National Research Laboratory of Molecular Microbiology and Toxicology, Department of Agricultural Biotechnology and Center for Food and Bioconvergence, Seoul National University, Seoul, Republic of Korea.
Microb Genom. 2021 May;7(5). doi: 10.1099/mgen.0.000572.
An SNP is a spontaneous genetic change having a potential to modify the functions of the original genes and to lead to phenotypic diversity of bacteria in nature. In this study, a phylogenetic analysis of serovar Enteritidis, a major food-borne pathogen, showed that eight strains of . Enteritidis isolated in South Korea, including FORC_075 and FORC_078, have almost identical genome sequences. Interestingly, however, the abilities of FORC_075 to form biofilms and red, dry and rough (RDAR) colonies were significantly impaired, resulting in phenotypic differences among the eight strains. Comparative genomic analyses revealed that one of the non-synonymous SNPs unique to FORC_075 has occurred in , which encodes a sensor kinase of the EnvZ/OmpR two-component system. The SNP in leads to an amino acid change from Pro248 (CCG) in other strains including FORC_078 to Leu248 (CTG) in FORC_075. Allelic exchange of between FORC_075 and FORC_078 identified that the SNP in is responsible for the impaired biofilm- and RDAR colony-forming abilities of . Enteritidis. Biochemical analyses demonstrated that the SNP in significantly increases the phosphorylated status of OmpR in . Enteritidis and alters the expression of the OmpR regulon. Phenotypic analyses further identified that the SNP in decreases motility of . Enteritidis but increases its adhesion and invasion to both human epithelial cells and murine macrophage cells. In addition to an enhancement of infectivity to the host cells, survival under acid stress was also elevated by the SNP in . Together, these results suggest that the natural occurrence of the SNP in could contribute to phenotypic diversity of . Enteritidis, possibly improving its fitness and pathogenesis.
SNP 是一种自发的遗传变化,具有改变原有基因功能的潜力,从而导致自然界中细菌表型的多样性。在本研究中,对主要食源性病原体肠炎沙门氏菌血清型 Enteritidis 的系统发育分析表明,韩国分离的 8 株 Enteritidis 菌株,包括 FORC_075 和 FORC_078,其基因组序列几乎完全相同。然而,有趣的是,FORC_075 形成生物膜和红色、干燥、粗糙(RDAR)菌落的能力显著受损,导致 8 株菌株之间出现表型差异。比较基因组分析表明,FORC_075 中一个独特的非同义 SNP 发生在 中,该基因编码 EnvZ/OmpR 双组分系统的传感器激酶。 中的 SNP 导致其他菌株(包括 FORC_078)中的 Pro248(CCG)突变为 FORC_075 中的 Leu248(CTG)。在 FORC_075 和 FORC_078 之间交换 ,确定 中的 SNP 是导致肠炎沙门氏菌生物膜和 RDAR 菌落形成能力受损的原因。生化分析表明,肠炎沙门氏菌中 中的 SNP 显著增加了 OmpR 的磷酸化状态并改变了 OmpR 调控子的表达。表型分析进一步表明, 中的 SNP 降低了肠炎沙门氏菌的运动性,但增加了其对人上皮细胞和鼠巨噬细胞的粘附和侵袭能力。除了增强对宿主细胞的感染力外, 中的 SNP 还提高了其在酸性应激下的存活率。综上所述, 中的 SNP 的自然发生可能导致肠炎沙门氏菌表型的多样性,从而可能改善其适应性和致病性。