Does inhibition of phosphatidylserine synthase induce autophagy?

为了研究磷脂酰丝氨酸合成缺陷与自噬性细胞死亡之间的关系，我们集中研究了一种磷脂酰丝氨酸合酶活性缺陷的CHO突变体。当突变体细胞在缺乏磷脂酰丝氨酸的培养基中培养时，LC 3-II，一种有前途的自噬标记物，在24小时内增加。在LC 3-II诱导后24- 48小时，细胞活力降低。结果提示，磷脂酰丝氨酸脱肽诱导细胞死亡时，自噬可能发挥细胞保护作用。

To investigate the relation between a defect in phosphatidylserine synthesis and autophagic cell death, we focused on a CHO mutant that has a defect in an activity of phosphatidylserine synthase. When the mutant cells were cultured in a medium lacking phosphatidylserine, LC3-II, a promising autophagic marker, was increased within 24h. At 24-48h after induction of LC3-II, cell viability was decreased. The results suggested that the autophagy play a cytoprotective role, when phsophatidylserine depeletion-induced cell death.