Blasdel Bob G, Chevallereau Anne, Monot Marc, Lavigne Rob, Debarbieux Laurent
Laboratory of Gene Technology, Department of Biosystems, Leuven, Belgium.
Institut Pasteur, Molecular Biology of the Gene in Extremophiles Unit, Department of Microbiology, Paris, France.
ISME J. 2017 Sep;11(9):1988-1996. doi: 10.1038/ismej.2017.63. Epub 2017 May 12.
Although the evolution of tailed bacteriophages has increasingly been better understood through comparisons of their DNA sequences, the functional consequences of this evolution on phage infectious strategies have remained unresolved. In this study, we comprehensively compared the transcriptional strategies of two related myoviruses, PAK_P3 and PAK_P4, infecting the same Pseudomonas aeruginosa host strain. Outside of the conservation of their structural clusters, their highly syntenic genomes display only limited DNA similarity. Despite this apparent divergence, we found that both viruses follow a similar infection scheme, relying on a temporal regulation of their gene expression, likely involving the use of antisense transcripts, as well as a rapid degradation of 90% of the host non-ribosomal mRNA, as previously reported for PAK_P3. However, the kinetics of the mRNA degradation is remarkably faster during PAK_P4 infection. Moreover, we found that each virus has evolved specific adaptations, as exemplified by the distinct patterns of their core genes expression as well as the specific manipulation of the expression of iron-related host genes by PAK_P4. This study enhances our understanding of the evolutionary process of virulent phages, which relies on adjusting globally conserved ancestral infection mechanisms.
尽管通过比较尾噬菌体的DNA序列,人们对其进化的理解越来越深入,但这种进化对噬菌体感染策略的功能影响仍未得到解决。在本研究中,我们全面比较了两种感染同一铜绿假单胞菌宿主菌株的相关肌病毒PAK_P3和PAK_P4的转录策略。除了结构簇的保守性外,它们高度同线的基因组仅显示出有限的DNA相似性。尽管存在这种明显的差异,但我们发现这两种病毒都遵循类似的感染模式,依赖于对其基因表达的时间调控,可能涉及反义转录本的使用,以及如先前报道的PAK_P3那样对90%的宿主非核糖体mRNA的快速降解。然而,在PAK_P4感染期间,mRNA降解的动力学明显更快。此外,我们发现每种病毒都进化出了特定的适应性,例如它们核心基因表达的不同模式以及PAK_P4对铁相关宿主基因表达的特定调控。这项研究增进了我们对烈性噬菌体进化过程的理解,其进化依赖于对全球保守的祖先感染机制的调整。