Viruses are a major control on populations of microbes. Often, their virulence is examined in controlled laboratory conditions. Yet, in nature, environmental conditions lead to changes in host physiology and fitness that may impart both costs and benefits on viral success. Phosphorus (P) is a major abiotic control on the marine cyanobacterium Synechococcus. Some viruses infecting Synechococcus have acquired, from their host, a gene encoding a P substrate binding protein (PstS), thought to improve virus replication under phosphate starvation. Yet, pstS is uncommon amongst cyanobacterial viruses. Thus, we asked how infections with viruses lacking PstS are affected by P scarcity. We show that production of infectious virus particles of such viruses is reduced in low P conditions. However, this reduction in progeny is not caused by impaired phage genome replication, thought to be a major sink for cellular phosphate. Instead, transcriptomic analysis showed that under low P conditions a PstS-lacking cyanophage increased the expression of a specific gene set that included mazG, hli2, and gp43 encoding a pyrophosphatase, a high-light inducible proteinand DNA polymerase respectively. Moreover, several of the upregulated genes were controlled by the hosts phoBR two-component system. We hypothesise that recycling and polymerization of nucleotides liberates free phosphate and thus allows viral morphogenesis, albeit at lower rates than when phosphate is replete or when phages encode pstS. Together, our data shows how phage genomes, lacking obvious P-stress related genes, have evolved to exploit their host’s environmental sensing mechanisms to coordinate their own gene expression in response to resource limitation.

中文翻译：

---

聚球藻病毒对环境应激的协调转录反应

病毒是微生物种群的主要控制者。通常，它们的毒力是在受控实验室条件下进行检查的。然而，在自然界中，环境条件会导致宿主生理和健康的变化，这可能会给病毒的成功带来成本和收益。磷 (P) 是对海洋蓝藻聚球藻的主要非生物控制剂。一些感染聚球藻的病毒从宿主那里获得了编码 P 底物结合蛋白 (PstS) 的基因，该基因被认为可以改善磷酸盐饥饿下的病毒复制。然而，pstS 在蓝藻病毒中并不常见。因此，我们询问缺乏 PstS 的病毒感染如何受到 P 稀缺的影响。我们发现，在低磷条件下，此类病毒的感染性病毒颗粒的产生会减少。然而，后代数量的减少并不是由噬菌体基因组复制受损引起的，噬菌体基因组复制被认为是细胞磷酸盐的主要来源。相反，转录组分析表明，在低磷条件下，缺乏 PstS 的噬菌体增加了特定基因组的表达，其中包括分别编码焦磷酸酶、高光诱导蛋白和 DNA 聚合酶的 mazG、hli2 和 gp43。此外，一些上调的基因是由宿主 phoBR 双组分系统控制的。我们假设核苷酸的回收和聚合会释放游离磷酸盐，从而允许病毒形态发生，尽管其速率低于磷酸盐充足或噬菌体编码 pstS 时的速率。总之，我们的数据显示了缺乏明显的 P 应激相关基因的噬菌体基因组如何进化为利用宿主的环境传感机制来协调自身的基因表达以应对资源限制。