NIH Research Festival
Maternal effect genes expressed during oogenesis are often an imperative for progression through early development and female fertility. The subcortical maternal complex (SCMC) is encoded by at least four maternal effect genes (Mater, Floped, Filia, Tle6) and targeted mutation of Mater in mice results in female infertility with embryos unable to develop beyond the 2-cell stage. Normally after fertilization, the zona pellucida surrounding early embryos becomes unreceptive to additional sperm which provides a definitive block to polyspermy. This block arises from exocytosis of ovastacin (encoded by Astl) from cortical granules located in the periphery of ovulated eggs. This metalloendoprotease cleaves the extracellular zona pellucida protein ZP2 and prevents sperm binding. Transgenic Astl-mCherry mice which provide a fluorescent marker of cortical granules were crossed with mice lacking Mater. Whereas cortical granules co-localize with MATER in the cortex of wildtype eggs, they are mis-localized throughout the endomembrane system in MATER-deficient eggs. In vitro fertilization and in vivo mating assays revealed that significantly more sperm penetrated and fused with eggs lacking MATER compared to wildtype eggs. Time-lapse confocal microscopy of parthenogenetically activated eggs documented that mCherry fluorescence disappears rapidly (10-20 minutes) from the cortex of activated Astl-mCherry eggs which corresponds to the time over which ZP2 is cleaved. In the absence of MATER, however, ovastacin-mCherry persists throughout activated eggs for a prolonged period and ZP2 remains uncleaved. Thus, MATER plays an important role in tethering cortical granules in the egg cortex to ensure timely exocytosis of ovastacin in the post-fertilization block to polyspermy.
Scientific Focus Area: Developmental Biology
This page was last updated on Friday, March 26, 2021