Sec1, a member of the Sec1 family, is involved in synaptic transmission and general secretion [1]. It lacks a transmembrane domain but can be membrane-bound, potentially due to interaction with syntaxin. The Sec1 proteins play a positive role in exocytosis, and their loss-of-function mutations can block protein transport in yeast [1].

In a mouse model of inflammatory bowel disease (IBD), Sec1 knockout led to the deterioration of IBD and elevated immune responses in the colonic mucosa. Silencing Sec1 in murine colon cancer cell lines increased the secretion of inflammatory cytokines. Also, Sec1 expression promoted the proliferation of colon epithelial cells, inhibited cell apoptosis, and facilitated the repair of inflammatory injury [2]. In addition, Sec1 knockout mice had significant weight gain, abdominal fat accumulation, and changes in gut microbial flora abundance and metabolic function [3].

In conclusion, Sec1 plays important roles in regulating intestinal mucosal immunity in IBD and impacts gut microbiota-related physiological conditions. The gene knockout mouse models have revealed its functions in these biological processes and disease conditions, providing valuable insights into understanding the mechanisms underlying IBD and gut microbiota-related disorders.

References:

1. Halachmi, N, Lev, Z. . The Sec1 family: a novel family of proteins involved in synaptic transmission and general secretion. In Journal of neurochemistry, 66, 889-97. doi:. https://pubmed.ncbi.nlm.nih.gov/8769846/

2. Cai, Jing, Wu, Hao, Wang, Chenxing, Jin, Yingli, Qian, Cao. 2023. Sec1 regulates intestinal mucosal immunity in a mouse model of inflammatory bowel disease. In BMC immunology, 24, 51. doi:10.1186/s12865-023-00578-9. https://pubmed.ncbi.nlm.nih.gov/38066482/

3. Ren, Zhanshi, Fan, Hairui, Gu, Shanshen, Bao, Wenbin, Wu, Shenglong. 2022. Expression Analysis and the Roles of the Sec1 Gene in Regulating the Composition of Mouse Gut Microbiota. In Genes, 13, . doi:10.3390/genes13101858. https://pubmed.ncbi.nlm.nih.gov/36292744/