报告题目：The phospholipid asymmetry in cell fusion
报告人：张洋 深圳湾实验室特聘研究员
报告地点：36365线路检测中心入口生命科学楼408会议室
报告时间：2023年10月10日下午1:30
主办单位：36365线路检测中心入口
报告人简介：
张洋，深圳湾实验室特聘研究员，博士生导师。本科及博士毕业于华中科技大学生物医学工程专业，2015年-2022年在杜克大学生物化学系从事博士后研究。现就职于深圳湾实验室分子生理学研究所。课题组主要从事离子通道与磷脂翻转酶在生殖发育中的功能研究。先后在Neuron, Science Advances, eLife, PNAS, Cancer Discovery等期刊发表论文18篇。先后荣获Joy Cappel 青年科学家奖，Burroughs Wellcome Fund合作研究奖， Gordon Research Conference Best Poster Presentation奖等。担任法国国家科研署、欧盟脑计划外部评审专家。
报告摘要：
Cell fusion is fundamental to the reproduction, development, and homeostasis of multicellular organisms. In addition to various cell type-specific fusogenic proteins, cell surface externalization of phosphatidylserine (PS), a universal eat-me signal in apoptotic cells, has been observed in different cell fusion events. Nevertheless, the molecular underpinnings of PS externalization and cellular mechanisms of PS-facilitated cell-cell fusion are unclear. Our lab report that TMEM16F, a Ca2+-activated phospholipid scramblase (CaPLSase), plays an essential role in placental trophoblast fusion by translocating PS to cell surface independent of apoptosis. We also identify one of the physiological activation mechanisms of TMEM16F in human trophoblast fusion. Our findings provide insight into understanding cell fusion mechanism of other cell types and demonstrate one approach to understand TMEM16F’s biological functions in wide-ranging physiological and pathological processes, including blood coagulation, bone mineralization, HIV infection, trophoblast fusion, and SARS-CoV2-mediated syncytialization.
