The bacterium Vibrio cholerae can colonize the human intestine and cause cholera, but spends much of its life cycle in seawater. The pathogen must adapt to substantial environmental changes when moving between seawater and the human intestine, including different availability of carbon sources such as fructose. Here, we use in vitro experiments as well as mouse intestinal colonization assays to study the mechanisms used by pandemic V. cholerae to adapt to these environmental changes. We show that a LacI-type regulator (FruI) and a fructose/H⁺ symporter (FruT) are important for fructose uptake at low fructose concentrations, as those found in seawater. FruT is downregulated by FruI, which is upregulated when O₂ concentrations are low (as in the intestine) by ArcAB, a two-component system known to respond to changes in oxygen levels. As a result, the bacteria predominantly use FruT for fructose uptake under seawater conditions (low fructose, high O₂), and use a known fructose phosphotransferase system (PTS, Fpr) for fructose uptake under conditions found in the intestine. PTS activity leads to reduced levels of intracellular cAMP, which in turn upregulate virulence genes. Our results indicate that the FruT/FruI system may be important for survival of pandemic V. cholerae in seawater.

细菌霍乱弧菌可寄居在人体肠道而引起的霍乱，但花费大量海水其生命周期。在海水和人体肠道之间移动时，病原体必须适应重大的环境变化，包括果糖等碳源的不同可用性。在这里，我们使用体外实验以及小鼠肠道定植分析来研究大流行霍乱弧菌用于适应这些环境变化的机制。我们表明 LacI 型调节剂 (FruI) 和果糖/H ⁺同向转运体 (FruT) 对低果糖浓度下的果糖摄取很重要，就像在海水中发现的那样。FruT 被 FruI 下调，当 O ₂ArcAB 是一种已知对氧气水平变化做出反应的双组分系统，因此浓度很低（如在肠道中）。因此，细菌在海水条件下（低果糖、高 O ₂）主要使用 FruT 摄取果糖，并使用已知的果糖磷酸转移酶系统（PTS、Fpr）在肠道条件下摄取果糖。PTS 活性导致细胞内 cAMP 水平降低，进而上调毒力基因。我们的结果表明 FruT/FruI 系统可能对海水中大流行霍乱弧菌的存活很重要。