Zhu Dongdong, Zhang Zhengyang, Li Ping, Du Xinjun
State Key Laboratory of Food Nutrition and Safety, College of Food Science and Engineering, Tianjin University of Science and Technology, Tianjin 300457, China.
Microorganisms. 2024 Nov 30;12(12):2464. doi: 10.3390/microorganisms12122464.
, an opportunistic foodborne pathogen, has a strong resistance to osmotic stress and desiccation stress, but the current studies cannot elucidate this resistance mechanism absolutely. A mechanosensitive channel MscM was suspected of involving to desiccation resistance mechanism of To investigate the specific molecular mechanism, the mutant strain (Δ) was constructed using the homologous recombination method, and the complementary strain was obtained by gene complementation, followed by the analysis of the difference between the wild-type (WT), mutant, and complementary strains. Compared to the wild-type bacteria (WT), the inactivation rate of the Δ strain decreased by 15.83% ( < 0.01) after desiccation stress. The absence of the gene led to an increase in the membrane permeability of mutant strains. Through turbidity assay, it was found that the intracellular content of potassium ion (K) of the Δ strain increased by 2.2-fold ( < 0.05) compared to the WT strain, while other metal ion contents, including sodium ion (Na), calcium ion (Ca), and magnesium ion (Mg), decreased by 48.45% ( < 0.001), 24.29% ( < 0.001), and 26.11% ( < 0.0001), respectively. These findings indicate that the MscM channel primarily regulates cell membrane permeability by controlling K efflux to maintain the homeostasis of intracellular osmotic pressure and affect the desiccation tolerance of bacteria. Additionally, the deletion of the gene did not affect bacterial growth and motility but impaired surface hydrophobicity (reduced 20.52% compared to the WT strain, < 0.001), adhesion/invasion capability (reduced 26.03% compared to the WT strain, < 0.001), and biofilm formation ability (reduced 30.19% compared to the WT strain, < 0.05) of the bacteria. This study provides a reference for the role of the gene in the desiccation resistance and biofilm formation of .
作为一种机会性食源性病原体，对渗透胁迫和干燥胁迫具有很强的抗性，但目前的研究尚不能完全阐明这种抗性机制。一种机械敏感通道MscM被怀疑参与了[病原体名称]的抗干燥机制。为了研究其具体分子机制，采用同源重组方法构建了[病原体名称]突变株（Δ[基因名称]），并通过基因互补获得了互补株，随后分析野生型（WT）、突变株和互补株之间的差异。与野生型细菌（WT）相比，干燥胁迫后Δ[基因名称]株的失活率降低了15.83%（P<0.01）。[基因名称]基因的缺失导致突变株细胞膜通透性增加。通过比浊法测定发现，与WT株相比，Δ[基因名称]株的细胞内钾离子（K⁺）含量增加了2.2倍（P<0.05），而其他金属离子含量，包括钠离子（Na⁺）、钙离子（Ca²⁺）和镁离子（Mg²⁺）分别降低了48.45%（P<0.001）、24.29%（P<0.001）和26.11%（P<0.0001）。这些结果表明，MscM通道主要通过控制K⁺外流来调节细胞膜通透性，以维持细胞内渗透压的稳态，并影响细菌的干燥耐受性。此外，[基因名称]基因的缺失不影响细菌的生长和运动能力，但损害了细菌的表面疏水性（与WT株相比降低了20.52%，P<0.001）、黏附/侵袭能力（与WT株相比降低了26.03%，P<0.001）和生物膜形成能力（与WT株相比降低了30.19%，P<0.05）。本研究为[基因名称]基因在[病原体名称]的抗干燥和生物膜形成中的作用提供了参考。
