Expression Analysis and the Roles of the Sec1 Gene in Regulating the Composition of Mouse Gut Microbiota

The Sec1 gene encodes galactose 2-L-fucosyltransferase, whereas expression during development of the Sec1 gene mouse and its effect on the composition of the gut microbiota have rarely been reported. In this study, we examined Sec1 gene expression during mouse development, constructed Sec1 knockout mice, and sequenced their gut microbial composition. It was found that Sec1 was expressed at different stages of mouse development. Sec1 knockout mice have significantly higher intraperitoneal fat accumulation and body weight than wild-type mice. Analysis of gut microbial composition in Sec1 knockout mice revealed that at the phylum level, Bacteroidetes accounted for 68.8%and 68.3% of gut microbial composition in the Sec1&minus:/&minus: and Sec1+/+ groups, respectively, and Firmicutes accounted for 27.1% and 19.7%, respectively: while Firmicutes/Bacteroidetes were significantly higher in Sec1&minus:/&minus: mice than in Sec1+/+ mice (39.4% vs. 28.8%). In verucomicrobia, it was significantly higher in Sec1&minus:/&minus: mice than in Sec1+/+ group mice. At the family level, the dominant bacteria Prevotellaceae, Akkermansiaceae, Bacteroidaceae, and Lacilltobacaceae were found to be significantly reduced in the gut of Sec1&minus:/&minus: mice among Sec1+/+ gut microbes, while Lachnospiraceae, Ruminococcaceae, Rikenellaceae, Helicobacteraceae, and Tannerellaceae were significantly increased. Indicator prediction also revealed the dominant bacteria Akkermansiaceae and Lactobacillaceae in Sec1+/+ gut microorganisms, while the dominant bacteria Rikenellaceae, Marinifilaceae, ClostridialesvadinBB60aceae, Erysipelotrichaceae, Saccharimonadaceae, Clostridiaceae1, and Christensenellaceae in Sec1&minus:/&minus: group. This study revealed that the Sec1 gene was expressed in different tissues at different time periods in mice, and Sec1 knockout mice had significant weight gain, significant abdominal fat accumulation, and significant changes in gut microbial flora abundance and metabolic function, providing a theoretical basis and data support for the study of Sec1 gene function and effects on gut microbiota-related diseases.