Data from: Fragility of foot process morphology in kidney podocytes arises from chaotic spatial propagation of cytoskeletal instability

The kidney podocyte's function depends on finger-like projections (foot processes) that interdigitate with those from neighboring cells to form the glomerular filtration barrier. The integrity of the barrier depends on spatial control of dynamics of actin cytoskeleton in the foot processes. We determined how imbalances in regulation of actin cytoskeletal dynamics can result in pathological morphology. We obtained 3-D electron microscopy images of podocytes and used quantitative features to build dynamical models to investigate how regulation of actin dynamics within foot processes controls local morphology. We find that imbalances in regulation of actin bundling, lead to chaotic spatial patterns that could impair the foot process morphology. Simulation results are consistent with experimental observations for cytoskeletal reconfiguration by dysregulated RhoA or Rac1, and they predict compensatory mechanisms for biochemical stability. We conclude that podocyte morphology, optimized for filtration, is intrinsically fragile, whereby local transient biochemical imbalances may lead to permanent morphological changes associated with pathophysiology.肾足细胞（kidney podocyte）的功能依赖于其指状突起——足突（foot processes）——与邻近细胞的足突相互交错，从而形成肾小球滤过屏障（glomerular filtration barrier）。该屏障的完整性取决于足突内肌动蛋白细胞骨架（actin cytoskeleton）动力学的空间调控。我们探究了肌动蛋白细胞骨架动力学调控失衡如何导致病理形态学改变。我们获取了肾足细胞的三维电子显微镜图像，并利用定量特征构建动力学模型，以研究足突内肌动蛋白动力学的调控如何控制局部形态。我们发现肌动蛋白束集（actin bundling）调控失衡会引发混沌空间模式，这可能会破坏足突形态。仿真结果与失调的RhoA或Rac1引发的细胞骨架重排的实验观测相符，并预测了维持生化稳定性的补偿机制。我们得出结论：为滤过功能优化的肾足细胞形态本质上较为脆弱，局部短暂的生化失衡可能引发与病理生理学相关的永久性形态改变。