由细胞施加的apico-basal力驱动上皮质折叠
Bruno Monier1, Melanie Gettings1, Guillaume Gay2
11] Université de Toulouse, UPS, LBCMCP, F-31062 Toulouse, France [2] CNRS, LBCMCP, F-31062 Toulouse, France.
Nature
|January 22, 2015
概括
异位细胞通过肌酸二线缆施加拉力,积极启动组织折叠. 这种新的机制揭示了细胞死亡如何驱动形态发生和组织重塑.
科学领域:
- 发展生物学 发展生物学
- 细胞生物学 细胞生物学
- 生物物理学的生物物理.
背景情况:
- 表皮的折叠对于在发育过程中形成3D结构至关重要.
- 由肌肉蛋白II和粘附结所驱动的角收缩是已知的机制.
- 在折叠中细胞重塑的初始触发因素尚不清楚.
研究的目的:
- 为了研究质细胞在启动上皮质折叠中的作用.
- 阐明细胞机制,通过这些细胞影响组织形态发生.
- 确定参与发育组织重塑的新信号通路.
主要方法:
- 发育中的组织的实时成像,以观察细胞动态.
- 使用理论生物物理3D模型进行模拟.
- 分析肌肉蛋白II分布和组织张力变化.
主要成果:
- 异位细胞通过apico-basal myosin II电缆产生暂时的拉力.
- 这些力量诱导组织张力增加和周围细胞中的肌酸二酶稳定.
- 来自亡细胞的依赖肌酸二的信号启动了细胞的重组和折叠.
结论:
- 亡细胞积极推动上皮质折叠,挑战了被动淘汰的观点.
- 通过髓二号信号传递,由亡细胞启动的新型形态发生机制被确定.
- 这项研究强调了细胞死亡在调节组织张力和重塑中的积极作用.
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