miR-497 regulates fatty acid synthesis via LATS2 in bovine mammary epithelial cells.
Zhi ChenShuangfeng ChuYusheng LiangTianle XuYujia SunMingxun LiHuimin ZhangXiaoLong WangYongjiang MaoJuan J LoorYun WuZhangping YangPublished in: Food & function (2021)
Both mRNA and miRNA play an important role in the regulation of mammary fatty acid metabolism and milk fat synthesis. Although studies have shown a strong transcriptional control of fatty acid metabolism, less is known about the regulatory mechanisms of milk fat synthesis as a function of miRNA-mRNA interactions. In this study, we carried out transcriptome sequencing using mammary tissues from the early lactation period, peak lactation, mid-lactation and late lactation in dairy cows and identified key genes regulating milk fatty acid metabolism. A total of 32 differentially co-expressed gene were screened out. Large tumor suppressor kinase 2 (LATS2) was chosen for further study using luciferase reporter assays, qRT-PCR and western blotting. The aim was to demonstrate that miR-497 is an upstream regulator of LATS2, i.e. miR-497 and LATS2 are a potential miRNA/mRNA regulatory pair. The results indicated that miR-497 could inhibit the production of triglycerides (TAG) and unsaturated fatty acids in bovine mammary epithelial cells (BMECs). In contrast, LATS2 can promote the production of TAG and unsaturated fatty acids. "Rescue" experiments further verified the miR-497/LATS2 regulatory network. Overall, data underscored that the miR-497/LATS2 pathway exerts control on milk fat metabolism and provides a theoretical approach for improving milk quality via genetic means.
Keyphrases
- fatty acid
- dairy cows
- cell proliferation
- long non coding rna
- long noncoding rna
- transcription factor
- genome wide
- human milk
- adipose tissue
- magnetic resonance
- single cell
- magnetic resonance imaging
- copy number
- binding protein
- high throughput
- rna seq
- electronic health record
- tyrosine kinase
- genome wide identification
- high density
- climate change
- big data
- contrast enhanced
- heat stress
- heat shock