铜绿假单胞菌中S型绿脓杆菌素与荧光嗜铁素的功能协同性分析

在铜绿假单胞菌(Pseudomonas aeruginosa)中，S型绿脓杆菌素S2和S4与细菌中的铁载体荧光嗜铁素(pyoverdine)使用相同的摄取通道，表明二者之间存在某些联系。本研究表征了细菌中3个S型绿脓杆菌素(Pys2、PA3866、PyoS5)的单细菌基因表达分布，并研究了S2型绿脓杆菌素对细菌摄取荧光嗜铁素的影响。结果表明，在DNA损伤压力下，S型绿脓杆菌素基因的表达在细菌种群中呈现出高度分化，外源加入S2型绿脓杆菌素会减少细菌对荧光嗜铁素的摄取，因此S2型绿脓杆菌素的存在会阻止不合成荧光嗜铁素的“欺骗者”摄取环境中荧光嗜铁素，进而减弱其对活性氧(reactive oxygen species,ROS)压力的抵抗能力。另外我们发现，在细菌中过表达SOS响应(SOS response)调节因子PrtN时，荧光嗜铁素相关合成基因的表达量显著降低，进而导致荧光嗜铁素的总合成量和外分泌量显著降低。以上结果表明细菌中SOS压力响应系统与铁摄取系统的功能是存在相互联系的。

Functional synergism of pyoverdine and the S-type pyocins of Pseudomonas aeruginosa

Pyocin S2 and S4 in Pseudomonas aeruginosa use the same uptake channels as the pyoverdine does in bacteria, indicating a possible connection between them. In this study, we characterized the single bacterial gene expression distribution of three S-type pyocins (Pys2, PA3866, and PyoS5) and examined the impact of pyocin S2 on bacterial uptake of pyoverdine. The findings demonstrated that the expression of the S-type pyocin genes was highly differentiated in bacterial population under DNAdamage stress. Moreover, exogenous addition of pyocin S2 reduces the bacterial uptake of pyoverdine so that the presence of pyocin S2 prevents the uptake of environmental pyoverdine by non-pyoverdine synthesizing ''cheaters'', thereby reducing their resistance to oxidative stress. Furthermore, we discovered that overexpression of the SOS response regulator PrtN in bacteria significantly decreased the expression of genes involved in the synthesis of pyoverdine, significantly decreasing the overall synthesis and exocytosis of pyoverdine. These findings imply a connection between the function of the iron absorption system and the SOS stress response mechanism in bacteria.