哺乳期
PI3K/AKT/mTOR通路
磷酸化
P70-S6激酶1
细胞生物学
化学
蛋白激酶B
基因敲除
乳腺
细胞信号
信号转导
细胞内
亮氨酸
生物
核糖体蛋白s6
细胞培养
蛋白质生物合成
生物化学
mTORC1型
分子生物学
基因表达
作者
Yongding Ke,B. Chen,Xinping Wang,Xingyue Jiang,Tingting Liu,Yi Pan,Yixuan Li,Zhaoxin Yang,Xi Chen,Xingtang Fang,Yanhong Wang,Chunlei Zhang
标识
DOI:10.1021/acs.jafc.5c08723
摘要
Sestrin 2, coded by the SESN2 gene, as a leucine sensor, can recognize and bind intracellular free leucine, regulate the mammalian target of rapamycin (mTOR) signaling pathway, and participate in protein synthesis, but its molecular mechanism in the mammary gland is still unclear. The aim of this study is to investigate the molecular mechanism of SESN2 on milk protein synthesis in bovine mammary epithelial cells (MAC-T) and further confirm its lactation-regulating function in the mouse mammary gland. In this study, it was found that, after SESN2 knockdown (KD), the phosphorylation levels of mTOR protein and downstream signaling molecule S6K were increased and the expression of α- and β-casein was increased in MAC-T cells. At the same time, the expression and distribution of LAT1 (the primary transporter of leucine) in the KD cell membrane increased. In mouse mammary tissue, milk production and the expression of α- and β-casein increased after SESN2 knockout (KO). In addition, the ability of leucine sensing was weakened in SESN2 KO mice, and phosphorylation of the mTOR protein and downstream signaling molecule S6K was decreased after the addition of the LAT1 selective inhibitor BCH to the mouse mammary gland explants. In summary, this is the first demonstration of SESN2-LAT1 cross-talk in milk protein synthesis and lactation. This study provides a new idea for further revealing the regulation mechanism of lactation and milk protein synthesis and provides a new target for the genetic section of dairy cattle.
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