F-actin polymers, assembled from soluble G-actin monomers, are essential players in cellular processes including vesicular transport and chromosome segregation, and are required for egg production from oocytes. A new study by the team of Binyam Mogessie (Scheffler et al., 2022) now proposes that the large mammalian oocyte nucleus helps maintain cytoplasmic F-actin organisation. By using live-cell and fixed-cell imaging, the authors first show that oocyte nuclei contain prominent F-actin structures. Surprisingly, disrupting the cytoplasmic F-actin network using the drug cytochalasin D leads to excessive nuclear F-actin assembly; this is a consequence of G-actin monomer transport into the nucleus, as confirmed by imaging labelled constructs. The authors also find that artificially overexpressing G-actin monomers in the nucleus is sufficient to induce polymerisation of nuclear F-actin. Conversely, reducing G-actin monomer transfer by blocking nuclear import leads to assembly of a dense cytoplasmic F-actin network that is incompatible with oocyte development. Finally, nuclear F-actin structures decline with female reproductive age, possibly due to disruptions in nuclear actin polymerisation. Collectively, this work points to the oocyte nucleus functioning in a G-actin-buffering process to continuously modulate the cytoplasmic actin network, with disruption of this buffer having important implications for female age-related infertility.