Data underlying the publication: "Mechanosensitive interactions between Jag1 and Myo1c control Jag1 trafficking in endothelial cells"

Morphogenesis of the cardiovascular system is responsive to hemodynamic cues sensed by endothelial cells. The organization of morphogenic signaling proteins is regulated by membrane presentation and internalization. Here we aimed to characterize factors that regulate this flow dependent protein localization by identifying differential interactors with the Notch ligand Jagged1 in response to shear stress. We cultured endothelial cells expressing Jagged1-APEX2 for proximity labeling on an orbital shaker shear stress platform. Myo1c was identified and confirmed through coimmunoprecipitation as a Jagged1 interacting factor under static conditions, with reduced interaction after exposure to shear. Jagged1 polarization downstream of shear followed by nucleograde transport was inhibited by Myo1c knockout. Further, Myo1c knockdown reduced membrane levels of Jagged1 under static, but not shear conditions. Together, our data reveal a role for Myo1c in the hemodynamic control of Jagged1 localization in endothelial cells.<br>This dataset contains data from <em>in vitro</em> experiments studying the interaction between Myo1c and Jagged1 under fluid flow shear stress.

心血管系统的形态发生过程可响应内皮细胞感知的血流动力学信号。形态发生相关信号蛋白的组装过程受膜呈递与内化作用调控。本研究旨在通过鉴定响应切应力（shear stress）时与Notch配体Jagged1的差异互作蛋白，表征调控该流动依赖性蛋白定位的因子。我们在轨道摇床式切应力平台上培养表达Jagged1-APEX2的内皮细胞以开展邻近标记（proximity labeling）实验。通过免疫共沉淀（coimmunoprecipitation）实验，鉴定并验证了Myo1c为静态条件下与Jagged1互作的因子，且该互作在细胞暴露于切应力后显著减弱。切应力下游的Jagged1极化及其后续的核定向转运过程可被Myo1c基因敲除（knockout）抑制。此外，静态条件下Myo1c基因敲低（knockdown）会降低Jagged1的膜定位水平，但该效应在切应力条件下并未出现。综上，本研究数据揭示了Myo1c在内皮细胞中通过血流动力学调控Jagged1定位的功能。
本数据集包含在流体流动切应力条件下研究Myo1c与Jagged1互作的体外（in vitro）实验数据。