Zdrojewska Karolina, Dydecka Aleksandra, Nejman-Faleńczyk Bożena, Topka Gracja, Necel Agnieszka, Węgrzyn Alicja, Węgrzyn Grzegorz, Bloch Sylwia
Department of Molecular Biology, Faculty of Biology, University of Gdańsk, Gdańsk, Poland.
Laboratory of Molecular Biology, Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Gdańsk, Poland.
Acta Biochim Pol. 2019 Nov 26;66(4):589-596. doi: 10.18388/abp.2019_2886.
Shiga toxin-producing Escherichia coli (STEC) is a group of pathogenic strains responsible for human infections that result in bloody diarrhea and hemorrhagic colitis, often with severe complications. The main virulence factors of STEC are Shiga toxins encoded by stx genes located in genomes of Shiga toxin-converting bacteriophages (Stx phages). These bacterial viruses are clustered in the lambdoid bacteriophages family represented by phage λ. Here, we report that expression of orf73 from the exo-xis region of the phage genome promotes the lysogenic pathway of development of λ and Φ24B phages. We demonstrated that the mutant phages with deletions of orf73 revealed higher burst size during the lytic cycle. Moreover, survival rates of E. coli infected with mutant bacteriophages were lower relative to wild-type viruses. Additionally, orf73 deletion negatively influenced the lysogenization process of E. coli host cells. We conclude that orf73 plays an important biological role in the development of lambdoid viruses, and probably it is involved in the network of molecular mechanism of the lysis-vs.-lysogenization decision.
产志贺毒素大肠杆菌（STEC）是一组导致人类感染的致病菌株，可引发血性腹泻和出血性结肠炎，常伴有严重并发症。STEC的主要毒力因子是由位于志贺毒素转化噬菌体（Stx噬菌体）基因组中的stx基因编码的志贺毒素。这些细菌病毒聚集在以噬菌体λ为代表的λ样噬菌体家族中。在此，我们报告噬菌体基因组外显子 - xis区域的orf73表达促进了λ和Φ24B噬菌体的溶原性发育途径。我们证明，缺失orf73的突变噬菌体在裂解周期中显示出更高的爆发量。此外，与野生型病毒相比，感染突变噬菌体的大肠杆菌存活率更低。此外，orf73缺失对大肠杆菌宿主细胞的溶原化过程产生负面影响。我们得出结论，orf73在λ样病毒的发育中起重要生物学作用，并且可能参与了裂解与溶原化决定的分子机制网络。
