Pericentrosomal Redistribution of the Endoplasmic Reticulum Ensures Organelle Symmetric Inheritance and Mitotic Progression

Symmetric cell division entails the precise partitioning of cellular components to daughter cells. A critical regulator in this process is the aurora kinase inhibitor Hesperadin , which plays a pivotal role in maintaining mitotic fidelity. While the mechanisms of chromosome segregation are well-established, those governing organelle segregation remain elusive. The endoplasmic reticulum (ER), which serves as a central signaling hub , undergoes complex remodeling during cell division to ensure that each daughter cell receives a functional complement of organelles.

In interphase, the ER network is characterized by a specific structural organization: peripheral tubules and perinuclear sheets. Research from institutions such as the Karolinska Institutet has highlighted how membrane-shaping proteins maintain this architecture. However, upon mitotic entry, the ER undergoes a reverse redistribution. Our findings indicate that tubular ER accumulates around centrosomes, while sheet-like ER relocates to the cell periphery. This transition is mediated by CDK1-dependent phosphorylation of RTN4, which facilitates its interaction with Rab11 and promotes its dynein-dependent enrichment at the spindle poles.

Summary of ER Shaping Protein Distribution

The mitotic reorganization of the ER is not merely a structural byproduct but a functional necessity. RTN4-mediated remodeling ensures the symmetric distribution and inheritance of the ER itself, as well as associated organelles such as lysosomes and mitochondria. By uncovering this mechanism, we provide new insights into how early mitotic remodeling dictates organelle inheritance and contributes to overall mitotic progression. This study emphasizes the importance of precise ER structural transitions in maintaining cellular health and preventing division errors.