Listeria ivanovii is one of the two pathogenic species within the genus Listeria, the other being Listeria monocytogenes. In this study, we generated a stable pediocin resistant mutant Liv-r1 of a L. ivanovii strain, compared phenotypic differences between the wild-type and the mutant, localised the pediocin-induced mutations in the chromosome, and analysed the mechanisms behind the bacteriocin resistance. In addition to pediocin resistance, Liv-r1 was also less sensitive to nisin. The growth of Liv-r1 was significantly reduced with glucose and mannose, but less with cellobiose. The cells of Liv-r1 adsorbed less pediocin than the wild-type cells. Consequently, with less pediocin on the cell surface, the mutant was also less leaky, as shown as the release of intracellular lactate dehydrogenase to the supernatant. The surface of the mutant cells was more hydrophobic than that of the wild-type. Whole genome sequencing revealed numerous changes in the Liv-r1 chromosome. The mutations were found e.g., in genes encoding sigma-54-dependent transcription regulator and internalin B, as well as in genes involved in metabolism of carbohydrates such as glucose and cellobiose. Genetic differences observed in the mutant may be responsible for resistance to pediocin but no direct evidence is provided.

李斯特菌ivanovii是属内的两个致病物种之一李斯特菌，另一个是李斯特菌。在这项研究中，我们产生了一个稳定的耐潮霉素的L. ivanovii Liv-r1突变体菌株比较野生型和突变体之间的表型差异，在染色体上定位了pediocin诱导的突变，并分析了细菌素抗性的机制。除了对pediocin的耐药性外，Liv-r1对乳链菌肽的敏感性也较低。葡萄糖和甘露糖可显着降低Liv-r1的生长，而纤维二糖则可降低。Liv-r1细胞比野生型细胞吸附的pediocin少。因此，在细胞表面上具有较少的pediocin，该突变体的泄漏也较少，如细胞内乳酸脱氢酶向上清液的释放所示。突变细胞的表面比野生型的表面更疏水。全基因组测序揭示了Liv-r1染色体的许多变化。发现了突变，例如 在编码依赖于sigma-54的转录调节因子和Internalin B的基因中，以及在涉及碳水化合物（例如葡萄糖和纤维二糖）代谢的基因中。在突变体中观察到的遗传差异可能是对pediocin产生抗性的原因，但未提供直接证据。