| First Author | Ohsugi M | Year | 2008 |
| Journal | Development | Volume | 135 |
| Issue | 2 | Pages | 259-69 |
| PubMed ID | 18057100 | Mgi Jnum | J:130427 |
| Mgi Id | MGI:3771666 | Doi | 10.1242/dev.011445 |
| Citation | Ohsugi M, et al. (2008) Maternally derived FILIA-MATER complex localizes asymmetrically in cleavage-stage mouse embryos. Development 135(2):259-69 |
| abstractText | Initial cell lineages that presage the inner cell mass and extra-embryonic trophectoderm are established when eight blastomeres compact to form polarized morulae in preimplantation mouse development. FILIA has been identified as a binding partner to MATER (maternal antigen that embryos require; also known as NLRP5), which is encoded by a maternal effect gene. Products of each gene are detected in growing oocytes and, although transcripts are degraded before fertilization, the cognate proteins persist in early blastocysts. The two proteins co-localize to the cytocortex of ovulated eggs, where the stability of FILIA is dependent on the presence of MATER. After fertilization, FILIA-MATER complexes become asymmetrically restricted in the apical cytocortex of two-cell embryos due to their absence in regions of cell-cell contact. This asymmetry is reversible upon disaggregation of blastomeres of the two- and four-cell embryo. Each protein persists in cells of the preimplantation embryo, but the continuous cell-cell contact of ;inner' cells of the morulae seemingly precludes formation of the subcortical FILIA-MATER complex and results in cell populations that are marked by its presence (;outer') or absence (;inner'). Thus, the FILIA-MATER complex provides a molecular marker of embryonic cell lineages, but it remains to be determined if the molecular asymmetry established after the first cell division plays a role in cell fate determinations in the early mouse embryo. If so, the plasticity of the FILIA-MATER complex localization may reflect the regulative nature of preimplantation mouse development. |
