Maternal Effect Genes in Mammalian Embryogenesis

FILIA已被鉴定为MATER（胚胎需要的母体抗原）的结合伴侣，MATER由母体效应基因编码。每个基因的产物在生长的卵母细胞中被检测到，尽管转录本在受精前被降解，但同源蛋白在早期胚泡中持续存在。这两种蛋白质共定位于排卵卵的细胞皮质，其中FILIA的稳定性取决于MATER的存在。受精后，FILIA/MATER复合物变得不对称地限制在两细胞胚胎的顶端细胞皮质中，由于它们在细胞-细胞接触区域中的缺失。这种不对称性在二细胞和四细胞胚胎的卵裂球解聚时是可逆的。每种蛋白质都存在于植入前胚胎的细胞中，但桑椹胚内细胞的连续细胞-细胞接触似乎排除了皮质下FILIA/MATER复合体的形成，并导致细胞群以其存在（外部）或不存在（内部）为标志。因此，FILIA/MATER复合物提供了胚胎细胞谱系的分子标记物，但尚待确定的是，在第一次细胞分裂后建立的分子不对称性是否在早期小鼠胚胎的细胞命运决定中起作用。如果是这样，FILIA/MATER复合体定位的可塑性可能反映了植入前小鼠发育的调节性质。

FILIA has been identified as a binding partner to MATER (Maternal Antigen That Embryos Require) which is encoded by a maternal effect gene. Products of each gene are detected in growing oocytes and, although transcripts are degraded prior to 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 pre-implantation mouse development.