Mitosis is the fundamental process by which genetic information is passed from a parental cell to two daughter cells. The crucial role of the microtubule cytoskeleton and the centrosomes in this process is well known, and still early mouse embryo lack centrosomes. In a study published in Cell researches have found an explanation to this paradox.

The microtubule cytoskeleton plays a major role in mitosis by aligning and carefully separating the duplicated sister chromatids. Centrosomes in turn play an important role in this process by nucleating and anchoring the microtubule filaments of the mitotic spindle. However, centrosomes are in fact missing from the early mouse embryo, at a stage in development when missegregation of chromosomes will have major consequences. This enigma that has been puzzling scientists for more than a decade, but it is becoming increasingly evident that another type of filaments can help overcome the lack of microtubule-organization by centrosomes.

In the study published in Cell, researchers identified a network of nuclear actin filaments that are essential for robust chromosome segregation in early mouse embryonic cells (Hernandez, 2025). Assembly of the nuclear F-actin network is mediated by Formin-2 and mDia-2, upon which interactions with prophase chromosomes occur through Myosin-10. Following nuclear breakdown, contraction of the network by actin disassembly ensures that the acentric chromosomes are organized toward the cell center, in a process that is completely independent of microtubules. Moreover, an additional network of actin filaments that forms around the metaphase microtubule spindle seems to control spindle size, a function that is otherwise mediated by astral microtubules. This complements the microtubule-centric view of mitosis, and provides evidence that alternative mechanisms can enable reliable chromosome segregation and genetic propagation during mitosis.

Below is a staining of human Formin-2 (FMN2). In the Human protein Atlas, Formin-2 localizes to actin filaments, cytosol, and plasma membrane. However, it has been shown to be recruited to the nucleoplasm in response to DNA damage, where it mediates clustering of damaged chromosomal regions (Aymard, 2017). Thus nuclear F-actin may have a role in chromosome clustering also in human cells.

Ulrika Axelsson