ELF5 gene promotes milk lipid synthesis in goat mammary epithelial cells by transcriptomic analysis

IF 3.4 2区 生物学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Cunxia Ma, Yuzhu Guo, Tongtong Tu, Shuangshuang Cui, Jintao Zhong, Yunhai Zhang, Ning Song, Hongyu Liu
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引用次数: 0

Abstract

E74-like factor 5 (ELF5) is an Ets transcription factor of epithelial development, while the function of ELF5 gene in goat milk fat synthesis remains to be elucidated. In goat mammary epithelial cells, we performed RNA sequencing and analyzed differentially expressed genes (DEGs) after ELF5 gene overexpression. ELF5 gene significantly up-regulated the synthesis of triglyceride, total cholesterol, free fatty acid, and lipid droplets. We obtained 929 DEGs after ELF5 gene overexpression in GMECs. Among the DEGs, SPP1, ELOVL1, PNPLA2, FOXO1, PTGS2, SEMA6A, ACSL5, and GPNMB genes that are related to lipid metabolism were identified. Enrichment analysis showed MAPK and FoxO signaling pathways were up-regulated by ELF5 gene overexpression in GMECs. These findings offer evidence that ELF5 gene could be a candidate gene for the regulation of milk lipid synthesis in goats, and provide molecular targets for the breeding of goats with high milk fat.
ELF5基因促进山羊乳腺上皮细胞脂质合成的转录组学分析
e74样因子5 (E74-like factor 5, ELF5)是一种与上皮发育相关的Ets转录因子,而ELF5基因在羊乳脂肪合成中的功能尚不清楚。在山羊乳腺上皮细胞中,我们进行了RNA测序,并分析了ELF5基因过表达后的差异表达基因(DEGs)。ELF5基因显著上调甘油三酯、总胆固醇、游离脂肪酸和脂滴的合成。ELF5基因在gmec中过表达后获得929个deg。在deg中,鉴定出与脂质代谢相关的SPP1、ELOVL1、PNPLA2、FOXO1、PTGS2、SEMA6A、ACSL5和GPNMB基因。富集分析显示,ELF5基因过表达上调了MAPK和FoxO信号通路。这些结果表明,ELF5基因可能是山羊脂合成调控的候选基因,为高脂山羊的育种提供了分子靶点。
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来源期刊
Genomics
Genomics 生物-生物工程与应用微生物
CiteScore
9.60
自引率
2.30%
发文量
260
审稿时长
60 days
期刊介绍: Genomics is a forum for describing the development of genome-scale technologies and their application to all areas of biological investigation. As a journal that has evolved with the field that carries its name, Genomics focuses on the development and application of cutting-edge methods, addressing fundamental questions with potential interest to a wide audience. Our aim is to publish the highest quality research and to provide authors with rapid, fair and accurate review and publication of manuscripts falling within our scope.
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