A fructose/H(+) symporter controlled by a LacI-type regulator promotes survival of pandemic Vibrio cholerae in seawater.
A fructose/H(+) symporter controlled by a LacI-type regulator promotes survival of pandemic Vibrio cholerae in seawater.
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由 LacI 型调节因子控制的果糖/H( ) 同向转运蛋白可促进大流行性霍乱弧菌在海水中的存活。
DOI:
10.1038/s41467-021-24971-3
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发表时间:
2021-07-30
影响因子:
16.6
通讯作者:
Wang L
中科院分区:
文献类型:
--
作者:
Liu Y;Liu B;Xu T;Wang Q;Li W;Wu J;Zheng X;Liu B;Liu R;Liu X;Guo X;Feng L;Wang L
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. The bacterium Vibrio cholerae can colonize the human intestine and cause cholera, but spends much of its life cycle in seawater. Here, Liu et al. identify a fructose uptake system that is important for the growth of the bacteria in seawater, where fructose concentrations are low.
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