Molecular Biology of the Oocyte

母体效应基因：在小鼠卵细胞减数分裂成熟过程中终止的转录，只有在双细胞胚胎的胚胎基因组被强力激活后才能恢复。卵母细胞和胚胎基因转录之间的间隙指示了在哺乳动物早期发育中储存的母体因子的作用。这些成分由母体效应基因编码，在卵子发生过程中积累，并为受精、胚胎基因组激活和卵裂期胚胎发生提供必要的途径。

Maternal Effect Genes: Transcription that terminates during meiotic maturation of mouse eggs, resumes only after robust activation of the embryonic genome of the two-cell embryo. This interregnum between oocyte and embryonic gene transcription dictates a role for stored maternal factors in early mammalian development. Encoded by maternal effect genes, these components accumulate during oogenesis and provide pathways essential for fertilization, activation of the embryonic genome and cleavage stage embryogenesis. Fertilization: The taxon-specificity of sperm-egg recognition in mammals is mediated primarily by the zona pellucid, an extracellular matrix surrounding ovulated eggs. However, despite extensive investigation, there is no unifying model for the molecular basis of sperm interactions with the zona matrix that result in mammalian fertilization. Current studies investigate: 1) the molecular biology of the formation of the extracellular zona pellucida; 2) molecular requirements of the zona pellucida matrix to support taxon-specific sperm-egg recognition; 3) mechanism that result in acrosome exocytosis necessary for gamete fusion; and 4) the processes by which post-fertilization polyspermy is prevented. Early Development: Activation of the embryonic genome in mice begins late in the one-cell zygote and is fully underway by the two-cell cleavage stage. Initial cell lineages that presage the inner cell mass and extra-embryonic trophectoderm are established when eight blastomeres compact to form polarized morulae in pre-implantation mouse development. The role of maternal effect genes in these processes in mammals constitute a rapidly evolving area of inquiry. Current studies investigate: 1) novel maternal effect genes that affect early mouse development; 2) components of a recently described maternally encoded subcortical complex; and 3) mechanisms by which the loss of the complex affects cleavage stage embryogenesis.