Sarkar Apurba, Jana Aniket, Agashe Atharva, Wang Ji, Kapania Rakesh, Gov Nir S, DeLuca Jennifer G, Paul Raja, Nain Amrinder S
School of Mathematical and Computational Sciences, Indian Association for the Cultivation of Science, Jadavpur, Kolkata 700032, India.
Department of Mechanical Engineering, Virginia Tech, Blacksburg, VA 24061.
bioRxiv. 2024 Apr 15:2024.04.12.589246. doi: 10.1101/2024.04.12.589246.
Accurate positioning of the mitotic spindle within the rounded cell body is critical to physiological maintenance. Adherent mitotic cells encounter confinement from neighboring cells or the extracellular matrix (ECM), which can cause rotation of mitotic spindles and, consequently, titling of the metaphase plate (MP). To understand the positioning and orientation of mitotic spindles under confinement by fibers (ECM-confinement), we use flexible ECM-mimicking nanofibers that allow natural rounding of the cell body while confining it to differing levels. Rounded mitotic bodies are anchored in place by actin retraction fibers (RFs) originating from adhesion clusters on the ECM-mimicking fibers. We discover the extent of ECM-confinement patterns RFs in 3D: triangular and band-like at low and high confinement, respectively. A stochastic Monte-Carlo simulation of the centrosome (CS), chromosome (CH), membrane interactions, and 3D arrangement of RFs on the mitotic body recovers MP tilting trends observed experimentally. Our mechanistic analysis reveals that the 3D shape of RFs is the primary driver of the MP rotation. Under high ECM-confinement, the fibers can mechanically pinch the cortex, causing the MP to have localized deformations at contact sites with fibers. Interestingly, high ECM-confinement leads to low and high MP tilts, which mechanistically depend upon the extent of cortical deformation, RF patterning, and MP position. We identify that cortical deformation and RFs work in tandem to limit MP tilt, while asymmetric positioning of MP leads to high tilts. Overall, we provide fundamental insights into how mitosis may proceed in fibrous ECM-confining microenvironments in vivo.
有丝分裂纺锤体在圆形细胞体内的准确定位对于生理维持至关重要。贴壁有丝分裂细胞会受到相邻细胞或细胞外基质(ECM)的限制,这可能导致有丝分裂纺锤体旋转,进而导致中期板(MP)倾斜。为了了解在纤维限制(ECM限制)下有丝分裂纺锤体的定位和方向,我们使用了柔性的模仿ECM的纳米纤维,这些纤维在使细胞体自然变圆的同时将其限制在不同水平。圆形有丝分裂体通过源自模仿ECM纤维上粘附簇的肌动蛋白收缩纤维(RFs)固定在原位。我们发现ECM限制模式在三维空间中对RFs的影响程度:在低限制和高限制下分别为三角形和带状。对中心体(CS)、染色体(CH)、膜相互作用以及有丝分裂体上RFs的三维排列进行的随机蒙特卡罗模拟重现了实验观察到的MP倾斜趋势。我们的机理分析表明,RFs的三维形状是MP旋转的主要驱动因素。在高ECM限制下,纤维可以机械挤压皮质,导致MP在与纤维的接触部位出现局部变形。有趣的是,高ECM限制会导致MP出现低倾斜和高倾斜,这在机理上取决于皮质变形程度、RF模式和MP位置。我们确定皮质变形和RFs协同作用以限制MP倾斜,而MP的不对称定位会导致高倾斜。总体而言,我们提供了关于有丝分裂在体内纤维状ECM限制微环境中如何进行的基本见解。