University of Groningen, University Medical Center Groningen, Department of Medical Microbiology, Hanzeplein 1, P.O. Box 30001, 9700 RB, Groningen, The Netherlands.
Department of Biology and Biochemistry, University of Bath, Bath, UK.
Sci Rep. 2019 Feb 26;9(1):2845. doi: 10.1038/s41598-019-39169-3.
Sublancin 168 is a highly potent and stable antimicrobial peptide secreted by the Gram-positive bacterium Bacillus subtilis. Production of sublancin gives B. subtilis a major competitive growth advantage over a range of other bacteria thriving in the same ecological niches, the soil and plant rhizosphere. B. subtilis protects itself against sublancin by producing the cognate immunity protein SunI. Previous studies have shown that both the sunA gene for sublancin and the sunI immunity gene are encoded by the prophage SPβ. The sunA gene is under control of several transcriptional regulators. Here we describe the mechanisms by which sunA is heterogeneously expressed within a population, while the sunI gene encoding the immunity protein is homogeneously expressed. The key determinants in heterogeneous sunA expression are the transcriptional regulators Spo0A, AbrB and Rok. Interestingly, these regulators have only a minor influence on sunI expression and they have no effect on the homogeneous expression of sunI within a population of growing cells. Altogether, our findings imply that the homogeneous expression of sunI allows even cells that are not producing sublancin to protect themselves at all times from the active sublancin produced at high levels by their isogenic neighbors. This suggests a mutualistic evolutionary strategy entertained by the SPβ prophage and its Bacillus host, ensuring both stable prophage maintenance and a maximal competitive advantage for the host at minimal costs.
短小芽孢杆菌素 168 是一种高效且稳定的抗菌肽，由革兰氏阳性细菌枯草芽孢杆菌分泌。短小芽孢杆菌素的产生使枯草芽孢杆菌在与其他在同一生态位（土壤和植物根际）中茁壮成长的细菌竞争时具有显著的生长优势。枯草芽孢杆菌通过产生同源免疫蛋白 SunI 来保护自身免受短小芽孢杆菌素的侵害。先前的研究表明，短小芽孢杆菌素的 sunA 基因和 SunI 免疫基因均由噬菌体 SPβ 编码。sunA 基因受多个转录调控因子的控制。在这里，我们描述了 sunA 在群体中异质表达的机制，而编码免疫蛋白的 sunI 基因则均匀表达。sunA 异质表达的关键决定因素是转录调控因子 Spo0A、AbrB 和 Rok。有趣的是，这些调控因子对 sunI 表达的影响很小，并且对生长细胞群体中 sunI 的均匀表达没有影响。总的来说，我们的研究结果表明，sunI 的均匀表达使得即使不产生短小芽孢杆菌素的细胞也能始终保护自己免受其同源邻居高水平产生的活性短小芽孢杆菌素的侵害。这表明 SPβ 噬菌体及其枯草芽孢杆菌宿主采用了一种互利的进化策略，确保了噬菌体的稳定维持和宿主的最大竞争优势，同时成本最小化。
