细胞有丝分裂过程中Aurora-A激酶驱动内质网动态形变促进染色体排列的机制研究

细胞分裂需要将遗传物质、细胞器和其它细胞成分准确分配到两个子细胞中。内质网在有丝分裂过程中发生结构和功能的改变。然而，内质网和遗传物质如何协同完成有丝分裂过程尚不清楚。我们前期研究发现：内质网在有丝分裂过程中发生以塑型蛋白Atlastin（ATL）和Reticulon（RTN）为基础的动态形变；内质网动态形变稳定纺锤体，促进染色体排列，维持遗传的稳定；Aurora-A激酶通过磷酸化Rab1A驱动内质网动态形变；线虫模型证实内质网动态形变在生物进化中保守。据此我们提出假说：在有丝分裂过程中，Aurora-A激酶磷酸化激活Rab1A,调控内质网塑形蛋白ATL和RTN的功能转换，驱动内质网动态形变，稳定纺锤体，促进染色体排列。本研究拟从分子和细胞水平，利用线虫和小鼠模型，探讨内质网动态形变的意义和调控机理，并将从细胞器和遗传物质协同分配的角度，进一步解析真核细胞有丝分裂这一复杂过程。

Cell division requires accurate allocation of genetic material, organelles and other cellular components into two daughter cells. Endoplasmic reticulum (ER) is the largest organelle in cells, which changes its structure and function during mitosis. however, how the endoplasmic reticulum and genetic material cooperate to complete the mitotic process is unclear. Our previous studies found that: endoplasmic reticulum exhibited biphasic dynamic during cell mitosis, which based on ER shaping protein Atlastin (ATL) and Reticulon (RTN); endoplasmic reticulum biphasic dynamic stabilized spindle, promoted chromosome alignment and maintained genetic stability; Aurora-A kinase promoted endoplasmic reticulum biphasic dynamic through phosphorylating Rab1A; C. elegant model indicited that mitotic endoplasmic reticulum biphasic dynamic was conserved in biological evolution. Therefore, we supposed that Aurora-A kinases activated Rab1A during mitosis, and then regulated the functional transformation of endoplasmic reticulum shaping protein ATL and RTN, promoted endoplasmic reticulum biphasic dynamic, stabilized spindle and ensured chromosome arrangement. This study intends to explore the significance and regulatory mechanism of endoplasmic reticulum dynamic using C. elegant and mouse models. Our study will further analyze the complex process of eukaryotic mitosis from the point of view of the synergistic distribution of organelles and genetic materials.