粘附能量控制了脂质结合介导的内细胞分裂
Raluca Groza1, Kita Valerie Schmidt1,2, Paul Markus Müller1
1Institute of Biochemistry, Freie Universität Berlin, Thielallee 63, 14195, Berlin, Germany.
Nature communications
|March 30, 2024
概括
结合细胞膜的球状颗粒可以使它们变形,引发克拉素独立的内细胞分裂. 这种结合诱导的膜变形足以进行内化,揭示了病原体进入的共同生物物理机制.
科学领域:
- 细胞生物学 细胞生物学
- 生物物理学的生物物理.
- 细胞内核的分子机制 细胞内核的分子机制
背景情况:
- 细菌毒素和病毒利用多价值脂质结合来变形细胞膜,促进了克拉素独立的内细胞分裂.
- 膜变形和随后的内细胞内化之间的精确机械联系仍然不完全理解.
研究的目的:
- 研究由多价值脂质结合诱导的膜变形和克拉特林独立内细胞分裂之间的机械联系.
- 为了确定由球状颗粒诱导的结合诱导的膜变形是否足以进行细胞内化.
主要方法:
- 使用脂质定受体 (GPI定抗GFP纳米体) 和多价值球状结合剂 (40nm粒子与180个GFP分子) 开发合成细胞系统.
- 由不同的受体-连接体亲属关系 (跨越7个数量级) 引发的膜变形和内细胞分裂的定量分析.
- 在合成系统中观察颗粒粘附,膜变形和克拉特林独立内细胞分裂.
主要成果:
- 合成球状颗粒成功地与细胞结合,在粘附时诱导显著的血膜变形,并通过克拉素独立的内细胞化内化.
- 识别出了膜粘附能量的明确值,超过这个值后,膜变形可靠地导致内细胞分裂.
- 球状粒子的多价值结合被证明足以诱导膜变形和随后的内部化.
结论:
- 由多价值球状颗粒引起的结合诱导的膜变形是克拉斯林独立内细胞分裂的足够机制.
- 这种生物物理机制可能是各种脂质结合毒素和病原体的内细胞分裂的基础.
- 该研究阐明了由膜相互作用介导的病原体和毒素进入的常见途径.
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