The multifaceted C. elegans major sperm protein: an ephrin signaling antagonist in oocyte maturation
- The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK CB10 1SA
This extract was created in the absence of an abstract.
In sexually reproducing animals, the ability to coordinate oocyte maturation and sperm availability has profound effects on reproductive success. In Caenorhabditis elegans, cell–cell signaling is crucial for promoting germ-line development, oocyte maturation, and ovulation. In this issue of Genes & Development, Miller et al. (2003) provide new insights into the role that sperm play in oocyte maturation and ovulation. Even before sperm and oocyte have the opportunity to meet, sperm establish their presence by signaling to oocytes and the somatic gonad. In turn, oocytes respond by resuming meiotic cell cycle progression and preparing for fertilization.
Meiotic arrest and oocyte maturation
The study of oocyte maturation has resulted in several important discoveries in cell biology, relevant to translational control, cell cycle regulation, and other areas (Stebbins-Boaz and Richter 1997;Nebreda and Ferby 2000). For example, the study of oocyte maturation in the frog Rana pipiens led to the landmark discovery of MPF (maturation promoting factor), which foreshadowed the identification of cyclins and their role in cell cycle regulation (Masui and Markert 1971). Less is known about the extracellular signaling mechanisms that control oocyte maturation, but these must also be important and are worthy of investigation.
In animals, oocytes undergo an arrest in cell cycle progression at the first meiotic prophase. Although this arrest is a universal characteristic of oocyte development, a wide variety of somatic and sperm-dependent mechanisms have evolved across the animal kingdom to alleviate this block and to promote oocyte maturation. In frogs, oocyte maturation is triggered by the somatic release of gonadotropins, which leads to the synthesis and release of progesterone from follicle cells. In turn, cAMP levels fall, and there is a rise in the accumulation of the translationally regulated Mos oncogene (Nebreda and Ferby 2000). An obvious change at this point is nuclear envelope breakdown (NEBD, or germinal …
