Parasitism by bacteriophages has led to the evolution of a variety of defense mechanisms in their host bacteria. However, it is unclear what factors lead to specific defenses being deployed upon phage infection. To explore this question, we co-evolved the bacterial fish pathogen Flavobacterium columnare and its virulent phage V156 in presence and absence of a eukaryotic host signal (mucin) for sixteen weeks. The presence of mucin leads to a dramatic increase in CRISPR spacer acquisition, especially in low nutrient conditions where over 60% of colonies obtain at least one new spacer. Additionally, we show that the presence of a competitor bacterium further increases CRISPR spacer acquisition in F. columnare. These results suggest that ecological factors are important in determining defense strategies against phages, and that the phage-bacterium interactions on mucosal surfaces may select for the diversification of bacterial immune systems.

噬菌体的寄生导致了宿主细菌多种防御机制的进化。然而，尚不清楚哪些因素导致噬菌体感染后部署特定防御。为了探索这个问题，我们在存在和不存在真核宿主信号（粘蛋白）的情况下共同进化细菌性鱼类病原体柱状黄杆菌及其剧毒噬菌体 V156 16 周。粘蛋白的存在导致 CRISPR 间隔区获得量急剧增加，特别是在低营养条件下，超过 60% 的菌落获得至少一个新间隔区。此外，我们发现竞争细菌的存在进一步增加了柱状镰刀菌中 CRISPR 间隔区的获得。这些结果表明，生态因素对于确定针对噬菌体的防御策略非常重要，并且粘膜表面上的噬菌体-细菌相互作用可能会选择细菌免疫系统的多样化。