Department of Biology, Biotechnical Faculty, University of Ljubljana, Ljubljana, Slovenia.
Harvard Medical School, Office for Research Initiatives and Global Programs, Boston, MA, 02115, USA.
Commun Biol. 2024 Oct 25;7(1):1388. doi: 10.1038/s42003-024-07082-9.
Betatectiviruses are prophages consisting of linear extrachromosomal genomes without obvious plasmid modules. It remains unclear how betatectiviruses are maintained in low-copy numbers in host cells and how they are vertically transmitted. Phage GIL01 is a model betatectivirus that infects the mosquito pathogen Bacillus thuringiensis serovar israelensis. Previous studies identified two closely spaced promoters, P1 and P2, responsible for the expression of GIL01 genes required for prophage replication and the switch from the lysogenic to lytic cycle. Here, we report that the GIL01-encoded 58-amino acid long gp1 protein forms a large nucleoprotein complex that represses its transcription from the strong promoter P2. Notably, ectopic expression of gp1 resulted in the loss of GIL01 in exponential cultures and immunized cells against infection with GIL01, indicating that gp1 plays a repressive role in the phage cycle. This finding is consistent with mutations in gp1 committing GIL01 to the lytic cycle and we show that maintenance of this phage variant in the bacterial population is contingent on the accumulation of deletions in the P1-P2 region. The fact that gp1 is conserved across most sequenced betatectiviruses suggests that the regulatory mechanism of gp1 that controls prophage maintenance is widespread among these bacteriophages.
β 噬体病毒是由没有明显质粒模块的线性染色体外基因组组成的原噬菌体。β 噬体病毒如何在宿主细胞中以低拷贝数维持以及如何垂直传播仍然不清楚。噬菌体 GIL01 是一种感染苏云金芽孢杆菌以色列亚种的模式β噬体病毒。先前的研究确定了两个紧密间隔的启动子 P1 和 P2，它们负责表达 GIL01 基因，这些基因对于原噬菌体的复制以及从溶原到裂解周期的转变是必需的。在这里，我们报告 GIL01 编码的 58 个氨基酸长的 gp1 蛋白形成一个大的核蛋白复合物，抑制其从强启动子 P2 的转录。值得注意的是，gp1 的异位表达导致指数培养物中 GIL01 的丢失和免疫细胞对 GIL01 的感染，表明 gp1 在噬菌体周期中发挥抑制作用。这一发现与 gp1 突变使 GIL01 进入裂解周期一致，我们表明这种噬菌体变体在细菌群体中的维持取决于 P1-P2 区域缺失的积累。gp1 在大多数已测序的β噬体病毒中保守，这表明 gp1 控制前噬菌体维持的调节机制在这些噬菌体中广泛存在。
