An influenza-derived membrane tension-modulating peptide regulates cell movement and morphology via actin remodeling
An influenza-derived membrane tension-modulating peptide regulates cell movement and morphology via actin remodeling
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DOI：
10.1038/s42003-019-0486-3
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发表时间：
2019-06-26
影响因子：
5.9
通讯作者：
Futaki, Shiroh
中科院分区：
文献类型：
--
作者：
Masuda, Toshihiro;Baba, Kentarou;Futaki, Shiroh
细胞膜张力与细胞运动和形态发生等多种细胞活动密切相关。因此，膜张力的调节可能是操纵细胞事件的新途径。在这里，我们表明，来自流感M2蛋白（M2[45-62]）的两亲性肽在细胞中的多个位点产生片状伪足。通过光镊评价M2[45-62]对细胞膜张力的影响。膜张力传感器蛋白FBP 17参与M2[45-62]驱动的板状伪足形成。M2中的赖氨酸至精氨酸取代[45-62]进一步增强了其板状伪足形成的活性。通过划痕迁移和transwell迁移试验评价，M2[45-62]具有降低细胞运动性的能力。M2处理后还观察到神经突生长增加[45-62]。上述结果表明M2[45-62]通过调节细胞膜张力调节细胞运动和形态的潜力。
Tension in cell membranes is closely related to various cellular events, including cell movement and morphogenesis. Therefore, modulation of membrane tension can be a new approach for manipulating cellular events. Here, we show that an amphipathic peptide derived from the influenza M2 protein (M2[45-62]) yields lamellipodia at multiple sites in the cell. Effect of M2[45-62] on cell membrane tension was evaluated by optical tweezer. The membrane tension sensor protein FBP17 was involved in M2[45-62]-driven lamellipodium formation. Lysine-to-arginine substitution in M2[45-62] further enhanced its activity of lamellipodium formation. M2[45-62] had an ability to reduce cell motility, evaluated by scratch wound migration and transwell migration assays. An increase in neurite outgrowth was also observed after treatment with M2[45-62]. The above results suggest the potential of M2[45-62] to modulate cell movement and morphology by modulating cell membrane tension.