Levandosky Katherine, Copos Calina
Department of Mathematics, Northeastern University, Boston, Massachusetts, United States of America.
Department of Biology, Northeastern University, Boston, Massachusetts, United States of America.
PLoS Comput Biol. 2024 Dec 17;20(12):e1012216. doi: 10.1371/journal.pcbi.1012216. eCollection 2024 Dec.
Symmetry breaking, which is ubiquitous in biological cells, functionally enables directed cell movement and organized embryogenesis. Prior to movement, cells break symmetry to form a well-defined cell front and rear in a process called polarization. In developing and regenerating tissues, collective cell movement requires the coordination of the polarity of the migration machineries of neighboring cells. Though several works shed light on the molecular basis of polarity, fewer studies have focused on the regulation across the cell-cell junction required for collective polarization, thus limiting our ability to connect tissue-level dynamics to subcellular interactions. Here, we investigated how polarity signals are communicated from one cell to its neighbor to ensure coordinated front-to-rear symmetry breaking with the same orientation across the group. In a theoretical setting, we systematically searched a variety of intercellular interactions and identified that co-alignment arrangement of the polarity axes in groups of two and four cells can only be achieved with strong asymmetric regulation of Rho GTPases or enhanced assembly of complementary F-actin structures across the junction. Our results held if we further assumed the presence of an external stimulus, intrinsic cell-to-cell variability, or larger groups. The results underline the potential of using quantitative models to probe the molecular interactions required for macroscopic biological phenomena. Lastly, we posit that asymmetric regulation is achieved through junction proteins and predict that in the absence of cytoplasmic tails of such linker proteins, the likeliness of doublet co-polarity is greatly diminished.
对称性破缺在生物细胞中普遍存在,其功能上能够实现细胞的定向运动和有序的胚胎发育。在运动之前,细胞通过一个称为极化的过程打破对称性,形成明确的细胞前端和后端。在发育和再生组织中,集体细胞运动需要相邻细胞迁移机制极性的协调。尽管有几项研究揭示了极性的分子基础,但较少有研究关注集体极化所需的跨细胞间连接的调控,从而限制了我们将组织水平动态与亚细胞相互作用联系起来的能力。在这里,我们研究了极性信号如何从一个细胞传递到其邻居,以确保整个群体以相同方向协调地从前向后打破对称性。在理论框架下,我们系统地研究了各种细胞间相互作用,发现只有通过对Rho GTPases进行强不对称调控或增强跨连接的互补F-肌动蛋白结构的组装,才能实现两个和四个细胞群体中极性轴的共排列。如果我们进一步假设存在外部刺激、细胞间内在变异性或更大的群体,我们的结果仍然成立。这些结果强调了使用定量模型来探究宏观生物现象所需分子相互作用的潜力。最后,我们推测不对称调控是通过连接蛋白实现的,并预测在没有此类连接蛋白细胞质尾巴的情况下,双联体共极性的可能性会大大降低。