持续的细胞接触使得基于E-cadherin/HMR-1和PAR-3的E-cadherin/HMR-1和PAR-3的对称性在正在发展中的C. elegans表皮内被打破
Victor F Naturale1, Melissa A Pickett2, Jessica L Feldman1
1Department of Biology, Stanford University, Stanford, CA 94305, USA.
Developmental cell
|August 8, 2023
概括
细胞接触持续时间的不对称性指导着C. elegans的组织极性. PAR-3和E-cadherin/HMR-1形成局部极性复合体,它们迁移以建立整个组织组织.
科学领域:
- 发展生物学 发展生物学
- 细胞生物学 细胞生物学
- 皮质生物学 皮质生物学
背景情况:
- 多细胞发育依赖于整个组织的模式.
- 细胞必须建立极性轴,并与空间和时间上的邻居协调它们.
研究的目的:
- 为了确定C. elegans肠表皮的全组织模式的机制.
- 了解细胞接触不对称如何告知极性建立.
主要方法:
- 使用了C. elegans肠表皮模型系统.
- 研究了PAR-3支架蛋白和E-cadherin/HMR-1跨膜蛋白的作用.
- 分析了局部极性复合体 (LPC) 和它们的迁移.
主要成果:
- 鉴定了一种由细胞接触生命周期不对称性驱动的模式机制.
- 在同型接触时,PAR-3和HMR-1在LPC中招募顶点决定因素.
- LPCs通过HMR-1迁移到中间线,建立整个组织的极性.
- HMR-1的非粘合性信号促进了组织层面的通信.
结论:
- 对称性破坏源于PAR-3依赖的细胞内极化和HMR-1-介导的组织通信.
- 不同的细胞接触寿命,受到邻居交换和细胞分裂的影响,决定了LPC的持久性和对称性破坏.
- 这种机制在没有明显的分子不对称的情况下为表皮质两极化提供了一个框架.
关键词:
这里是C. elegans.这是E-cadherin.在HMR-1中,它是HMR-1.在 PAR-3 中,我们可以看到 PAR-3 .细胞接触细胞接触在表皮质上.形态发生 (morphogenesis) 是一种形态的产生.极性的极性 极性的极性对称性打破 破坏对称性更多相关视频
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