Cdc42 移动性和膜流调节分裂酵母细胞形状和生存率
David M Rutkowski1, Vincent Vincenzetti2, Dimitrios Vavylonis1
1Department of Physics, Lehigh University, Bethlehem PA, USA.
bioRxiv : the preprint server for biology
|July 28, 2023
概括
细胞极化依赖于Cdc42 GTPase激活和膜流动. 降低Cdc42的移动性会损害两极分化,但减少GTPase激活蛋白 (GAPs) 会挽救生命力,揭示流动性.
科学领域:
- 细胞生物学 细胞生物学
- 系统生物学 系统生物学
- 生物物理学的生物物理.
背景情况:
- Cdc42 GTPase激活驱动着极化细胞外和膜流.
- 膜流影响了与膜相关的蛋白质的分布.
- 了解Cdc42分泌极化系统中的自我组织至关重要.
研究的目的:
- 在膜流下研究Cdc42分泌偏振系统的自我组织特性.
- 模拟Cdc42激活,水解和流动诱导的位移之间的相互作用.
- 确定Cdc42流动性在*Schizosaccharomyces pombe*中的极化中的作用.
主要方法:
- 开发了一种反应-扩散粒子模型,包括正反,GTPase激活蛋白 (GAPs) 和流动诱导的位移.
- 经过实验修改了Cdc42的膜结合特性,通过改变其前化部位.
- 利用计算机模拟和在裂变酵母中的实验观测.
主要成果:
- 模型模拟表明两极分化取决于低流动性GAPs的流动诱导的耗尽.
- 减少Cdc42的移动性导致Cdc42激活水平的降低和更广泛的极化斑块.
- Cdc42-1ritC细胞是可行的和两极分化的,Cdc42-2ritC表现为极化不良,Cdc42-3ritC是不可行的.
- GAP的耗尽增加了Cdc42的活性,但导致了极化损失,实验证实了这一点.
- 删除Cdc42 GAPs恢复了Cdc42-3ritC细胞的活力.
结论:
- 膜流是Cdc42驱动的模式形成的组成部分.
- Cdc42的移动性是调节极化的一个关键因素.
- 在Cdc42活性和GAP调节之间的平衡对于细胞活力和两极分化至关重要.
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