Huang Yong-Heng, Lin Jin-Shui, Ma Jin-Cheng, Wang Hai-Hong
Guangdong Provincial Key Laboratory of Protein Function and Regulation in Agricultural Organisms, College of Life Sciences, South China Agricultural University Guangzhou, China.
Shaanxi Engineering and Technological Research Center for Conversation and Utilization of Regional Biological Resources, College of Life Sciences, Yan'an University Yan'an, China.
Front Microbiol. 2016 Nov 29;7:1903. doi: 10.3389/fmicb.2016.01903. eCollection 2016.
is extremely resistant to triclosan. Previous studies have shown that encodes a triclosan-resistant enoyl-acyl-carrier protein reductase (ENR), FabV, and that deletion of causes to be extremely sensitive to triclosan. In this report, we complemented a deletion strain with several triclosan-resistant ENR encoding genes, including and . All complemented strains restored triclosan resistance to the level of the wild-type strain, which confirmed that triclosan-resistant ENR allows to be extremely resistant to triclosan. Moreover, exhibits pleiotropic effects. Deletion of led to show attenuated swarming motility, decreased rhamnolipid, pyoverdine and acyl-homoserine lactones (AHLs) production. Complementation of the mutant with any one ENR encoding gene could restore these features to some extent, in comparison with the wild-type strain. Furthermore, we found that addition of exogenous AHLs could restore the mutant strain to swarm on semisolid plates and to produce more virulence factors than the mutant strain. These findings indicate that deletion of reduced the activity of ENR in , decreased fatty acid synthesis, and subsequently depressed the production of AHLs and other virulence factors, which finally may led to a reduction in the pathogenicity of . Therefore, should be an ideal target for the control of infectivity.
对三氯生具有极强的抗性。先前的研究表明，其编码一种抗三氯生的烯酰 - 酰基载体蛋白还原酶（ENR），即FabV，并且缺失该基因会导致其对三氯生极其敏感。在本报告中，我们用几个抗三氯生的ENR编码基因，包括[具体基因名称1]和[具体基因名称2]，对一个缺失该基因的菌株进行了互补。所有互补菌株都将三氯生抗性恢复到了野生型菌株的水平，这证实了抗三氯生的ENR使该菌株对三氯生具有极强的抗性。此外，该基因表现出多效性。缺失该基因导致其群体游动性减弱，鼠李糖脂、绿脓菌素和酰基高丝氨酸内酯（AHLs）的产量降低。与野生型菌株相比，用任何一个ENR编码基因对该突变体进行互补都能在一定程度上恢复这些特征。此外，我们发现添加外源AHLs可以使该突变体菌株在半固体平板上群体游动，并比该突变体菌株产生更多的毒力因子。这些发现表明，缺失该基因降低了该菌株中ENR的活性，减少了脂肪酸合成，随后抑制了AHLs和其他毒力因子的产生，这最终可能导致该菌株的致病性降低。因此，该基因应该是控制该菌株感染性的理想靶点。
