shiga toxin 2 genes (stx2) are carried in λ-like bacteriophages (stx2-phages) inserted into the EHEC genome as prophages. Factors that cause DNA damage induce the lytic cycle of stx2-phages, leading to Stx2 production. The phage Q protein is critical for transcription antitermination of stx2 and phage lytic genes. This study reports that deficiency of two endoribonucleases (RNases), E and G, significantly delayed cell lysis and impaired production of both Stx2 and stx2-phages, unlike deficiency of either enzyme alone. Moreover, scarcity of both enzymes reduced the concentrations of Q and stx2 transcripts and slowed cell growth.
产肠出血性大肠杆菌（EHEC）是一组肠道病原体，可导致多种疾病，包括肾衰竭和神经损伤。EHEC 产生关键的毒力因子，志贺毒素（Stx）1 或 2，Stx2 的合成与更严重的疾病表现有关。感染患者只能接受支持性治疗，因为一些常规抗生素会促进毒素的产生。志贺毒素 2 基因（stx2）携带在 λ 样噬菌体（stx2-噬菌体）中，插入 EHEC 基因组作为前噬菌体。导致 DNA 损伤的因素诱导 stx2-噬菌体的裂解周期，导致 Stx2 的产生。噬菌体 Q 蛋白对于 stx2 和噬菌体裂解基因的转录终止反终止至关重要。本研究报告称，两种内切核糖核酸酶（RNases）E 和 G 的缺乏显著延迟了细胞裂解，并损害了 Stx2 和 stx2-噬菌体的产生，而单独缺乏任何一种酶都不会产生这种影响。此外，两种酶的缺乏减少了 Q 和 stx2 转录本的浓度，并减缓了细胞生长。
