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Abstract：
The suppressor of cytokine signaling 3 (SOCS3) is a key signaling molecule that regulates milk synthesis in dairy livestock. However, the molecular mechanism by which SOCS3 regulates lipid synthesis in goat milk remains unclear. This study aimed to screen for key downstream genes associated with lipid synthesis regulated by SOCS3 in goat mammary epithelial cells (GMECs) using RNA sequencing (RNA-seq). Goat SOCS3 overexpression vector (PC-SOCS3) and negative control (PCDNA3.1) were transfected into GMECs. Total RNA from cells after SOCS3 overexpression was used for RNA-seq, followed by differentially expressed gene (DEG) analysis, functional enrichment analysis, and network prediction. SOCS3 overexpression significantly inhibited the synthesis of triacylglycerol, total cholesterol, non-esterified fatty acids, and accumulated lipid droplets. In total, 430 DEGs were identified, including 226 downregulated and 204 upregulated genes, following SOCS3 overexpression. Functional annotation revealed that the DEGs were mainly associated with lipid metabolism, cell proliferation, and apoptosis. We found that the lipid synthesis-related genes, STAT2 and FOXO6, were downregulated. In addition, the proliferation-related genes BCL2, MMP11, and MMP13 were upregulated, and the apoptosis-related gene CD40 was downregulated. In conclusion, six DEGs were identified as key regulators of milk lipid synthesis following SOCS3 overexpression in GMECs. Our results provide new candidate genes and insights into the molecular mechanisms involved in milk lipid synthesis regulated by SOCS3 in goats.
摘要：
细胞因子信号传导抑制因子3（SOCS3）是调节乳畜乳合成的关键信号分子。然而,SOCS3调节羊奶中脂质合成的分子机制尚不清楚。本研究旨在使用RNA测序（RNA-seq）筛选山羊乳腺上皮细胞（GMEC）中与SOCS3调节的脂质合成相关的关键下游基因。将山羊SOCS3过表达载体(PC-SOCS3)和阴性对照(PCDNA3.1)转染到GMEC中。SOCS3过表达后细胞的总RNA用于RNA-seq，然后进行差异表达基因（DEG）分析，功能富集分析，和网络预测。SOCS3过表达显著抑制三酰甘油的合成,总胆固醇,非酯化脂肪酸，和积累的脂滴。总的来说,确定了430个DEG,包括226个下调基因和204个上调基因，SOCS3过表达后。功能注释显示DEGs主要与脂质代谢有关,细胞增殖，和凋亡。我们发现与脂质合成相关的基因，STAT2和FOXO6下调。此外,增殖相关基因BCL2，MMP11和MMP13上调，凋亡相关基因CD40下调。总之,在GMEC中过表达SOCS3后，六个DEGs被确定为乳脂合成的关键调节剂。我们的结果提供了新的候选基因和对山羊中SOCS3调节的乳脂合成的分子机制的见解。
