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Lemon exosome-like nanoparticles enhance stress survival of gut bacteria by RNase P-mediated specific tRNA decay

机译:柠檬外渗纳米颗粒通过RNase P介导的特异性TRNA衰减增强了肠细菌的应力存活

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摘要

Diet and bile play critical roles in shaping gut microbiota, but the molecular mechanism underlying interplay with intestinal microbiota is unclear. Here, we showed that lemon-derived exosome-like nanoparticles (LELNs) enhance lactobacilli toleration to bile. To decipher the mechanism, we used Lactobacillus rhamnosus GG (LGG) as proof of concept to show that LELNs enhance LGG bile resistance via limiting production of Msp1 and Msp3, resulting in decrease of bile accessibility to cell membrane. Furthermore, we found that decline of Msps protein levels was regulated through specific tRNAserUCC and tRNAserUCG decay. We identified RNase P, an essential housekeeping endonuclease, being responsible for LELNs-induced tRNAserUCC and tRNAserUCG decay. We further identified galacturonic acid-enriched pectin-type polysaccharide as the active factor in LELNs to increase bile resistance and downregulate tRNAserUCC and tRNAserUCG level in the LGG. Our study demonstrates a tRNA-based gene expression regulation mechanism among lactobacilli to increase bile resistance.
机译:饮食和胆汁在成形肠道微生物群中发挥关键作用,但肠道微生物群的相互作用的分子机制尚不清楚。在这里,我们表明柠檬衍生的外渗纳米颗粒(LELNS)增强乳杆菌含有叶片。为了破译该机制,我们使用Lactobacillus rhamoosus gg(lgg)作为概念的证据,以表明Lelns通过限制MSP1和MSP3的产生来增强LGG胆管抗性,导致细胞膜的胆汁脱离性降低。此外,我们发现通过特定的TrnAserucc和TnaSerucg衰减调节MSP蛋白水平的下降。我们鉴定了RNase P,这是一种必要的内脏内核酸酶,负责叶列诱导的TrnAserucc和TrnaSerucg衰减。我们进一步将富含环弧菌酸富集的果胶型多糖作为叶列的主动因子,以增加胆汁抗性和下调的TNASERUCC和TRNASERUCG水平。我们的研究表明,乳酸杆菌基于基于TRNA的基因表达调控机制,以增加胆汁抗性。

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