Darland-Ransom Monica, Wang Xiaochen, Sun Chun-Ling, Mapes James, Gengyo-Ando Keiko, Mitani Shohei, Xue Ding
Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.
Science. 2008 Apr 25;320(5875):528-31. doi: 10.1126/science.1155847.
The asymmetrical distribution of phospholipids on the plasma membrane is critical for maintaining cell integrity and physiology and for regulating intracellular signaling and important cellular events such as clearance of apoptotic cells. How phospholipid asymmetry is established and maintained is not fully understood. We report that the Caenorhabditis elegans P-type adenosine triphosphatase homolog, TAT-1, is critical for maintaining cell surface asymmetry of phosphatidylserine (PS). In animals deficient in tat-1, PS is abnormally exposed on the cell surface, and normally living cells are randomly lost through a mechanism dependent on PSR-1, a PS-recognizing phagocyte receptor, and CED-1, which contributes to recognition and engulfment of apoptotic cells. Thus, tat-1 appears to function in preventing appearance of PS in the outer leaflet of plasma membrane, and ectopic exposure of PS on the cell surface may result in removal of living cells by neighboring phagocytes.
磷脂在质膜上的不对称分布对于维持细胞完整性和生理功能以及调节细胞内信号传导和重要细胞事件（如凋亡细胞清除）至关重要。磷脂不对称性是如何建立和维持的尚未完全清楚。我们报告称，秀丽隐杆线虫P型三磷酸腺苷酶同源物TAT-1对于维持磷脂酰丝氨酸（PS）的细胞表面不对称性至关重要。在缺乏tat-1的动物中，PS异常暴露于细胞表面，正常存活的细胞会通过一种依赖于PSR-1（一种PS识别吞噬细胞受体）和CED-1（有助于识别和吞噬凋亡细胞）的机制随机丢失。因此，tat-1似乎在防止PS出现在质膜外小叶中发挥作用，而PS在细胞表面的异位暴露可能导致相邻吞噬细胞清除存活细胞。
