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投稿时间：2022-05-12
投稿时间：2022-05-12
中文摘要: 为更好地阐释阪崎克罗诺杆菌的耐干燥机制，该研究通过同源重组的方法敲除阪崎克罗诺杆菌ATCC BAA-894的ESA-00281基因，来探究该基因的功能及其在耐干燥中的作用。结果表明，该基因的缺失降低了耐干燥能力，与野生株相比，突变株干燥死亡率提高8.76%，表明此基因在阪崎克罗诺杆菌的耐干燥中发挥重要的正向调节作用。此外，该基因对阪崎克罗诺杆菌的生物膜形成及表面疏水性具有正向调节作用，但对膜透过性和运动性没有影响，表明该基因可能通过改变表面疏水性来调节生物膜的形成和对介质的黏附，从而正向调节菌株的耐干燥能力。
Abstract:To explain the desiccation resistance mechanism of Cronobacter sakazakii，this study knocked out the ESA-00281 gene of C.sakazakii ATCC BAA-894 by homologous recombination to explore its function and role in desiccation resistance.The results showed that the desiccation tolerance was reduced in the context of ESA-00281 gene deletion.Compared with the desiccation-induced mortality of the wild strain，that of the mutant strain was increased by 8.76%，indicating that this gene played an important positive regulatory role in the desiccation tolerance of C.sakazakii.In addition，the ESA-00281 gene positively regulated the biofilm formation and surface hydrophobicity of C.sakazakii，but showed no effect on membrane permeability and motility.It was suggested that this gene might positively regulate the desiccation tolerance of the strain by regulating the biofilm formation and adhesion to the medium via altering the surface hydrophobicity.
keywords: Cronobacter sakazakii gene knockout ESA-00281 biofilm surface hydrophobicity desiccation resistance
文章编号：202219025 中图分类号： 文献标志码：
基金项目:国家自然科学基金面上项目（31972167）；河北省重点研发计划项目（20372801D）
| 作者 | 单位 |
| 吕文1，张正阳1，李萍1，杜欣军1*，王硕2* | 1.食品营养与安全国家重点实验室，天津科技大学食品科学与工程学院，天津 300457；2.天津市食品科学与健康重点实验室，南开大学医学院，天津 300071 |
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