• Register
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.


Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.


Role of Filia, a maternal effect gene, in maintaining euploidy during cleavage-stage mouse embryogenesis.

During oogenesis, mammalian eggs accumulate proteins required for early embryogenesis. Although limited data suggest a vital role of these maternal factors in chromatin reprogramming and embryonic genome activation, the full range of their functions in preimplantation development remains largely unknown. Here we report a role for maternal proteins in maintaining chromosome stability and euploidy in early-cleavage mouse embryogenesis. Filia, expressed in growing oocytes, encodes a protein that binds to MATER and participates in a subcortical maternal complex essential for cleavage-stage embryogenesis. The depletion of maternal stores of Filia impairs preimplantation embryo development with a high incidence of aneuploidy that results from abnormal spindle assembly, chromosome misalignment, and spindle assembly checkpoint (SAC) inactivation. In helping to ensure normal spindle morphogenesis, Filia regulates the proper allocation of the key spindle assembly regulators (i.e., AURKA, PLK1, and gamma-tubulin) to the microtubule-organizing center via the RhoA signaling pathway. Concurrently, Filia is required for the placement of MAD2, an essential component of the SAC, to kinetochores to enable SAC function. Thus, Filia is central to integrating the spatiotemporal localization of regulators that helps ensure euploidy and high-quality cell cycle progression in preimplantation mouse development. Defects in the well-conserved human homologue could play a similar role and account for recurrent human fetal wastage.

Pubmed ID: 19376971


  • Zheng P
  • Dean J


Proceedings of the National Academy of Sciences of the United States of America

Publication Data

May 5, 2009

Associated Grants

  • Agency: Intramural NIH HHS, Id:

Mesh Terms

  • Animals
  • Aurora Kinase A
  • Aurora Kinases
  • Cell Cycle Proteins
  • Cleavage Stage, Ovum
  • Embryo, Mammalian
  • Embryonic Development
  • Female
  • Mad2 Proteins
  • Mice
  • Mice, Mutant Strains
  • Ploidies
  • Protein-Serine-Threonine Kinases
  • Proteins
  • Proto-Oncogene Proteins
  • Spindle Apparatus
  • Tubulin