CRISPR/Cas9-meditated gene knockout in pigs proves that LGALS12 deficiency suppresses the proliferation and differentiation of porcine adipocytes

文献类型： 外文期刊

第一作者： Wu, Wenjing

作者： Wu, Wenjing;Yin, Yajun;Zhang, Jin;Huang, Jing;Pan, Jianzhi;Yang, Ruifei;Li, Qiuyan;Zhang, Jin

作者机构：

关键词： LGALS12; CRISPR/Cas9; Knockout; Pig fat

期刊名称：BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS （ 影响因子：4.8； 五年影响因子：5.0 ）

ISSN： 1388-1981

年卷期： 2024 年 1869 卷 3 期

页码：

收录情况： SCI

摘要： LGALS12, also known as galectin12, belongs to the galectin family with beta-galactoside-binding activity. We previously reported that LGALS12 is an important regulator of adipogenesis in porcine adipocytes in vitro, but its value in pig breeding needed to be explored in vivo. In this study, we used CRISPR/Cas9 to construct porcine fetal fibroblasts (PFFs) with a 43 bp deletion in LGALS12 exon 2. Using these PFFs as donor cells, a LGALS12 knockout pig model was generated via somatic cell nuclear transfer. Primary cultures of porcine intramuscular (IM) and subcutaneous (SC) adipocytes were established using cells from LGALS12 knockout pigs and wild-type pigs. A comparison of these cells proved that LGALS12 deficiency suppresses cell proliferation via the RASp38MAPK pathway and promotes lipolysis via the PKA pathway in both IM and SC adipocytes. In addition, we observed AKT activation only in IM adipocytes and suppression of the Wnt/beta-catenin only in SC adipocytes. Our findings suggest that LGALS12 deficiency affects the adipogenesis of IM and SC adipocytes through different mechanisms.

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